IMR Press / RCM / Volume 2 / Issue S2 / pii/1561516082443-1724126136

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 imrpress.com as a courtesy and upon agreement with MedReviews, LLC.

Open Access Review
The Treatment Targets in Acute Decompensated Heart Failure
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1 The Ahmanson-UCLA Cardiomyopathy Center, Division of Cardiology, UCLA School of Medicine, Los Angeles, CA
Rev. Cardiovasc. Med. 2001, 2(S2), 7–12;
Published: 20 February 2001
Abstract
Acute decompensated heart failure is characterized by hemodynamic abnormalities as well as neuroendocrine activation, which contribute to heart failure symptoms, progressive cardiac dysfunction, and sudden death. The therapeutic goals in patients hospitalized with decompensated heart failure are to reverse acute hemodynamic abnormalities, relieve symptoms, and initiate treatment that will slow disease progression and improve long-term survival. Traditional hemodynamic targets in acute heart failure have been reduction in left and right ventricular filling pressures, reduction in systemic vascular resistance, and increase in cardiac output. Treatments aimed at these targets in patients with acute decompensated heart failure include diuretics, vasodilators, and inotropic agents. In patients hospitalized with acute decompensated heart failure, persistently elevated left ventricular filling pressure has been shown to be highly predictive of an increased risk of fatal decompensation and sudden death. Measures of systemic perfusion, arterial pressure, and vascular resistance have not. Thus, there is a more compelling physiologic rationale for the use of vasodilators than for inotropic agents in these patients. 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 naturiesis, lacks direct positive inotropic effects, and does not result in reflex neuroendocrine activation.
Keywords
Hemodynamics
Heart failure
Pulmonary capillary wedge pressure
Mortality
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