Full transcript
0:05Hello everyone and welcome to our module
0:07on blood flow mechanics.
0:09There are lots of mathematical equations
0:11that describe the flow of fluids through
0:14vessels like blood vessels in the body.
0:16But there are basically two that have
0:18importance when it comes to
0:19cardiovascular physiology. So the first
0:21important equation that has to do with
0:23blood flow through vessels is simply
0:25called the flow equation and it deres
0:27from Ohm's law. So you probably learned
0:29Ohm's law as it relates to electricity
0:31in a physics class, but it also relates
0:33to fluid mechanics and blood flow. So
0:35Ohm's law says that the voltage in an
0:37electrical circuit is equal to the
0:39current I times the resistance R. This
0:42is just basically a simple expression of
0:44a fact that if you want to drive flow
0:47through a system, whether it's
0:48electricity or fluid flow, the amount of
0:51energy you need, that's the voltage, is
0:52equal to how fast you want to go, that's
0:54the current, times the resistance to
0:56flow, that's R. So we can modify Ohm's
0:58law and apply it to fluid flow like the
1:00flow of blood through a blood vessel.
1:02And if we apply it to fluid flow, the
1:04change in pressure in a system is equal
1:06to the flow rate Q times the resistance
1:08R. And this equation is often applied to
1:11the body as a whole because the entire
1:12cardiac output flows through the body as
1:14a whole. And therefore the resistance to
1:16flow is equal to the total resistance of
1:19blood vessels in the body. And we'll
1:20talk more about this later on in this
1:23video. So when we're talking about the
1:24body as a whole, the change in pressure
1:26as blood flows through the body is equal
1:28to the cardiac output times what's known
1:31as the TPR. TPR is total peripheral
1:34resistance. It's the sum of the
1:36resistances to flow of all the vessels
1:38in the body. So if we put this all
1:40together, we get the flow equation which
1:41says delta P equals cardiac output time
1:44TPR. And we'll be coming back to this
1:46more and more throughout the course of
1:47this video. And just to make this more
1:49clear, let's imagine that we have a
1:51blood vessel. And let's imagine that we
1:52have a pressure of 10. As blood flows
1:54into the vessel. And let's imagine that
1:56when blood flows out of the vessel, we
1:58have a pressure of five. This change in
2:00pressure of five is equal to the flow
2:03rate Q, the flow rate of fluid moving
2:05through that vessel times the resistance
2:07R. That's the flow equation. And we're
2:09going to come back to this more and more
2:10as we go through this video today. The
2:13second equation that's important for
2:15physiologic flow of blood through the
2:17body is simply a geometry equation. So
2:20the velocity of blood moving through
2:22blood vessels times the area of the
2:24blood vessels is equal to the flow rate.
2:26So this is just a mathematical
2:28geometrical sort of equation. The
2:30velocity in meters/s time the area in me
2:33squar equals the flow rate in meters
2:35cubed/s. So just like the flow equation,
2:38we'll come back to this geometrical
2:40equation later on in this video. Now
2:42let's talk about two important concepts
2:44that relate to the flow of blood through
2:46vessels in the body. And those are the
2:47concepts of resistance and compliance of
2:49blood vessels. When blood flows into a
2:52blood vessel, some of those vessels are
2:54very very stiff, sort of like a lead
2:56pipe. Other vessels are very distensible
2:58and stretchy and they can stretch to
3:00absorb the fluid as it moves through the
3:02vessel. Vessels that are very stiff have
3:04a high resistance to flow and they also
3:07have a low compliance. The term
3:09compliance means the distensibility of
3:11vessels and resistance and compliance
3:13are related. So stiff vessels have a
3:16high resistance to flow and a low
3:17compliance. They are not very stretchy
3:19at all. Stretchy vessels have a low
3:21resistance to flow and a high
3:23compliance. And these are the two
3:24concepts of resistance and compliance
3:26that are important to blood flow
3:28mechanics. High resistance vessels tend
3:30to have a low compliance and vice versa.
