Full transcript
0:05Hello everyone and welcome to our module
0:07on regulation of blood pressure. Blood
0:10pressure is the driving force for blood
0:12flow and normal blood pressure is
0:14required for profusion of tissues in the
0:16body. However, as you likely know, your
0:18blood pressure can change depending on
0:20environmental conditions. For example,
0:22when you take in more or less sodium and
0:24water, this could raise or lower your
0:25blood pressure. Turns out, however, that
0:28the body has a sophisticated set of
0:30mechanisms to keep the blood pressure
0:32relatively constant. The nervous system
0:34can modify the vascular system so that
0:36blood pressure stays relatively constant
0:38despite being in different environmental
0:40settings where blood pressure might go
0:42up and down for other reasons. In order
0:45for your brain to be able to control
0:46blood pressure, it first must sense the
0:49blood pressure. And the way this is done
0:50in the body is through structures called
0:52barrow receptors. Barerrower receptors
0:55are found in a number of places in the
0:56body and they can be stretched when
0:58blood pressure rises and when they are
1:00stretched they send more signals to the
1:02central nervous system in the brain and
1:04therefore the brain knows what your
1:05blood pressure is. The brain can then
1:07respond via the autonomic nervous
1:09system, the sympathetic and
1:10parasympathetic systems to modify blood
1:13pressure and keep it relatively constant
1:15over time. There are a number of ways
1:17that the autonomic nervous system
1:18modifies blood pressure. The autonomic
1:20nervous system can change the heart rate
1:22and the contractility of the left
1:23ventricle. The nervous system can modify
1:26arterial tone. The degree of vasoc
1:28constriction and vasoddilation can raise
1:30or lower the blood pressure. The
1:32autonomic nervous system can also modify
1:34the venus tone. So your veins hold lots
1:37of blood volume under normal
1:38circumstances. When those veins
1:40constrict, we say that the body has
1:42increased venus tone. And this pushes
1:44blood volume out of the veins and into
1:46the heart and raises the preload to the
1:48left ventricle. And then finally, barrel
1:50receptors are also found in the kidneys
1:52and the kidneys can release more rein
1:54when the blood pressure changes and they
1:56want to maintain a normal blood
1:57pressure. The major barrel receptors
1:59that I'll talk about in this video are
2:01those that are found in the aortic arch
2:03and the corateed sinus. These barrel
2:05receptors are important for quick
2:06responses to changes in blood pressure.
2:09They allow a rapid response of the body
2:11via the autonomic nervous system. There
2:13are also barrel receptors found in the
2:15kidneys which can modify renin release.
2:17These are part of a slower response to
2:19changes in blood pressure via the renin
2:21angotensin eldoststerone system which I
2:23talk about in detail in some of the
2:25kidney videos. If you look at this
2:27drawing I've shown in the screen here,
2:28this is the aortic arch and this is
2:30where the aortic arch barrel receptors
2:32are found and they can send signals to
2:34the brain to modify the output of the
2:37autonomic nervous system. It turns out
2:39that the barrel receptors in the aortic
2:41arch are best at sensing elevated blood
2:43pressure. When your blood pressure
2:44rises, that's when these barrel
2:46receptors are most effective. They have
2:49relatively poor sensing of low blood
2:50pressure. Basically, when your blood
2:52pressure falls below the normal range,
2:54these barrel receptors aren't able to
2:56modify their signaling very much and
2:57therefore they do a poor job of telling
2:59the brain when there is very low blood
3:01pressure. The other barrel receptors are
3:03found in the corateed sinus shown here
3:05on the drawing. These are the most
3:06important barrel receptors overall.
3:08These barrel receptors can modify their
3:10signals to the brain over a much wider
3:12range of blood pressure compared with
3:14the aortic arch and they are useful
3:16therefore for sensing both low and high
3:18blood pressure and directing the
3:20autonomic nervous system to respond.
