There are three major fluid compartments; intravascular, interstitial, and intracellular. Fluid movement from the intravascular to interstitial and intracellular compartments occurs in the capillaries. A capillary “membrane,” which consists of the endothelial glycocalyx, endothelial cells, and the subendothelial cell matrix, separates the capillary intravascular space from the interstitial fluid compartment. This capillary “membrane” is freely permeable to water and small-molecular-weight particles such as electrolytes, glucose, acetate, lactate, gluconate, and bicarbonate. Gases such as oxygen and carbon dioxide diffuse freely through this membrane, following their concentration gradient, to enter or exit the intravascular compartment.
The interstitial compartment is the space between the capillaries and the cells. Fluids support the matrix and cells within the interstitial space. The intracellular compartment is separated from the interstitial space by a cell membrane. This membrane is freely permeable to water but not to small- or large-molecular-weight particles. Any particle movement between the interstitium and the cell must occur through some transport mechanism (eg, channel, ion pump, carrier mechanism).
Fluids are in a constant state of flux across the capillary endothelial membrane, through the interstitium, and into and out of the cell. The amount of fluid that moves across the capillary “membrane” depends on a number of factors, including capillary colloid oncotic pressure (COP), hydrostatic pressure, and permeability, which is dictated by factors such as the endothelial glycocalyx layer (EGL) and pore sizes between the cells. The natural particles in blood that create COP are proteins: primarily albumin but also globulins, fibrinogen, and others. The hydrostatic pressure within the capillary is the pressure forcing outward on the capillary membrane generated by the blood pressure and cardiac output. Fluid moves into the interstitial space when intravascular hydrostatic pressure is increased over COP, when membrane pore size increases, the EGL is disrupted, or when intravascular COP becomes lower than interstitial COP. The EGL is now known to play an important role in controlling fluid and other molecule (eg, albumin) transport across the capillary layer, and the oncotic pressure of the glycocalyx plays a larger role than the oncotic pressure of the interstitium; various disease processes and therapy (such as IV fluid administration) can significantly disrupt the EGL, resulting in altered transcapillary movement.