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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 signs or symptoms, 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.


ADHF is characterized by a rapid decline in condition due to fluid retention and/or compromised tissue perfusion. Acute decompensation is frequently a consequence of disease progression or stems from medication or lifestyle nonadherence. A number of medications can also provoke ADHF by promoting fluid retention (eg, nonsteroidal anti-inflammatory drugs [NSAIDs]) or decreasing contractility (eg, diltiazem, verapamil). Alternatively, ADHF may occur abruptly due to 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 (CO) and vital organ perfusion, activation of these systems ultimately results in a deterioration of 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.

Clinical Presentation

Patients with ADHF can be classified into one of four hemodynamic subsets based on signs and symptoms of congestion (“dry” versus “wet”) and/or low CO (“warm” versus “dry”), and treatment differs based on whether patients are “warm and wet,” “cold and wet,” “warm and dry,” or “cold and dry.” Signs and symptoms of congestion often predominate. Pulmonary edema presents as dyspnea, orthopnea, and crackles on auscultation. Peripheral edema, ascites, and hepatomegaly/hepatojugular reflux are signs of systemic fluid overload. “Congested” patients may also present with systemic hypertension. Evidence of low CO includes increased serum creatinine (SCr) and hepatic transaminases, altered mental status, and cool extremities. Additionally, gut ischemia can occur leading to pain or vomiting with eating.


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 ...

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