Acute decompensated heart failure (ADHF) is the leading cause of hospital admission in patients age 65 and older.1 It is estimated that Americans are hospitalized for approximately 6.5 million patient-days per year due to this condition.2 In 2009, the projected sum of direct and indirect costs from heart failure (HF) admissions is $36.2 billion with the majority of cost associated with hospitalization care.3
Unfortunately, patients who are hospitalized for ADHF have a high readmission rate in the 6 months following discharge.2 Depending on the severity of disease, rates of in-hospital mortality range from 2% to 19%.4 Despite the serious nature of the problem, relatively few prospective, randomized, clinical trials have been conducted to address the optimal treatment strategy for ADHF.
ADHF is commonly characterized by a relatively rapid (over days to weeks) decrease in cardiac output (CO) which triggers a variety of compensatory mechanisms in an attempt to maintain hemodynamic stability. Ultimately, activation of these compensatory neurohormonal pathways may result in fluid retention and vasoconstriction, both of which can further compromise cardiac function. Acute decompensation is frequently a consequence of disease progression in patients with chronic heart failure (HF).5 It may also stem from medication or lifestyle noncompliance, such as failing to take evidence-based chronic heart failure medications as prescribed or indulging in excessive sodium or water intake (or both).
|ADHF = acute decompensated heart failure|
|BP = blood pressure|
|BNP = brain natriuretic peptide|
|CO = cardiac output|
|CI = cardiac index|
|EF = ejection fraction|
|HF = heart failure|
|HR = heart rate|
|PCWP = pulmonary capillary wedge pressure|
|RAAS = renin-angiotensin-aldosterone system|
|SNS = sympathetic nervous system|
|SVR = systemic vascular resistance|
|SV = stroke volume|
Alternatively, ADHF may occur abruptly as a result of an acute insult such as the onset of atrial fibrillation, acute coronary syndrome, pneumonia, myocarditis, acute valvular dysfunction, acute kidney failure, or pulmonary embolism, among others.6
All of the above etiologies involve damage to or increased strain on cardiac tissue, triggering a series of neurohormonal responses. In response to a reduction in cardiac output and resultant hypoperfusion, activation of the sympathetic nervous system (SNS) and the renin-angiotensin-aldosterone system (RAAS) manifests as increased secretion of norepinephrine as well as angiotensin II and aldosterone, respectively. These effects are beneficial in maintaining cardiac output and vital organ perfusion in the short term; however, chronic activation of these systems worsens cardiac function in the long term. Chronic SNS activation can cause vasoconstriction, thereby increasing systemic vascular resistance (SVR, also known as afterload) and negative myocardial remodeling, and worsening pump dysfunction.5 Activation of the RAAS also results in vasoconstriction as well as collagen deposition with fibrosis and further remodeling of myocardial tissue. In addition, RAAS activation causes renal sodium and water retention which increases ...