3:22Shown on this slide is a schematic of
3:24how the body responds to changes in
3:26blood pressure. And I'll use this
3:28schematic to talk about a number of
3:29different physiologic situations. So
3:32your blood pressure is sensed by the
3:34aortic arch and the corateed sinus as we
3:36just described. Those signals from those
3:38barrel receptors are sent through the
3:40brain via apherrant fibers. Anytime you
3:42hear of an aphrant nerve fiber that is a
3:44fiber that is arriving at the brain with
3:46information. The corateed sinus sends
3:49its signals via cranial nerve 9, the
3:51glossal fangial nerve. The aortic arch
3:53sends its signals via cranial nerve 10,
3:55the vagus nerve. Once those signals
3:57arrive in the brain, the sympathetic and
4:00parasympathetic branches of the
4:02autonomic nervous system are modified to
4:04respond. Those systems respond via
4:06epherent fibers. Anytime you hear of an
4:08epherent nerve fiber, that is a nerve
4:10fiber exiting the brain. You can just
4:12remember apherent for arrives and
4:14epherent for exits. The portion of the
4:17brain that senses these signals coming
4:19from barrel receptors in the corateed
4:21sinus and aortic arch is called the
4:22nucleus solitarius and it's found in the
4:24medulla. It sends signals via those
4:27epherent fibers of the autonomic nervous
4:29system that direct the response to
4:30changes in blood pressure. These are
4:32responses like constriction or dilation
4:34of veins and arteries or changes in
4:36heart rate and contractility.
4:38So let's go through some physiologic
4:40changes and talk about how this system
4:42responds. So first let's imagine that
4:44your blood pressure goes up. Maybe
4:46you're very angry at someone and your
4:47blood pressure starts to get high. How
4:49will the body respond? Well, first of
4:51all that high blood pressure is sensed
4:52in the kidney which can modify salt and
4:55water retention via the renanotens and
4:57eldoststerone system. That's a much
4:58slower response and not a major part of
5:01the quick response to short-term
5:02elevations in blood pressure. The faster
5:05responses come from the aortic arch and
5:07the corateed sinus which will both sense
5:09the high blood pressure and signal the
5:11brain via the vagus nerve and the
5:12glossopringial nerve. The sympathetic
5:15and parasympathetic systems will then
5:16respond and what they will do is
5:18arteries will dilate. This will bring
5:20the blood pressure down. Veins will
5:22dilate. This will pull more blood in the
5:24venus system and reduce the preload to
5:26the left ventricle and that will lower
5:28the blood pressure. And in the heart,
5:30these systems will lower the heart rate
5:31and decrease the contractility. So the
5:33combined effect of all these changes is
5:36that your blood pressure will then be
5:37brought down once it is sensed by these
5:39systems. Now let's talk about what
5:41happens when there is hemorrhage and
5:43loss of blood. This will lower the blood
5:45pressure and the system will respond to
5:46the drop in blood pressure. So how will
5:48this take place? First of all, the
5:50kidneys will sense the fall in blood
5:51pressure and they will respond by
5:53modifying the renin eldoststerone system
5:55to increase salt and water retention.
5:57This is slow and takes longer time to
5:59occur. The quicker response occurs
6:02through the nervous system. So remember
6:03the aortic arch is not great at sensing
6:05low blood pressure. So it won't be able
6:07to sense low blood pressure very well.
6:09But the corateed sinus is very good at
6:10sensing low blood pressure and it will
6:12modify signals to the brain via the
6:14cranial nerve 9, the glossopringial
6:16nerve. This will lead to an alteration
6:19in the output of the autonomic nervous
6:20system. So veins will constrict and they
6:22will push blood volume into the heart.
6:24Arteries will constrict and this will
6:26raise the blood pressure. And in the
6:27heart, the sympathetic nervous system
6:29will raise heart rate and contractility.
6:30And this will also try to combat the
6:32fallen blood pressure that occurs in the
6:34setting of hemorrhage. These systems can
6:36also be modified by corateed massage. So
6:39if you press on a patient's neck and
6:41massage the corateed sinus, you will
6:43trick the corateed sinus into thinking
6:45the blood pressure is high. Basically
6:47you are manually stretching those barrel
6:49receptors the same way they would be
6:50stretched if the blood pressure was high
6:52and in some cases this happens to
6:54patients when they are shaving or
6:55buttoning a tight shirt and actually
6:57patients can faint because of the
6:58response of this system. So let's go
7:00through that response now. So when you
7:02massage the corateed sinus you trick the
7:04system into thinking that the blood
7:06pressure has been raised. This is sensed
7:08by the aortic arch and the corateed
7:09sinus and then the brain responds
7:11through the autonomic nervous system the
7:13same way it responds to high blood
7:14pressure. or veins dilate, arteries
7:16dilate and the heart rate and the
7:17contractility fall. So all of these
7:19things can reduce the blood pressure and
7:21that's the reason that patients
7:22sometimes have syncopy when they press
7:24on their corateed sinus. One of the ways
7:26that physiologists initially determined
7:28how this system works was by performing
7:30studies on animals where they oluded the
7:32corateed artery. This would trick the
7:34corateed sinus into thinking the blood
7:36pressure was low. So let's talk about
7:38how one of these corateed occlusion
7:39studies would work. So if you olude the
7:42corateed artery you will trick the body
7:44into thinking blood pressure is low at
7:45the corateed sinus. So the corateed
7:47sinus will sense the low blood pressure
7:49and send signals via the glossophrenial
7:51nerve to the brain. The output of the
7:53autonomic nervous system will be
7:54modified and what the body will do is
7:56constrict veins to send blood volume
7:58back to the heart constrict arteries and
8:00also raise the heart rate and
8:01contractility. So the net effect of
8:03oluding a corateed artery is that the
8:05heart rate goes up, blood vessels
8:06constrict and the blood pressure rises.
