The difference between oncotic and hydrostatic pressure
The normal values for colloid osmotic and hydrostatic pressures in the resting state . Plasma colloid osmotic pressure: Before surgery, in connection with Circulating blood volume (CBV) for estimation of blood loss during. Identify the primary mechanisms of capillary exchange; Distinguish between capillary hydrostatic pressure and blood colloid osmotic As we discuss osmotic pressure in blood and tissue fluid, it is important to . Interactive Link Questions. Oncotic pressure can be measured with a colloid osmometer. Normal Relationship between the concentration of plasma proteins in solution and the .. At the arteriolar end of the capillaries the hydrostatic pressure of the blood is sufficient to.
As a consequence, the increase in transcapillary filtration is much greater in chronic versus acute venous hypertension.
Interstitial Fluid Colloid Osmotic Pressure in Healthy Children
The mechanisms responsible for the reduction in intestinal vascular resistance that account for the changes in capillary pressure and capillary filtration coefficient that lead to enhanced capillary filtration in chronic portal hypertension involve the formation of vasodilator substances and other factors and are reviewed elsewhere [ 18192181,]. Nevertheless, the associated increase in transmicrovascular filtration rate largely accounts for the elevated transcapillary escape rate of proteins noted in this disorder through convective coupling of fluid and protein flux.
Elevated capillary pressure and filtration rate occur early in the course of development of diabetes mellitus and is thought to be an important stimulus for capillary basement membrane thickening, the ultrastructural hallmark of diabetic microangiopathy [ 27]. Microvascular rarefaction, or loss of capillaries, has been reported to accompany the development of arterial hypertension, diabetes mellitus, and the metabolic syndrome [ 827327073].
The attendant reductions in the surface area available for exchange may partially offset the effect of capillary hypertension to increase interstitial fluid volume in these conditions.
Interstitial Fluid Colloid Osmotic Pressure in Healthy Children
Very large increases in venous pressure may induce increments in capillary filtration far in excess of what would be predicted from the associated increase in capillary pressure. This is due to pressure-induced increases in microvascular permeability that are manifest in the Starling equation by increases in hydraulic conductivity and reductions in the osmotic reflection coefficient. Organs such as the liver, which have discontinuous capillaries characterized by large gaps between endothelial cells and reflection coefficients approaching 0.
Large increases in venous pressure are thought to enlarge these pores in microvascular wall, which is referred to as the stretched pore phenomenon [, ]. Individual organs demonstrate a differential sensitivity to the effect of elevated venous pressure with regard to induction of the stretch pore phenomenon. For example, no increase in permeability occurs in microvessels of the feet during quiet standing, even though capillary pressure in the feet increases by more than 50 mmHg relative to values measured when supine, owing to the large hydrostatic column in arteries and veins.
However, pulmonary capillaries may demonstrate a stretched pore phenomenon during conditions such as left ventricular failure, an effect that exacerbates pulmonary edema formation in this condition [ ].
As noted above, myogenic constriction of arterioles in response to elevations in arterial or venous pressure constitutes an important safety factor against edema formation in hydrostatic edema by limiting the increase in capillary pressure and by reducing the number of perfused capillaries, and thus the available surface area for fluid filtration, that might otherwise occur in response to arterial or venous hypertension or increased venous resistance Figure 4.Forces of Filtration
However, it is important to note even modest increments in capillary pressure, which might appear to be small and inconsequential, can result in substantial increases in fluid filtration rates across the microvasculature.
This is because normal net filtration pressure is quite small, averaging 0. Thus, increasing capillary pressure by just 2 mmHg, as noted above in arterial hypertension, results in an initial fold increase in fluid movement from the blood into the interstitium.
Capillary hypertension results in the formation of a protein-poor ultrafiltrate that upon entry into the interstitial space raises interstitial fluid volume. Owing to the compliance characteristics of the interstitium, small increments in interstitial volume produce very large increases in tissue pressure, which effectively reduces the transcapillary hydrostatic pressure gradient, thereby limiting further accumulation of fluid Figure 4.
This effect is exacerbated in response to elevations in venous outflow pressure through the phenomenon of venous bulging. That is, the volume in veins increases immediately on elevation of venous pressure, which produces a coincident increase in interstitial pressure caused by expansion of engorged venules and veins into the interstitial spaces Figure 4.
