Fluid Overload

نویسندگان

  • Claudio Ronco
  • Maria Rosa Costanzo
  • Rinaldo Bellomo
  • Alan S. Maisel
چکیده

Despite its high prevalence and significant rates of associated morbidity and mortality, the syndrome of decompensated heart failure (HF) remains poorly defined and vastly understudied. HF is due to several mechanisms including pump dysfunction disorder, neurohormonal activation disorder, and salt-water retention disorder. The first step of the syndrome includes cardiac damage and remodeling in terms of coronary disease systo diastolic dysfunction and myocardial metabolism alterations. Neurohormonal activation and hydrosaline retention occur during successive steps in response to cardiac injury for compensatory reasons. Both mechanisms provide inotropic support to the failing heart increasing stroke volume, and peripheral vasoconstriction to maintain mean arterial perfusion pressure. However, they are deleterious to cardiocirculatory homeostasis in the late stage. Further factors involve structural changes, such as loss of myofilaments, apoptosis and disorganization of the cytoskeleton, as well as disturbances in Ca homeostasis, alteration in receptor density, signal transduction, and collagen synthesis. Each disorder contributes at a different time to HF development and worsening. Clinical presentation depends on pulmonary congestion, organ perfusion, presence of coronary disease, fluid retention and systemic pressure. For these reasons, the picture of HF is widely varied. Copyright © 2010 S. Karger AG, Basel Heart failure (HF) is the leading cause of hospital admissions in the Medicare population. In addition to its high prevalence, hospitalization for decompensated HF is associated with extraordinarily high rates of morbidity and mortality. Estimates of the risk of death or rehospitalization within 60 days of admission for this disease vary from 30 to 60%, depending on the population studied in the US [1, 2]. Despite its high prevalence and significant rates of associated morbidity and mortality, its pathophysiologic mechanisms and treatment options remain poorly defined and vastly understudied. In addition, there is no

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تاریخ انتشار 2010