8:09You can also affect this system by
8:11severing cranial nerve 9. This can
8:13sometimes occur accidentally during
8:14surgery. So when you do this, the
8:16corateed sinus will stop sending signals
8:18to the brain and that will trick the
8:20brain into thinking that the blood
8:22pressure is low and the brain will
8:23respond the same way it always does to
8:25low blood pressure by constricting veins
8:27and arteries and raising the heart rate
8:28and contractility. So the result of
8:30severing the glossophringial nerve is
8:32that the heart rate will go up, the
8:34blood vessels will vasoc constrict and
8:35the blood pressure will rise. And just
8:37for completeness sake, let's talk about
8:39what would happen if you severed cranial
8:41nerve 10. If this happened, the aortic
8:43arch would not be able to transmit
8:45signals to the brain. And this could
8:47lead the brain to think that there was
8:48low blood pressure. But remember what I
8:50said before that the aortic arch barrel
8:52receptors do a relatively poor job of
8:54signaling the brain that there is low
8:55blood pressure. So this really wouldn't
8:57have much effect on this system overall
8:59in terms of tricking the brain into
9:00thinking there is low blood pressure.
9:02The main consequence of severing cranial
9:04nerve 10 is that you disrupt
9:06parasympathetic intervation to the heart
9:09and the stomach. This is a procedure
9:10called a veattomy. It leads to unopposed
9:13sympathetic cardiac stimulation. So
9:15basically at rest your heart wants to
9:17beat at about 110 or 120 beats per
9:19minute, but it does not because it's
9:21constantly stimulated at a low level by
9:23the vagus nerve and that makes the
9:24resting heart rate about 70 to 80. If
9:26you disrupt the vagus nerve, then the
9:28resting heart rate will rise. In
9:31addition, if you disrupt a vagus nerve,
9:32there's no parasympathetic intervation
9:34to the stomach, and this shuts down acid
9:36production. Years ago, before there were
9:39ulcer medications, patients would have a
9:41veattomy. In other words, surgeons would
9:43cut their cranial nerve 10 in order to
9:45shut down acid production in the stomach
9:47in an attempt to improve ulcers. But the
9:50big picture here to remember is that
9:51severing cranial nerve 10 has very
9:53little effect in the system overall
9:55because the aortic arch isn't good at
9:56signaling low blood pressure. The main
9:58effect is to cut off parasympathetic
10:00intervation to the heart and the
10:01stomach. Now let's talk about coronary
10:04blood flow because blood flow in the
10:05coronary arteries has some special
10:07properties. So shown on the screen here
10:09is a classic slide that you can find in
10:11many physiology textbooks. At the top of
10:13the image is the aortic pressure and you
10:16can see that when the QRS complex occurs
10:18cy begins and the aortic pressure rises
10:21and this is when most blood flow in
10:22organs in the body occurs. As the
10:24pressure rises that's more driving
10:26force. And so if you look at blood flow
10:28through most organs in the body, it
10:29occurs in cy. The coronary arteries are
10:32special. This is coronary blood flow
10:34shown at the bottom of the screen.
