Interactive Biology, by Leslie Samuel » IBTV
By Leslie Samuel
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Podcast Description
In these short videos, I break down biological concepts in a simple way. The goal is to make biology fun and understandable.
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| 1 | Video060 Hemoglobin and the Oxygen-Dissociation Curve | httpv://www.youtube.com/watch?v=MKGhoC1Bf-I Click Here to Download This Video Ever wonder how the oxygen binds to our blood cells and sent to the different parts of our body? Watch and learn with Leslie as he explains how this happens and uses the Oxygen-Dissociation Curve to describe this event. Have fun! Transcript of Today's Episode Hello and welcome to another episode of Interactive-Biology T.V. where we’re making Biology fun! My name is Leslie Samuel and in this episode, Episode 60, I’m going to be talking about hemoglobin and what’s called the oxygen-dissociation curve. So, let’s get right into it. We’ve already done an introduction to the respiratory system and we’ve shown how the heart beats and sends the blood. When the right ventricle sends the blood, it sends it to the lungs that comes back to the left atria and then, the left ventricle pumps and that sends the blood through the rest of the body. We’ve also looked in the lungs and seen how we have the trachea going into the bronchi and then that splits off into the bronchioles, and as you can see here, that gives us the alveoli and it’s in the alveoli where we have the exchange between the oxygen coming into the bloodstream, via the capillaries that we have here, and the carbon dioxide leaving the capillaries going into the lungs and being sent from the body. Now, when the blood comes in here, it is picking up oxygen, and the type of blood cells that are picking up the oxygen, would be the red blood cells. Here you can see a picture of a few red blood cells, of course, it’s simplified. It’s not showing the white blood cells or anything else. It’s just showing the red blood cells and these are the blood cells that pick up that oxygen. In the red blood cells, we have special molecule. That molecule is called hemoglobin. You can see a three-dimensional image here of the structure of hemoglobin so, this is, (let me write it here), hemoglobin. This molecule, it’s actually a protein, and this protein is the protein that is responsible for picking up the oxygen. Now, let’s go into a little more detail. You can see here, that we have these four structures. Those four structures are called, (let’s do that in blue), those are heme groups. All right, so these are the four heme groups. The special thing about these heme groups is that those are the parts where the oxygen is attracted, so, we have O2 that actually comes and binds to the heme groups. As you would imagine since we have four heme groups, we can take a total of four oxygen molecules. So, this is one oxygen molecule here, and we can have another oxygen molecule here, here, and also here. So, this hemoglobin molecule once again, has a capacity to hold four oxygen molecules. What’s interesting about the hemoglobin is that whenever one oxygen binds to a heme group, that causes the entire hemoglobin structure to undergo a conformational change so, basically changing the site of the molecule whenever one oxygen binds. As you can see here, this is the heme group but, there’s stuff around on it, and you can imagine that it would be relatively hard for the oxygen to get in there and find the right spot. However, when one binds, it causes a change which opens it up a little bit to make it a little easier for another oxygen to come in and bind. And, when that other oxygen comes in and bind, it causes another conformational change, making it easier for another oxygen to come and bind and, once again, once that oxygen comes and binds here, it makes it easier for another oxygen to come in here and bind to it. So, in other words, as it starts taking up oxygen, it makes it easier for it to take up more oxygen. And then, of course, the opposite will be true. If we have a hemoglobin molecule that has four oxygen attached and, for some reason it gives up one oxygen, that’s going to cause a change that makes it a little harder for the other oxygen to bind. In other words, | 6/7/11 | Free | View In iTunes |
