![]() ![]() ![]() Its value is typically close to the average transmural pressure at the level of systemic post-capillary venules, and the pressure gradient between those venules and the right atrium (central venous pressure) is the driving force returning blood to the heart ( 10). Mean circulatory filling pressure is in turn defined as the average transmural pressure of the circulatory system when the heart and blood flow is stopped, and it is determined by blood volume and autonomic control of vascular smooth muscle. Hypervolemia is a state of excessive blood volume and elevated mean circulatory filling pressure (MCFP). However, some have argued that rather than focusing on development of edema as a foundational feature of fluid overload, clinicians should be more concerned about the presence of hypervolemia ( 9). In fact, FO is almost universally defined in such terms in clinical studies of humans ( 7, 8). The importance of FO has been underlined by a growing number of reports of observational studies that associate the condition with higher morbidity and mortality in hospitalized patients, an association that held true in recent meta-analyses of 44 studies in children ( 6) and 31 in adults ( 7).Ĭlinically, FO is usually defined by some combination of edema, excessive weight gain, or excessively positive fluid balance in a patient that has received intravenous fluid therapy. Although for many years FO has been recognized as a potential complication of anuria in chronic hemodialysis patients, in this century the phrase has more often been used to describe a complication of fluid therapy in any patient at risk for hypervolemia or edema. The concept of FO as a clinical entity to be avoided appeared in earnest within the medical literature during the 1970's, with 54 PubMed citations from that decade using that phrase. Although evolutionary pressure likely selected for the adaptive responses to hypovolemia following injury or illness, there was no such selection pressure to respond to hypervolemia in the same setting, a situation now commonly referred to as fluid overload (FO). However, the application of modern intensive care sets the stage for harm when potentially limitless amounts water and sodium can be administered to patients whose upset biology favors retention of both. These responses may serve to defend blood volume and maintain hydration when access to water is impaired by debility, and in the absence of medical care likely confer some survival advantage. The mammalian stress response to injury, hypovolemia, or critical illness includes retention of sodium and water and, at least early on, increased thirst ( 1– 5). The risk of FO may be minimized by limiting resuscitation fluid to the smallest amount needed to optimize cardiac output and then limiting maintenance fluid to the amount needed to replace ongoing normal and pathological losses of water and sodium. Numerous observational clinical studies in humans have demonstrated an association between FO, adverse events, and mortality, as have two retrospective observational studies in dogs and cats. Most clinical studies of the association of FO with fluid therapy and risk of harm define it in terms of an increase in body weight of at least 5–10%, or a positive fluid balance of the same magnitude when fluid intake and urine output are measured. FO may be a consequence of spontaneous disease, or may be a complication of intravenous fluid therapy. In clinical practice it is usually suspected when a patient shows evidence of pulmonary edema, peripheral edema, or body cavity effusion. ![]() Fluid overload (FO) is characterized by hypervolemia, edema, or both. ![]()
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