Water and Electrolyte Metabolism in Con - gestive Heart Failure
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چکیده
SINCE 1944 when Warren and Stead' first attributed the fluid retention of chronic congestive heart failure to a specific renal dysfunction, an ever increasing interest has centered upon the kidney in an attempt to elucidate its part in the production of edema. Seven years later, although there has been no general agreement on the mechanism, it is believed by many workers that in heart failure there is an initial retention of sodium as a result of decreased glomerular filtration or increased tubular reabsorption of this ion or both, with a subsequent retention of water that results in increased extracellular fluid volume and pitting edema.1-9 According to current concepts the fluid retaining effect of sodium depends upon its position as the principal component of osmotically active base in the extracellular fluid compartment. Alterations in sodium content are reflected by retention or release of water if osmotic constancy (constant concentration of the sodium ion) is maintained. Retention of potassium, calcium, or magnesium does not lead to fluid retention since the physiologic concentration and range of these ions is so small that each contributes a negligible fraction to osmotic activity of this body fluid compartment. Having accepted sodium as the keystone in the development of edema it follows that the extracellular fluid concentration of this ion should be elevated, or at least in the high
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تاریخ انتشار 2005