IMR Press / RCM / Volume 3 / Issue S4 / pii/1561516743268-1945402137

Reviews in Cardiovascular Medicine (RCM) is published by IMR Press from Volume 19 Issue 1 (2018). Previous articles were published by another publisher in Open Access under a CC-BY (or CC-BY-NC-ND) licence, and they are hosted by IMR Press on as a courtesy and upon agreement with MedReviews, LLC.

Open Access Review
Pharmacologic Therapies for Acutely Decompensated Heart Failure
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1 Division of Cardiology, UCLA School of Medicine, Los Angeles, CA
Rev. Cardiovasc. Med. 2002, 3(S4), 18–27;
Published: 20 August 2002
The management of acutely decompensated heart failure in the emergency medical setting poses a major clinical challenge. Acutely decompensated heart failure is characterized by hemodynamic abnormalities and neuroendocrine activation that contribute to heart failure symptoms, end-organ dysfunction, arrhythmias, and progressive cardiac failure. The therapeutic goals in patients presenting with acutely decompensated heart failure are to stabilize the patient, reverse acute hemodynamic abnormalities, rapidly reverse dyspnea and/or hypoxemia caused by pulmonary edema, and initiate treatments that will decrease disease progression and improve survival. Pharmacologic therapies to impact the hemodynamic abnormalities and symptoms in patients with acutely decompensated heart failure include diuretics, inotropic agents, vasodilators, and natriuretic peptides. In patients with acutely decompensated heart failure, it has recently been demonstrated that elevation in left ventricular filling pressure is the hemodynamic abnormality that most directly impacts heart failure symptoms and is highly predictive of increased risk of fatal decompensation and sudden death. Measures of systemic perfusion, arterial pressure, and vascular resistance have not been predictive of symptoms or clinical outcomes. An ideal agent for acute decompensated heart failure would be one that rapidly reduces pulmonary wedge pressure, results in balanced arterial and venous dilation, promotes natriuresis, lacks direct positive inotropic effects, and does not result in reflex neuroendocrine activation.
Acute heart failure
Emergency department
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