| 2 | Video059 An Introduction to the Respiratory System | httpv://www.youtube.com/watch?v=aoa50sd7lWM Click Here to Download This Video We are off to start learning from a new set of videos about another part of the human body system and here, Leslie opens a new topic with a brief introduction of the Respiratory System. Watch and enjoy! Transcript of Today's Episode Hello and welcome to another episode of Interactive-Biology T.V. where we’re making Biology fun! My name is Leslie Samuel and in this episode, Episode 59, I’m going to be giving an introduction to the respiratory system. So, we’re changing gears now. We just finished talking about the circulatory system and, now, we’re going to talk about a system that is very closely linked to the circulatory system that is, the respiratory system. So, let’s get right into it. Here, we’re looking at a bunch of ladies. These ladies are exercising. They are working out in the gym. Some of them are on the, like over here you can see we have one on an elliptical then, we have some riding exercise, bikes and lifting some dumbbells here and boxing a punching bag, punching a punching bag and there’s a lot going on right here. There’s one thing that these ladies all have in common, well, there are a number of things that these ladies have in common. They’re all attractive that’s one. They’re all exercising but, the thing that I want to focus on is that they are all breathing. I hope that make sense. They are all breathing, they are working out and in order to be able to get the energy that they need, they need to be breathing in oxygen. There are a number of things that have to happen in that process and we are going to talk about that today. So, whether you’re exercising or you’re just standing still or even if you are sleeping, you need to be breathing if you’re going to be alive of course, and we’re going to be talking about that today. So, let’s get right into it. In order for us to have energy, there is a process that needs to happen and this process is called, ‘cellular respiration.’ Now, we’re not going to go into too much detail in terms of cellular respiration in this episode but, we are going to come back to it. The main thing that I want us to look at is the formula for cellular respiration, and that formula is: If you’re a biologist, you’re into Biology, you’re in a Biology class, or whatever the case might be, I think, it’s imperative for you to know this formula. So, memorize this formula: Now, let’s give some names to these bad boys. This guy over here (C6H12O6), that is none other glucose, okay so that a carbohydrate, it’s a type of sugar. O2, you should know that is oxygen. And then, of course CO2 is carbon dioxide and H2O, if you don’t know this, something is wrong, that is water. Well, maybe nothing is wrong, maybe you just never heard of it before. But, anyhow so, we have glucose that’s reacting with oxygen and the products, so these are the reactants on the left, the products on the right are carbon dioxide and water. And this right here is the general equation for cellular respiration. It is an oversimplification but, it gives you the things that are necessary and the things that are produced. Now, glucose, where do we get this from? Well, of course, we eat, right? We take in some food and we get glucose. So, let’s say we get this (glucose) from eating, oxygen, we get this from breathing, there’s oxygen in the air and, when we breathe, we bring in that oxygen that we need. Carbon dioxide, this is actually a waste product. We’re producing this but, we don’t actually use it. When we breathe, we breathe that out and that goes into the air, and that’s used by plants and plants can use that for photosynthesis. Water, do we need water? Yes, of course we need water. I’m not going to write anything right here because it’s just water. Water is essential for life and we are actually producing water in this process of cellular respiration. In doing this enti | 6/6/11 | Free | View In iTunes |
| 3 | Video058 Net Hydrostatic Pressure and Filtration Pressure | httpv://www.youtube.com/watch?v=OP4Xh4oawG8ha Click Here to Download This Video 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 great | 5/31/11 | Free | View In iTunes |
| 4 | Video057 Pressure Reflexes and Mean Arterial Pressure | httpv://www.youtube.com/watch?v=DfAyZwsIYR4 Click Here to Download This Video 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, | 5/26/11 | Free | View In iTunes |
| 5 | Video056 Regulating Peripheral Resistance – Part 2 | httpv://www.youtube.com/watch?v=MRcra9oxrXY Click Here to Download This Video 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. | 5/26/11 | Free | View In iTunes |
| 6 | Video055 Regulating Peripheral Resistance – Part 1 | httpv://www.youtube.com/watch?v=14Z8GNLU4os Click Here to Download This Video 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 changi | 5/26/11 | Free | View In iTunes |
| 7 | Video054 Blood Pressure and Mean Arterial Pressure | httpv://www.youtube.com/watch?v=BnPdf8Te93I Click Here to Download This Video [DAP isPaidUser="Y" hasAccessTo="3" errMsgTemplate=""]…private…[/DAP] 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 i | 5/25/11 | Free | View In iTunes |