10:35During cy which is right here, you
10:37actually have relatively low flow in the
10:39coronary arteries. And most of the blood
10:41flow in the coronary arteries occurs
10:42here, which is in diastily. That's very
10:45unusual. The reason for this is because
10:47when the mocardium contracts in cy, it
10:50actually diminishes blood flow. That's
10:51why you see this funny shape to the
10:52curve here. and then blood flow goes up
10:55to a higher level in diastily. So the
10:57coronary arteries are special in that
10:59most of the blood flow occurs in
11:00diastilly. This also means that when the
11:03heart is tacocartic for example in the
11:05setting of infection or trauma diastily
11:07is shorter. There's less time spent in
11:09diastilly. So blood flow in the coronary
11:11arteries actually declines in the
11:13setting of tacicardia because of less
11:15time in diastily. For this reason the
11:18blood vessels have to respond by
11:19vasoddilating and we'll talk more about
11:21that in a minute. Shown on the left side
11:23of the screen is a drawing of the
11:25coronary arteries. Note that they sit on
11:26the outside of the heart. This is called
11:28the epicardium. Furthest away from the
11:30epicardium is the subendocardium. This
11:33is this layer on the inside of the
11:35chambers of the heart like the left and
11:37right ventricle. It's important that you
11:38understand that the coronary arteries
11:40are out here and the subendocardium is
11:42the furthest away from those vessels.
11:44This means that the subendocardium
11:46receives relatively less blood flow
11:48compared to the epicardium. And
11:50importantly, the subendocardium is the
11:51most vulnerable to eskeeia. If there's a
11:54fallen coronary blood flow, as occurs in
11:56anga and other eskeemic syndromes, the
11:58most vulnerable portion is the
12:00subendocardium. This layer here on the
12:02inside of the chambers of the heart.
12:04This table lists some special features
12:06of the blood flow to different organs.
12:08So the lung receives 100% of the cardiac
12:10output. Remember, all of the cardiac
12:12output goes through the lungs and then
12:14it drains to the left atrium and left
12:15ventricle and then goes to the body. The
12:17liver receives the largest portion of
12:19the systemic blood flow of any organ.
12:22The kidneys receive the highest blood
12:24flow by weight. And then finally, the
12:26heart is famous as the organ that
12:27extracts the most oxygen from blood. The
12:30heart extracts about 80% of the oxygen
12:32from blood. What this means is that when
12:35the heart has increased demand for
12:36oxygen, it cannot meet that demand by
12:38taking more oxygen out of the blood
12:40because it's already maximally doing
12:41that. Therefore, the only way the heart
12:43can increase oxygen supply is through
12:45vasoddilation. This is the major
12:47mechanism by which the heart increases
12:49the blood delivery to the myioardium.
12:53Some tissue beds and organs in the human
12:55body have a special property called
12:56autoregulation that allows these organs
12:59to maintain constant blood flow over a
13:01range of blood pressures. So in these
13:03organs when blood pressure goes up this
13:05transiently increases the flow but that
13:08increase in flow is sensed by the organ
13:10and in response blood vessels vasoc
13:12constrict and bring the flow back down
13:14to the normal range and the way these
13:16tissue beds and organs work is that they
13:18use the levels of local metabolites to
13:19sense the blood pressure and the blood
13:21flow and they use that to modify the
13:23degree of vasoc constriction. So what
13:26you would expect to see if you grafted
13:27blood flow versus blood pressure. For
13:29example, if blood pressure were on the
13:30x- axis and flow were here. What you
13:33should see is as blood pressure goes up,
13:34flow should go up because blood pressure
13:36is the driving force. But in these
13:38organs, what you see is that as blood
13:40pressure goes up, flow is constant. And
13:41the reason is because of autoregulation.
13:44Shown on this table are some organs in
13:46the body and some details about how they
13:48autoregulate. So the heart and the brain
13:50are famous as excellent autoregulators.
13:53The heart can sense levels of carbon
13:55dioxide, adenazine and nitric oxide. And
13:57the brain can sense carbon dioxide and
13:58pH levels. And these two organs use
14:01these elements in the bloodstream to
14:02determine the blood flow. And they vasoc
14:04constrict or vasoddilate to keep blood
14:06flow constant. The kidneys are also
14:08excellent at autoregulation. The kidneys
14:10can sense blood pressure. I mentioned
14:12earlier that the kidneys have barrel
14:14receptors. The kidneys can also sense
14:16the amount of sodium chloride being
14:18delivered to the maculadensa. And
14:19through both of these mechanisms, the
14:21kidneys can maintain constant blood flow
14:23over a range of blood pressures. The
14:25lungs have some unusual local factors
14:28that lead to autoregulation. When there
14:29is hypoxia in the lungs, this leads to
14:31vasoc constriction. This is a unique
14:33property of the lungs. Most tissue beds
14:35vasoddilate in the setting of hypoxia to
14:38bring in more blood, but not the lungs.
