cardiovascular system we need to not lose sight of one of the major functions which is to simply circulate blood throughout our body and with the circulation of blood that indicates circulation of plasma so plasma is the liquid portion of the blood, and realizing that as we get this blood to the various tissue beds, there's going to be exchange of fluids. And that exchange is going to happen at the level of the capillary. So we're going to talk right now about how does this exchange of fluids occur across the capillary. Now if we look at what a typical systemic capillary looks like, we'll see that as is the case with all capillaries, the capillary consists of a single cell thickness and these cells that line all of the vascular system are called endothelial cells. And in our typical systemic capillary we have little spaces between these cells, these little pores, which allow movement of of water.
When we're talking about diffusion, we're typically referring to the movement of solutes in and out of the capillary, and recall that just from our basic principles of how we can move things across membranes, realize that whether or not there's pores present or not, lipophilic substances can easily diffuse in and out of the capillary because they can go straight through the cell membrane. Hydrophilic substances can diffuse through the pores or potentially they can have carriers that can move things across. The one thing that cannot move easily are proteins. So proteins in this picture doesn't have a protein. reflect the size appropriately, the proteins that are in our capillaries are actually quite large, the most important protein being albumin.
So albumin, in essence, is trapped within the capillary in most cases, and because of that, that's going to play an important role with regards to the movement of fluid. When we talk about bulk flow, bulk flow is describing the movement of water across the capillary wall. So it's the movement of water between the intravascular space and the interstitial space. And the reason that water is going to move across this area is because of pressure gradients. So we need to look and see what are these pressures that cause water to either move into or out of the capillary.
These pressures were described by Dr. Starling and so we refer to them as a group as Starling forces. So this is a picture depicting a typical capillary bed. So on this side would be the arterial side, and this side would be the venous side.
So this would be our typical systemic capillary, indicating that the oxygenated blood is coming in, signified by the red color, and then as we drop off oxygen, which will be a topic we cover later, we have deoxygenated blood leaving. Now the process of fluid leaving a capillary, we refer to that as filtration. Absorption is when we take that fluid from the interstitial space and put it back into the capillary.
So one of the forces that's going to be important with this is called our capillary hydrostatic pressure. So hydrostatic pressure as a group, that's a type of a pressure that we describe with fluid exerting pressure on a container wall. So in this case, our container is the capillary, and so blood and plasma is flowing into the capillary, and because of the pressure head, the mean arterial pressure which is pushing this blood forward, there is pressure exerted on the capillary.
walls from the plasma. So we call this the capillary hydrostatic pressure and highlighted by coloring this in red, capillary hydrostatic pressure is a force which is tending to push fluid out of the capillary or to favor filtration. Now the pressure at the arterial side of the capillary, I've given that a number of about 32 millimeters of mercury.
The number itself is not real important, but just giving some idea of the relative pressure. So that's the capillary hydrostatic pressure at the arterial end, but if we measure that same pressure at the venous end, we see it goes down to 12. So what we'll see is that this capillary hydrostatic pressure, which I'm now indicating by these red arrows, starts out as quite high. and it goes along the capillary bed, it becomes less and less.
So capillary hydrostatic pressure favors filtration. We also can describe an interstitial hydrostatic pressure. So this would be the pressure that the fluid in the interstitial space is exerting back onto the capillaries.
I guess an easy way to think about this is that under normal circumstances we consider our interstitial space as being kind of this ill-defined borderless compartment. It's not, but that's a good way to think about it. And because of that, we typically view the interstitial hydrostatic pressure under normal conditions as being negligible or zero.
Now, if it was present, if there was some pathologic condition where we did increase that hydrostatic pressure, realize that that would tend to favor absorption because it would tend to restrict the movement of fluid out of the capillary. Our other main pressure is one that we call oncotic pressure, and sometimes this is referred to as osmotic pressure. Oncotic pressure is just more specific and likely a better term because it describes a pressure that's created by protein which is trapped in the capillary.
So we have protein that's in the capillary and this protein under normal circumstances remains in the capillary. And think of this protein as working like a sponge. So it basically holds on, it draws water toward it.
So this plasma oncotic pressure, and this is typically depicted by the pi sign, is going to be a force which is going to favor absorption. Now the protein, because it tends to pull fluid into the capillary, we're going to give that pressure as a negative number. And notice that I have this shown as being constant from the arterial end to the venous end. This isn't... necessarily exactly correct, but it gets the point across is the fact that in our systemic capillaries there's exchange of fluid, but the amount of fluid that leaves the capillary is not too great, and therefore the protein concentration doesn't change much.
much. So we can appropriately consider that the osmotic pressure or the oncotic pressure stays relatively stable across the length of the capillary. Now this is a force which is going to be favoring absorption, so we're going to show these arrows as going in the opposite direction.
So plasma oncotic pressure favors absorption. Interstitial oncotic pressure, again this is one of those pressures that under normal circumstances we don't have much protein in the interstitial space and therefore we consider this pressure to be practically speaking zero. However, if protein that got into the interstitial space, and we may see that with certain pathologic conditions, it would tend to draw fluid out so it would tend to favor filtration. Now the way that we determine which direction fluid is going to be moving with bulk flow is by simply looking at the strength of these different forces.
