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.

Pulmonary artery pressure‐guided heart failure management: US cost‐effectiveness analyses using the results of the CHAMPION clinical trial

“…Despite increased utilization of pharmacological2, 3, 4, 5, 6, 7, 8, 9 and device therapy options10, 11, 12, 13 that improve clinical outcomes in randomized controlled trials, morbidity and mortality in HF remain a major burden to patients, their caregivers, and national healthcare systems. Patients with HF frequently experience worsening symptoms related to accumulation of excess intravascular volume and congestion, requiring hospitalization to provide intravenous medical support to restore normal volume 14, 15, 16, 17, 18, 19. Heart failure is cited as the most frequent cause of hospitalization in the US Medicare population, resulting in >1 million admissions per year (accounting for 1–2% of all hospitalizations) 20, 21.…”

A case of severe preeclampsia presenting as acute pulmonary oedema

“…2 It is now recognised that not only is fluid accumulation and retention, a mechanism for acute pulmonary oedema, but so too is fluid redistribution from the systemic circulation to the pulmonary circulation due to venoconstriction or vasoconstriction in a person who is euvolaemic. 3,4 Therapies for the treatment of acute pulmonary oedema reverse one or more of these factors, with re-absorption of pulmonary oedema both a passive and an active process. 5 Frequently, more than one risk factor is present, with iatrogenic fluid administration a major preventable factor.…”

Management of acute heart failure-Is there a paradigm shift around the corner?

“…Fluid redistribution is induced by vascular mechanisms (vasoconstriction) as well as neurohormonal and inflammatory activation, renal dysfunction, and possibly inappropriate use of some medications. Fluid redistribution in particular causes elevated LV filling pressure with consequent gradual increase in the PCWP [31][32][33]. The resulting congestion is an obvious pathophysiological continuum consisting of three distinct stages: hemodynamic congestion [34], clinical congestion [34], and residual congestion.…”