14:40The idea here is that when there is
14:41hypoxy in the lungs, the lungs do not
14:43want blood flow going to those regions
14:45because they may not have adequate
14:46ventilation. Skeletal muscle can
14:49autoregulate by sensing levels of
14:50lactate, adenazine and potassium. And
14:53then finally I want to mention the skin.
14:55So the skin has poor autoregulatory
14:57capacity. Basically blood flow in the
14:59skin is very dependent on blood pressure
15:01in the body. The only exception I want
15:03to mention here is that the sympathetic
15:04nervous system interervates the skin. So
15:06when your sympathetic nervous system is
15:08activated, your skin can become cool
15:10because the skin has intervation by the
15:12system and vasoc constriction occurs.
15:15The last topic for this video is
15:16capillary fluid exchange. So, as you
15:19know, blood flows into capillaries in
15:20the body and then exits the capillaries
15:22into the Venus system. And as blood
15:24moves through those capillaries, blood
15:26and tissue elements need to move into
15:28and out of the capillaries. So, what
15:29forces control this movement? Well, it
15:32turns out there are two forces that
15:34drive fluid into or out of capillaries.
15:36The first force is called the
15:37hydrostatic pressure. This is denoted by
15:40a capital letter P. And down in my
15:42drawing here, I've got a capillary and
15:43the surrounding interstatial space. P
15:46subc denotes the hydrostatic pressure in
15:48the capillary. P subi denotes the
15:50hydrostatic pressure in the interstitial
15:52space. The hydrostatic pressure is the
15:54pressure generated by molecules against
15:56the capillary walls. This is like your
15:58blood pressure. And this pressure tends
16:00to be higher in the capillary than in
16:01the interstitial space. So it tends to
16:03push fluid out of the capillaries. The
16:05second of the two forces that control
16:07fluid movement into and out of
16:08capillaries is the anotic pressure which
16:11is denoted by pi shown in my drawing.
16:13I've got pi subc here for the enotic
16:16pressure in the capillaries and pi subi
16:18out here for the enotic pressure in the
16:19interstitial space. Solutes especially
16:22albamin are found in the capillaries and
16:24they tend to draw fluid into the
16:26capillaries. Albumin cannot cross out of
16:28the capillaries. So it gets stuck behind
16:30and there's a lot of albumin in here and
16:32that tends to draw fluid in. So this
16:34enotic pressure tends to be higher in
16:36the capillaries and lower in the
16:38interstitial space and it resists the
16:40movement of fluid out of the
16:41capillaries. So what we've got is
16:43hydrostatic pressure pushing fluid out.
16:46Anotic pressure resisting that movement
16:48out and trying to hold fluid in. The
16:49balance of these two forces determines
16:51whether fluid will move into capillaries
16:53and out of tissue beds or out of
16:55capillaries and into tissue beds. So
16:57I've summarized these points on this
16:59slide to emphasize them. Hydrostatic
17:01pressure is the pressure of fluid
17:02pushing against the walls like walls of
17:04the capillaries. And high pressure which
17:06is found in the capillaries tends to
17:08drive fluid toward lower pressure which
17:10is found in the interstitial space.
17:12Anotic pressure is pressure generated by
17:14solutes pulling fluid in. And high
17:17pressure draws fluid away from low
17:19pressure. And this is something that's
17:20confusing about enotic pressure. So in
17:23the case of enotic pressure, a high
17:25pressure draws fluid toward it, not away
17:27from it. As is the case with hydrostatic
17:29pressure. You're probably used to
17:30thinking that fluid moves away from high
17:32pressure towards low pressure. That's
17:34the case for hydrostatic pressure. But
17:35the opposite is true when we describe
17:37onotic pressure. So if you look at my
17:40drawing at the bottom of the screen, we
17:41can actually write an equation for the
17:42net pressure across the capillary walls.
