http://www.youtube.com/watch?v=OP4Xh4oawG8

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How do the differences in hydrostatic and osmotic pressures affect the flow of blood within the circulatory system and to the different parts of the body? What is filtration pressure and how are these affected during abnormal conditions such as having a high blood pressure?

Watch and learn with Leslie as he explains further about this topic. Have fun!

Transcript of Today’s Episode

Hello and welcome to another episode of Interactive-Biology TV where we’re making Biology fun! My name is Leslie Samuel and in this episode, Episode 058, I’m going to be talking about “Net Hydrostatic Pressure and Filtration Pressure.” Let’s get right into it.

Now, we’ve been looking at the circulatory system and we’ve shown that the blood leaves the heart and then, it goes via the aorta to the arteries and then, to the capillaries, to the venules, to the veins and then, to the vena cava, and then, ultimately, back to the heart. If you need a review of that, you can always check out Episode 054 where we go into more detail about that.

What we’re going to be doing today is we’re going to be looking at what happens between the arterioles, the capillaries, and the venules. That’s what we’re showing here. We have an artery leading to the arteriole and then, that goes to the capillary bed and then, that goes via the venules to the vein. What we’re going to look at is what happens specifically right here. The goal here is we want to get blood coming to the tissues delivering nutrients and so on, oxygen to the tissues and then, taking stuff away. So, taking away waste and so on.

What I’m going to do here is I’m going to simplify this a little bit. I’m going to show this like this. I’m going to take from the arterioles to the venules. I’m going to simplify it showing one arteriole that connects to one capillary, and then, that’s going to connect to one venule. I’m simplifying this significantly. Here we have the arteriole, here we have the venule, and here we have the capillary (I’m not going to put the ‘c’ here, but, here we have the capillary).

The main things that we’re going to focus on are the different pressures that we have in this setup. Now, of course the heart is pumping and the blood is coming in this direction, and then, it’s going via the capillaries. This is where the exchange happens because this is where we have the tissue and, this is where we want to get stuff delivered and we want to pick up stuff to take away from the tissues.

The first thing we’re going to talk about is ‘net hydrostatic pressure.’ I’m just going to write NHP for net hydrostatic pressure. When we’re talking about hydrostatic pressure, we are talking about pressure due to the fluids. Of course, in the blood we have fluids. In the tissue we also have fluids. The net hydrostatic pressure, as the blood is coming in here, of course there’s going to be a blood pressure because the heart is beating, it’s pumping the blood, and we’ve looked at blood pressure in previous episodes, and as the blood goes through the capillaries, there’s going to be friction that it’s encountering. It’s going to be bumping against the walls of the capillaries, and that is going to actually reduce the pressure. What we’re going to end up with is a high amount of pressure here and that’s going to drop down as we go along the capillaries. But, not only that, we have tissue here that’s filled with fluid also and that’s also going to exert a pressure on the capillaries.

The net hydrostatic pressure, we’re talking about the total hydrostatic pressure, that is going to be equal to the blood pressure, so the blood is pumping out, and we’re going to subtract the tissue pressure. So, the blood pressure, how much it’s pumping out and how much it’s pushing in from the fluids in the tissues. That net hydrostatic pressure is going to be greatest going out closer to the arterioles. So, we have a lot of hydrostatic pressure pushing out and, as we go down, and the blood is bumping against the walls and so on, that amount of pressure is going to decrease. This is what I’m illustrating here, it’s going down, going down, and when I reached to the end, we’re going to have the least amount of hydrostatic pressure which makes sense, as I said before, the blood is coming via the arteries to the arterioles. It’s coming because the heart is pumping it, and with that pumping we’re going to get a lot of pressure.

That’s going to be highest here, but, because this tube is so small, we have a tiny tube almost to the point that the blood cells can only get through one at a time. That is going to cause a lot of friction, and that is going to decrease the amount of pressure. If I take something and I push it across a surface, because there’s going to be friction with that surface it’s going to slow down. And, that’s exactly what we’re getting here. The amount of pressure is going to decrease as we go away from the arterioles and towards the venules. So, the net hydrostatic pressure is what we’re looking at here.

We’re going to get stuff leaving, but, not everything can leave. Blood cells aren’t going to leave but, water is small enough to get through the pores in the capillaries. So, water is going to leave. It’s going to take some oxygen with it. It’s going to take nutrients with it and so on. That is going to leave the capillaries which is exactly what we want because we want to deliver that stuff to the tissues or to the muscles or to whatever it is this capillary is going through. This is a good thing but, as the water is leaving, of course, we’re going to get less and less water inside the capillaries. Because of that, we’re going to have a change in osmotic pressure. Now, if you remember osmosis is the movement of water across a selectively permeable membrane. We have a selectively permeable membrane here.

What is going to happen is water leaves here, there’s going to be a little bit of osmotic pressure for water to come back in. As more water leaves, we’re going to get an increase in osmotic pressure and then, we’re going to get an even greater increase in osmotic pressure. That’s going to continue of course, and this is exactly what we’re going to see.

As the net hydrostatic pressure goes down, the net osmotic pressure is going to increase and increase and increase. When we take this together, we’re going to get the filtration pressure, (I’m going to write FP), and that’s going to be equal to net hydrostatic pressure minus net osmotic pressure: FP = NHP – NOP. These are not the official symbols. This is just what I’m writing for simplification. But, you can see that we’re going to get a filtration pressure. If we’re over here and we’re taking this hydrostatic pressure minus this osmotic pressure, we’re going to see that we’re going to have a net filtration pressure moving stuff out. That’s going to decrease as we go here to where in the center, the filtration pressure is going to be zero because we have this amount coming out and this amount going in. And, just to make that more equal, I’m just going to draw the rest of that arrow here. Then, of course, as we go down here, we have more pressure, going in, the osmotic pressure is significantly greater, so, we’re going to get a filtration pressure that’s pointing into the capillaries, moving stuff in.

So, over here, we’re moving stuff out. Over here, we’re moving stuff in. And if I were to draw a graph, I’m just going to draw a graph over this, I’m not sure why I did that as a dotted line, this is the y-axis and we’re dealing with filtration pressure, and let’s say this is the zero line. What we’re going to have is a filtration pressure that looks something like this. Here we have it moving out, so it’s going to be somewhere around here, and of course, that’s going to go down to zero at this point, and then, continue going down, showing that we have a negative filtration pressure or in other words, a pressure moving stuff into the capillaries. Here is ‘moving out of’ and here we’re ‘moving stuff into.’

This point right here, where we have a filtration pressure of zero, that is called the ‘dynamic center.’ This is where the net hydrostatic pressure is equal to the net osmotic pressure — equal but, and opposite of course — and that is called the dynamic center. In a perfect world, this dynamic center is exactly where we want it to be so that, we have a good amount of distance for stuff to leave and a good amount of distance for stuff to come in. So, we’re delivering the nutrients and the stuff that we need to the tissue, and we’re taking away the waste and the stuff that we don’t want sending that away from the tissues.

I want to look at a different scenario, where we have the same setup. We have the arteriole, the capillary and the venule going back to the veins, and vena cava, and back to the heart. But, in this situation, we’re going to be dealing with someone that has high blood pressure. So, here, we’re going to have a significant amount of net hydrostatic pressure pushing stuff out. So, it’s much higher. What that’s going to do, as you can see here is the pressures are going to be greater all the way along. Yes, it’s decreasing but, because we’re starting with a higher amount, we’re also going to end with a higher amount.

We also have the osmotic pressure doing the same thing that it was doing before and, stuff is leaving, and let’s say, we have it here, and this is kind of extreme and let’s say that because of this high blood pressure, we still have the filtration pressure here, we have the osmotic pressure here. But, the dynamic center, instead of being over in the center, the dynamic center is somewhere around here. Now, that is a significant problem because this is what we have. In this entire section we have this fluid leaving and, it’s not until here that we have a net amount of fluid coming in. What’s that going to do is it’s going to cause more fluid to be leaving than the amount of fluid that’s coming in, and that is going to result in accumulation of fluid in the tissues or, we can also call that, edema. So, this can be a result of high blood pressure because we have more fluid leaving the capillaries than coming into the capillaries. We have more going towards the tissues and that can cause a significant amount of problems resulting in edema.

So, the take home message, net hydrostatic pressure is blood pressure minus tissue pressure. That’s what we’re showing here. And, if we want to find the filtration pressure, we take net hydrostatic pressure minus net osmotic pressure. That will give us that filtration pressure. To this side of the dynamic center, the filtration pressure is moving fluids and dissolved molecules out of the capillaries. As we come to this side, it’s moving fluids into the capillaries. If we have high blood pressure, that can shift the dynamic center significantly resulting in accumulation of the fluids in the tissues or edema.

That is pretty much it for this episode. As usual, I’d like to invite you to visit the website at Interactive-Biology.com for more Biology videos and other resources. That’s it for this video and I’ll see you on the next one.

http://www.youtube.com/watch?v=DfAyZwsIYR4

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Here is an interesting concept about pressure reflexes that you might want to watch. It is related to the mean arterial pressure of a man. Learn more by watching another one of Leslie’s easy videos to help you understand these concepts easier.

Have fun!

Transcript of Today’s Episode

Hello and welcome to another episode of Interactive-Biology TV where we’re making Biology fun! My name is Leslie Samuel and in this episode, Episode 57, I’m going to talk about, ‘Pressure Reflexes and Mean Arterial Pressure.’ We’ve been talking about mean arterial pressure a lot, we’ve spoken about cardiac output and peripheral resistance. You can always revisit previous episodes to find out more about them.

Today, we are talking about pressure reflexes. We’ll look exactly at why we call it pressure reflexes. Here we have the heart (I feel like I keep saying that in very episode recently) and the heart, it pumps the blood throughout the body. We have the aorta.

One of the arteries that I have not been talking about would be the carotid artery. This is the common carotid. I’m just going to come here and draw a line here and say, that we’re dealing with carotid arteries. Of course, here, we are dealing with the aorta.

There is something very special that we have in these two arteries. In both the aortic and the carotid bodies, we have receptors that we call ‘baroreceptors.’ From the time you hear the prefix ‘baro-,’ you should know that it has something to do with pressure. For example, a barometer measures pressure and, here we have baroreceptors and these baroreceptors respond to changes in, you guessed it! Pressure. That is why they are called baroreceptors.

What’s going to happen is, if we have an increase in the mean arterial pressures, so we have a significant increase in mean arterial pressure, what that’s going to do, these baroreceptors are going to start firing. We’re going to have an increase in the firing of these baroreceptors. In other words, they’re going to be sending signals. Those signals are going to a region in the brain stem that we call the medulla. This is known as the “blood pressure regulating center.” Of course, it regulates other things but, it also regulates pressure.