| 8 | Video053 Cardiac Output | httpv://www.youtube.com/watch?v=Wx1_8iTUanA Click Here to Download This Video 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 chan | 5/23/11 | Free | View In iTunes |
| 9 | Video052 The Cardiac Cycle | httpv://www.youtube.com/watch?v=kcWNjt77uHc Click Here to Download This Video 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 t | 5/23/11 | Free | View In iTunes |
| 10 | Video051 Isovolumetric Contraction | httpv://www.youtube.com/watch?v=SctzRlx3F1s Click Here to Download This Video 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, | 4/8/11 | Free | View In iTunes |
| 11 | Video050 Regulating Stroke Volume, Skeletal Muscle Pump and Frank-Starling Mechanism | httpv://www.youtube.com/watch?v=SvOaUrfywd8 Click Here to Download This Video 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, | 4/7/11 | Free | View In iTunes |
| 12 | Video049 What Stroke Volume is and How to Calculate It | httpv://www.youtube.com/watch?v=JFIciyGWJb4 Click Here to Download This Video 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, | 4/4/11 | Free | View In iTunes |
| 13 | Video048 How to Read an Electrocardiogram (ECG/EKG) | httpv://www.youtube.com/watch?v=4vkbywows-o Click Here to Download This Video 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. | 4/1/11 | Free | View In iTunes |
| 14 | Video047 Action Potentials and Contraction in Cardiac Muscle Cells | httpv://www.youtube.com/watch?v=xpR8d9KsUrQ Click Here to Download This Video 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, | 3/31/11 | Free | View In iTunes |
| 15 | Video046 How Adrenaline and Acetylcholine Affect Heart Rate | httpv://www.youtube.com/watch?v=2MkYAXTCYcQ Click Here to Download This Video 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. | 3/30/11 | Free | View In iTunes |
| 16 | Video045 The Pacemaker Potential of the SA Node and the AV Node | httpv://www.youtube.com/watch?v=0xUifyll2Oc Click Here to Download This Video 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 rushin | 3/29/11 | Free | View In iTunes |
| 17 | Video044 How Blood Flows Through the Heart | httpv://www.youtube.com/watch?v=VUtehbgbpRk Click Here to Download This Video 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. | 3/28/11 | Free | View In iTunes |
| 18 | Video043 The Details of Muscle Contraction | httpv://www.youtube.com/watch?v=f0mDFP7qn1Y Click Here to Download This Video Join Leslie as he shares this last video on muscle contraction explaining with full clarity the smallest details on how this 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 43, I am going to go into the details of muscle contraction. This is going to be the last video in the muscle contraction series, so, enjoy! Let’s get right into it. You can always go back to Episode 42 to refresh your memory but, we said that the functional unit of contraction is called the sarcomere and, that is what we’re looking at right now. This unit is one sarcomere. We said that we have a thick filament that is called myosin and, we have a thin filament that is called actin. We said that, when muscle contraction happens, the more the neuron releases neurotransmitter that stimulates calcium release. When that happens, the fibers slide against each other just like this. So, as the muscle fibers becomes shorter, that is the muscle contracting. And you can clearly see that in this animation. The reason we said that this can happen is because on the myosin filaments, we have these heads and those heads extend and bind to the actin. When they bind, they kind of flex so, it moves in this direction and that pulls the actin shortening the sarcomere. What we are going to do today is we’re going to look at the details of what is happening there. We are going to look at six steps in muscle contraction. This is another image that’s showing something similar to what we’ve looked at. We have the myosin heads. Let me do that in a different color so that you can make sure to see it because we have a lot of red there. We have the myosin heads that are binding to the actin filaments. Here, we are going to be looking at that in more details. We have the actin. Yes, it’s a different spelling because it’s from a different language but, on the actin filaments, there are two things that are very important. We have tropomyosin as you see here so that’s this long strand here. On top of the tropomyosin, we have troponin. This is a complex that we find all along the actin filaments. Here’s the situation. Because this is here, the myosin heads want to bind to the actin. There’s