3:32One of the classic applications of the
3:34concept of compliance to cardiovascular
3:36physiology is the pulse pressure. The
3:39pulse pressure is the systolic blood
3:40pressure minus the diastolic blood
3:42pressure. And in a normal patient with a
3:44blood pressure of 120 over 80, the pulse
3:46pressure would be equal to 40. It turns
3:49out as we age, older patients develop an
3:51increase in the pulse pressure. It also
3:53turns out that patients with
3:55hypertension develop an increase in the
3:56pulse pressure. And the reason for this
3:58is because older patients and
4:00hypertensive patients have a change in
4:02their vessel compliance. They have
4:04decreased compliance of their blood
4:05vessels and this leads to a rise in the
4:08pulse pressure. To understand this
4:09better, you need to appreciate that the
4:11compliance of a blood vessel can
4:13actually be calculated as the change in
4:15volume divided by the change in
4:17pressure. So let's consider a stiff
4:19blood vessel which as we said before has
4:20a very low compliance. These types of
4:23vessels have a high pulse pressure. So
4:25why is that the case? That's because a
4:27small change in volume is all you get
4:29for a given pressure applied to the
4:31walls. Let's look at this equation at
4:33the bottom of the screen here. So the
4:35compliance is equal to the change in
4:36volume in a blood vessel divided by the
4:38change in pressure. If we rearrange this
4:41for the delta P, we see that the delta P
4:43is equal to the change in volume divided
4:45by the compliance. Now any blood vessel
4:48needs to get a constant change in volume
4:50through that vessel. Think about your
4:52body. You need to get your entire
4:53cardiac output through your body, no
4:55matter what the compliance of the
4:56vessels is. So if you want to get that
4:58same change in volume through a set of
5:00blood vessels that has a very low
5:02compliance, the only way you are going
5:04to do this is by raising the change in
5:06pressure as blood moves through that
5:08vessel. So by this equation, you can see
5:11that when the compliance goes down, the
5:13delta P for a blood vessel must go up in
5:15order to move the same volume through
5:17that blood vessel. And that's why the
5:18pulse pressure increases when you have
5:21stiff vessels that have low compliance.
5:23The opposite is true for stretchy
5:24vessels. Stretchy vessels have a high
5:26compliance and they tend to have a low
5:28pulse pressure. That's because you get a
5:30large change in volume for any given
5:31pressure applied to the walls. And
5:33here's one more way you can think about
5:35this to keep it straight in your mind.
5:37The pulse pressure varies with vessel
5:38compliance as we've been talking about.
5:40And stiff vessels have a low compliance.
5:42So, let's imagine we've got a very
5:44distensible vessel, a stretchy vessel,
5:46and we shove a bunch of blood into that
5:48vessel. Well, because the vessel is
5:50stretchy, it can absorb the blood volume
5:52without increasing the pressure so much.
5:54So, we get a normal blood pressure and a
5:56normal pulse pressure like 120 over 80
5:58with a pulse pressure of 40. Now, let's
6:01imagine we've got a very stiff rigid
6:02vessel. You tend to find vessels like
6:04this in older patients and patients with
6:06hypertension. Well, now when we shove
6:08this blood volume in, the vessel cannot
6:10stretch and distend. Therefore, the
6:11pressure inside the vessel goes up a
6:13lot. These molecules are being packed
6:15close together because the vessel cannot
6:17stretch. Therefore, we get a higher
6:19pulse pressure and we get a blood
6:20pressure like 170 over 100 with a pulse
6:23pressure of 70. This is what you see in
6:25older patients and patients with
6:26hypertension. It all ties back to the
6:28concept of compliance. Now, let's go
6:31back to that flow equation I talked
6:33about at the beginning of this module
6:34and talk in more detail about the
6:36concept of total peripheral resistance.
6:38So, like I told you at the beginning of
6:40this video, the flow equation states
6:42that delta P is equal to blood flow
6:44times resistance. And when we're talking
6:46about the entire body, the blood flow
6:48through the entire body is the cardiac
6:50output. And the resistance to flow, the
6:52resistance contributed by all the
6:54vessels and organs in the body is called
6:55the total peripheral resistance. And
6:58anytime this total peripheral resistance
7:00goes up, it means the heart has to
7:02generate more pressure to maintain flow.
7:04In other words, if peripheral resistance
7:06goes up and we want to keep the cardiac
7:08output constant, then we have to raise
7:10the driving pressure. And when the heart
7:12needs to create more pressure, it means
7:13the heart has to do more work. So
7:15anytime the peripheral resistance goes
7:17up, anytime the total peripheral
7:18resistance of the body increases, the
7:20heart has to do more work to drive the
7:22normal cardiac output through the body.