That then, is going to cause a combination of two things. It’s going to cause an increase in parasympathetic activity and going to cause naturally a decrease in sympathetic activity. If you remember from one of the early episodes, sympathetic activity causes stuff like increase in heart rate, increase in blood pressure, and so on. Parasympathetic activity calms stuff down so, it reduces blood pressure, it reduces heart rate, breathing rate, and so on. So, we have an increase in mean arterial pressure, so an increase in blood pressure, the baroreceptors are going to respond by sending signals to the medulla. That’s going to cause an increase in parasympathetic activity, calming stuff down, and a decrease in sympathetic activity. Sympathetic activity would normally increase pressure, and speeds stuff up but, here we’re slowing that down. So, the net result of these two things is we’re going to get a reduction in cardiac output and also in peripheral resistance. Then, of course, that is going to cause a reduction in mean arterial pressure.

This is why we call it a reflex because we have an increase in mean arterial pressure, and that’s going to cause a number of things that’s going to eventually cause a reduction in mean arterial pressure. The relationships between these quantities here, we’ve looked at a number of times, and, just to revisit that:

M.A.P. =CP x PR,

Mean arterial pressure is equal to cardiac output times peripheral resistance. Since we’re decreasing both cardiac output and peripheral resistance, we are also going to decrease mean arterial pressure.

That’s pretty much it for this episode. Of course, you can always visit the website at Interactive-Biology.com for more Biology videos, more Biology resources, and more Biology fun. That’s it for now and I’ll see you in the next one.

http://www.youtube.com/watch?v=MRcra9oxrXY

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Here is the second part of Regulating Peripheral Resistance. Leslie explains two more ways on how it can be influenced and how it affects someone’s blood pressure and mean arterial pressure. Watch to learn more!

Have fun!

Transcript of Today’s Episode

Hello and welcome to yet another episode of Interactive-Biology TV where we’re making Biology fun! My name is Leslie Samuel and in this episode, Episode 56, I’m going to continue talking about, ‘Regulating Peripheral Resistance.’ This is part 2, and I think this is going to be the final part about this. So, let’s get directly into the content for today.

In the last episode, we emphasized, we re-emphasized the fact that mean arterial pressure is equal to cardiac output times peripheral resistance (M.A.P. = CO x PR). We’ve spoken about the fact that we are modifying peripheral resistance. We’re looking at the different ways in which peripheral resistance is influenced. In the last episode, you can go back to Episode 55, we spoke about vasoconstriction and we said that that is going to cause an increase in peripheral resistance. We spoke about vasodilation which is going to cause a decrease in peripheral resistance.

We’re going to talk about two other ways in which we can influence peripheral resistance. The first way that we are going to talk about today is called, blood viscosity. By viscosity what I mean is basically the thickness of the blood. This is very logical.

For example, a few weeks ago I was in Colombia and we remember we went to a restaurant and I ordered a mango milk shake. The milk shake was very, very, very thick. I was sucking on the straw trying to get it out and it was really hard to get that mango, I mean it was a very good tasting mango milkshake but, it was hard to get it in my mouth because of how thick it was.

This is the same thing. The thicker the blood is, the more resistance we’re going to have to blood flow. If we increase blood viscosity, we’re going to increase peripheral resistance significantly. By the viscosity, specifically, I am talking about the ratio of RBCs (red blood cells) to the blood plasma:

RBCs : plasma

By plasma, we’re basically talking about the fluid. If we have more red blood cells, or we increase the ratio of red blood cells to plasma, we are increasing the thickness of the blood. So, the overall message is, and let me just divide this in two, if we increase blood viscosity, that of course is going to result in an increase of peripheral resistance. On the other hand, if we (let’s use a different color), decrease blood viscosity, that is going to cause a decrease in peripheral resistance.

What is an example of a way we can increase blood viscosity? Well, for example if we are dehydrated. What that’s going to do is it’s going to reduce the amount fluid in the blood, so the plasma is going to be less. That is going to cause an increase ratio of red blood cells to the plasma, we’re going to have an increase in blood viscosity, and that’s going to cause an increase in peripheral resistance.

What can cause decrease in blood viscosity? For example, loss of blood volume due to anemia or if there’s hemorrhage, that’s another example (forgive my R’s… My students always make fun of me for my R’s). If there’s anemia or hemorrhage, that’s going to cause a decrease in blood viscosity causing a decrease in peripheral resistance. So, the first that we’re looking at today is by influencing blood viscosity.

The second way is by looking at the total blood vessel length. The message here is, the longer the blood vessels, the higher is the peripheral resistance. So, if you increase the blood vessel length, you are going to naturally increase peripheral resistance. That should also make sense. If something is much longer, you have a tube that’s very long, it’s going to be much harder to get the blood through. If my straw for my mango shake was extremely long, let’s say that straw was two-feet long, that would take a lot of work for me to get that great tasting mango shake into my mouth because it’s longer, increase in peripheral resistance.

Now, how would this translate to the human being? I’ll give you a very good example in America and other places also. If someone is overweight, what that’s going to do is that’s going to naturally increase blood vessel length. I’m going to give you some numbers right now that can be very disturbing. Or, it can’t be very disturbing depending on how you look at it. If you gain 2.2 pounds of weight of additional fat, that is going to add approximately, and this is very scary, 400 miles of blood vessels. That’s one kilogram of fat and approximately 650 kilometers of blood vessels. So, you can see, by gaining weight, you’re gaining more blood vessels. That’s basically increasing the blood vessel length, and that is going to increase peripheral resistance. And we know what increase in peripheral resistance will do to mean arterial pressure and to blood pressure because, we keep coming back to this:

M.A.P = CO x PR

More fat, longer blood vessels, increased peripheral resistance, and that is going to cause an increase in mean arterial pressure.

I guess, the take home message for today is, watch your weight.

That’s pretty much it for this episode. As usual, I want to invite you to check out the website at Interactive-Biology.com for more Biology videos and other resources. You can join the community over there, ask your questions in the forums, and just take part in everything that we have going there. That’s it for this video and I’ll see you in the next one.

http://www.youtube.com/watch?v=14Z8GNLU4os

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As promised, here is a video focusing on peripheral resistance. Understand what it is and how it affects mean arterial pressure by watching along and listening as Leslie once again explains the concept with full clarity.

Enjoy!

Transcript of Today’s Episode

Hello and welcome to another episode of Interactive-Biology TV where we’re making Biology fun! My name is Leslie Samuel, and in this episode, Episode 55, I’m going to be talking about, ‘Regulating Peripheral Resistance,’ and this is going to be part 1. Initially, I was going to make one video about peripheral resistance, but, then I started going into it and I decided to split it up into at least two parts. So, this is going to be the first part. It might end up being two parts, it might end up being three parts. We’ll see how it all turns out.

We’ve been talking about the cardiovascular system or the circulatory system. We have spoken a lot about the heart and the blood vessels that lead from the heart and to the heart. We said that when the heart beats, and let’s say the ventricles contract, that sends the blood, if it’s the left ventricle, it sends the blood into the aorta which then sends the blood into the rest of the body. It’s going to the organs, and to the tissues. It’s taking oxygen and nutrients to the organs and the muscles, and so on. And, of course, it’s bringing waste away from the muscles and organs also.

What we’re going to do today, we’ve been talking about cardiac output, we’ve been talking about the mean arterial pressure and in the last episode, we focused on mean arterial pressure and we said that:

M.A.P. (mean arterial pressure) = CO x PR

This is one of the formulas that we use for calculating mean arterial pressure. Just as a reminder, the other one is:

M.A.P. = Diastolic pressure + 1/3 (systolic pressure – diastolic pressure)

You can go back to Episode 54 for more of an explanation on this two. We’re not going to focus on this guy right here. We are focusing on this indirectly. Why? Because today, we’re going to talk about peripheral resistance. We already defined what peripheral resistance is. Peripheral resistance is basically opposition to blood flow. Of course, you have the heart that’s beating and sending the blood through these blood vessels. But, of course, it’s not a frictionless environment. There’s going to be friction between the blood and the walls of the blood vessels that is going to cause resistance. If something is trying to get through a tube, there is resistance. This is exactly what we have here, the blood is trying to get through many tubes all throughout the body. Of course, that is going to encounter resistance. Just to give you an idea, if you were to take all of the blood vessels out of your body and just make it in one long line, it would be long enough to wrap around the globe twice. So, we have a significant amount of blood vessels going through the body. That is what peripheral resistance is.

What we are going to do is we are going to talk about how we can regulate peripheral resistance. So, I said, we have the heart and that sends the blood to the rest of the body. There are a number of different types of vessels that we can encounter. We have, of course, the aorta, and we’ve looked at this. From the aorta, it’s going to go to the arteries. From the arteries, it’s going to go to arterioles, and from the arterioles, it’s going to go to the capillaries, and then, from the capillaries, (let’s use a different color here), that’s going to take us to the venules, to the veins, and then, via the vena cava, and then, that is going to go back to the heart. That cycle continues.

When it comes to peripheral resistance, the place that we’re going to focus on will be the arterioles. The aorta and the arteries are relatively thick. Yes, they are flexible but, we don’t have much in terms of changing the diameter of these guys. The arterioles has a smooth muscle layer, a significant smooth muscle layer, that we can constrict or we can dilate. If we constrict it, the diameter is going to be smaller. If that’s the case, that is going to increase peripheral resistance. If we expand it, if we relax the muscles, we dilate the muscles, the arterioles are going to expand, and, of course that is going to decrease peripheral resistance. It’s really simple. It is harder to get something through a very narrow tube than it is to get something through a thicker tube. So, by constricting the arterioles, that is going to increase the peripheral resistance; by dilating the arterioles, that is going to decrease peripheral resistance. Just to give you a visual here. Here we have an artery. We’re delivering blood to a specific tissue whatever that is. So, we have some tissue cells here. From the arteries, it goes via arterioles and then, we have the capillaries going to the venule and then, to the vein, and as I said before, then back to the vena cava and back to the heart. The magic is happening right here in the arterioles. If we have some constriction, that is going to increase peripheral resistance. If we have dilation, that’s going to decrease peripheral resistance.

Now that we know that, let’s talk about some specific instances and some specific ways in which we can have these kinds of effect.

We’re going to look at two hormones. We’re going to look at epinephrine which is another name for adrenaline, and you’ve heard a lot about adrenaline. And, we’re also going to look at norepinephrine. So, these are the two that we’re going to look at today.

