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  • Title: Salt and water balance in congestive heart failure.
    Author: Dyckner T, Wester PO.
    Journal: Acta Med Scand Suppl; 1986; 707():27-31. PubMed ID: 2943141.
    Abstract:
    The majority of symptoms related to congestive heart failure (CHF) can be derived from the excessive accumulation of fluid in the body. The retention of fluid is the result of the activation of a complex system of compensatory mechanisms working on the kidneys and altering the hemodynamic situation in the body. The compensatory mechanisms are essentially the same as those activated in acute blood loss. The common denominator for CHF and acute blood loss is a decrease of the effective arterial blood volume (EABV), a parameter defined as blood volume in relation to vascular capacity. In the early stages of CHF there is an increased sympathoadrenergic tone, leading to a peripheral vasoconstriction and a decrease of blood flow to the kidneys. Due to a preferential constriction of the efferent arterioles, the filtration fraction is increased and the glomerular filtration rate remains unchanged. However, there is an increased colloid osmotic pressure and a decreased intravascular hydrostatic pressure in the peritubular capillaries. These alterations result in an increased reabsorption of sodium and water in the kidneys. Furthermore, the blood flow in the kidneys is rerouted from the cortical to the juxtamedullary nephrons, which have larger glomeruli and longer loops of Henle. This will further increase the retention of salt and water. The renin-angiotensin-aldosterone (R-A-A) system is also activated due to the decrease of EABV. Angiotensin II exerts about the same effects as norepinephrine--vasoconstriction, rerouting of blood within the kidney and preferential vasoconstriction of the efferent arterioles--all changes contributing to the retention of salt and water.(ABSTRACT TRUNCATED AT 250 WORDS)
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