Read e-book online Clinical Physiology of Acid-Base and Electrolyte Disorders PDF

By Burton Rose, Theodore Post

ISBN-10: 0071346821

ISBN-13: 9780071346825

This beautifully written textual content provides scholars, citizens, and practitioners the sting in figuring out the mechanisms and medical administration of acid-base issues. provides the middle details to appreciate renal and electrolyte body structure, and reports the remedy purpose for all significant acid-base and electrolyte disturbances. the total textual content is exhaustively revised, and now contains questions and solutions in each one bankruptcy.

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Extra resources for Clinical Physiology of Acid-Base and Electrolyte Disorders

Sample text

The filtration fraction), since these parameters will tend to change in opposite directions. The opposing effects of efferent arteriolar tone on Pgc and RPF also mean that the direct relationship between this resistance and the GFR (Fig. 2-7) must be modified, since the RPF is an independent determinant of GFR. As an example, although efferent arteriolar constriction increases Pgc, the concomitant elevation in renal vascular resistance will reduce RPF, which will tend to lower the GFR. Depending upon the magnitude of efferent constriction, the net effect may be an increase, no change, or, if RPF is sufficiently reduced, even a fall in GFR.

The closed symbols represent animals given an intrarenal infusion of an angiotensin II antagonist; autoregulation of RBF was maintained (with an increase in the baseline level because of the fall in renal vascular resistance), but the GFR was less well regulated. Although not shown, autoregulation also applies when the renal artery pressure is initially raised. (Adapted from Hall JE, Guyton AC, Jackson TE, et al, Am J Physiol 233:F366, 1977. 128 As illustrated in Fig. 129 The preferential increase in efferent arteriolar resistance induced by angiotensin II contributes to 43 44 autoregulation of GFR by preventing any fall in Pgc; consequently, infusion of an angiotensin II antagonist or an ACE inhibitor leads to less effective maintenance of the GFR.

117 The reduction in permeability becomes a limiting factor, because it is now severe enough to prevent filtration equilibrium from being reached. 118 On the other hand, volume depletion due to vomiting or diarrhea can result in hemoconcentration and a rise in the plasma protein concentration. This increases Ï p, contributing to the decrease in GFR that may be seen in this setting. REGULATION OF GLOMERULAR FILTRATION RATE AND RENAL PLASMA FLOW Regulation of renal hemodynamics is primarily achieved via changes in arteriolar resistance, which can affect both RPF [from Eq.

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Clinical Physiology of Acid-Base and Electrolyte Disorders by Burton Rose, Theodore Post


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