Figure 220

In volume expansion, total body sodium (Na) content is increased. In primary renal Na retention, volume expansion is modest and edema does not develop because blood pressure increases until Na excretion matches intake. In secondary Na retention, blood pressure may not increase sufficiently to increase urinary Na excretion until edema develops.

CLINICAL SIGNS OF VOLUME EXPANSION

CLINICAL SIGNS OF VOLUME DEPLETION

LABORATORY SIGNS OF VOLUME DEPLETION OR EXPANSION

Pulmonary crackles Ascites

Jugular venous distention Hepatojugular reflux Hypertension

Orthostatic decrease in blood pressure and increase in pulse rate Decreased pulse volume Decreased venous pressure Loss of axillary sweating Decreased skin turgor Dry mucous membranes

Hypernatremia

Hyponatremia

Acid-base disturbances

Abnormal plasma potassium

Decrease in glomerular filtration rate

Elevated blood urea nitrogen-creatinine ratio

Low functional excretion of sodium (FE^)

Clinical signs of volume expansion.

| FIGURE

1 FIGURE

Clinical signs of volume depletion. Note that laboratory test results for volume expansion and contraction are similar. Serum sodium (Na) concentration may be increased or decreased in either volume expansion or contraction, depending on the cause and intake of free water (see Chapter 1). Acid-base disturbances, such as metabolic alkalosis, and hypokalemia are common in both conditions. The similarity of the laboratory test results of volume depletion and expansion results from the fact that the "effective" arterial volume is depleted in both states despite dramatic expansion of the extracellular fluid volume in one.

w from a reduction in mean arterial pressure (MAP). Some disorders decrease cardiac output, such as congestive heart failure owing to myocardial dysfunction; others decrease systemic vascular resistance, such as high-output cardiac failure, atriovenous fistulas, and cirrhosis. Because MAP is the product of systemic vascular resistance and cardiac output, all causes lead to the same result. As shown in Figures 2-3 and 2-4, small changes in MAP lead to large changes in urinary Na excretion. Although edema-tous disorders usually are characterized as resulting from contraction of the effective arterial volume, the MAP, as a determinant of renal perfusion pressure, may be the crucial variable (Figs. 2-26 and 2-28 provide supportive data). The mechanisms of edema in nephrotic syndrome are more complex and are discussed in Figures 2-36 to 2-39.

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