17:45And this net pressure is going to
17:47determine whether fluid moves out of the
17:48capillaries or into the capillaries. So
17:51net pressure is equal to the hydrostatic
17:53pressure difference PC c minus pi plus
17:57the anotic pressure difference pi i
17:59minus pi c. And then we can say that the
18:01flow will be equal to that net pressure
18:04times some factor that has to do with
18:06the permeability of the capillaries. We
18:08call that k subf. So you may find this
18:10easier to understand if we just put some
18:12numbers in. So if we say that PC is 100
18:14and PI is 50 and PIC C is 50 and pi I is
18:1830 then the net pressure difference is
18:2050 minus 20 or 30. So we have a positive
18:23net pressure which means fluid is going
18:25to move on balance out of the
18:27capillaries because the hydrostatic
18:29pressure driving fluid out is 50 and the
18:31enotic pressure pulling fluid in is only
18:3420. And then if we multiply that net
18:36pressure of 30 by a permeability factor
18:38KF, we could determine the flow. No one
18:40ever actually does this and calculates
18:42the flow. This is just to give you a
18:43concept of all the different factors
18:45that can dictate fluid movement into or
18:47out of capillaries. And one of the major
18:50clinical applications of the principle
18:52of capillary movement is edema. This is
18:54very common in a number of disorders.
18:56Edema occurs when there is excess fluid
18:58movement out of capillaries. This leads
19:01to tissue swelling. If you have excess
19:03movement out of capillaries in the lungs
19:05that causes pulmonary edema. This occurs
19:07in heart failure and a number of other
19:09conditions. If you have excess movement
19:11of fluid out of the systemic
19:13capillaries, then gravity will draw all
19:15that fluid down to the ankles and the
19:17lower extremities and you will get lower
19:18extremity edema as shown in this picture
19:20here. That also occurs in heart failure
19:22and some other disorders. And all of
19:24these problems have to do with
19:26alterations of those variables leading
19:28to excess movement out of the
19:30capillaries and into tissue beds. So
19:32many students find this equation at the
19:34top of the screen confusing. Luckily,
19:36you don't really need to know it. All
19:37you need to know is what happens in
19:39different pathologic conditions to
19:41modify this equation and drive fluid out
19:44of capillaries. So when the capillary
19:46hydrostatic pressure goes up P subc that
19:49leads to pulmonary edema and lower
19:51extremity edema. That's what happens in
19:53heart failure and I talk about this in
19:54the heart failure videos. If you have a
19:57loss of plasma proteins, you will get a
19:59very low PI subc. That can happen in the
20:01nefotic syndrome and liver failure where
20:04you have low levels of proteins in the
20:05blood. If the permeability of the
20:08capillary to fluids becomes increased
20:10that can lead to edema and that's what
20:13happens when patients are exposed to
20:14toxins or when they have certain types
20:16of infections or burns. In all these
20:18situations capillary permeability rises
20:21and that's the mechanism of edema
20:22formation. And then finally if you have
20:25increased interstitial osmotic pressure
20:27pi subi this will tend to draw fluid out
20:30of the capillaries and cause edema. And
20:32that's what happens when there's an
20:33obstruction of the lymphatic system. All
20:36the proteins in the interstitial space
20:38drain into the lymphatic system. If it's
20:39obstructed, proteins will build up out
20:42here and that will draw fluid out of the
20:43capillaries. I'll finish with this slide
20:46and mention a term that you will hear
20:47many times on your clinical rotations
20:49and that term is third spacing. This is
20:51a term we use to describe when patients
20:53have excess capillary leak for any
20:55reason. So this term gets its name
20:57because the intracellular fluid is said
20:59to be the first space. That's about
21:01twothirds of your body fluid. The
21:03extracellular fluid is the second space.
21:05It's about onethird of your body fluid.
21:07So the third space are spaces in the
21:09body where fluid should not be. They
21:11normally have no body volume, but they
21:13will accumulate fluid in certain
21:15pathologic conditions. So on your
21:16clinical rotations, you will hear
21:18residents and attendings say this
21:20patient is third spacing. And what they
21:22mean is fluid is moving into places
21:23where it should not be. For example, the
21:25patient may have plural eusions or
21:27ascites or cerebral edema. They may have
21:30low intravascular volume but high total
21:32volume because all of the volume is
21:34found in the tissue beds. And there are
21:36a number of systemic inflammatory
21:38conditions like the posttop state or
21:39sepsis where basically all the
21:41capillaries in the body begin to leak
21:43and that's when third spacing occurs. So
21:45I say this to you now just so you've
21:46heard this term when you get to your
21:48clinical rotations. And that concludes
21:50our video on regulation of blood