First, we’re going to focus on epinephrine. The interesting thing about these things, I’m going through one example of one pathway for each but, epinephrine, for example, in certain instances, it can be a vasoconstrictor. In other instances, it can be a vasodilator. What we’re going to do, the typical one that you hear about is the vasoconstriction. I’m going to talk a little bit about how this causes vasodilatation.

Epinephrine binds to what we call, beta-2 receptors and these are on the smooth muscles of the arterioles and then, what that’s going to do is it’s going to activate a G-protein which then is going to activate an enzyme called adenylate cyclase. What this enzyme is going to do, it’s going to take ATP, adenosine triphosphate, which is the energy currency of the body and convert that into a different form. That’s going to be a cyclic AMP. What that’s going to do is it’s going to activate calcium pumps in the cisternae of the smooth muscle cells. That is going to cause the calcium to be pumped back into the cisternae which is going to decrease calcium level. So, we’re going to get calcium decrease. If you remember from one of the earlier episodes, calcium in the muscle causes muscle contraction. If we’re decreasing the calcium, we’re not going to get contraction which would cause constriction. We’re going to get vasodilation. When we have vasodilation, of course, what that’s going to do is it’s going to decrease peripheral resistance because we have a wider tube, blood can flow much easier. So, that’s going to cause a decrease in peripheral resistance. This is one example of one way in which epinephrine can affect peripheral resistance.

Let’s talk about norepinephrine. (Let’s come over here). Norepinephrine is going to activate a different type of receptor. We’re going to call those alpha-receptors. That is going to activate a G-protein, once again. However, in this case, the G-protein is not going to activate adenylate cyclase. It’s going to activate phosphatidylinositol and then, that is going to activate the molecule IP3. That is going to do the exact opposite. That is going to cause calcium release from the cisternae. Of course, now, we have calcium release that is going to cause contraction which in this case would be vasoconstriction. Of course, then, the effect of that is going to be to increase peripheral resistance.

We’ve been looking at the formula: M.A.P. (mean arterial pressure) = CO x PR. In these situations, we are affecting PR, which is peripheral resistance and if you increase peripheral resistance, which would be the effect of norepinephrine in this specific situation, that is going to cause an increase in the mean arterial pressure. If you decrease peripheral resistance as in this situation, that is going to cause a decrease in mean arterial pressure.

So, by influencing vasodilation or vasoconstriction, what we’re doing is we are making the diameter of the blood vessels smaller or larger. That is going to influence peripheral resistance. If it’s smaller, we have more resistance. It’s harder to get stuff through. If it’s larger, it’s going to be easier to get stuff through because there’s less resistance to flow.

There’s one more thing that I want to add to this. Here we have an example of atherosclerosis and that is where we have plaque buildup in the arteries. So, here you can see the plaque, and that is building up in the arteries. What that’s going to do is, it’s going to cause for us to have a narrowed arteries. So, the diameter is going to be significantly smaller. This can happen as a result of having too much cholesterol in our diets. That’s just an example but, that is going to cause a smaller opening. Of course, if you have a smaller opening, what that’s going to do is, it’s going to increase peripheral resistance. If you increase in peripheral resistance, and we know that:

M.A.P. = CO x PR,

You increase this over here, that is going to increase the mean arterial pressure. So, you’re basically increasing the blood pressure when there is plaque in the arteries. You’re doing that by increasing peripheral resistance.

Take home message is: Watch your diet, exercise, live a healthy lifestyle, so that this doesn’t happen, so that this doesn’t go up and so that your blood pressure, your mean arterial pressure does not go up. That’s the health nugget for this lesson.

That’s pretty much it for this episode. As usual, you can visit the website at Interactive-Biology.com for more Biology videos and other resources that we’re adding over there. This is Leslie Samuel. Thank you for watching and I’ll see you on the next one.

http://www.youtube.com/watch?v=BnPdf8Te93I

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What does blood pressure really mean? What does it actually measure? Watch, listen, and learn as Leslie once again explains clearly and makes it so simple for everyone of us to understand easily about the principles behind this new episode.

Have fun!

Transcript of Today’s Episode

Hello and welcome to another episode of Interactive-Biology TV where we’re making Biology fun! My name is Leslie Samuel, and in this episode, Episode 54, I’m going to be talking about ‘Blood Pressure and Mean Arterial Pressure.’ These are the two things I’m going to cover today. Blood pressure… You know, when you go to the doctor’s office, one of the first thing they do is they take your blood pressure. And, you know what? After today, you’re going to know exactly what they’re doing and what it means, if you don’t already know. So, let’s get right into the topic for today.

Here, we have the heart. We’ve been speaking about the heart because we’re talking about the cardiovascular system or the circulatory system and the heart has a very important job. It’s pumping the blood throughout the body. The blood carries oxygen and nutrients to the muscles and to the other organs that need this in order for you to live; in order for you to do all the things that you are doing right now.

Here is the heart. If we take the heart and we put it inside the human body, you can see here, we have the human heart and it is serving the purpose of pumping the blood through these arteries, to the rest of the body. Of course, the blood is coming back via these veins to the heart. That process goes over and over. It’s also sending the blood to the lungs so that it can get the oxygen that it needs and then send that to the body and so on. We’ve kind of spoken about that in previous episodes.

Today, we want to talk about blood pressure. First, I’m going to define blood pressure and I’m going to do it simply by writing here. Here, we have the blood and over here, we have blood vessels. As the heart is beating, and it’s sending that blood out to the body, it’s going via these blood vessels, and because it’s being pumped, that is going to exert a pressure on the blood vessels. We’re going to call this pressure a ‘hydrostatic pressure.’ The reason we call it a hydrostatic pressure is because blood is a fluid, and when fluids exert pressure on something, that is called, ‘hydrostatic pressure.’ Okay, so, the blood is being pumped. It’s going through these blood vessels. It’s hitting against the walls of the blood vessels, the inner lining of the blood vessels. That is exerting a pressure on those blood vessels. This is what we mean when we say ‘blood pressure.’

When the doctor is taking your blood pressure, or the nurse is taking your blood pressure, they are checking to see how much pressure is exerted on the blood vessels by the blood. That is a very important measure when it comes to the health of your body.

When the blood leaves the heart, as we’ve shown before, the blood then goes into the aorta which is this vessel that’s leaving from the heart, and then, that goes down here. This is also the… this is called the descending aorta and it goes via these other blood vessels to the rest of the body. It would make sense to understand that the closer you are to the heart, the more you’re going to feel that pressure. If you are right by the heart, you’re going to feel more pressure than if you are all the way down here in the toes, right? Because here is where the heart is beating, and the farther away you go from that, the lower the pressure is going to be.

Let’s look at how this works. What I’m going to do is I’m going to draw a little graph here. (I just realized that I can use a ruler on my tablet which makes sense but, I just never thought about it). Here we have the y-axis and then, here, we are going to draw the x-axis. What I’m going to do is kind of chart the blood pressure as the blood is going from the heart to the, first it’s going to go via the aorta (let me write ‘aorta’), and that’s right here. As it leaves the aorta, it’s going to go to some little smaller vessels and those are called arteries. From there, it’s going to go even smaller to the arterioles. From there, it’s going to go to the capillaries (I’m just going to write here ‘cap’). That is where it actually crosses over from being in the arteries section, arteries and arterioles, to where it’s going into the veins. But, before it goes to the veins, it’s going to go via the venules and then, the veins. When it’s in the venules and the veins, it’s because it’s going back to the heart eventually via the vena cava.

We’re going away from the heart via the aorta and then, we go to the arteries. We’re going away — a very easy way of remembering this is the ‘a’ in ‘arteries,’ ‘arterioles,’ and ‘aorta’ is going ‘away’ from the heart. When it reaches the tissues and the organs, it’s going to have an exchange in the capillaries where it then goes into the venules, to the veins, and then, back via the vena cava to the heart.

Let’s look at pressure on the y-axis. I’m going to give these some values of 20 (let me just write them in here first. Okay, it’s not fully evenly spaced), 20, 40, 60, 80, 100, 120, and 140. On the y-axis we’re dealing (I’m just going to write it over here), with pressure in millimeters of Mercury (mm Hg).

When the heart contracts, we have ventricular contraction and that’s when we’re going to get the greatest amount of pressure because the ventricles are larger than the atria. When they contract sending the blood to the rest of the body, that’s going to give you the systolic pressure, which is going to be the greatest pressure. We’re going to see here, (let me draw this in… Let’s go with red), the ventricles are contracting so the pressure is going to increase significantly and then, as the atria contract, you’re going to get that little bump there. That process continues as the heart beats, continues as the heart beats. We’re in the arteries.

As we go away from the arteries and into the arterioles, what you’re going to see, we’re getting away from the heart a little bit, the pressure is going to start kind of going down, going down. As you go away, you’re going to see smaller fluctuations. You’re not getting as great of an effect. As we reach into the capillaries, it’s kind of dying down even more and the pressure is going to continue going down and down until, on the way back to the heart, there’s hardly any pressure remaining. I mean, in comparison to up here, where we had pressures of up to 120 mm Hg, or sometimes even more in this situation, in comparison, the farther away we get from the heart and as the blood is being pushed back to the heart, we don’t get these fluctuations in pressure and there’s significantly less pressure as the blood is going back to the heart.

When the doctor takes your pressure and the doctor says, “You are in excellent health. Your blood pressure is great,” what are the numbers that you usually hear? The numbers that you usually hear are 120 over 80 (120/80). What that refers to, of course at the top, we have the systolic pressure and here we have the diastolic pressure – systolic pressure and diastolic pressure. Systolic is during systole contraction so, that’s the higher point. Diastolic is during relaxation where we have a lower point. If you have that 120/80, you are a happy camper. All is well with the world, at least where your blood pressure is concerned. That is what we want to have.

That is blood pressure. When you’re measuring blood pressure, you’re measuring the difference between systole and diastole – contraction and relaxation.

Now, let’s talk a little bit about ‘mean arterial pressure.’ (I’m just going to write M.A.P. for short). Mean arterial pressure, when you hear the word ‘mean,’ you always think average. The mean arterial pressure is basically the average pressure in the arteries. We’re not looking at the fluctuations. We are looking at the average. If we were to take the average here, I’m just going to plot a second line, it would look something like this. So, straight line here and as it goes down, it’s going to look a little like this until where we have a straight line here, it follows that straight line. That gives us the average pressure in the arteries.

There’s a formula that we use to calculate mean arterial pressure. Mean arterial pressure, M.A.P., is going to be equal to CO times PR.