So what we'll notice is that the hydrostatic pressure toward the arterial end is greater than the osmotic pressure. So on the arterial end of the capillary we're going to tend to have filtration. As we move along the capillary those forces change so that on the venous side of the capillary our oncotic pressure is greater than the hydrostatic pressure and so that's going to tend to draw fluid back in. So filtration on the arterial end of the capillary, absorption on the venous end.
Now over the course of a day, we typically can filter about three liters more fluid than what we absorb. So there's about three liters a day that's out in the interstitial space that's not absorbed by the capillary. This extra fluid is fluid that is going to be picked up by the lymphatic system. And the lymphatic system is the third group of vessels, one that's oftentimes overlooked when we talk about the cardiovascular system.
But these are vessels that are very thin. walled, very low pressure. They're throughout our body and they help pick up this extra fluid.
Now if we have an excess of fluid in the interstitial space that's not picked up by our capillaries or by our lymphatic system, we refer to this as edema. So this is a diagram that just basically gives an idea of the extent of the lymphatics throughout our body. So lymphatics are virtually everywhere, and they're going to drain, and they're going to pull everything back up, and eventually this fluid enters back into the circulatory system, typically through the left internal jugular vein, through a structure called the thoracic duct. The name of that structure is not important. But just realize that this fluid is returned back into the circulation.
And this just depicts how the lymphatic system will drain back in, and this is showing the thoracic duct here, back into the circulatory system. Now let's see what happens if we have a change in Starling forces. So this diagram depicts our heart.
This would be the mean arterial pressure pushing blood toward the capillaries. This would be the venous flow back to the heart. Here we're depicting our capillary hydrostatic pressure with the blue lines and we notice how that pressure decreases as we go from the arterial end to the venous end.
And then we have our oncotic pressure which is showing it pulling back in, our capillary or plasma oncotic pressure. So in this way that we're drawn we show the net effect, filtration occurs on the arterial side, absorption occurs on the venous side. But realize that with heart failure, and the way we can think about heart failure for our class is just think that the heart's not adequately able to pump blood out. So what happens is that the venous blood, you can think of that as basically getting backed up. And realize that as we increase this amount of blood in the venous system, we're going to be increasing the pressure in the venous system.
So what typically is a very low pressure, that pressure increases some. So what force, what Starling force is that going to impact? Well, that's going to impact our capillary hydrostatic pressure.
So as blood is coming through the capillary and trying to get out, it can't as easily because of this increased pressure here. So it tends to build up pressure within the capillary. So that causes us to have an increase in capillary hydrostatic pressure.
And so that alters the relationship between these two forces. And that's going to result in us having more filtration than absorption. This filtration that occurs is greater than what our lymphatic system can pick up, and that results in edema. Now, this is just a few pictures clinically to kind of show you how this may show up in a clinical situation. This is a normal chest x-ray.
This is looking at somebody's chest from straight on. The black area is the lung fields, or are the lung fields, and this is the heart here in the center. And so typically the lungs are filled with air.
So these areas are fairly dark because they primarily consist of air. This is a chest x-ray where we'll notice there's a difference here. You'll notice that particularly here on this side, we see a lot more white.
We can actually see a little bit of that streaking throughout. But this is because instead of having nice thin air sacs in the lung, they now have excess fluid. That's a result of heart failure.
You can also maybe notice that this heart appears to be a bit larger than what we see here. So this is edema that's forming in the lung tissue. So this is something we call pulmonary edema, and we'll see that with congestive heart failure.
This is another example that we may see. This is a patient's ankle, and if you look closely, what you can notice is there are little impressions here within this patient's leg. That's where a physician has placed their fingers and applied pressure.
So we refer to that as pitting, P-I-T-T-I-N-G, pitting edema, so that by applying pressure we can actually create pits in the patient's skin. So this is again a sign of edema of excess fluid in the interstitial space. Another way that we can see troubles is maybe not with the heart causing troubles with our hydrostatic pressure, but we may have a condition such as with liver failure where we're not making adequate amount of protein.
So if we don't have adequate amount of protein, or perhaps we have a trouble with our kidney where our kidney is allowing us to lose protein, regardless in either way, we have decreased protein content within the blood. So what pressure has that now affected? It hasn't affected the hydrostatic pressure, but it's definitely affected the plasma oncotic pressure.
So as a result, that pressure will decrease. And notice now that that then has caused a disturbance in the normal relationship between those two pressures. So in this case, we're going to see more filtration because of our reduced plasma oncotic pressure.
So this can also lead to edema. And just for interest's sake, one of the interesting things we see in patients who have liver disease that have this trouble is they develop fluid inside of their peritoneal cavity. So this is, if you were to examine this patient and push on their stomach and kind of tap it, you would actually sense that there's actually fluid in there that's just freely floating.
And that also is a result of altered Starling forces. Again, for just simply interest's sake, this is a patient who has previously undergone surgery for breast cancer. And in previous years, and this isn't done nearly as frequently now as it used to be, when a woman would have surgery for breast cancer, they would remove that breast and also remove all of the lymph nodes located in the axilla.
The lymph nodes, when you take those out, you are disrupting the lymphatics. So you're disrupting the lymphatic flow from the arm. So this is a case of edema being created, not because of a change in hydrostatic pressure or oncotic pressure, but simply because the lymphatics are blocked off and they're not able to get that fluid out, that extra fluid out, as they normally would.