![]() ![]() The importance of an adequate BV in maintaining normal organ perfusion is well recognized, and several early studies by Warren et al. Total BV normally accounts for 6-7% of lean body weight and 11-12% of total body fluids. As a result, a cycle of decompensation (acute on chronic) provoking a clinical response of aggressive short-term diuretic treatment of congestive symptoms occurs, which is then followed by the gradual recurrence of fluid accumulation and/or fluid redistribution, which in turn promotes another cycle of decompensation (fig. This chronic volume excess is often only marginally mitigated with standard diuretic and vasodilator therapies. The latter may be slowly progressive and delayed in presentation, but once it develops in chronic HF, marked fluid retention has often already occurred and, depending on the volume capacity of the interstitial compartment, can reflect multi-liter fluid excess. ![]() Volume overload leads to hemodynamic congestion with increased central filling pressures and the eventual development of symptomatic clinical congestion. While this process occurs initially as compensatory mechanisms to maintain effective circulating BV, over time, they become detrimental with the development of pathologic inappropriate BV and interstitial fluid expansion contributing to volume overload and organ congestion. Given that only 30-40% of total BV normally resides in the arterial circulation, and even less in the presence of systolic HF with relative arterial underfilling, considerable overall volume expansion is required to maintain effective tissue perfusion dynamics. The expansion of the interstitial fluid compartment with an associated increase in interstitial tissue pressure thus provides a mechanistic basis for sustaining the compensatory expansion of intravascular volume over time. While an initial sympathetic-driven vasoconstriction maintains organ perfusion pressure in the short term, a more gradual accumulation of extracellular/interstitial compartment fluid also occurs, which supports a compensatory expansion of intravascular plasma volume (PV). This response occurs in conjunction with baroreceptor activation and neurohormonal stimulation, which further promote renal sodium and water retention. The kidney acts as an early responder to the myocardial dysfunction and the resulting arterial underfilling with a reduction in effective circulating blood volume (BV). The features of chronic heart failure (HF) reflect a syndrome characterized by the renal retention of sodium and water with resulting intravascular and interstitial fluid volume expansion and redistribution. Key Message: Not all volume overload is the same, and the measurement of intravascular volume identifies heterogeneity to guide tailored therapy. The quantitative assessment of intravascular volume is an effective tool to help guide individualized, appropriate therapy. Clinical bedside evaluations and right heart hemodynamic assessments can alert of changes in volume status, but only the quantitative measurement of total blood volume can help identify the heterogeneity in plasma volume and red blood cell mass that are features of volume overload in chronic HF. The dynamics of interstitial and intravascular fluid compartment interactions and fluid redistribution from venous splanchnic beds to the central pulmonary circulation need to be taken into account in strategies of volume management. Summary: The pathophysiology of volume regulation is complex, and the simple concept of passive intravascular fluid accumulation is not adequate. Background: Volume overload and fluid congestion remain primary clinical challenges in the assessment and management of patients with chronic heart failure (HF). ![]()
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