M.A.P. = CO x PR

Now, two of these you know already: M.A.P., mean arterial pressure; and CO, you should know that that is cardiac output. PR is one that we haven’t covered. PR is ‘peripheral resistance.’ As I said,

M.A.P. = CO x PR

We’re going to go more into peripheral resistance in the next episode so, I’m not going to deal too much with this. The main thing that you want to know is the two factors that are going to influence mean arterial pressure is cardiac output and peripheral resistance. Peripheral resistance is basically, we’re going to define that as, opposition to blood flow. The blood is flowing but, of course there’s going to be some resistance, there’s going to be friction between the blood and the walls of the blood vessels and so forth.

There’s another way of calculating mean arterial pressure. Mean arterial pressure is also equal to diastolic blood pressure, so, that’s during diastole, relaxation, plus 1/3 times systolic blood pressure minus diastolic blood pressure (my handwriting is getting kind of sloppy there but, you get the point).

M.A.P. = diastolic BP + 1/3 (systolic BP – diastolic BP)

Once again, if you’re looking at that graph where we had something kind of looking like this, in the beginning, and if this is 80 and this is 120, the mean arterial pressure is going to be equal to 80 plus 1/3 of 120 minus 80, is 40, and that’s going to be equal to 80 plus let’s see, 1/3 of 40, let’s go with 13.3, I’m just going to leave that at 13, so, mean arterial pressure would be equal to 93 mm Hg.

M.A.P. = 80 + 1/3 (40) = 80 + 13 = 93

That’s mean arterial pressure. Two ways to calculate it: Cardiac output times peripheral resistance. We’ve dealt with cardiac output, that’s the amount of blood pumped by the heart every minute and we’re multiplying that by peripheral resistance which is the opposition to blood flow. In Episode 55, we’re going to go a little more into peripheral resistance or, we can take the diastolic blood pressure plus one-third of the difference between the systolic and diastolic blood pressures which in this case would be 80 plus a third of 40 which would be approximately 13, which gives us 93 mm Hg:

M.A.P. = 80 + 1/3 (40) = 80 + 13 = 93 mm Hg

That’s pretty much it for this episode. Of course, if you want to check out some more Biology videos and other resources like quizzes and the community that we have at Interactive-Biology, you can check out the website at Interactive-Biology.com.

That’s all for now, and I’ll see you on the next one.

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Learn more about calculating cardiac output and how changing stroke volume and heart rate can increase or decrease its value.

Have fun!

Transcript of Today’s Episode

Hello and welcome to another episode of Interactive-Biology TV where we’re making Biology fun! My name is Leslie Samuel, and in this episode, Episode 53, I’m going to talk about the ‘Cardiac Output.’ I’m first going to talk about what it is and then, I’m going to talk about how to calculate it, and some of the things that are going to influence cardiac output. So, let’s get right into it.

Here, we’re looking at a picture of the heart. A diagram of the heart during systole, so it’s during contraction, ventricular contraction, and what’s happening here, is as the ventricles contract, the left ventricle is sending blood to the aorta which then goes to the rest of the body, the right ventricle of course, is sending the blood to the lungs so that, it can get oxygenated, come back to the heart and then, be sent to the rest of the body.

Now, we’re going to talk about cardiac output today so, let me write that here, ‘Cardiac Output.’ It kind of is exactly what it sounds like. Cardiac output is talking about the volume of blood that’s being ejected from the ventricles every minute. So, we’re talking about the amount of blood that’s being sent from the left ventricle to the rest of the body via the aorta, and also we’re talking about the amount of blood that’s being sent from the right ventricle to the lungs. You expect those to be the same or else that can lead to some other problems. That we’re not going to get into in this episode.

Right now, we are just going to try to look at how to calculate cardiac output. It’s a pretty simple formula and it involves two things that we’ve already looked at in previous episodes. Cardiac output is equal to SV, which is stroke volume, times HR, which is heart rate:

CO = SV x HR

Now, stroke volume tells you the amount of blood that’s ejected with each beat. So, we’re talking about milliliters of blood per beat, and then, with heart rate, we’re talking about how many times the heart is beating in one minute. So, we calculate that as beats per minute. So, stroke volume is the amount of blood ejected from the ventricles, let’s say the left ventricle in each beat, with each beat. And, the heart rate tells us how many times the heart is beating, how many times the ventricles are contracting in one minute. If we, multiply these out of course, if you apply some simple algebra, we’re going to be canceling out the beats, so, cardiac output is calculated in milliliters per minute – some pretty straightforward algebra there.

Now, let’s plug in some values. The average adult male has a stroke volume of approximately 70 millliters per beat and an average heart rate of 75 beats per minute. Now, if you want to calculate cardiac output, the amount of blood ejected from the ventricle each minute, cardiac output would be equal to 70 milliliters per beat times 75 beats per minute and that’s going to give us a value of 5,250 milliliters per minute. Of course, you can make that into 5.25 L per minute. So, this is the average adult male at rest, 5.25 L/min cardiac output. Now keep in mind that the average adult male has about 5L of blood in their body. So, every minute the heart is re-circulating pretty much all of the blood if you’re just at rest. All right, so the heart is doing a significant amount of work. It’s sending the blood to the muscles, that organs that need to get oxygen and the nutrients that come via the blood.

We know how to calculate cardiac output. Now, if you want to change cardiac output or if you want to influence cardiac output, it should be obvious that we can do that in three ways by influencing stroke volume, by influencing heart rate, or by influencing both of them. So, if you make a change, to the stroke volume or the heart rate, that of course, in turn is going to make a change to cardiac output.

Now, we’ve also looked at factors that are going to influence volume and heart rate. We’ve spoken about those factors in Episodes, I think it’s 46 and Episode 50. Episode 46 talks about how we can influence heart rate. Episode 50 talks about influencing stroke volume. You can always revisit those and see how that works.

When you’re exercising, you’re going to have a little bit of a different situation. You know when you’re starting to exercise and you’re doing some aerobic activity, your heart rate is going to increase, your cardiac output is also going to increase because you’re increasing stroke volume and your heart rate so, that’s going to give you some different values.

Let’s take an example where we’re trying to calculate cardiac output again. As usual, cardiac output is equal to stroke volume. We’re going to take that and multiply that by heart rate. Same exact situation.

CO = SV x HR

But, okay, I’m showing ladies here exercising but, we’re going to stick with the example for the calculations, we’re going to stick with males, and we’re going to see during moderate exercise, the stroke volume might increase to a point of let’s say about 100 mL/beat, and let’s say the heart rate increases before it was 75 and let’s say we have, let’s go with a 100 because that’s easy to calculate, a hundred beats per minute (100 beats/min). So, we have more of an intense situation, it’s not a very stressful situation but, you’re doing some exercise. So, that’s going to influence cardiac output of course. Cardiac output is going to be equal to:

CO = 100 mL/beat x 100 beats/minute

Giving us a cardiac output of 10 L/min. So, by doing a little bit of exercise, we’ve almost doubled the cardiac output. In other words, your blood is being pumped throughout your body twice in that minute with moderate exercise.

As you exercise and you train, hopefully we’re doing this on a regular basis, hopefully, like three times a week, **hint, hint, hint** but, as you’re doing this more regularly, there are going to be some adaptations that happen. One of the main adaptations is that your stroke volume increase, (I’m just going to put an up arrow here showing that your stroke volume increases). In other words, everytime that your heart pumps, it pumps more blood than the average untrained individual.

What that can do in turn is that can actually cause a lower resting heart rate. All right, so, a trained person on average has a lower heart rate than an untrained person. However, they’re still able to get the same cardiac output. In other words, your heart is becoming more efficient at pumping the blood. Everytime it contracts the ventricles, it’s sending a significant amount more than the untrained person and you can achieve the same effect if not even a better effect with less work.

So, the take home message there I guess you could say is, do like this ladies, get into the gym and start doing some exercise. That’s always good and it’s going to pay off in the long run.

That’s not what I intended to teach but, hey it’s something that’s good for us to learn. That’s pretty much it for this episode. As usual, you can visit the website at Interactive-Biology.com for more Biology resources and a bunch of other resources that we’re adding there. We’re adding quizzes and we have just added a brand new Biology community where you can ask questions, get answers, give input. Join the community and make the community stronger and much more fun.

Thank you for watching this episode and I’ll see you on the next one.

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Ever wonder what happens in a heartbeat? What happens inside our heart when we hear the ‘lub-dub’ sound?

Watch and see as Leslie describes in full detail what a cardiac cycle is and how this is reflected in one heartbeat.

Have fun!

Transcript of Today’s Episode

Hello and welcome to another episode of Interactive-Biology TV where we’re making Biology fun! My name is Leslie Samuel, and in this episode, Episode 52, I’m going to be talking about the ‘Cardiac Cycle.’ When I say the cardiac cycle, I’m talking about all of the events that happen with one complete heartbeat. So, we’re going to go into the details of this. There are a lot of details but, we’re going to try to break it down, one step at a time to make it as easy and as fun as possible. Let’s get right into it.

Here, we are looking at the entire cardiac cycle. We have this graph here that shows a number of details and, to make this as easy as possible, what we’re going to do is we’re going to take everything and break it down one section at a time. I want you to follow me on this. Like I said, we’re talking about one complete heartbeat and with one complete heartbeat, I’m talking about the contraction and the relaxation of the atria and the contraction and the relaxation of the ventricles. Anytime I say contraction, I’m referring to systole which is the CMS contraction; and, when I say relaxation, I am referring to diastole.

What we’re going to do is first, I’m going to describe what all these things show, and then, we’re going to take it one stage at a time.

Here, we’re looking at the phonocardiogram. In other words, we’re looking at the sounds that we hear when the heart beats, when we’re looking through the different stages of the heartbeat. Then, here we’re looking at the electrocardiogram, and we’ve looked at that in a previous episode. You can always revisit that to get a good understanding of how the electrocardiogram or the ECG or the EKG works.

Then, we’re looking at the ventricular volume. In other words, we’re looking at the amount of blood, the volume of blood in the ventricle, specifically we’re looking at the left ventricle. Then, here in blue, we are looking at ventricular pressure. So, that’s the pressure in the left ventricle. Here in gray, we’re looking at the atrial pressure, so, the pressure in the atria. Then, last but not least, we’re looking at the aortic pressure, and that’s the pressure in the aorta which is this structure right here, which sends the blood from the heart to the rest of the body.

That’s an overview of what we’re going to be looking at. Now, we’re going to take it one section at a time. This has a lot of details in it. It summarizes the entire cardiac cycle so, we’re going to take it one step at a time and get a good understanding of what is going on. Actually, I am going to start right in this section here. The reason I’m going to start here is because here we have showing the P, Q, R, S complex and the T wave. This is one full cycle but, this is labeled differently so, we’re going to look at that.

