الفهرس 
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Abstract
Acute decompensated heart failure (ADHF) is a common and potentially fatal cause of acute respiratory distress. It is characterized by the development of dyspnea, often associated with accumulation of fluid within the lung’s interstitial and alveolar spaces, as a result of acutely elevated cardiac filling pressure (cardiogenic pulmonary edema). However, ADHF can also present as elevated left ventricular filling pressures and dyspnea without pulmonary edema.
ADHF is most commonly due to left ventricular systolic or diastolic dysfunction, with or without additional cardiac pathology, such as coronary artery disease or valve abnormalities.
A variety of conditions or events can cause pulmonary edema due to an elevated pulmonary capillary wedge pressure in the absence of heart disease, including primary fluid overload (eg, due to blood transfusion), severe hypertension, and severe renal disease.
ADHF is defined as a sudden worsening of heart failure (HF) symptoms and is usually caused by cardiogenic pulmonary edema with rapid fluid accumulation in the lungs, although it can occur without pulmonary edema.
Hypertension, ischemia, and/or ventricular dysfunction causes a decrease in cardiac output, which leads to an activation of the neurohormonal pathway. The sympathetic system increases norepinephrine to improve peripheral perfusion via vasoconstriction and activates the renin-angiotensin-aldosterone system to increase renal perfusion through water retention.
An acute increase in left ventricular filling pressure causes protein-poor fluid to leak into the lung alveoli and interstitium, but no compromise of pulmonary membrane integrity occurs. Compensatory mechanisms increase heart rate and systemic vascular resistance in an attempt to improve cardiac output, and a vicious cycle ensues.
Common causes of ADHF include left ventricular or diastolic dysfunction with or without coronary artery disease (CAD) or valvular abnormalities. Although most patients hospitalized with ADHF have a worsening of preexisting heart failure (HF) up to 20% of patients have no prior diagnosis of HF.
ADHF can also occur in patients without any preexisting cardiac disease, including conditions such as severe hypertension, fluid overload, severe renal disease, or renal artery stenosis. Factors precipitating an event involve a change in the flow of blood through the heart; ADHF can be induced by hypertensive crisis, myocardial infarction (MI) or ischemia, atrial obstruction, acute mitral regurgitation, fluid overload, or non-adherence to HF medications.
Certain medications, such as beta-blockers, nondihydropyridine calcium channel blockers, and nonsteroidal anti-inflammatory drugs (NSAIDs), can also precipitate ADHF.
Management of ADHF is guided by the patient’s hemodynamic status, which is evaluated using cardiac index (CI) and pulmonary capillary wedge pressure (PCWP) values. While the standard of care has not changed significantly over the past several years, a new focus on the pharmacoeconomic impact of HF has shown that not all treatments are equal.
Pharmacotherapy should be chosen based on the diagnosed subset, either treating fluid overload or hypoperfusion. Patients having both fluid overload and perfusion dysfunction and, therefore, require therapy for both symptoms.
Future research will need to focus on novel pharmacological therapies, especially for patients hospitalized with HF; regenerative cell-based therapies to restore myocardium; and new device platforms that will either improve existing technologies (e.g., CRT, ICD, left ventricular assist device) or introduce simpler, less morbid devices that are capable of changing the natural history of HF.