7:24So just to emphasize this point, when
7:26it's easy to push blood out of the
7:28heart, less oxygen is required by the
7:30myioardium. When there's an increase in
7:32the resistance to blood flow through the
7:34body, in other words, when the total
7:35peripheral resistance goes up, then the
7:37heart has to do more work and the heart
7:39needs more oxygen. So, what are the
7:41things in the body that affect the total
7:43peripheral resistance? In other words,
7:45what makes it harder for blood to flow
7:47out of the heart and through the body?
7:48Well, the first thing is the types of
7:50vessels, the pipes and tubes. The second
7:52thing is the thickness of blood, and
7:54this is called the blood viscosity. So,
7:56there are many different types of
7:58vessels in the human body. Some of them
8:00have a very high resistance to blood
8:01flow and others have a very low
8:03resistance to blood flow. And the way
8:05you can best appreciate this is by
8:07looking at the pressure change as blood
8:09flows through vessels in the body. So as
8:12blood leaves the heart and flows through
8:13the aorta, the blood pressure falls to
8:16about 100 millimeters of mercury
8:18systolic. As that blood moves into the
8:21large arteries, there's only a tiny
8:22change in pressure, just a few
8:24millimeters of mercury. And this is
8:25because the large arteries provide very
8:27little resistance to flow. But remember
8:29what I said before, when there's high
8:31resistance to flow, you're going to have
8:33a high delta P or a big pressure change.
8:36If you've got a very low resistance to
8:38flow, there'll be a very small pressure
8:39change. And that's the case in the large
8:41arteries. As that entire cardiac output
8:43moves from the large arteries to the
8:45small arteries, there's a pressure
8:47change of about 10 to 20 millimeters of
8:49mercury. But the biggest pressure change
8:51occurs when blood passes through the
8:53arterials. The pressure change across
8:55the arterials is about 35 mm of mercury.
8:58And I've highlighted this in red because
9:00you should remember that the arterials
9:02are the set of vessels in the body that
9:04provide the greatest resistance to flow.
9:06They are said to be resistance blood
9:07vessels and the pressure change will
9:09always be highest across the arterials
9:11compared to other types of blood vessels
9:14that also see the entire cardiac output
9:16move through them. So I've summarized
9:18these points on this slide. The
9:20arterials are said to be the resistance
9:21vessels. They are the major determinant
9:23of the total peripheral resistance.
9:25There's a large pressure drop or large
9:27pressure change as blood flows across
9:29these vessels. And as you may know, the
9:32autonomic nervous system can modify the
9:34arterials and shrink them. That's called
9:36vasoc constriction or enlarge them.
9:38That's called vasoddilation. And when
9:40these vessels shrink, the resistance
9:41goes up even more. And when these
9:43vessels dilate, the total peripheral
9:45resistance falls. Viscosity is the
9:48thickness of blood. Think about the
9:50difference between water and maple
9:52syrup. Water has relatively low
9:54viscosity and therefore it flows easily
9:56through a vessel with low resistance to
9:58flow. Maple syrup on the other hand is
10:00thick and sticky and therefore it has
10:02more viscosity and greater difficulty
10:04flowing through a blood vessel. There
10:06will be more resistance to flow when
10:07pushing something like maple syrup
10:09through a blood vessel. Most of the
10:11blood in our body is made up of water
10:12and the viscosity is relatively low. But
10:14there are a couple of pathologic
10:16conditions where the viscosity may be
10:18higher or lower and this can affect the
10:20resistance to flow. So first of all,
10:22patients who are anemic have relatively
10:24fewer red cells in their blood and this
10:26can lower the viscosity and therefore
10:28lower the resistance to blood flow. A
10:31number of pathologic conditions create a
10:32high viscosity situation. First of all,
10:34polyythemeia. Patients with polyythemeia
10:37have excess red cells and sometimes also
10:39white blood cells and platelets and this
10:41can raise the viscosity of blood and
10:43increase the resistance to flow. The
10:45same is true in multiple myyoma.