I’m going to start by looking at the electrocardiogram. First thing we’re going to see is we have the P wave, and if you remember from a previous episode, the P wave represents atrial depolarization. So, we’re talking about the depolarization of the atria. Once this happens, that is going to cause the atria to contract. So, let’s jump up here and look at the atrial pressure. You can see here, right after the P wave we get this increase in pressure in the atria. That is when the atria are contracting and that is why we see that increase in pressure as a result of the depolarization of the atria. Once again, the P wave represents atrial depolarization that is going to cause atrial contraction or, as you can see here, atrial systole. What that’s going to do is that’s going to push the last bit of blood from the atria, which is this part over here (I’ll show it with a blue pointer), from the atria into the ventricle. So, we’re going from the left atria, left atrium to the left ventricle when that contracts. That is why we see this quick increase in the amount of blood in the left ventricle. So, we get an increase in ventricular volume right after the atria contracts.

We’ve described this section here which is the atrial systole. And then, after the P wave, we then get the QRS complex. Once again, we’ve covered this in a previous episode, I think it’s Episode 48 where we talked about the EKG. The QRS complex represents the depolarization of the ventricles. And of course, once the ventricles depolarize, that’s going to cause the ventricles to start to contract just like after atrial depolarization, we get atrial contraction.

Now, after ventricular depolarization, we also get ventricular contraction. So, that is where we’re starting this phase of systole where the ventricles are contracting. However, there is a short period here, and you can see here the same period. It’s called isovolumic or isovolumetric contraction. That is when these valves, the atrioventricular valves and the semilunar valves are closed as there’s a buildup in pressure. You can see there’s a significant increase in pressure here during the stage of isovolumetric contraction. Of course, the volume of blood in the ventricles is staying the same. So, here, you see the left ventricular volume is staying the same. At a certain point, we will have enough pressure in the ventricle to cause the semi-lunar valve to open so that you can pump the blood into the aorta. Now, at what point is that? Well, you can see here the aortic pressure is somewhere around 80 mm Hg as you can see here. So, once we have enough pressure to overcome the pressure in the aorta, that’s going to cause the valve to open, and then the blood can be sent to the aorta which can then go to the rest of the body.

In the case of the ventricular volume, when those valves open, and the blood leaves, that’s going to cause the ventricular volume, the amount of blood in the ventricles, to decrease significantly. Why? Because the ventricles are contracting, we’re sending the blood out to the body so, that it can go to the muscles, the organs that need blood and oxygen, and all that good stuff. That is the result of the ventricles contracting, so you can see the increase in pressure, the blood being ejected so, you can see the decrease in ventricular volume, and that happens right after the QRS complex which is the depolarization of the ventricles.

So, thus far, we’ve looked at the P wave, atrial depolarization causing atrial systole or atrial contraction. Then, we’ve looked at the QRS complex which then causes ventricular contraction and increase in pressure. Here you have isovolumetric contraction where the valves are close and no blood is exiting the ventricles and then, you have the semilunar valves opening when the pressure in the ventricles can overcome the amount of pressure in the aorta, and that causes ventricular ejection. You can see the term here, ‘ejection’ that means that the blood is being ejected from the ventricles. You can see there’s a significant decrease in ventricular volume.

Then, we have this T wave that represents the repolarization of the ventricles. When the ventricles repolarize, that’s also going to cause the ventricles to relax so, you can see now the amount of pressure in the ventricle is going down significantly. Then, at a certain point, we didn’t talk about this in Episode 51 where we spoke about isovolumetric contraction, the same thing is going to happen on the opposite end where we have isovolumetric relaxation. And, that’s because the valves are closed, the pressure is decreasing, so, you’re going to get a significant drop in pressure while the volume of blood in the ventricle is staying constant. Then, once that’s done, the ventricles are relaxed, the atria are also relaxed the, we can get ventricular filling where blood is being sent back. You can see here during relaxation, this is where the filling happens, blood is coming back from the body, blood is coming back from the lungs and entering the ventricle, so the ventricular volume is going to start going up again, it’s going to increase as you see here, the full thing, increases until we get that P wave again which causes atrial depolarization, and the cycle continues.

Now, there’s one thing we didn’t look at as yet, and that’s the phonocardiogram. You can see here, we have a signal here, a signal here, a third signal here, and there’s actually even a fourth signal. What these represent would be the sounds of the heartbeat. When you listen to the heartbeat, you usually hear a ‘lub-dub’ sound: ‘lub-dub,’ ‘lub-dub,’ ‘lub-dub.’ What that refers to would be the first and the second sound that you see here. Yes, there’s a third sound and there is a fourth sound but, you don’t hear those because they’re not strong sounds. The two main sounds that you hear are the first and the second. What that refers to is the closing of these valves. So, at this point after the QRS complex where the ventricles depolarize and the ventricles start to contract, when they start to contract, that’s going to cause an increase in force closing the valve, closing this atrioventricular valve, and when that valve shuts, you’re going to hear that first sound, the ‘lub’ sound. Then, here, where the ventricles relax after sending all of that blood out, you’re going to get a closing of the semilunar valves and you’re going to hear the second sound which is the ‘dub’ sound. So, you get ‘lub-dub,’ ‘lub-dub,’ ‘lub-dub.’ That is the heartbeat that you hear. This third sound here is when the ventricles are being filled, and as the ventricles are being filled, there’s going to be some turbulence in there and that’s going to cause a third sound but, you don’t hear that as much because there are no valves that are closing or anything of that sort. It’s just blood that’s flowing. The fourth sound that there is represents the filling of the atria with blood. Of course, since the atria are significantly smaller than the ventricles, that sound is going to be even softer. So, you don’t even see it in this phonocardiogram.

This shows the entire cardiac cycle. I hope that now that we’ve gone through all of the details, this entire graph does not look as intimidating as it might have looked when we first started. You can always revisit some of the previous episodes. In Episode 48, we deal with the electrocardiogram, we talk about isovolumetric contraction in Episode 51, and there are a few other episodes covering other details involved in this process.

That’s all for this video. Of course, you can visit the website at Interactive-Biology.com for more Biology videos and other resources. That’s it for now, and I’ll see you on the next one.

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Isovolumetric contraction is that stage when the ventricles continue to contract even though the blood volume stays the same. How and when exactly do this happen?

Watch to learn more.

Enjoy!

Transcript of Today’s Episode

Hello and welcome to another episode of Interactive-Biology TV where we’re making Biology fun. My name is Leslie Samuel and in this episode, Episode 51, I am going to talk about isovolumetric contraction. So, let’s get right into it.

What we’re looking at here is diastole at the top and systole at the bottom. So, this is where the ventricles are relaxing and this is where the ventricles are contracting. As you can see, blood is flowing into the atria and then, into the ventricles. Then, when the ventricle contracts, that pushes the blood into the aorta so that, it can go to the rest of the body and also, send blood to the lungs.

There’s something very significant that’s happening here. When the blood comes in, you can see this atrioventricular valve is open to let that blood get in to the ventricle. Once the ventricles contract, that causes this atrioventricular valve to close and of course, the same thing over here, so that the blood does not flow back into the atria.

We see here that this semilunar valve is open. However, that does not happen immediately. When the ventricle contracts, it needs to build up enough pressure to open that valve so that, the blood can flow out of the ventricle and to the rest of the body.

What we’re going to look at over here is what we’ve looked at before where right after the ventricular contraction happens, the cycle starts over and the ventricle fills with blood. So, you’re going to see an increased volume in the ventricle. And then, at a certain point, the atria are going to contract so, when the right atrium contracts, that forces even more blood faster into the ventricle. So, when the left atrium contracts, that forces more blood faster into the left ventricle and then, the ventricle contracts. When it contracts, that is going to push blood out of the ventricle and it’s going to go to the rest of the body. This is the end diastolic volume here and here we have the end systolic volume.

Let’s look at what’s happening in the ventricle when it comes to pressure. During the relaxation period, the diastole, we’re not going to have any pressure in the ventricle. So, we hardly have any so, I’m going to put that around zero. Then, at a certain point, let’s say at this point here, we have the atrium contracting, and when the atrium contracts, that’s going to cause an increase in pressure in the ventricle. Not a huge increase, but, an increase nonetheless. Then, the ventricle is going to contract. When the ventricle contracts, that’s going to cause an increase in pressure in the ventricle.

Let me draw that here. Here, we have that increase in pressure but, as you can see, it’s not until we reach this point that the valve actually opens, the semilunar valve opens, so that the blood can flow out. This is the point that we need to reach. Let’s say that that point is somewhere around 80 mL of mercury so, the pressure has to reach approximately 80. When that happens, the semilunar valves open and the blood gets ejected. We still have some increase in pressure and then, at a certain point, the muscle relaxes, we get diastole, and the pressure comes back down.

This time period, between where the ventricle contracts but the blood does not get ejected, and this point, we call this, (let me do that in a different color), we call this isovolumetric contraction. Why do we call it isovolumetric contraction? “Iso-” refers to the fact that it’s the same; “volumetric ” refers to volume so, the volume stays the same; “contraction” because the ventricle is actually contracting even though the volume is staying the same. The reason the volume is staying the same, is because the valves are closed so, the blood cannot leave until it reaches that point where the semilunar valve opens. Once that opens, the blood can flow out to the rest of the body.

That’s it! That’s the concept of isovolumetric contraction. That is all I want to cover in this episode. As usual, I’d like to invite you to visit the website at Interactive-Biology.com for more Biology videos and the many other resources we’re adding over time. Our goal is to help make Biology fun. That’s it for this video and I’ll see you on the next one.

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Here, Leslie discusses how stroke volume can be regulated. Depending on which factors are changed, blood volume entering the heart may increase and in effect increasing heart contraction too.

Watch, listen, and learn how this happens. Enjoy!

Transcript of Today’s Episode

Hello and welcome to Interactive-Biology TV where we’re making Biology fun. My name is Leslie Samuel and in this episode, Episode 50, I’m going to talk about regulating stroke volume, the skeletal muscle pump and Frank-Starling mechanism. So, let’s get right into it.

So, we’ve been looking at stroke volume and we’ve been looking at the fact that blood enters into the heart, comes in through the atria and then, into the ventricle and then, it gets pumped out, as you can see here, to the aorta, to the rest of the body, and to the lungs, and so on.

Then, we looked at how to determine the stroke volume, and we said, if we have blood entering into the ventricle, the ventricle is being filled and then, at a certain point, the ventricle contracts shooting that blood out to go to the rest of the body and we have the EDV and the ESV, the end diastolic volume and the end systolic volume, the difference between the two, that’s this difference here, that is the stroke volume (SV).

