Contraction of extracellular fluid (ECF) and plasma volumes can be achieved with dietary salt restriction and diuretic therapy. This may be of great benefit to patients with chronic or acute congestive heart failure. Volume contraction reduces central and pulmonary venous capillary pressures which reverses pulmonary congestion and edema, as well as peripheral edema, ascites, and hepatic congestion.
ECF and plasma volumes can be manipulated by varying salt intake. When normal individuals switch from a normal salt intake to a low salt diet, urine sodium excretion does not fall immediately to match the lower intake level. Usually, a brief period of negative salt and water balance ensues. During this time, ECF and plasma volumes decrease and this activates vasoconstricting and salt retaining mediators which include renin, angiotensin, aldosterone, catecholamines, sympathetic nerves, etc. Salt excretion gradually decreases and after several days is reduced to levels equal to those ingested. At this point sodium balance is restored. Note that although balance is reestablished, the ECF volume, plasma volume, and weight are lower than they were on a normal salt intake. These parameters will remain "reduced" as long as salt intake remains at the lower level.
An increase in salt intake produces the opposite sequence. Urine salt excre tion initially lags behind the higher levels of salt intake. Positive salt balance increases the ECF volume, plasma volume, and weight. Vasoconstricting and salt retaining factors are suppressed while vasodilating and salt excretory factors are activated. Renal salt excretion increases and after several days matches the higher intake level. Balance is thus reestablished at higher ECF and plasma volumes and weight. These parameters all remain greater than baseline as long as the increased level of salt intake continues.
Figure 7 shows the relationship between urinary sodium output (which under balance conditions becomes equivalent to sodium intake) and ECF volume. The slope of the relationship indicates that the change in ECF sodium content is equal to about (1.3) X (change in sodium intake). Thus, if sodium intake increases by 100 mmol/day, the Na+ content of the ECF will increase by about 130 mmol. This will expand ECF volume by about 900 ml (assuming that the
ECF Volume. Liters ECF Volume, Liters
FIGURE 7. (A) The effect of dietary Na excretion (intake) on ECF volume in normal subjects and patients with CHF. Steady-state conditions exist so that Na excretion becomes equivalent to Na ingestion. The dashed lines indicate daily Na intake of about 1 and 5 g, respectively. The ECF volume of normal individuals expands when Na intake increases, but edema will not develop unless Na intake is enormous. The patient with mild congestive heart failure in this example develops edema at an intake of 200-300 mEq (5-8 g) of Na/day. The patient with severe heart failure remains edematous despite severe Na restriction. (B) The effect of diuretics and salt intake in patients with severe congestive heart failure. Diuretics shift the relationship to the left so for any given level of Na excretion (intake) ECF volume is lower. Loop diuretics may also alter the slope of the relationship. The flatter slope indicates that any change in salt intake will cause larger change in ECF volume. Note the important impact of salt intake on ECF volume whether or not diuretics are utilized (see text). •, Normal subject; ■, patient with mild CHF; patient with severe CHF; O, patient with severe CHF treated with a thiazide; A, patient with severe CHF; □, patient with severe CHF treated with a loop diuretic. (Adapted from Ellison, D. H. (1994). "Diuretics drugs in the treatment of edema: From clinic to bench and back again." Am. J. Kidney Dis. 23, 624-625, Figures 1 and 2.)
plasma [Na] = 140 mEq/liter). A 100 mmol/day decrease in dietary Na+ reduces ECF sodium content and volume by similar amounts .
Figure 7 also shows the abnormal relationship which exists between ECF volume and sodium intake in patients with congestive heart failure. The line defining this relationship shifts to the right so that any given level of sodium excretion (i.e., intake) is associated with a larger ECF volume. The slightly flatter slope also indicates that any change in salt intake will generate a greater change in ECF volume. Reducing salt intake will clearly decrease ECF volume. However, in patients with severe CHF even extreme salt restriction may not reduce ECF volume adequately. Relationships similar to those shown in Fig. 7 also exist between salt intake and measurements of plasma volume or body weight.
In a carefully controlled environment, sodium intake can be reduced to about 250 mg (about 10 mEq) per day. However, a more reasonable goal for the outpatient setting is 1000-1500 mg (about 40-65 mEq) of Na+ per day. Accurate quantitation of dietary salt intake may prove difficult. Under relative steady-state conditions, daily salt intake can be assumed to equal the sodium content of a 24-hr urine collection (as in Fig. 7). However, equivalence between salt intake and renal excretion does not exist during periods of rapid weight gain or loss (i.e., when sodium and fluid balance is positive or negative) or if sodium is lost via nonrenal routes such as diarrhea, vomiting, NG suction, etc.
When dietary salt restriction cannot reduce ECF and plasma volumes to a desired level, then diuretic therapy is indicated. Figure 7 also shows the effect of diuretics on the relationship between sodium excretion (again assume this is equivalent to intake) and ECF volume in patients with heart failure. Chronic diuretic treatment shifts this relationship to the left, so that any given level of sodium intake will result in lower steady state ECF volumes (and plasma volume and weight). When dietary salt intake remains constant, the initiation of a diuretic produces a relatively short-lived period of negative sodium balance. This decreases the patient's weight, reduces ECF and plasma volumes, and activates salt retaining mediators. Sodium balance is then restored at a lower weight and lower ECF and plasma volumes. Chronic diuretic therapy does not produce persistent negative sodium balance, which would, of course, be fatal. Note that dietary sodium continues to have an important impact on the size of the ECF and plasma volumes after initiation of diuretics. The level of salt intake affects the reduction in volume which will be generated by a diuretic. Ditary salt intake also impacts the frequency and severity of diuretic-associated side effects (see Diuretic Complications, below).
Another action of diuresis is a reduction in systemic vascular resistance and cardiac afterload which often improves cardiac output (Fig. 3). However, over-diuresis can reduce arterial blood pressures to levels which compromise organ perfusion so that diuretic therapy must be carefully monitored.
Loop diuretics of the furosemide class also produce acute venodilation by nondiuretic mechanisms. This effect is due to increased in synthesis and release of vasodilatory prostaglandins from the kidney. These acute hemodynamic effects reduce venous return to the heart and thereby decrease central venous and pulmonary capillary pressures [2, 6]. Thus, diuretics may have at least three different beneficial actions in patients with heart failure:
1. Diuresis and natruresis reduce ECF and plasma volumes, reduce cardiac preload, and improve pulmonary and systemic congestive symptoms.
2. Diuretics reduce systemic vascular resistance and cardiac afterload which often increases cardiac output.
3. Furosemide class loop diuretics cause renal release of prostaglandins and prostacyclines which result in systemic venodilation. The fall in preload can rapidly improve congestive symptoms.
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