10:46Patients with this condition have lots
10:48of extra proteins in their blood and
10:49therefore the viscosity of blood can go
10:51up. And then finally, spherocytosis is
10:54sort of famous for being a high
10:55viscosity situation in terms of blood
10:57flow mechanics. Patients with
10:59spherocytosis have red blood cells that
11:01form spheres instead of the normal by
11:03concave disc. These cells are more rigid
11:05and they don't deform normally as they
11:07move through capillaries. That makes it
11:08harder for blood to move through the
11:11vasculature and that raises the
11:12viscosity of blood and the resistance to
11:14blood flow. Puazul was a French
11:17mathematician and he created Puazoul's
11:19law which describes how the resistance
11:21to flow varies with certain elements of
11:24a system and this law applies to blood
11:26flow through the human body. So remember
11:28that the flow equation says the change
11:29in pressure is equal to the flow rate
11:32times resistance. We can rearrange this
11:34equation and solve for resistance to
11:36flow and state that it's equal to the
11:38pressure change divided by the flow
11:39rate. Well, Poul's law further relates
11:42that resistance to various elements of a
11:44system. So, Pazu's law says that
11:46resistance is equal to 8 * the viscosity
11:49time the length of the tubes that blood
11:51is flowing through divided by pi * the
11:54radius of the blood vessels to the
11:56fourth power. So, we've already talked
11:58about how when viscosity goes up,
12:00resistance to flow goes up. And that
12:01fits with puzzle's law. The other
12:04important element of Puzzle's law is the
12:06radius here. Remember, radius is in the
12:08denominator and it's raised to the
12:09fourth power. So changes in radius have
12:12a very powerful effect on resistance.
12:15When the radius of a blood vessel falls,
12:17the resistance to flow is going to go up
12:19a lot because radius is to the fourth
12:21power. When the radius to flow
12:23increases, then the resistance to flow
12:25is going to fall significantly once
12:27again because radius is raised to the
12:29fourth power.
12:31Now let's talk about series and parallel
12:34circuits. So the organs in the human
12:36body are arranged in parallel and this
12:38is a very good thing because by
12:40arranging organs in parallel you greatly
12:43reduce the resistance to flow and this
12:45makes the heart more efficient because
12:47it doesn't have to generate so much
12:48blood pressure. So when blood leaves
12:51your heart if our organs were arranged
12:52in series the blood would then go to the
12:55kidneys for example and then to the gut
12:57and then to the liver and then it would
12:58all come back to the heart. This would
13:00be bad because the resistance to flow in
13:02this system would be very very high.
13:04Instead, what happens is that blood
13:05leaves the heart and then it branches
13:07and flows through organs in parallel.
13:09So, some goes up here for example
13:11through the kidneys, some goes here
13:12through the gut, some goes down here and
13:14goes through the liver and then it all
13:16comes back together to re-enter the
13:18heart and go to the lungs. These organs
13:19are arranged in parallel and that is a
13:21much lower resistance to flow compared
13:23to in series and that makes things
13:25easier for the heart. We can describe
13:27this mathematically because resistances
13:30to flow add up differently when
13:32structures are arranged in series
13:34compared to in parallel. So structures
13:36arranged in parallel have a total
13:38resistance that obeys this equation here
13:41where one over the total resistance
13:42equals 1 over the resistance of the
13:45first structure plus one over the second
13:47structure. In series, resistances add up
13:49such that R total equals R1 + R2. So
13:53this is easier to understand if we put
13:55some numbers in. So let's suppose that
13:56we have two structures with a resistance
13:59of two and two. We'll just arbitrarily
14:01assign them to number two. What's the
14:02total R? Well, if we arrange these
14:05structures in parallel like the human
14:06body, then 1 / R total equals 1 /2 + 1
14:09over2. And if you solve this, R total is
14:12equal to 1. Now, if we put those two
14:14structures in series, R total is R1 plus
14:17R2, which is 2 plus 2 plus 4. So look at
14:19this. The same organs with the same
14:21resistance if arranged in parallel have
14:24a resistance of one. If arranged in
14:26series, the resistance is four times
14:28higher. So once again, parallel
14:30arrangement of structures is much more
14:32efficient because it lowers the
14:33resistance to flow. And this is why the
14:35human body is set up this way. Now let's
14:38go back to the flow equation that we
14:39talked about at the beginning of this
14:41video. Delta P is equal to flow rate
14:43times resistance. And let's talk about
14:45how you can use this to calculate
14:47resistance cardiac output or delta P for
14:50the body and the lungs. This is the way
14:52that the flow equation is often applied
14:54to the body and the lungs. And the
14:56reason it's so often applied to these
14:57two systems is because for both of these
14:59systems, Q is the cardiac output. The
15:01entire cardiac output goes through the
15:03lungs and obviously the entire cardiac
15:04output goes through the body as a whole.
