INTRODUCTION AND EPIDEMIOLOGY
Acute heart failure covers a wide spectrum of illness, ranging from a gradual increase in leg swelling, shortness of breath, or decreased exercise tolerance to the abrupt onset of pulmonary edema. While alternative terms such as decompensated heart failure, acute heart failure syndrome, or hospitalized with heart failure have been used nearly interchangeably over the last decade, 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 The term congestive heart failure is outdated and describes patients with signs and symptoms of fluid accumulation.
Most ED visits for acute heart failure result in hospital admission.1 With the aging population, increased survival from acute myocardial infarction, and evidence-based outpatient treatment options, the prevalence of heart failure is expected to increase over the next decade.2,3,4 ED physicians drive most disposition decisions.5,6 There have been tremendous advances in outpatient management of heart failure patients. While long-term heart failure management has improved through the use of β-blockers, angiotensin-converting enzyme inhibitors, spironolactone, and cardiac resynchronization therapy,2,3 acute therapy is largely unchanged. Acute therapies include nitrates, diuretics, and positive-pressure ventilation, the same as in 1974.7 Only one therapy, nesiritide, has been approved for heart failure treatment in the last three decades, but it is not significantly better than standard treatment.8
Heart failure has a poor prognosis, with approximately 50% of patients diagnosed dying within 5 years.9 Hospitalization also marks an inflection point in a patient's HF trajectory, with those hospitalized having higher mortality than a matched nonhospitalized cohort.10
Heart failure is a complicated 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. A clinically useful definition of heart failure is as follows: a complex clinical syndrome that results from any structural or functional impairment of ventricular filling or ejection of blood. The cardinal manifestations of heart failure are dyspnea and fatigue, which may limit exercise tolerance, and fluid retention, which may lead to pulmonary and/or splanchnic congestion and/or peripheral edema.2 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 become maladaptive, contribute to long-term disease progression, and contribute to acute exacerbations.
Threats to cardiac output from myocardial injury or stress trigger a neurohormonally mediated cascade that includes activation of the renin-angiotensin-aldosterone system and the sympathetic nervous systems. Levels of norepinephrine, vasopressin, endothelin (a potent vasoconstrictor), and tumor necrosis factor-α are increased. Although not measured in routine care, elevated levels of these hormones correlate with higher mortality.
The combined clinical effects of neurohormonal activation are sodium and water ...