In essence, venous engorgement shifts the interstitial compliance curve to the left, so that a smaller change in interstitial volume produces a larger increase in interstitial pressure. Increased interstitial fluid pressure increases lymph flow by three mechanisms. First, increased tissue pressure provides the driving pressure for flow into initial lymphatics.
Second, increased pressure in the interstitial compartment creates radial tension on the anchoring filaments connecting the extracellular matrix to lymphatic endothelial cells, locally increasing initial lymphatic diameter and opening gaps between interdigitating and overlapping junctions between adjacent lymphatic endothelial cells Figure 3.
These tensional forces create a small, transient suction pressure for movement of interstitial fluid through enlarged gaps between adjacent endothelial cells, which act as a second, one-way valve system to ensure unidirectional flow from the interstitium into lymphatics.
Third, as fluid moves into initial lymphatics, it increases volume in upstream lymphangions, promoting their contractile activity and lymph flow. The presence of valves between adjacent lymphangions assures one-way flow. As noted above, capillary hypertension results in the movement of protein-poor fluid into the interstitial spaces, reducing the concentration of tissue proteins and decreasing tissue colloid osmotic pressure Figure 4.
Because solute is excluded from a large portion of gel water in the extracellular matrix, the rapidity of the decrease in tissue protein concentration that occurs in response to increased interstitial fluid volume is enhanced, thereby augmenting the effectiveness of protein washdown as an edema safety factor.
It is important to note that the effectiveness of decreases in tissue osmotic pressure as an edema safety factor is reduced in severe capillary hypertension, owing to the stretched-pore phenomenon discussed above, which increases convective-coupled protein transport into the tissue spaces.
Hypoproteinemia Marked reductions in the circulating levels of proteins, especially albumin, is another cause of edema that relates to intravascular factors Figure 4. Hypoproteinemia may result from rapid loss of proteins across a compromised glomerular barrier in diseased kidneys, impaired hepatic synthesis of plasma proteins in liver disease, severe malnutrition or protein-losing enteropathy which limits the availability of substrate for protein synthesisor from infusion of intravenous fluids lacking macromolecules.
Like capillary hypertension, this effect is opposed by elevations in tissue hydrostatic pressure, which increases lymph flow, both of which serve to limit the accumulation of tissue fluid Figure 4. Enhanced capillary filtration also acts to dilute the concentration of proteins in the extracellular spaces, an effect that is magnified by increasing the accessible volume in the extracellular matrix gel Figures 2.
The ensuing reduction in interstitial colloid osmotic pressure acts to reduce net filtration pressure, thereby minimizing edema formation.
Unlike the response to vascular hypertension, there is no stimulus for myogenic arteriolar vasoconstriction and venous bulging does not occur in hypoproteinemia, which reduces the margin of safety for edema formation in response to this edemagenic stress.
As a consequence, tissues are less able to compensate for reductions in plasma colloid osmotic pressure that are equivalent to a given increase in capillary hydrostatic pressure.
Permeability Edema and Inflammation Disruption of the microvascular barrier is a pathologic sequela in a large number of disease states, commonly accompanies trauma, and can be induced by a wide variety of endogenously produced mediators and pharmacologic agents.
In the Starling equation Equation 1. Rapid reductions in the reflection coefficient decrease the effectiveness of the colloid osmotic pressure gradient in opposing filtration. The reduction in the restrictive properties of the endothelial barrier allows movement of a protein-rich filtrate into the tissue spaces, which increases interstitial colloid osmotic pressure Figure 4.
The resultant reduction in the colloid osmotic pressure gradient increases net filtration pressure, an effect that is exacerbated by the fact that many if not most of the mediators that increase microvascular permeability also act as vasodilators and reduce arteriolar resistance Figure 4. As a consequence, capillary pressure is elevated, which further increases net filtration pressure.
In addition, vasodilatation tends to recruit capillaries, thereby increasing microvascular surface area available for fluid and protein flux into the tissues.
The latter change contributes to a further increase in the capillary filtration coefficient which is equal to the hydraulic conductivity times surface area, LpSthereby magnifying the effect of increased net filtration pressure to promote volume flux.
The marked enhancement in transcapillary fluid filtration results in increased convective transport of protein through the enlarged pores in the microvascular barrier Figure 4. Under such conditions, the effect of increases in interstitial fluid pressure and lymph flow to provide a margin of safety against edema formation are rapidly overwhelmed and marked swelling of the interstitial spaces ensues.