Looking at the stroke volume, if we want to increase or decrease the stroke volume, we can do it in two ways. We can either change the end diastolic volume or the end systolic volume. I guess, you can say we can do it in three ways. We can do one of those two or we can do both of them. If we adjust those, that’s going to change what the stroke volume is.

So, the question today is, how do we change the end diastolic volume and the end systolic volume. Now, I want to look at a number of ways to change the end diastolic volume and the end systolic volume thus changing the systolic volume. But, I’m just going to discuss a few of them so that you can kind of get the concept.

The first where we can do that is by increasing the amount of time that we have before the ventricular contraction. So, if we have more time, we have more time for the ventricles to be filled. So, here it is being filled until about 120 mL. If we increase the amount of time that we have, it might go upto a 140 mL before the ventricles can contract. Then, when the ventricles contract, you can see, we have a greater stroke volume. So, just by increasing the amount of time, that can increase the amount of blood entering into the heart which increases the end diastolic volume and we’re going to show a little later how that even decreases the end systolic volume. So, that’s the first way – by having more space between the heart beats. In other words, by having a lower heart rate.

Another way of increasing the end diastolic volume, let me just write that here, is by causing more blood to be sent back to the heart. How do we do that? Well, there are a number of mechanisms.

The way I want to talk about is called the Skeletal Muscle Pump. What that is, it’s a mechanism for increasing what we call, venous return. The difference between arteries and veins, arteries are the vessels that are going away from the heart and veins are the vessels that are returning to the heart. So, arteries take the blood to the muscles and to the organs and the tissues that need the blood and the oxygen that comes with the blood and once those nutrients and the oxygen are used by the organs and so on, the blood returns to the heart via the veins.

What I’m going to do right now is, I’m going to draw a vein. The cool thing about these veins is that in the veins, we have these valves. So, I’m going to draw these valves. The way these valves are constructed is so that, the blood can only flow in one direction. The blood can enter the veins and go in this direction with no problem. But, if you try to go back in the opposite direction, that won’t work because these valves are actually going to stop them. Now, associated with these veins, we have skeletal muscles. So, this is some skeletal muscle here and this is, I’m just going to draw these strands to show that it’s striated and here, we have more skeletal muscles on this side (Forgive my poor drawing skills). Here we have skeletal muscle on this side and skeletal muscle on this side.

What this does is, it actually contracts in a way that helps to push the blood in the direction that it needs to go. This is something that happens, for example, when you’re exercising, you want more blood going back to the heart so that it can be pumped to the lungs, pick up more oxygen and then be sent back to the rest of the body. So, when you’re working out, you’re exercising, the skeletal muscle pumps are doing their work and they’re helping to push that blood so the blood can go faster, more blood can be going to the heart. That is what we call, increasing venous return. We’re increasing the amount of blood that’s returning to the heart via the veins. There are a number of things that regulate this process. But, this is the concept. Skeletal muscle pump increases the amount of blood returning to the vein. That has to do with increasing the end diastolic volume, the EDV. The other factor that influences stroke volume is the ESV, the end systolic volume.

Let’s look at one of the ways where that is controlled. We’ve looked at muscle contraction and we said that the functional unit of contraction is the sarcomere. This is one sarcomere here. We looked in Episode 041 at how this process happens. When muscle contraction happens, we have this that we call, myosin. This is the myosin filament. The blue here, we call actin. This is “A” for actin and this is “M” for myosin. On the myosin we have myosin heads and those myosin heads associate with the actin and they pull so that, this process can happen where we have the sliding filaments. The filaments slide against each other , the muscle contracts and then the muscle relaxes. This is the exact same process that happens in the heart. If you need a review of this process, you can go back to Episode 041 to check out those details.

Now, the way the structure of this sarcomere is set up, in order for us to have the maximum amount of contraction, we have to have optimum overlap. Here, we have the overlapping between the myosin heads and the actin. In order to get the best, the strongest contraction, we have to have maximum overlap.

This is how this works. When the heart gets filled with blood, this stretches out more. So, the end of this sarcomere might be over here because there’s more blood in the heart. That stretching of the muscle causes an increase in contraction for a number of reasons.

Imagine if the end of this actin was over here. There’s an increase distance between these two points so that, it has a farther distance to travel as the sarcomere gets shorter. That’s going to cause a stronger contraction and if you have a stronger contraction, it’s going to send more blood out of the heart, leaving less blood in the heart. In addition to this, we’ve spoken about how calcium is involved in this process. And, you can check out Episode 043 for more details on this. Calcium ions (Ca2+) are released from the sarcoplasmic reticulum. That binds to troponin which is on here, blocking the binding sites for the myosin head. When calcium comes, that exposes the binding site so that the myosin heads can bind freely. The stretching of the heart increases the affinity of this troponin for calcium ions.

If have an increased the affinity for calcium ions, you’re going to have more myosin heads being able to bind to the binding sites on the actin and that is also going to increase the contraction. This is called the Frank-Starling mechanism. It’s called that because it was named after the two guys who first described that process. What it says is that, if the heart gets filled with more blood, that is natuarally going to cause a stronger contraction sending more blood out of the heart and increasing the stroke volume even further by decreasing the end systolic volume. We looked at how this happens. You have better overlap and you have a greater affinity for calcium which is going to cause a stronger contraction.

Once again, if you need to understand the details of how calcium is involved in this process, go back into Episode 043 where I go into those details.
That’s pretty much it for this video. As usual, I want to invite you to visit the website at Interactive-Biology.com for more Biology videos and all of the other resources we’re adding there on a regular basis so that we can help make Biology fun. That’s it for this video , and I’ll see you on the next one.

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Stroke Volume = EDV – ESV

What do these mean? Watch to learn more and understand about stroke volume.

Enjoy!

Transcript of Today’s Episode

Hello and welcome to another episode of Interactive-Biology TV where we’re making Biology fun. My name is Leslie Samuel and before I get into this episode, I just want to send a shout out to Richard Morris and his friend, Nathan. Richard sent me an email a few days ago letting me know that they appreciate the videos and that they have watched every single video that I have published here at the Interactive Biology TV. And that is just awesome. Richard and Nathan, I hope you have gotten a tremendous amount of value and, I hope that you continue to get a tremendous amount of value from the videos that you are watching here at Interactive-Biology TV.

I know there are so many of you out there that have been watching the videos and, I want to let you know how much I appreciate every minute that you spend watching these videos. Thank you for every comment that has been left. Thank you for every question that have been asked and all of the feedback that I’ve been getting. It is just tremendous to know that this is helping so many people all over the world. So, thank you, thank you, thank you.

Inside this episode, Episode 49, I’m going to be talking about what is stroke volume and how to calculate it. So, let’s just get right into it.

When I’m talking about stroke volume, I’m talking about the amount of blood that is pumped by one ventricle during each heart beat. So, we know that the heart beats and, we know that blood comes into the heart, and when the ventricle contracts, it pushes that blood out to the rest of the body and to the lungs. We’ve looked at this in detail, in Episode 44. If you need to review that, you can go back to Episode 44 to check out those details.

Here, we’re looking at the heart. Right now, we’re just going to look at the left ventricle. What is happening is blood is coming into the left atrium and then into the left ventricle. When it reaches in the left ventricle, after a short period of time, the ventricles contract and that pushes blood, as you can see here, pushes the blood out into the aorta and that then goes to the rest of the body.

That’s a brief overview but, once again, you can go back to Episode 44 to check out more details about that.
There are a few definitions that I want you to know. Definition number one: systole. Systole is the contraction of the heart. Then we have diastole and that’s the relaxation of the heart. So, systole is contraction, diastole is relaxation then, we have the End Diastolic Volume or the EDV which is the amount of blood in the ventricle right before ventricular contraction. So, right before the ventricle contracts, the amount of blood that we have in the ventricle, we call that the End Diastolic Value which makes sense. It’s right at the end of diastole so, that’s the End Diastolic Volume.

Then, of course we have the End Systolic Volume which is the amount of blood left in the ventricle right after the ventricular contraction. So, when the ventricles contract, and it pushes the blood out to the lungs and out to the rest of the body, the amount of blood we have left over, that is the end systolic volume which, once again, makes sense because its at the end of systole.

With those definitions, let’s look at the graph.

All right. So, what we have here is a graph. On the x-axis we have time and on the y-axis we have volume in milliliters so, we’re looking for the amount of blood in the ventricle.

For this example, we’re going to talk about the left ventricle which is the one that pushes the blood into the aorta to go to the rest of the body.

Let’s say, ventricular contraction has just finished. When that contraction is finished, the ventricles start to get filled with blood again. After that contraction, another cycle starts where blood flows into the ventricle. Here we have blood getting into the ventricle. At a certain point, we’re going to have a more rapid filling, and when it reaches this point, and we’re not going to talk about too many details where this part is concerned. We’re going to talk more about that in a later episode. But, let’s say this is the point where the ventricle contracts. What’s going to happen here is, when the ventricle contracts, that’s going to push the blood out of the ventricle and it’s going to go to the rest of the body.

Here we have a certain amount of blood and here we have a certain amount of blood. The amount of blood that we have in here, right before the contraction, we’re going to call that the EDV. Once the contraction is over, we’re going to call that the ESV.

The way we calculate the stroke value is SV is equal to EDV minus ESD:
SV= EDV – ESD

If the end diastolic volume is 120 mL of blood and the end systolic volume is around, let’s say, it’s 50 mL. The stroke value is going to be 120ml minus 150 mL and that is going to be equal to 70 mL. I just realized here that I wrote 5. I meant to put 50 so, I’m just going to put that 0 here. So 120 minus 50 = 70. Seventy would be my stroke volume.
Again, ventricle fills with blood, the ventricle contracts. At a certain point, the ventricle contracts that pushes the blood out of the ventricle and to the rest of the body. At the end of the contraction, we have an end systolic volume. If the end systolic volume is 50 mL and the end diastolic volume is 120 mL, the stroke volume will be 120 minus 50 and that is going to be equal to seventy.

That’s pretty much it for this episode. Of course, if you want to see more, you can go to Interactive-Biology.com where we have more Biology videos and many other resources. We’re adding to the resources on a regular basis to try to help make Biology fun. That’s it for this video and I’ll see you on the next one.

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Have you seen an ECG reading? What do those lines mean? How does it measure heart activity?

Watch and learn as Leslie once again teaches us about this topic.

Enjoy!

