The pathophysiology of acute heart failure—Is it all about fluid accumulation?

• Published in: The American heart journal 2008, Vol.155 (1), p.9-18
• Main Authors: Cotter, Gad, MD, Felker, G. Michael, MD, Adams, Kirkwood F., MD, Milo-Cotter, Olga, MD, O'Connor, Christopher M., MD
• Format: Article
• Language: English
• Subjects: Acute coronary syndromes; Acute Disease; Aged; Arrhythmias, Cardiac - mortality; Arrhythmias, Cardiac - physiopathology; Biological and medical sciences; Cardiology. Vascular system; Cardiovascular; Edema, Cardiac - mortality; Edema, Cardiac - physiopathology; Female; Heart; Heart failure; Heart Failure - mortality; Heart Failure - physiopathology; Heart Failure - therapy; Heart failure, cardiogenic pulmonary edema, cardiac enlargement; Heart Function Tests; Hospitalization; Hospitalization - statistics & numerical data; Humans; Hypoxia; Ischemia; Male; Medical sciences; Middle Aged; Myocardial Ischemia - mortality; Myocardial Ischemia - physiopathology; Pathogenesis; Prognosis; Risk Assessment; Severity of Illness Index; Studies; Survival Analysis
• ISSN: 0002-8703; 1097-6744
• DOI: 10.1016/j.ahj.2006.02.038

Despite significant advancement in chronic heart failure (HF), no breakthroughs have occurred in the last 2 decades in our understanding of the pathophysiology, classification, and treatment of acute HF (AHF). Traditional thinking, which has been that this disorder is a result of gradual fluid accumulation on a background of chronic HF, has been called into question by recent large registries enrolling less selected patient populations. It is increasingly recognized that many patients with this syndrome are elderly, have relatively preserved ejection fraction, and have mild or no preexisting chronic HF. In this review, we propose 2 primary subtypes of AHF: (1) acute decompensated cardiac failure, characterized by deterioration of cardiac performance over days to weeks leading to decompensation; and (2) acute vascular failure, characterized by acute hypertension and increased vascular stiffness. Registry data suggest that the latter is the more common form of AHF in the general population, although the former is often overrepresented in studies focused in academic tertiary care centers. Regardless of the clinical subtype, a variety of pathophysiologic mechanisms may play a role in this disorder, many of which remain poorly understood. In this review, we describe current understanding of the pathophysiology of AHF, including a critical evaluation of the data supporting both traditional and novel mechanisms, and suggest a framework for integrating these mechanisms into an overall model of AHF.