Heart failure (HF) is a progressive syndrome resulting from abnormal cardiac structure or function impairing the ability of the ventricle to fill with or eject blood. Acute decompensated heart failure (ADHF) characterizes patients with worsening HF, often requiring hospitalization. Patients with persistent symptoms or refractory HF despite optimal oral therapies are classified as stage D by the American College of Cardiology/American Heart Association staging system. Additionally, ADHF patients have symptoms with minimal activity or at rest and thus are most commonly classified as New York Heart Association class III or IV.
Etiology and Pathophysiology
ADHF is characterized by a rapid decline in condition due to fluid retention and/or compromised cardiac function. Acute decompensation is frequently a consequence of disease progression or stems from medication or lifestyle nonadherence. Alternatively, ADHF may occur abruptly as a result of an acute insult (eg, atrial fibrillation, acute coronary syndrome).
While the sympathetic nervous system (SNS) and renin-angiotensin-aldosterone system (RAAS) are initially activated to maintain cardiac output and vital organ perfusion, activation of these systems ultimately deteriorate cardiac function. The SNS increases systemic vascular resistance (SVR, afterload) causing pump dysfunction. The RAAS results in vasoconstriction and sodium and water retention leading to increased intravascular fluid volume (preload). Furthermore, arginine vasopressin is secreted causing vasoconstriction, free water retention, and hyponatremia.
B-type natriuretic peptide (BNP) is secreted from ventricular tissue in response to fluid overload and ventricular wall stretch. The physiologic effect of BNP is to induce natriuresis as well as venous and arterial vasodilation. However, the release of endogenous BNP only mildly attenuates the negative compensatory neurohormonal cascade.
HF is a clinical diagnosis and no single test establishes its presence or absence. Nearly all patients with HF present with dyspnea. The absence of dyspnea makes HF highly unlikely and other explanations for the patient’s symptoms should be sought first.
When used in conjunction with patient history and physical examination, BNP can be helpful in distinguishing ADHF from other conditions. A BNP concentration below 100 pg/mL is highly predictive for the absence of fluid overload. Unfortunately, BNP concentrations may be falsely elevated due to non-HF causes such as pneumonia or pulmonary embolism.
Placement of a pulmonary artery catheter (PAC, also known as a Swan-Ganz catheter) may be helpful in distinguishing a patient’s hemodynamic profile in ADHF. While hemodynamic parameters may assist in the development of a pharmacotherapy plan, use of a PAC does not improve outcomes. Consequently, a PAC should only be employed in patients: (1) not responding to initial therapy, (2) whose volume status cannot be determined by history and physical examination, or (3) who experience hemodynamic instability during treatment.
Patients with low cardiac index (CI) less than 2.2 L/min/m2 are referred to as “cold” because ...