The Hospitalized Patient

(1) The diagnosis of HF is primarily based on signs and symptoms derived from a thorough history and physical examination. Clinicians should determine the following:
(a) adequacy of systemic perfusion
(b) volume status
(c) the contribution of precipitating factors and/or comorbidities
(d) if the heart failure is new onset or an exacerbation of chronic
(e) whether it is associated with preserved ejection fraction. Chest
radiographs, electrocardiogram, and echocardiography are
key tests in this assessment.

(2) Concentrations of B-type natriuretic peptide (BNP) or N-terminal pro-B-type natriuretic peptide (NT-proBNP) should be measured in patients being evaluated for dyspnea in which the contribution of HF is not known. Final diagnosis requires interpreting these results in the context of all available clinical data and ought not to be considered a stand-alone test.

(3) Acute coronary syndrome precipitating HF hospitalization should be promptly identified by electrocardiogram and cardiac troponin testing, and treated as appropriate to the overall condition and prognosis of the patient.

(4) It is recommended that the following common potential precipitating factors for acute HF be identified as recognition of these comorbidities is critical to guide therapy:
(a) acute coronary syndromes/coronary ischemia
(b) severe hypertension
(c) atrial and ventricular arrhythmias
(d) infections
(e) pulmonary emboli
(f) renal failure
(g) medical or dietary noncompliance.

(5) Oxygen therapy should be administered to relieve symptoms related to hypoxemia.

(6) Whether the diagnosis of HF is new or chronic, patients who present with rapid decompensation and hypoperfusion associated with decreasing urine output and other manifestations of shock are critically ill and rapid intervention should be used to improve systemic perfusion.

(7) Patients admitted with HF and with evidence of significant fluid overload should be treated with intravenous loop diuretics. Therapy should begin in the emergency department or outpatient clinic without delay, as early intervention may be associated with better outcomes for patients hospitalized with decompensated HF. If patients are already receiving loop diuretic therapy, the initial intravenous dose should equal or exceed their chronic oral daily dose. Urine output and signs and symptoms of congestion should be serially assessed, and diuretic dose should be titrated accordingly to relieve symptoms and to reduce extracellular fluid volume excess.

(8) Effect of HF treatment should be monitored with careful measurement of fluid intake and output; vital signs; body weight, determined at the same time each day; clinical signs (supine and standing) and symptoms of systemic perfusion and congestion. Daily serum electrolytes, urea nitrogen, and creatinine concentrations should be measured during the use of IV diuretics or active titration of HF medications.

(9) When diuresis is inadequate to relieve congestion, as evidenced by clinical evaluation, the diuretic regimen should be intensified
using either:
(a) higher doses of loop diuretics
(b) addition of a second diuretic (such as metolazone, spironolactone, or intravenous chlorothiazide)
(c) continuous infusion of a loop diuretic.

(10) In patients with clinical evidence of hypotension associated with hypoperfusion and obvious evidence of elevated cardiac filling pressures (e.g., elevated jugular venous pressure; elevated pulmonary artery wedge pressure), intravenous inotropic or vasopressor drugs should be administered to maintain systemic perfusion and preserve end-organ performance while more definitive therapy is considered.

(11) Invasive hemodynamic monitoring should be performed to guide therapy in patients who are in respiratory distress or with clinical evidence of impaired perfusion in whom the adequacy or excess of intracardiac filling pressures cannot be determined from clinical assessment.

(12) Medications should be reconciled in every patient and adjusted as appropriate on admission to and discharge from the hospital.

(13) In patients with reduced ejection fraction experiencing a symp- tomatic exacerbation of HF requiring hospitalization during chronic maintenance treatment with oral therapies known to improve outcomes, particularly ACEIs or ARBs and beta-blocker therapy, it is recommended that these therapies be continued in most patients in the absence of hemodynamic instability or contraindications.

(14) In patients hospitalized with HF with reduced ejection fraction not treated with oral therapies known to improve outcomes, particularly ACEIs or ARBs and beta-blocker therapy, initiation of these therapies is recommended in stable patients prior to hospital discharge.

(15) Initiation of beta-blocker therapy is recommended after optimiza-tion of volume status and successful discontinuation of intravenous diuretics, vasodilators, and inotropic agents. Beta-blocker therapy should be initiated at a low dose and only in stable patients. Particular caution should be used when initiating beta-blockers in patients who have required inotropes during their hospital course.

(16) In all patients hospitalized with HF, both with preserved and low EF, transition should be made from intravenous to oral diuretic therapy with careful attention to oral diuretic dosing and monitoring of electrolytes. With all medication changes, the patient should be monitored for supine and upright hypotension, and worsening renal function and HF signs/symptoms.

(17) Comprehensive written discharge instructions for all patients with a hospitalization for HF and their caregivers is strongly recommended, with special emphasis on the following 6 aspects of care: diet; discharge medications, with a special focus on adherence, persistence, and uptitration to recommended doses of ACEI/ARB and beta-blocker medication; activity level; follow-up appointments; daily weight monitoring; and what to do if HF symptoms worsen.

(18) Postdischarge systems of care, if available, should be used to facilitate the transition to effective outpatient care for patients hospitalized with HF.

(1) When patients present with acute HF and known or suspected acute myocardial ischemia due to occlusive coronary disease, especially when there are signs and symptoms of inadequate systemic perfusion, urgent cardiac catheterization and revascularization is reasonable where it is likely to prolong meaningful survival.

(2) In patients with evidence of severely symptomatic fluid overload in the absence of systemic hypotension, vasodilators such as intrave- nous nitroglycerin, nitroprusside or nesiritide can be beneficial when added to diuretics and/or in those who do not respond to diuretics alone.

(3) Invasive hemodynamic monitoring can be useful for carefully selected patients with acute HF who have persistent symptoms despite empiric adjustment of standard therapies, and
(a) whose fluid status, perfusion, or systemic or pulmonary
vascular resistances are uncertain
(b) whose systolic pressure remains low, or is associated with
symptoms, despite initial therapy
(c) whose renal function is worsening with therapy
(d) who require parenteral vasoactive agents
(e) who may need consideration for advanced device therapy or

(4) Ultrafiltration is reasonable for patients with refractory congestion not responding to medical therapy.

(1) Intravenous inotropic drugs such as dopamine, dobutamine or milrinone might be reasonable for those patients presenting with documented severe systolic dysfunction, low blood pressure and evidence of low cardiac output, with or without congestion, to maintain systemic perfusion and preserve end-organ performance.

(1) Use of parenteral inotropes in normotensive patients with acute decompensated HF without evidence of decreased organ perfusion is not recommended.

(2) Routine use of invasive hemodynamic monitoring in normotensive patients with acute decompensated HF and congestion with symptomatic response to diuretics and vasodilators is not recommended.

JACC. 2009; 53; e1-e90