15:06So we can use the flow equation to
15:09estimate cardiac output or if we know
15:11the cardiac output, we can use the flow
15:13equation to estimate what the pressure
15:15change or the resistance is. So if we're
15:18going to apply the flow equation to the
15:20body as a whole, the pressure change as
15:22blood moves through the body as a whole
15:24is equal to the pressure in the aorta.
15:26In other words, the arterial pressure
15:28minus the right atrial pressure. After
15:30blood has moved through all the organs
15:32and vessels in the body, it returns to
15:33the heart at a pressure equal to the
15:35right atrial pressure. The resistance
15:37for the body as a whole, as I said
15:38before, is the total peripheral
15:40resistance. You should know that it's
15:41also sometimes called the systemic
15:43vascular resistance or SVR. These two
15:45terms mean the same thing. And then if
15:48we're talking about the lungs, the
15:49pressure change as blood moves through
15:50the lungs is equal to the pressure in
15:52the pulmonary arteries minus the
15:54pressure in the left atrium. After blood
15:56moves through the lungs, it returns to
15:58the left atrium at a pressure equal to
16:00the left atrial pressure. And the
16:02resistance as blood moves through the
16:03lungs is called the pulmonary vascular
16:05resistance or PVR. Now, there's a
16:07problem with what I've written on the
16:09screen here. As you may know, a normal
16:11arterial pressure in the body is about
16:13120 over 80. So, what number are we
16:16going to use for the arterial pressure?
16:18We need a single number to plug into the
16:20flow equation. The same problem comes up
16:22in the pulmonary arteries. The normal
16:24pulmonary artery pressure is about 24
16:26over 12. So what single number are we
16:28going to use for the flow equation? This
16:31is not so much of a problem in the right
16:32atrium or the left atrium. Pressure
16:34fluctuates slightly in the right atrium,
16:36but it's very close to a single number
16:39pressure of about six or five or so. In
16:42the left atrium, the pressure also
16:44fluctuates very slightly, but it's very
16:46close to a mean number of about 10 or
16:48so. So we don't have so much of a
16:49problem in the atria, but we do have a
16:51problem in the arteries. we need a
16:52single number to plug into the flow
16:54equation. So if we're going to use the
16:56flow equation and we need a value for
16:58the systemic arterial pressure or the
17:00pulmonary arterial pressure, we need to
17:03calculate the mean arterial pressure.
17:05And you might think that the mean
17:06arterial pressure should be halfway
17:08between the systolic and diastolic
17:10pressure. But it turns out that's not
17:11the case. The reason for this is because
17:13our body spends more time in diastilly
17:15than in cy. So the mean arterial
17:18pressure is calculated from the equation
17:20that mean arterial pressure is equal to
17:22diastolic blood pressure plus 1/3 of the
17:25difference between systolic and
17:26diastolic pressure. So for the total
17:29body if a patient had a normal arterial
17:31blood pressure of 120 over 80. The mean
17:34arterial pressure would be 80. That's
17:35the diastolic pressure plus 1/3 of the
17:38difference between 120 over 80 which is
17:4040. And this would work out to 93. If
17:42we're talking about the lungs and let's
17:44suppose a patient had a pulmonary artery
17:46pressure of 40 over 20, the mean
17:48pulmonary artery pressure would be 20
17:50plus 1/3 of 20 and that equals 27. So
17:52this is how you calculate a mean
17:54arterial pressure and this is what you
17:55need to do to use the flow equation for
17:57the lungs or the body because the
17:59pulmonary artery pressure and the
18:00systemic arterial pressure fluctuate a
18:03lot. You need a single number to plug
18:04into the flow equation. So now let's
18:07talk about how we would actually use the
18:09flow equation to estimate some values
18:12for the total body. So for the total
18:14body, the resistance is the total
18:15peripheral resistance. The change in
18:17pressure as blood flows through the
18:19total body is equal to the mean arterial
18:21pressure minus the right atrial
18:23pressure. And just to make this very
18:25clear, blood leaves the heart to go
18:26through the total body with a pressure
18:28of the mean arterial blood pressure. The
18:31blood then flows through the entire
18:33body. It flows through all the organs in
18:35the body and then the blood goes back to
18:36the heart and the pressure when it comes
18:38back to the heart is equal to the right
18:39atrial pressure. So the delta P is the
18:42difference between these two values. So
18:44suppose we have a normal cardiac output
18:46of 5 L per minute. And then let's
18:48further suppose that a patient has a
18:49blood pressure of 155 over 80 which
18:52gives a mean arterial pressure of 105.