some binding sites on the actin so, let’s say this is a binding site right here. But, what’s the problem? The tropomyosin is covering that binding site so, the myosin heads cannot bind. Okay, so, we have these myosin head-binding sites all along the actin; myosin heads want to bind, we have all these myosin heads ready to do their business but, they cannot because it’s blocked by the tropomyosin. All right so, let’s go now and look at the six steps of muscle contraction. Step number one. Calcium is released from the terminal cisternae. Remember we said that the terminal cisternae is a part of the sarcoplasmic reticulum and that is where calcium is stored. So, calcium is released. You can see here, we have this little binding site for the calcium so the calcium now comes and binds the troponin. So, here we have calcium and binding to the troponin. And then, what that does is it causes a conformational change. To put it more simply, we’re just moving the tropomyosin-troponin complex. So, that moves and, when that moves, it exposes the binding sites on the actin. That’s step number one. So, step number one: We had calcium in the terminal cisternae that is released when there’s a stimulus. The calcium ions bind to the troponin causing a conformational change in the troponin-tropomyosin complex. In other words, it’s moving out of the way. And then, the next step can happen. That step is, the myosin heads can bind to the binding sites on the actin. So, this is the one binding site. For simplification we’re just showing one myosin head but, | 3/23/11 | Free | View In iTunes |
| 19 | Video042 How the Release of Calcium Ions Results in Muscle Contraction | Now that you have an overview as to how muscle contraction works, here Leslie now discusses in more detail how it is affected in the presence of calcium. What really happens when these ions are released? Watch to learn more and enjoy! Enjoy! | 3/9/11 | Free | View In iTunes |
| 20 | Video041 An Introduction to Skeletal Muscle Contraction | Ever wonder how our muscles contract and what makes them do so? In this video, Leslie gives a clear overview of how muscle contraction works. Enjoy! | 3/8/11 | Free | View In iTunes |
| 21 | Video040 The Role of Hair Cells in Hearing | Do you ever wonder what happens to the hair cells inside our ears as we hear sound? What role do these tiny hairs have in hearing? Watch this short movie as Leslie explains clearly and vividly enough for us to understand the main role of these tiny hair cells as sound enters our ears. Enjoy! | 3/1/11 | Free | View In iTunes |
| 22 | Video039 The Function of the Organ of Corti | httpv://www.youtube.com/watch?v=fSO6i5qNWG0 Click Here to Download This Video The organ of corti - such a small part of the cochlea with such a major function. Watch as Leslie demonstrates how the vibrations in the cochlea affect the cilia on the hair cells, and how this process is translated to hearing. There's also a really cool video of a hair cell dancing to Rock Music. 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 39, I’m going to be talking about the function of the Organ of Corti. And don’t worry, I won’t be singing in this episode. That’s Episode 38. So, if you want to hear me sing, go to Episode 38 and enjoy! Today, we are just going to talk about the function of the Organ of Corti. So let’s get right into it! Now, we’ve been looking at this picture and we’ve been looking at the structure of the ear. We look at the fact that sound waves come in here; cause vibration in the tympanic membrane; causing the malleus, incus, and stapes to vibrate; and then causing the fluid inside of the cochlea to vibrate. In the last episode, we unrolled the cochlea and we looked at it like this. And we showed that, depending on where it vibrates, that’s going to send signals to the brain, and the brain can interpret that as a certain pitch, a certain frequency. Now, there are a few things that I want you to pay attention to in this episode that we did not pay attention to in the previous episodes. And that would be here. We have the scala vestibuli. That’s this cavity at the top here. And below the basilar membrane, we have the scala tympani. And that’s the cavity at the bottom of the cochlea, beneath the basilar membrane. And what I’m going to do in the next picture is, I’m going to actually take a cross-section. So I’m going to cut straight through the cochlea like this, and we are going to look at a cross- section of the cochlea. So let’s go to the next figure. Here, we are looking at the cross-section of the cochlea. And here, you can see we have the scala vestibuli. And here we have the scala tympani. And here, this is the basilar membrane. And right above