Permeability edema is exacerbated in inflammatory states that are characterized by leukocyte infiltration into the tissues Figure 4. Inflammation is a characteristic response to tissue injury and involves the release of a large number of mediators that not only increase microvessel permeability and cause vasodilatation, but also act to attract leukocytes to the damaged tissue Figure 4.
These phagocytic cells release a variety of hydrolytic enzymes as well as reactive oxygen and nitrogen species that degrade extracellular matrix components and the anchoring filaments that attach to lymphatic endothelial cells Figures 3. This reduces the radial tension on the valve-like overlapping and interdigitating cell membranes at the interendothelial junctions in initial lymphatics, which may compromise lymphatic filling. Thus, fluid generally moves out of the capillary and into the interstitial fluid.
This process is called filtration. Osmotic Pressure The net pressure that drives reabsorption—the movement of fluid from the interstitial fluid back into the capillaries—is called osmotic pressure sometimes referred to as oncotic pressure. Whereas hydrostatic pressure forces fluid out of the capillary, osmotic pressure draws fluid back in.
Osmotic pressure is determined by osmotic concentration gradients, that is, the difference in the solute-to-water concentrations in the blood and tissue fluid. A region higher in solute concentration and lower in water concentration draws water across a semipermeable membrane from a region higher in water concentration and lower in solute concentration. As we discuss osmotic pressure in blood and tissue fluid, it is important to recognize that the formed elements of blood do not contribute to osmotic concentration gradients.
Rather, it is the plasma proteins that play the key role. Solutes also move across the capillary wall according to their concentration gradient, but overall, the concentrations should be similar and not have a significant impact on osmosis.
Because of their large size and chemical structure, plasma proteins are not truly solutes, that is, they do not dissolve but are dispersed or suspended in their fluid medium, forming a colloid rather than a solution. The pressure created by the concentration of colloidal proteins in the blood is called the blood colloidal osmotic pressure BCOP. Its effect on capillary exchange accounts for the reabsorption of water. The plasma proteins suspended in blood cannot move across the semipermeable capillary cell membrane, and so they remain in the plasma.
As a result, blood has a higher colloidal concentration and lower water concentration than tissue fluid. It therefore attracts water. We can also say that the BCOP is higher than the interstitial fluid colloidal osmotic pressure IFCOPwhich is always very low because interstitial fluid contains few proteins. Thus, water is drawn from the tissue fluid back into the capillary, carrying dissolved molecules with it.
This difference in colloidal osmotic pressure accounts for reabsorption. Interaction of Hydrostatic and Osmotic Pressures The normal unit used to express pressures within the cardiovascular system is millimeters of mercury mm Hg.
When blood leaving an arteriole first enters a capillary bed, the CHP is quite high—about 35 mm Hg. Gradually, this initial CHP declines as the blood moves through the capillary so that by the time the blood has reached the venous end, the CHP has dropped to approximately 18 mm Hg. In comparison, the plasma proteins remain suspended in the blood, so the BCOP remains fairly constant at about 25 mm Hg throughout the length of the capillary and considerably below the osmotic pressure in the interstitial fluid.
The net filtration pressure NFP represents the interaction of the hydrostatic and osmotic pressures, driving fluid out of the capillary. Since filtration is, by definition, the movement of fluid out of the capillary, when reabsorption is occurring, the NFP is a negative number. NFP changes at different points in a capillary bed Figure Recall that the hydrostatic and osmotic pressures of the interstitial fluid are essentially negligible.
Thus, the NFP of 10 mm Hg drives a net movement of fluid out of the capillary at the arterial end. At this point, there is no net change of volume: Fluid moves out of the capillary at the same rate as it moves into the capillary.
Near the venous end of the capillary, the CHP has dwindled to about 18 mm Hg due to loss of fluid. Because the BCOP remains steady at 25 mm Hg, water is drawn into the capillary, that is, reabsorption occurs. Net filtration occurs near the arterial end of the capillary since capillary hydrostatic pressure CHP is greater than blood colloidal osmotic pressure BCOP.
The Role of Lymphatic Capillaries Since overall CHP is higher than BCOP, it is inevitable that more net fluid will exit the capillary through filtration at the arterial end than enters through reabsorption at the venous end.
Considering all capillaries over the course of a day, this can be quite a substantial amount of fluid: Approximately 24 liters per day are filtered, whereas