18:54And then let's suppose the right atrial
18:56pressure is five. From these numbers we
18:58can calculate the total peripheral
19:00resistance. It's equal to the delta P
19:02divided by the cardiac output. This is
19:04all according to the flow equation.
19:06That's equal to the mean arterial
19:07pressure minus right atrial pressure
19:09divided by 5, which is 105 - 5 over 5 or
19:1220. And in board exams, they're always
19:14going to give you numbers that work out
19:15very easily just like these. Notice that
19:17all the numbers you can basically
19:18calculate without a calculator and get
19:20an answer for the total peripheral
19:21resistance. We can do the same thing in
19:24the lungs. So in the lungs, the
19:25resistance is the pulmonary vascular
19:27resistance. The delta P is pulmonary
19:29artery pressure minus left atrial
19:30pressure. If we're given a cardiac
19:32output of five and a pulmonary artery
19:34pressure of 40 over 10, the mean
19:36pulmonary artery pressure is 20. The
19:38left atrial pressure is given as five.
19:40We can then calculate the pulmonary
19:42vascular resistance. And if you plug all
19:43these numbers in, you will get a PVR
19:45that's equal to three. And in many
19:47disease states, the PVR goes up. And
19:49there are many disease states where the
19:50TPR goes up or down. So this is why this
19:52flow equation is important. It helps us
19:54understand those disease states. And
19:57here I've summarized the variables that
19:58you need in order to apply the flow
20:00equation to either the lungs or the
20:02total body. So for both the lungs and
20:04the body, the flow rate is the cardiac
20:06output. The resistance to flow is PVR in
20:08the lungs and TPR in the body. The
20:11starting pressure as blood enters the
20:13system for the lungs is the pulmonary
20:14artery pressure. In the body, it's the
20:16mean aortic pressure. The ending
20:19pressure which is the pressure as blood
20:20exits the system is the left atrial
20:22pressure for the lungs and it's the
20:24right atrial pressure for the body. And
20:26then finally the delta P across the
20:28lungs is the mean pulmonary artery
20:29pressure minus left atrial pressure. For
20:31the body it's the mean aortic pressure
20:33minus right atrial pressure. Now let's
20:35go back to that geometric equation I
20:37described at the beginning of this video
20:38that relates velocity and area to flow
20:40rate. So like I talked about before flow
20:43rate in meters cub/s is equal to
20:45velocity in meters/s time me squared.
20:49And it turns out that area and velocity
20:51change as blood moves through different
20:53types of vessels. So the entire cardiac
20:56output has to move through the aorta and
20:57all the arterials and all the
20:59capillaries and all the veins. All of
21:01these systems have the same flow rate.
21:03In other words, the same volutric flow
21:05rate of the cardiac output. But the
21:07different types of vessels have
21:08different areas and therefore different
21:10velocities. And anytime the area for
21:12flow rate goes up, the velocity must go
21:14down according to this equation. So
21:17let's look at this table I've placed on
21:18the screen here describing the flow
21:20properties of different types of blood
21:22vessels. Flow is the same through all
21:24the types of blood vessels. There's no
21:26set that has higher or lower flow. All
21:28the types of blood vessels, arteries,
21:29veins, capillaries, have the entire
21:31cardiac output flowing through them. The
21:33total area for flow, however, is
21:35different through different vessel
21:36types. The capillaries it turns out have
21:39the highest area for flow. Even though
21:40capillaries are very very small there
21:42are millions of them in the body and
21:44therefore the total area is very high.
