Disorders of Sodium Balance
ECF volume is directly proportionate to total body sodium content. Variations in ECF volume result from changes in total body sodium content. A posi-tive sodium balance increases ECF volume, whereas a negative sodium balance decreases ECF volume. It is important to reemphasize that extracellular(plasma) Na+ concentration is more indicative of water balance than total body sodium content.
Net sodium balance is equal to total sodium intake (adults average 170 mEq/d) minus both renal sodium excretion and extrarenal sodium losses. (One gram of sodium yields 43 mEq of Na ions, whereas 1 g of sodium chloride yields 17 mEq of Na+ ions.) The kidneys’ ability to vary urinary Na + excretion from less than 1 mEq/L to more than 100 mEq/L allows them to play a critical role in sodium balance .
Because of the relationship between ECF volume and total body sodium content, regulation of one is intimately tied to the other. This regulation is achieved via sensors that detect changes in the most important component of ECF, namely, the “effective” intravascular volume. The latter corre-lates more closely with the rate of perfusion in renal capillaries than with measurable intravascular fluid (plasma) volume. Indeed, with edematous disorders (heart failure, cirrhosis, and kidney failure), “effec-tive” intravascular volume can be independent of the measurable plasma volume, ECF volume, and even cardiac output.
ECF volume and total body sodium content are ultimately controlled by appropriate adjustments in renal Na + excretion. In the absence of kidney disease, diuretic therapy, and selective renal isch-emia, urinary Na+ concentration reflects “effective” intravascular volume. A low urine Na+ concentra-tion (<10 mEq/L) is therefore generally indicative of a low “effective” intravascular fluid volume and reflects secondary retention of Na+ by the kidneys.
The multiple mechanisms involved in regulating ECF volume and sodium balance normally comple-ment one another but can function independently. In addition to altering renal Na+ excretion, some mechanisms also produce more rapid compensatory hemodynamic responses when “effective” intravas-cular volume is reduced.
Baroreceptors are the principal volume receptors in the body. Because blood pressure is the product of cardiac output and systemic vascular resistance , significant changes in intravascular vol-ume (preload) not only affect cardiac output but also transiently affect arterial blood pressure. Thus, the baroreceptors at the carotid sinus and afferent renal arterioles (juxtaglomerular apparatus) indirectly function as sensors of intravascular volume. Changes in blood pressure at the carotid sinus modulate sym-pathetic nervous system activity and nonosmotic ADH secretion, whereas changes at the afferent renal arterioles modulate the renin–angiotensin– aldosterone system. Stretch receptors in both atria are affected by changes in intravascular volume, and the degree of atrial distention modulates the release of atrial natriuretic hormone and ADH.
Regardless of the mechanism, effectors of vol-ume change ultimately alter urinary Na+ excretion. Decreases in “effective” intravascular volume decrease urinary Na+ excretion, whereas increases in the “effec-tive” intravascular volume increase urinary Na+ excre-tion. These mechanisms include the following:
Renin–angiotensin–aldosterone—Renin secre-tion increases the formation of angiotensin II. The latter increases the secretion of aldosterone and has a direct effect in enhancing Na+ reabsorption in the proximal renal tubules. Angiotensin II is also a potent direct vasoconstrictor and potentiates the actions of norepinephrine. Secretion of aldosterone enhances Na+ reabsorption in the distal nephron and is a major determinant of uri-nary Na+ excretion.
Atrial natriuretic peptide (ANP)—This peptideis normally released from both right and left atrial cells following atrial distention. ANP appears to have two major actions: arterial vasodilation and increased urinary sodium and water excretion in the renal collecting tubules. Na +-mediated afferent arte-riolar dilation and efferent arteriolar constriction can also increase glomerular filtration rate (GFR). Other effects include the inhibition of both renin and aldosterone secretion and antagonism of ADH.
Brain natriuretic peptide (BNP)—ANP, BNP, and C-type natriuretic peptide are structurally related peptides. BNP is released by the ventricles in response to increased ventricular volume and pressure, and ventricular overdistention, and also by the brain in response to increased blood pressure. BNP levels are usually approximately 20% of ANP levels, but dur-ing an episode of acute congestive heart failure BNP levels may exceed those of ANP. BNP levels can be measured clinically, and a recombinant form of BNP, nesiritide (Natrecor), is available to treat acute decompensated congestive heart failure.
Sympathetic nervous system activity—Enhanced sympathetic activity increases Na+ reab-sorption in the proximal renal tubules, resulting in Na+ retention, and increases renal vasoconstriction, which reduces renal blood flow . Conversely, stimulation of left atrial stretch recep-tors results in decreases in renal sympathetic tone and increases in renal blood flow (cardiorenal reflex) and glomerular filtration.
Glomerular filtration rate and plasma sodium concentration—The amount of Na+fi ltered in thekidneys is directly proportionate to the product of the GFR and plasma Na+ concentration. Because GFR is usually proportionate to intravascular vol-ume, intravascular volume expansion can increase Na+ excretion. Conversely, intravascular volume depletion decreases Na + excretion. Similarly, even small elevations of blood pressure can result in a relatively large increase in urinary Na+ excretion because of the resultant increase in renal blood flow and glomerular filtration rate. Blood pressure– induced diuresis (pressure natriuresis) appears to be independent of any known humorally or neurally mediated mechanism.
Tubuloglomerular balance—Despite wide varia-tions in the amount of Na+ fi ltered in nephrons, Na+ reabsorption in the proximal renal tubules is normally controlled within narrow limits. Factors considered to be responsible for tubuloglomerular balance include the rate of renal tubular flow and changes in peri-tubular capillary hydrostatic and oncotic pressures. Altered Na+ reabsorption in the proximal tubules can have a marked effect on renal Na+ excretion.
Antidiuretic hormone—Although ADH secre-tion has little effect on Na + excretion, nonosmotic secretion of this hormone (see above) can play an important part in maintaining extracellular volume with moderate to severe decreases in the “effective” intravascular volume.
Osmoregulation protects the normal ratio of sol-utes to water, whereas extracellular volume regula-tion preserves absolute solute and water content (Table 49–7). As noted previously, volume regulation generally takes precedence over osmoregulation.
Problems related to altered sodium balance result from its manifestations as well as the underlying disorder. Disorders of sodium balance present either as hypovolemia (sodium deficit) or hypervolemia (sodium excess). Both disturbances should be cor-rected prior to elective surgical procedures. Cardiac, liver, and renal function should also be carefully evaluated in the presence of sodium excess (gener-ally manifested as tissue edema).
Hypovolemic patients are sensitive to the vaso-dilating and negative inotropic effects of vapor anesthetics, propofol, and agents associated with histamine release (morphine, meperidine). Dosagerequirements for other drugs must also be reduced to compensate for decreases in their volume of dis-tribution. Hypovolemic patients are particularly sensitive to sympathetic blockade from spinal or epidural anesthesia. If an anesthetic must be admin-istered prior to adequate correction of hypovolemia, etomidate or ketamine may be the induction agents of choice for general anesthesia. Hypervolemia should generally be corrected preoperatively with diuretics. The major haz-ard of increases in extracellular volume isimpaired gas exchange due to pulmonary interstitial edema, alveolar edema, or large collections of pleu-ral or ascitic fluid.
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