Disorders of extracellular fluid volume are disorders of sodium balance and total body sodium content. The terms volume contraction and volume expansion are frequently employed as shorthand to indicate extracellular fluid (ECF) volume contraction and expansion, respectively. Because ECF volume control systems are largely distinct from systems that regulate plasma osmolality, disorders of ECF volume are commonly distinguished from disorders of water balance. The term dehydration is commonly used to indicate ECF volume depletion; strictly, its use should be reserved for depletion of water (as in diabetes insipidus) rather than ECF volume.
Disorders of ECF volume have long presented a challenge in the understanding of body fluid volume regulation. In the normal subject, if ECF is expanded, the kidney will excrete the excessive amount of sodium and water, thus returning ECF volume to normal. What has not been understood, however, is why the kidneys continue to retain sodium and water in edematous patients. Neither total ECF nor its interstitial component, both of which are expanded in the patient with generalized edema, is the modulator of renal sodium and water excretion. Rather, some body fluid compartment other than total ECF or interstitial fluid volume must be the regulator of renal sodium and water excretion.
The term effective blood volume was coined to describe this undefined body fluid compartment that signals the kidney, through unknown pathways, to retain sodium and water in spite of expansion of the total ECF volume. It was first suggested that the kidney is responding to a decline in cardiac output, providing an explanation for sodium and water retention in low-output cardiac failure. This idea, however, did not provide a universal explanation for generalized edema, because many patients with decompensated cirrhosis who avidly retain sodium and water have normal or elevated cardiac output. The venous component of the plasma in the circulation was also proposed as the modulator of renal sodium and water excretion because a rise in the left atrial pressure is known to cause a water diuresis and natriuresis, mediated in part by a suppression of vasopressin and an increase in secretion of atrial and B-type natriuretic peptides. These factors also cannot fully explain ECF volume homeostasis, because renal sodium and water retention are hallmarks of congestive heart failure—a situation in which pressures in the atria and venous component of the circulation are increased.
The arterial portion of body fluids is the remaining component that may be pivotal in the regulation of renal sodium and water excretion. The relation between cardiac output and peripheral arterial resistance [termed the effective arterial blood volume (EABV)] has been proposed as a regulator of renal sodium and water reabsorption. In this context, either a decrease in cardiac output or vasodilation of the arterial tree may cause arterial underfilling and thereby initiate and sustain a sodium and water-retaining state.
Two major compensatory processes respond to arterial underfilling. One is ...