Transcript of Today’s Episode

Hello and welcome to another episode of Interactive-Biology TV where we’re making Biology fun. My name is Leslie Samuel and in this episode, Episode 48, I’m going to show you how to read an electrocardiogram. For short, it’s called ECG or EKG. So, let’s get right into it.

First, I want to answer the question, what is an electrocardiogram? An electrocardiogram is a test that records the electrical activity of the heart. We looked at how the  SA node starts the signal and we looked at how that signal spreads to the rest of the heart. You can always go back to Episode 46 for more details on how that works.

The ECG is used to test for irregularities in how the heart functions. You’ve probably either seen this first hand in a hospital or on TV. You can look at the electrocardiogram and it will tell you if the heart is working the way it should. The way this is conducted is by placing skin electrodes on different parts of the body. These electrodes are able to detect the electrical activity of the heart. When you look at the electrocardiogram, it looks kind of like this {Leslie shows an animation of an electrocardiogram} and you’ve probably seen this. Normally when you see this, there’s a beep associated with it. There’s no beep in this animation but, you get the point.

What we’re going to do is we’re going to look at this and we’re going to look at each component of the electrocardiogram. Let’s look at it right now.

We’re looking at an electrocardiogram and you can see that we have a number of things. We have this peak over here. We’re going to call this the P wave, this peak right here. And then, we have this section that we’re going to call the QRS complex. Then, we have the T wave and sometimes we get this U wave. We’re going to talk about what these different waves show.

The P wave. We’ve looked at how the SA node generates the signal and then that signal spreads to the muscle cells in the atria. What this P wave shows us is the depolarization of the atria. Okay, so, when the atria depolarizes, we see this peak.

We have the QRS complex, you probably guessed it by now but, this shows the depolarization of the ventricles. That is what is represented by the QRS complex.

Then, we have the T-wave which comes after the QRS complex and this shows the repolarization of the ventricles.
Now, you’re probably wondering why the signals that come from the ventricles are significantly larger than this little signal that comes from the atria. But, if you look at the heart, you’ll see that the atria is significantly smaller than the ventricles. So, when the cells in the ventricles depolarize, that’s going to have a much greater effect on the EKG or the ECG because you have more cells depolarizing so you can get a stronger signal. And then of course, you get the repolarization.

The U wave is one that you don’t always see. It’s sometimes hard to see and in most cases, you don’t really see it. But, in some cases, you do see it. In some cases it can tell you something about when things are going wrong with the heart. We’re not going to go into all those details but, I included it here because it was shown in this pictures that I found and because it does show up sometimes. Some people think it’s the repolarization of the Purkinje fibers. And it’s also thought to be the repolarization of some other specialized muscle cells. But, we’re not going to go into that.

The main things are the P wave, the QRS complex and the T wave. The P wave being the depolarization of the atria; the QRS complex being the depolarization of the ventricles and; the T wave being the repolarization of the ventricles.

If you ever need a refresher on what the terms depolarization and repolarization mean, you can always go back and to Episodes 9 and 10 and that will give you more details.

Well, that’s all for this video. As usual, I’d like to invite you to check out the website at Interactive-Biology.com for more Biology videos and other resources to help make Biology fun.

This is Leslie Samuel. That’s it for this video and I’ll see you on the next one.

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Leslie explains how action potentials are generated by the cardiac cells of the heart and how the release of calcium can generate heart contraction.

Watch to learn more.

Enjoy!

Transcript of Today’s Episode

Hello and welcome to another episode of Interactive-Biology TV where were making Biology fun. My name is Leslie Samuel and in this episode, Episode 47, I’m going to be talking about action potentials and contraction in cardiac muscle cells. So, let’s get right into it.

I’m looking at the heart. We’ve looked at a number of things related to the heart. In the previous episode, we spoke about the SA node, which is what we see here, number one and, we spoke about the AV node, which is this part here, number two, and we spoke about these Purkinje fibers. I’m just going to write PF for now. So, this is the AV node, the SA node and the Purkinje fibers. You can go back to the previous episode to learn more about those, in case you’re not sure what they do; in case you’re not sure how they function.

There are a number of things that I want you to know here. We said that the SA node functions as the pacemaker. There’s an important feature about the heart muscle cells that you need to be aware of. That is the fact that these cells are all electrically connected. So, all of the muscle cells in the ventricle are electrically connected, all of the muscle cells in the atria are also electrically connected.

What that means is that if one of the cells in the ventricle gets stimulated, that signal is going to travel to all of the other cells in the ventricle. Not only that, but, if the SA node starts a signal, that signal is going to spread. This is why we get the heart contracting in response to the signal that’s generated by the SA node. Then, when it reaches the AV node and it spreads via the Purkinje fibers, that signal spreads to all of the muscle cells in the ventricles, causing the ventricles to contract.

There are some other important details that you need to know. When the signal is generated in the SA node and it spreads to the atria, the conduction velocity is one meter per second (1 m/s). So, the signal spreads at a speed of 1 m/s here. At the AV node, it slows down to where it’s somewhere around 0.04m/s. Then, in the Purkinje fibers, it speeds up significantly, and we get a conduction velocity of 5 m/s.

So, what this means is that we have a signal that starts here and spreads throughout the atria relatively quickly at 1 m/s but then, it slows down at the atrioventricular node to 0.04 m/s. So, there’s a delay here, and then, after it passes the atrioventricular node, that signal spreads rapidly to the ventricles. Now, why do we want this? As we mentioned before, the blood first goes to the atria and then, the atria contracts, sending the blood from the atria to the ventricles.

You don’t want the atria and the ventricles contracting at the same time. That would cause problems. You want the ventricles to get filled with the blood from the atria first and then, you want the ventricles to contract sending all that blood to the rest of the body and to the lungs. So, that’s how that works and that is why it’s good that we have this slowing down at the atrioventricular node.

Now that we know that and now that we understand that the muscle cells are all connected electrically, let’s move on and look at what happens inside the muscle cells.

We have a stimulus that comes from the AV node or the SA node and that spreads to the muscle cells. In response to that, what’s going to happen is that the membrane potential of the cardiac muscle cells is all of a sudden going to depolarize very quickly. So, we have that initial depolarization. When the muscle cells depolarize, as with skeletal muscles, we’re going to have calcium being released from the sarcoplasmic reticulum. For a refresher of how that works, you can go back to Episode 42 where I talked about calcium release and how that causes muscle contraction.

Once the calcium is released from the sarcoplasmic reticulum, that’s going to prevent the repolarization that normally happens rather quickly. With a normal neuron, the action potential lasts less than a millisecond. However, in cardiac muscle cells, we have calcium that’s being released that slows down the repolarization process and we get a phase that’s referred to as the ‘plateau.’ The membrane potential does not repolarize as quickly. Then, at a certain point, calcium gets pumped back into the sarcoplasmic reticulum, potassium also leaves as usual, and we get the repolarization of the cardiac muscle cells.

As you can see, the time scale that we have here shows that this action potential can last as much as 300 milliseconds as opposed to the one millisecond or less than one millisecond that we get with a neuron. That’s because of the calcium released. That’s because of this plateau phase.

Let’s see what that does for muscle contraction. Yes, we’re going to have a depolarization but then, we’re going to have the calcium released and that is going to cause the muscle cells to contract just like I showed in Episode 42. Once again, you can always go back at Episode 42 to revisit that concept.

This is what we’re going to do. I’m going to plot the tension in the cardiac muscle cells. So, we’re looking at the cardiac muscle and here, nothing is happening. But, as soon as calcium starts being released, that’s going to cause the muscle cells to contract. This is what’s going to happen. This is the tension and then, once calcium starts being pumped back into the sarcoplasmic reticulum, the muscle cell is going to relax and go back to its resting state.

So, we have the action potential lasting significantly longer than we’ve seen before, because of the calcium that’s released from the sarcoplasmic reticulum and that calcium then causes the muscle cells to contract and we get this tension in the muscle cells.

As the calcium gets pumped back into the sarcoplasmic reticulum and the potassium ions leave, that is going to cause the muscle cells to relax and go back to its original state.

And that’s pretty much it. The action potential causes calcium release. Calcium release causes muscle contraction.

That’s all I’m going to cover in this video. As usual, you can head back to the website at Interactive-Biology.com for more Biology videos and for more resources that we’re adding there on a regular basis. So, stay tuned. This is Leslie Samuel. That’s it for this video and I’ll see you on the next one.

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In this episode, Leslie discusses the effect of adrenaline and acetylcholine on heart rate. These two modifies the conductance of the ions across the membranes of the cells of the SA node causing either an increase or a decrease in heart rate.

Watch and learn how it all works.

Enjoy!

Transcript of Today’s Episode

Hello and welcome to another episode of Interactive Biology TV where we’re making Biology fun. My name is Leslie Samuel and in this episode, Episode 46, I’m going to talk about how adrenaline and acetylcholine affect heart rate. So, let’s get right into it.

In the last episode, Episode 45, we looked at this slide where I showed that in the SA node, we have a pacemaker potential that results in a spontaneous signal so that we have the heart beating in response to these action potentials that are automatically generated in the SA node.

If you haven’t looked at Episode 45, I would recommend for you to pause this right now and go and watch Episode 45 so that you’re going to get a full understanding of what we’re going to be talking about.

Let’s go to the next slide. I’m sure you’ve all been in situations where, let’s say you’re doing something and someone jumps up behind you and scares you. What happens? Your heart starts beating faster. The reason it starts beating faster is because adrenaline is released from the adrenal gland that’s located above the kidneys. When that adrenaline is released, that causes the conductance in the pacemaker cells to change. As you can see here, we have an increased conductance for sodium and calcium ions. That is going to cause those to rush into the cell much faster.

It’s going to look a little different than what we looked at before because the membrane potential is going to increase significantly faster so that we’re going to get a faster action potential. So, it might look something like this. As you can see, the signal happens much faster. Forgive my sloppy drawing here. So, we have signals being produced much faster and the heart rate increases. If you remember from the last one that I showed, I was able to show two action potentials on this. But, because sodium and calcium ions are rushing in much faster, the signals are going to be generated much faster because it’s going to reach the threshold much faster and we get an increased heart rate. So, that’s adrenaline.

Now, there’s an opposite effect where instead of adrenaline being released, we have acetylcholine being released. I didn’t plan for the acetylcholine to come in as a flame but, it did for some reason.

What happens when acetylcholine is released? As you can see up here, the conductance for potassium is going to increase significantly. You should know that potassium wants to leave the cell. So, this is going to increase hyperpolarization and is going to slow down depolarization.

