In certain pathological conditions like congestive heart failure and hepatic cirrhosis, the excretion of NaCl by the kidneys does not accurately reflect the volume of extracellular fluid (ECFV). Instead of increased NaCl excretion as expected, there is a reduction in renal excretion of NaCl. To understand this phenomenon, it is important to comprehend the concept of effective circulating volume (ECV). Unlike ECF, ECV cannot be measured or considered as a distinct fluid compartment in the body. ECV refers to the portion of ECF that is contained within the vascular system and effectively perfuses the tissues. It represents the activity of volume sensors located in the vascular system.

Patients with congestive heart failure often experience an increase in ECFV, resulting in increased plasma volume and accumulation of interstitial fluid in the lungs (pulmonary edema) and peripheral tissues (generalized edema). This excess fluid is caused by the kidneys retaining NaCl and water. The kidneys' response of retaining NaCl and water seems paradoxical considering the increased ECFV. However, this fluid is not present in the vascular system but rather in the interstitial fluid compartment. Additionally, poor cardiac performance can lead to reduced blood pressure and cardiac output. Consequently, the sensors located in the vascular system respond as they do in ECFV contraction, causing the kidneys to retain NaCl and water. In this situation, the ECV, as monitored by the volume sensors, is decreased.

In healthy individuals, ECV correlates directly with ECFV, specifically the volume of the vascular system (arterial and venous), arterial blood pressure, and cardiac output. However, this relationship does not hold true in certain pathological conditions. The subsequent sections of this chapter focus on the examination of the relationship between ECFV and renal NaCl excretion in healthy adults, where changes in ECV and ECFV occur simultaneously.

The monitoring of ECFV or ECV involves multiple sensors. Some of these sensors are situated in the vascular system, monitoring its fullness and pressure. These receptors are commonly known as vascular volume receptors or baroreceptors because they respond to pressure-induced stretching of the walls of the structure they are located in, such as blood vessels, cardiac atria, and ventricles.

Volume sensors, also known as baroreceptors, are found within the walls of the left and right atria, right ventricle, and large pulmonary vessels. These sensors respond to the distention of these structures due to the high compliance of the low-pressure side of the circulatory system. The baroreceptors transmit signals to the brainstem through afferent fibers in the glossopharyngeal and vagus nerves (cranial nerves IX and X). The activity of these sensors influences both sympathetic nerve outflow and the secretion of antidiuretic hormone (ADH or AVP). For instance, a decrease in filling of the pulmonary vessels and cardiac atria increases sympathetic nerve activity and stimulates AVP secretion. Conversely, distention of these structures decreases sympathetic nerve activity. Typically, a change in blood volume and pressure of 5% to 10% is required to elicit a response.
However, in some pathological conditions (e.g., congestive heart failure, hepatic cirrhosis), renal excretion of NaCl does not reflect the ECFV. In both of these situations the volume of the ECF is increased. However, instead of increased renal NaCl excretion, as would be expected, renal excretion of NaCl is reduced. To explain renal Na+ handling in these situations, it is necessary to understand the concept of effective circulating volume (ECV). Unlike ECF, ECV is not a measurable and distinct body fluid compartment. Effective circulating volume refers to that portion of the ECF that is contained within the vascular system and is “effectively” perfusing the tissues (effective blood volume and effective arterial blood volume are other commonly used terms). More specifically the ECV reflects the activity of volume sensors located in the vascular system (discussed later).
Patients with congestive heart failure frequently have an increase in ECFV that manifests as increased plasma volume and accumulation of interstitial fluid in the lungs (pulmonary edema) and peripheral tissues (generalized edema). This excess fluid is the result of NaCl and water retention by the kidneys. The kidneys’ response (i.e., retention of NaCl and water) is paradoxical because the ECFV is increased. However, this fluid is not in the vascular system but rather in the interstitial fluid compartment. In addition, blood pressure and cardiac output may be reduced because of poor cardiac performance. Therefore the sensors located in the vascular system respond as they do in ECFV contraction and cause NaCl and water retention by the kidneys. In this situation the ECV, as monitored by the volume sensors, is decreased.
In healthy individuals, ECV varies directly with ECFV and in particular the volume of the vascular system (arterial and venous), the arterial blood pressure, and cardiac output. However, as noted this is not the case in certain pathological conditions. In the remaining sections of this chapter the relationship between ECFV and renal NaCl excretion in healthy adults—where changes in ECV and ECFV occur in parallel—are examined.
ECFV (or ECV) is monitored by multiple sensors. A number of these sensors are located in the vascular system, and they monitor its fullness and pressure. These receptors are typically called vascular volume receptors, or because they respond to pressure-induced stretch of the walls of the structure in which they are located (e.g., blood vessels or the cardiac atria and ventricles), they are also referred to as baroreceptors.
Volume Sensors in the Low-Pressure Cardiopulmonary Circuit
Volume sensors (i.e., baroreceptors) are located within the walls of the left and right atria, right ventricle, and large pulmonary vessels, and they respond to distention of these structures (see 19).
Because the low-pressure side of the circulatory system has a high compliance, these sensors respond mainly to the “fullness” of the vascular system. These baroreceptors send signals to the brainstem via afferent fibers in the glossopharyngeal and vagus nerves (cranial nerves IX and X). The activity of these sensors modulates both sympathetic nerve outflow and AVP secretion. For example, a decrease in filling of the pulmonary vessels and cardiac atria increases sympathetic nerve activity and stimulates AVP secretion. Conversely, distention of these structures decreases sympathetic nerve activity. In general, 5% to 10% changes in blood volume and pressure are necessary to evoke a response.