Plasma-Interstitial Fluid Exchange

The aqueous solutions that compose the plasma and the interstitial fluid exchange readily through the thin walls of most of your body's capillaries.  The primary forces that govern this exchange are hydrostatic pressure (the blood pressure within the capillaries), and osmosis.

Hydrostatic Pressure at the Capillary:

The capillary wall acts as a filtration "barrier".  Most of the fluid within the capillaries is retained, but some filters through pores between the cells, pushed by the pressure difference between the capillary blood and the ISF.

Water and small solutes can pass freely through these pores.  The net effect of the hydrostatic pressure alone is a net loss of water and solute from plasma to the ISF.

The capillary wall (both cells and pores) are, however, impermeable to the plasma proteins and lipids.  Under normal conditions, these stay within the plasma.   Note that following injury, the capillaries can also leak protein.

The hydrostatic pressure in the capillaries is lower than that of the arteries, and decreases along the length of the capillary as blood flows through.  At the arteriolar end of the capillary, the pressure is usually about 35 mm Hg (due to the pressure drop caused by the resistance arterioles).  On the venule end of the capillary, the pressure is in the range of 15 mm Hg.  The mid-capillary pressure profile can be assumed to be linear (see figures below).

Osmotic forces in the capillaries:

Because the capillary wall is permeable to water, but essentially impermeant to the plasma proteins, these molecules generate an osmotic pressure.  Furthermore, since these proteins are negatively charged, they tend to hold additional cations in the plasma (the Gibbs-Donnan effect), further enhancing an osmotic gradient between the plasma and the interstitial fluid.

The combined effect (osmotic and Gibbs-Donnan) results in a pressure that draws water out of the interstitium and into the plasma.  This pressure is known as the Colloid Oncotic Pressure (often shortened to the Oncotic Pressure).

This pressure is proportional to the difference in protein concentration between the plasma and the ISF.  Compared to pure saline, the plasma exerts about 28 mm Hg Oncotic pressure, whereas the ISF has only about 3 mm Hg.  The net Oncotic Pressure is thus about 25 mm Hg.  This value remains roughly constant over the length of most capillary beds.

Starling's Relationship

The British physiologist Starling first identified the interrelationship between the hydrostatic pressure and the oncotic forces within the capillary.

Hydrostatic pressure tends to cause fluid to leave the plasma, and oncotic pressure pulls it back.  These two forces tend to balance each other.

The hydrostatic forces, however, are gradually decreasing over the length of the capillary, while the oncotic pressure remains constant.  If these pressures were graphed, they would look approximately like the following figure:

On the arteriole end, the hydrostatic pressure is higher than the oncotic, so there is fluid movement from plasma to interstitium.  The magnitude of this water flow is indicated by the light blue area on the left (downward arrows). On the venule end, the hydrostatic pressure has dropped below the oncotic.  Fluid moves back from the interstitium to the plasma. The magnitude of this reverse flow is indicated by the green area on the right (upward arrows).  

In a normal capillary bed, fluid gain and loss from the plasma are closely balanced, so there is little or no net change in plasma and ISF volumes.  Note that this can be seen graphically, since the blue and green (right and left) regions have equal areas.

Note that a small excess in fluid loss from plasma to ISF is normally drained back to the circulation via the lymphatics.

Starling forces in disease:

The balance described above can be altered by changes to the capillary pressure near the arterioles or near the venules, as well as alterations in the Oncotic Pressure.   The following examples illustrate the range of imbalances that can occur:

Increased Blood Pressure at the capillaries:  Vasodilation

Vasodilation reduces the pressure drop across the arterioles, bringing the capillaries closer to the arterial pressure.  The venous pressure may not be altered.  In this case, there is a greater region where fluid leaves the plasma, and a reduced regions where it returns.

This imbalance results in a net loss of fluid from the plasma.  The result is an expansion of the interstitial fluid in this tissue.  If this expansion continued, it would result in the clinical symptom known as edema.

Decreased Blood Pressure at the Capillaries:  Shock

When the central blood pressure declines, the pressure at the capillaries usually also decreases.  In addition, most vascular beds will participate in reflex attempts to maintain the central blood pressure via arteriolar vasoconstriction.  This further reduces the pressure at the start of the capillary.

The decrease in hydrostatic pressure results in a diminution in the region where fluid is lost from the plasma, and an expansion in the region where fluid returns back to the plasma.  There is a net gain of fluid to the plasma.

This net gain, taken over most of the body's vascular beds leads to an "auto-transfusion" that helps to compensate for plasma loss during hemorrhagic shock.

Increased Venous Pressure:  Congestive Heart Failure

When the heart's function is compromised, it cannot pump blood as effectively, so venous pressure rises.  This elevation in venous pressure is also felt at the capillaries, as illustrated above.

This rise in venous pressure diminishes the region where fluid is reabsorbed into the plasma.  As with the case (above) of vasodilation, this condition results in a net loss of fluid from plasma to ISF.  The resulting edema can be seen in the swollen ankles (and other tissues) that are symptomatic of congestive heart failure.

Decreased Oncotic Pressure:  Protein deficiency and tissue damage

When the plasma does not contain sufficient protein, or the interstitial fluids contain too much, then the difference in oncotic forces diminishes.  As shown above, this results in a net increase in the region where hydrostatic pressure exceeds oncotic.   Edema results.

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Copyright 1999, Joe Patlak, Department of Physiology, University of Vermont.
For comments, problems or questions regarding this web contact Joe Patlak.
Last updated: November 01, 2000.