21:46What this means is by this equation when
21:48the area goes up in the capillaries the
21:50velocity goes down. So the velocity in
21:53meters/s of blood flow through the
21:55capillaries is very slow and that's
21:57actually very helpful for gas exchange.
21:59The lowest area for flow is in the large
22:01arteries. This is counterintuitive.
22:03These are large vessels, so you might
22:04think they have a high area for flow,
22:06but they're actually relatively few of
22:08them. So when you sum up the total area,
22:10it's the smallest of all the different
22:11vessel types. Velocity is highest,
22:14therefore in the large arteries and
22:16lowest in the capillaries. It's
22:17basically the reverse of the situation
22:19for area. The resistance to flow, as I
22:21told you before, is highest in the
22:23arterials. Those are resistance vessels
22:25and they have the therefore the highest
22:28pressure drop as blood flows through
22:29them. The lowest resistance to flow is
22:31in the veins and therefore the smallest
22:33pressure changes as blood flows through
22:34the veins. The most important thing to
22:36know about the veins is that they hold a
22:38large volume of blood. They are
22:39basically a storage basin for blood and
22:42therefore in situations of volume loss,
22:44the veins can constrict and push more
22:46blood to the heart to help keep the
22:47volume status of the body normal. The
22:49last topic for this module is the law of
22:51lelass. The law of lelass explains the
22:54determinance of wall tension or wall
22:56stress. It can be applied to a blood
22:58vessel but in this module we're going to
22:59talk about how it applies to cardiac
23:01chambers like the left ventricle. The
23:03reason the law of lelass is important
23:05for understanding the left ventricle of
23:07the heart is because anything that
23:08raises the wall tension in the left
23:10ventricle will raise myocardial oxygen
23:12demand and this can potentially cause
23:14eskeemia or anga. So the law of lelass
23:17states that the wall tension of the left
23:19ventricle is proportional to the
23:21pressure generated by the left
23:22ventricular chamber times the radius of
23:24the left ventricle divided by 2 * the
23:26wall thickness. The letter h is used to
23:28denote wall thickness. So now let's talk
23:31about some pathologic processes that can
23:33raise the wall tension in the left
23:35ventricle via the law of lelass.
23:37Anything that raises the afterload of
23:39the left ventricle will increase the
23:40pressure that must be generated by the
23:42left ventricular chamber. This occurs in
23:44the setting of hypertension and aortic
23:46stenosis. These are the two classic
23:48conditions that raise the afterload on
23:50the left ventricle. Via the law of
23:52lelass when the afterload goes up and
23:54the pressure that must be generated by
23:56the left ventricle goes up the wall
23:57tension will rise because pressure is in
23:59the numerator. So when it goes up the
24:01wall tension goes up. This means that
24:03the mioardial oxygen demand of the left
24:05ventricle will be increased in the
24:07setting of these conditions like
24:08hypertension and aortic stenosis via the
24:10law of lelass. This is called pressure
24:12overload of the left ventricle. If the
24:15preload on the left ventricle rises
24:17significantly, this can stretch the
24:18chamber and increase the radius of the
24:20left ventricle. This will increase the
24:23wall tension via the law of lelass
24:24because when the radius goes up, the
24:26wall tension goes up. This is called
24:27volume overload of the left ventricle.
24:29The two classic conditions that cause
24:31this problem are chronic valvular
24:33disease from aortic or mitro
24:34regurgitation. In both of these valvular
24:36disorders, blood is leaking through
24:38either the aortic or mitro valve and
24:40therefore the left ventricle has greater
24:42preload and this can lead to increased
24:44wall tension via the law of lelass. The
24:46law of lelass also explains left
24:48ventricular hypertrophy which is a
24:50compensatory mechanism of the left
24:51ventricle to decrease the wall tension
24:53in the left ventricular chamber. Anytime
24:56the wall thickness goes up according to
24:58the law of lelass, wall tension will go
25:00down. The force inside the left
25:01ventricular chamber is distributed over
25:03more mass when left ventricular
25:05hypertrophy occurs. And this is commonly
25:07seen in settings of chronic pressure or
25:09volume overload. In my field of
25:11cardiology when we take images of the
25:12heart of patients who have aortic
25:14stenosis or hypertension or chronic
25:16valvular disease, we see increased
25:18thickness of the walls of the heart.
