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Acute heart failure covers a wide spectrum of illness severity, ranging from a gradual increase in leg swelling, shortness of breath, or decreased exercise tolerance to the abrupt onset of pulmonary edema. While the alternative terms decompensated heart failure, acute heart failure syndrome, or hospitalized with heart failure are often used in an overlapping manner, we refer to patients with either an acute exacerbation of chronic heart failure or a new-onset heart failure as having acute heart failure. The outdated term congestive heart failure describes patients with signs and symptoms of fluid accumulation.

Most ED visits for acute heart failure result in hospital admission.1 ED physicians drive most disposition decisions in this setting.2,3 With the aging population, increased survival from acute myocardial infarction, and outpatient treatment options, the prevalence of heart failure is expected to increase over the next decade.4-6 Although long-term heart failure management has improved through the use of β-blockers, angiotensin-converting enzyme inhibitors, spironolactone, and cardiac resynchronization therapy,4,5 acute heart failure therapy is largely unchanged and includes nitrates, diuretics, and positive-pressure ventilation.7 Only one new therapy, nesiritide, was recently approved for acute heart failure treatment, but it does not improve outcomes compared to standard treatment.8

Heart failure has a poor prognosis, with approximately 50% of patients dying within 5 years of diagnosis.9 Hospitalization is an inflection point in this disease, with those hospitalized having higher mortality than a matched nonhospitalized cohort.10


Heart failure is a complex clinical syndrome manifested by cardinal symptoms (shortness of breath, edema, and fatigue) occurring from functional or structural cardiac damage, impairing the ability of the heart to act as an efficient pump. Symptoms may limit exercise tolerance and lead to fluid retention, driving pulmonary and/or splanchnic congestion and/or peripheral edema.4 There are numerous responsive adaptations in the kidney, peripheral circulation, skeletal muscle, and other organs to maintain short-term circulatory function. Eventually, these responses may contribute to long-term disease progression and to acute exacerbations.

As cardiac output drops from myocardial injury or stress, a neurohormonally mediated cascade including activation of the renin-angiotensin-aldosterone and sympathetic nervous systems occurs. Responses include release of norepinephrine, vasopressin, endothelin (a potent vasoconstrictor), and tumor necrosis factor-α. Although not measured in routine care, elevated levels of these hormones correlate with higher mortality.

The clinical effects of neurohormonal activation are sodium and water retention coupled with increased systemic vascular resistance. These maintain blood pressure and perfusion, but at the cost of increasing myocardial workload, wall tension, and myocardial oxygen demand. Although some patients are initially asymptomatic, a secondary pathologic process called cardiac remodeling begins to occur, eventually triggering more dysfunction.

Natriuretic peptides are the endogenous counterregulatory response to neurohormonal activation in heart failure. Three types exist: atrial natriuretic peptide, primarily ...

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