title: Fluid overload in acute heart failure--re-distribution and other mechanisms beyond fluid accumulation.
abstract: Although fluid overload is one of the most prominent features of acute heart failure (AHF), its mechanism remains challenging, due to the lack of consistent data from prospective studies. Traditionally, fluid overload was thought to be mainly the result of either increased intake of fluid and salt or non-adherence with diuretic therapy. However, recent data showed little weight change before or during an AHF event suggesting that in many cases fluid overload is caused by other mechanisms such as fluid redistribution and neurohormonal or inflammatory activation. Redistribution may be the result of a combined vascular and cardiac process reducing capacitance in the venous system (and hence increasing preload) and increasing arterial stiffness and resistance (and hence afterload). When these vascular processes occur acutely and are superimposed on reduced cardiac function; fluid is redistributed to the lungs instigating pulmonary congestion. In this paper we elaborate on this possible pathophysiological mechanism and review its potential causes and amplifiers.
authors.affiliation: Momentum-Research Inc, Durham, NC 27707, USA. gadcotter@momentum-research.com
authors.forename: Gad
authors.initials: G
authors.lastname: Cotter
authors.forename: Marco
authors.initials: M
authors.lastname: Metra
authors.forename: Olga
authors.initials: O
authors.lastname: Milo-Cotter
authors.forename: Howard C
authors.initials: HC
authors.lastname: Dittrich
authors.forename: Mihai
authors.initials: M
authors.lastname: Gheorghiade
mesh_terms: D001127:Arginine Vasopressin / Q000097:blood; D001158:Arteries / Q000503:physiopathology; D018450:Disease Progression; D004489:Edema, Cardiac / Q000503:physiopathology; D004548:Elasticity; D006333:Heart Failure / Q000503:physiopathology*; D006801:Humans; D007676:Kidney Failure, Chronic / Q000453:epidemiology; D008168:Lung / Q000503:physiopathology; D011654:Pulmonary Edema / Q000503:physiopathology; D012084:Renin-Angiotensin System / Q000502:physiology; D014655:Vascular Resistance; D014665:Vasodilator Agents / Q000627:therapeutic use; D014883:Water-Electrolyte Imbalance / Q000503:physiopathology*
chemical_list: D014665:Vasodilator Agents; D001127:Arginine Vasopressin