25:20That is hypertrophy which is a
25:22compensatory mechanism of the left
25:23ventricle. There's lots of basic science
25:25research that looks at the cellular
25:27mechanisms by which wall tension drive
25:29the myioytes to hypertrophy. You don't
25:31need to know all that for step one, but
25:33you do need to be aware that when the
25:34left ventricle hypertrophies, it lowers
25:36the wall tension and compensates for the
25:39increased pressure or volume overload
25:40occurring inside the chamber.
25:43Now, it turns out that there are two
25:45ways by which the left ventricle can
25:47hypertrophy in disease states and it's
25:49very high yield to understand these. So,
25:51let's talk about this now. The first way
25:53the ventricle hypertrophies is called
25:55eccentric hypertrophy. And in eccentric
25:58hypertrophy basically what happens is
26:00the myioytes in the left ventricle
26:01become longer. And the reason they
26:03become longer is because more sarcimeirs
26:05are added and they are added in series.
26:08Let's look at my drawings on the screen
26:09here. On the left side of the screen
26:11I've drawn a normal LV cavity of normal
26:13size and it's got some sarcimeir
26:15present. When eentric hypertrophy occurs
26:18the LV cavity becomes dilated and the
26:21myioytes become longer. So if you were
26:23to weigh this heart in the middle of the
26:24screen, it would weigh more than the
26:25normal heart. That's because there is
26:27hypertrophy and the left ventricular
26:29mass is increased. However, if you
26:31measure the thickness of the walls, the
26:33wall thickness is not increased. And
26:35that's because the new sarcimeirs are
26:37being added in series. The myioytes are
26:39growing longer, but they're not becoming
26:40thicker.
26:42This type of hypertrophy classically
26:44occurs in situations where there is
26:46volume overload of the left ventricle.
26:48basically when the left ventricle is
26:50flooded with blood volume. And the two
26:52classic valve conditions that cause this
26:54are aortic regurgitation and mitro
26:56regurgitation. You can also see
26:58eccentric hypertrophy in many forms of
27:00cardiammyopathy including eskeemic
27:03cardiopathy and non-eskeemic
27:04cardiopathy. So when my patients with
27:06heart failure who have a reduced
27:08ejection fraction develop hypertrophy,
27:10the type of hypertrophy they usually
27:12have is eccentric hypertrophy. The
27:14second type of hypertrophy is called
27:16concentric hypertrophy. In contrast to
27:19eccentric hypertrophy, this typically
27:21occurs when the ventricle is pressure
27:23overloaded and there are chronically
27:25high pressures in the ventricle. If you
27:27look at the drawing on the bottom of the
27:29screen here, we've once again got our
27:30normal left ventricle on the left side
27:32of the screen. In concentric
27:33hypertrophy, you get something like what
27:35I've shown in the middle of the screen.
27:36Once again, left ventricular mass is
27:38increased. However, in this case, the LV
27:41cavity size is smaller, and that's
27:43because these walls have become thicker.
27:45And the reason they've become thicker is
27:46because sarcimeirs are added in
27:48parallel. We've got increased myasy
27:50size, but in this case, it's because
27:51sarcimeir are added in parallel and
27:53therefore the wall thickness goes up.
27:55And remember, in eccentric hypertrophy,
27:57the wall thickness does not increase.
27:59So, the two classic causes of concentric
28:01hypertrophy are systemic hypertension
28:03and aortic stenosis. In both of these
28:06conditions, the pressure inside the left
28:08ventricular cavity gets very high and
28:10that leads to concentric hypertrophy. No
28:12one really understands the biochemical
28:14mechanisms that lead to eccentric
28:16hypertrophy in some cases and concentric
28:18hypertrophy in other cases. But the
28:20bottom line is these high pressure
28:22disorders like hypertension and aortic
28:24stenosis are associated with concentric
28:26hypertrophy. In addition, anytime you
28:28have concentric hypertrophy and thick
28:30walls of the left ventricle, you get
28:32decreased compliance and a stiff
28:34ventricle. And for that reason in many
28:36cases of diastolic heart failure which I
28:38talk about in the heart failure section
28:39you see evidence of concentric
28:41hypertrophy when you do imaging of the
28:43heart. And that concludes our video on
28:45blood flow mechanics.