What’s going to happen is, instead of this rapid depolarization, we’re going to get a significantly slower depolarization so that, it takes much longer to reach the threshold. When it reaches the threshold, the usual process happens: voltage-gated calcium channels open and calcium rushes in to the cell. Then, we have our depolarization. Then, this process continues.

But, as you can see here, depolarization is much slower than over here. Here, depolarization is sped up because sodium and calcium are rushing into the cell much faster in response to adrenaline. Here, it’s going to be much slower because more potassium is leaving the cell causing depolarization to slow down and we get a slower heart rate.

Faster heart rate in response to adrenaline; slower heart rate in response to acetylcholine.

That’s pretty much it for this video. As usual, you can visit the website at Interactive-Biology.com for more Biology videos and all of the other resources we’re putting together over there. This is Leslie Samuel. That’s it for this video and I’ll see you on the next one.

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In this episode, Leslie talks about how a pacemaker potential can cause a heart to beat automatically. Details about how it is generated is discussed in this video. Just how does this happen, our heart beating again and again?

Watch to learn more.

Have fun and enjoy!

Transcript of Today’s Episode

Hello and welcome to another episode of Interactive-Biology TV where we’re making Biology fun. My name is Leslie Samuel and in this episode, Episode 45, I’m going to be talking about the pacemaker potential of the S.A. node and the A.V. node. We’re basically going to look at how this results in the heart beating automatically. So, let’s get right into it.

Let’s first talk about the S.A. node. The S.A. node stands for the sinoatrial node and you can see it in this figure over here, it is number one. That’s this cluster of cells. It is basically a specialized group of cardiac muscle cells that don’t contract which is kind of strange. They’re muscle cells and they don’t actually contract. But, what’s special about these cells is that they are adapted to automatically generate impulses. So, it can automatically cause signals that can spread throughout the heart, causing the heart to beat. The S.A. node functions as the pacemaker of the heart. Yes, we have the A.V. node and some other stuff that we are going to talk about but, these generates signals faster than any of the others so, it sets the pace for the heartbeat. As you can see, it is located in the right atrium.

So, now let’s talk about the A.V. node. The A.V. node is number two. So, it’s this cluster of cells here and it stands for the atrioventricular node. It is similar in function to the S.A. node in that it automatically generates impulses and it is located between the atria and the ventricles hence the name, atrioventricular node.

Let’s go back to the S.A. node and see how this results in the pacemaker potential. Before we look at that, I just want to point out that we have, in addition to the S.A. node and the A.V. node, we have some fibers that extend from the A.V. node and spread throughout the ventricle and those fibers are called Purkinje fibers. These are also very important in that they spread that signal throughout the rest of the ventricle.

Let’s talk about the S.A node. We said that that functions as a pacemaker. So, we are going to look at the pacemaker cells that we have in the S.A. node. What is special about these cells is that normally, there’s a significantly higher conductance for sodium than there is for potassium. Now, if you go back to Episode 006, I talk about Donnan equilibrium and driving force and I show how there’s normally a driving force for sodium to rush into the cell. I also show that potassium wants to leave the cell. Because the cell is much more permeable to sodium, we’re going to have a situation where there’s much more sodium coming in than potassium leaving.

Because we have more positives going in than leaving, what we’re going to get is a pacemaker potential where the cell normally depolarizes. Then, when it reaches the threshold, something interesting happens. Yes, we have the sodium rushing in and some potassium leaving but, now that we’ve reached the threshold, voltage-gated calcium channels open and calcium is going to rush into the cell. So, we’re going to get this rapid depolarization. In other words, we’re going to get an action potential.

At the peak, we’re going to get a different situation where, yes, we have sodium coming in and potassium leaving but, voltage-gated potassium channels are going to open so that the conductance for potassium increases significantly and potassium is going to rush out of the cell repolarizing the membrane.

At that point, we still have the sodium that’s coming in and the voltage-gated potassium channels close so, we have the initial situation where sodium is rushing into the cell, causing this depolarization then, the same thing happens. It reaches the threshold, voltage-gated calcium channels open depolarizing the cell membrane once again, causing that impulse. Voltage-gated potassium channels open causing potassium to rush out of the cell again. This process continues over and over and over. What ends up happening is we have this automatic signal that’s generated constantly resulting in the contraction of the heart. This causes the heart to beat.

It’s really that straightforward but, the main idea is that the cells in the S.A. node have a significantly higher conductance for sodium so it continuously depolarizes causing that impulse that causes the heart to beat.

That’s really all I want to talk about in this video. As usual, you can visit the website at Interactive-Biology.com for more Biology videos and other resources to help make Biology fun. This is Leslie Samuel. That’s it for this video and I’ll see you on the next one.

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How does the blood move around the body? What is the role of the heart in bringing blood to all the different parts of the body?

Watch and see as Leslie gives an overview of the Circulatory System, the first in this series.

Enjoy!

Transcript of Today’s Episode

Hello and welcome to another episode of Interactive Biology TV where we’re making Biology fun! My name is Leslie Samuel and in this episode, Episode 44, I am going to be talking about how blood flows through the heart. This is going to be the first video in the Circulatory System series. So, let’s get right into it.

Here, we are looking at two pictures of the heart. On your left, we’re looking at the heart when it’s being filled with blood. On the right, we’re looking at the heart when it’s pumping the blood out of the heart. We’re going to look at a number of details here just to give an overview of how the blood flows through the heart. In order to understand how the blood flows through the heart, we need to look at the valves that are found in the different parts of the heart.

First of all, allow me to point out that this is the right side of the heart so, this is right. Over here, we have the left side of the heart. Now, that looks a little strange because when you’re looking at the screen, this is your left and this is your right. But, this is looking at it as an individual that’s facing you. This would be his right side and this would be the left side.

There are a number of valves that are found throughout the heart. There are a number of parts of the heart that we need to know.

The first thing I want to point out is here, we have the right atrium and the left atrium. So, this chamber is the left atrium. This chamber is the right atrium. Then, we have the right ventricle and the left ventricle. Same thing over here, we have the right ventricle, left ventricle; right atrium and left atrium.

The next thing I want to point out is that between the atria and the ventricles, we have what we call the atrioventricular valve. And that makes sense since it’s between the atria and the ventricle. So, here we have an atrioventricular valve, here we have an atrioventricular valve. Now, on the right side, we also call this atrioventricular valve a tricuspid valve. We call it “tricuspid” because it has three cusps, in other words, three flaps. You’re only seeing two here but, that’s because this is a cross-section. Then, on the left side, we have what we call the left atrioventricular valve which is also known as the mitral valve or the bicuspid valve. I’m just giving you these different names so that if you go and read a textbook and it says one of these, you know exactly what it’s talking about. So, we have the tricuspid or the right atrioventricular valve and the bicuspid or the mitral or the left atrioventricular valve.

Then, we have valves that allow blood to leave the ventricles. On the right side, we have the right semilunar valve and that is also called the pulmonary valve. The reason it’s called a pulmonary valve is because it leads into the pulmonary artery. On the left, we have this semilunar valve which we can also call the aortic valve. We call it the aortic valve because it leads into the aorta.

So, these are the different names and I want you to know these names: tricuspid, bicuspid, mitral, atrioventricular, aortic, semilunar, which is the pulmonary and the aortic. Those are the valves that I want you to be familiar with.

The special thing about valves is that it allows for blood to flow in one direction. So, here you can see blood can flow into the ventricle but, it can’t flow back. If it tries to flow back, these valves are going to shut. So, all of these valves are one-way valves. They allow for blood to flow in one direction.

Now that we know the different valves, let’s look at how blood flow happens. Blood comes back from the body and it enters into the heart via the vena cava. So, you can see blood is flowing into the vena cava. We have the posterior vena cava and we have the anterior vena cava. Blood is coming in, entering into the right atrium.

As it enters into the right atrium, the atrium contracts and that pushes the blood into the right ventricle. Once the blood gets into the right ventricle, the ventricle contracts and that pushes the blood through the semilunar valve or the pulmonary valve into the pulmonary artery. And from here, that blood goes to the lungs. And, it goes also in this direction to the lungs.

Once the blood goes to the lungs, it picks up, you guessed it, oxygen because you’re breathing in the oxygen. That oxygen aids the blood. Once the blood gets oxygen aided, it leaves the lungs and goes via the pulmonary veins into the left atrium. The left atrium contracts sending the blood through the left atrioventricular valve into the left ventricle. Once the blood is in the left ventricle, the left ventricle contracts and that sends the blood through the semilunar valve or the aortic valve in this case, into the aorta, and then, that blood can go to the rest of the body.

I know this looks a little confusing with all of these arrows but, let’s follow that one more time. Blood comes from the body. It enters via the posterior and anterior vena cava into the right atrium. The right atrium contracts and that pushes the blood through the tricuspid valve or the right atrioventricular valve into the ventricle. The ventricle contracts and that pushes the blood via the semilunar valve or the pulmonary valve to the pulmonary arteries that go to the lungs, picks up oxygen, then it comes back oxygenated via the pulmonary veins into the left atrium. The left atrium contracts and that pushes the blood into the left ventricle. The ventricle contracts, pushing the blood via the aortic valve or the semilunar valve to the aorta and out to the rest of the body.

So, the function of the heart is basically to pump the blood to the body, to send the blood to the lungs to pick up oxygen, and then to send that oxygenated blood to the muscles and to the organs that need it. Once the muscles and the organs that need it, once they use that oxygen, the blood comes back via the vena cava to the heart. The process can continue over and over again.

I have these two over here and you can see, this shows the heart filling with blood and, this shows when the ventricles actually contract and send the blood out to the lungs and to the rest of the body via the aorta.

There’s one thing I’d like to emphasize though. I say that, first the right atrium contracts and then the right ventricle contracts, and I’m saying that just because I’m showing it one at a time. But, both atria contracts simultaneously and both ventricles contract simultaneously. So, that while this process is happening, this process is also happening. Blood is being pumped to the lungs. At the same time, it’s being pumped to the rest of the body.

That gives you a general introduction into the circulatory system by showing you how the heart pumps blood.

As usual, you can visit the website at Interactive-Biology.com for more Biology videos and other resources. That’s all for this video, my name is Leslie Samuel and I’ll see you on the next one.

There are some regular pictures and some 3d pictures of the human heart. If you click on the images, you will see them in Full Size. Feel free to download and use them as necessary. However, if you do that, make sure to retain the copyright info on those containing the copyright info.

Systole and Diastole

Heart

Heart - Numbered

Oblique View of Human Heart

Heart myocardium and coronary vessels diagram

Normal anatomy of the human heart, anterior view

Heart, Left Oblique View

Heart Apical 4-Chamber Anatomy

Heart Attack