the basilar membrane, we have the Organ of Corti. So that’s this section right here. We can’t see too many details about it, but that is the Organ of Corti. Here we can see more details. This entire structure is the Organ of Corti. But I just want you to pay attention to how it is laid out here, with the Organ of Corti here, scala vestibuli at the top. This is the basilar membrane. And here we have the scala tympani. One more place that I want you to pay attention to, here, is another cavity we call the cochlear duct. And once again, in here we have the Organ of Corti. So this is a cross-section of the cochlea, and that’s how it’s laid out. Now, I want to bring your attention to the Organ of Corti which is shown clearly right here. Once again, we can see here we have the basilar membrane, and on top of that we have the Organ of Corti. A few more things to point out here. This membrane here, it says membrana tectoria. We call this the tectorial membrane. And we look at the fact that, when sound enters the cochlea, that causes the basilar membrane to vibrate up-and-down. Now, when that vibrates up-and-down, that’s going to cause the Organ of Corti to move up and down. Then, here we have the tectorial membrane that’s attached only at one end. So, as the basilar membrane is going up-and-down and the Organ of Corti is going up-and-down, that is going to cause the tectorial membrane to move in a windshield- wiper-like fashion. So it’s just going to flap like a windshield wiper. Now, in the Organ of Corti, we have a number of different hair cells. We have inner hair cells, which would be this one here; and we have outer hair cells, which would be these four here. Now, as you can imagine, | 2/24/11 | Free | View In iTunes |
| 23 | Video038 How We Hear Different Pitches | How does the ear allow you to distinguish between various pitches? Watch this video and listen as Leslie details the processes in the inner ear that result in us being able to tell the difference. Enjoy! | 2/24/11 | Free | View In iTunes |
| 24 | Video037 How Sound is Transferred to the Inner Ear | In this episode, Leslie talks about how sound is transferred to the inner ear. Because there is fluid inside the cochlea, impedance matching has to take place for the vibration in the fluid to accurately represent the sound that you are hearing. Watch this video to learn how this process works. | 2/21/11 | Free | View In iTunes |
| 25 | Video036 An Overview of the Mechanism of Hearing | In this episode, Leslie talks about how we hear sounds. From the external ear to the eardrum, down to the 3 bony ossicles, then to the cochlea to be sent as signals towards the brain, it is all explained in this video. Enjoy! | 2/18/11 | Free | View In iTunes |
| 26 | Video035 On Center, Off Surround Ganglion Cells | In this episode, Leslie tells us about on center, off surround ganglion cells. See how the configuration of rods with respect to the ganglion cell's receptive field influences the type of response we get when those rods are stimulated. Enjoy! | 2/17/11 | Free | View In iTunes |
| 27 | Video034 How Lateral Inhibition Enhances Visual Edges | In this video, Leslie explains all about lateral inhibition using two rectangles. Watch to learn how this process helps us see edges of objects more clearly. Enjoy! | 2/16/11 | Free | View In iTunes |
| 28 | Video033 The Receptive Field of a Ganglion Cell | In this episode, Leslie explains more about the connections between rods and cones to bipolar cells, and between bipolar cells and ganglion cells. He also describes how these connections determine the receptive fields of each ganglion cell. Enjoy! | 2/16/11 | Free | View In iTunes |
| 29 | Video032 Visual Processing in the Retina | After the rods and the cones, there are a few other important cells involved in visual processing. In this video, Leslie explains about how the bipolar cells and ganglion cells contribute to this process. Enjoy! | 2/11/11 | Free | View In iTunes |
| 30 | Video031 How Rods and Cones Respond to Light | In this video, Leslie explains how rods and cones work, using the rods as an example. Watch to find out how rhodopsin, transducin, and phosphodiesterase, all play a major role in the process of vision. Enjoy! | 2/8/11 | Free | View In iTunes |
| 31 | Video030 How Eyes Work – An Introduction | In this video, Leslie explains all about how we are able to see with our eyes. Enjoy! | 2/4/11 | Free | View In iTunes |
| 32 | Video029 A General Overview of How Senses Work | In this video, Leslie explains the general mechanism of how senses work. Enjoy! | 2/3/11 | Free | View In iTunes |
| 33 | Video028 The Thalamus and Hypothalamus | In this video, Leslie explains about the thalamus and the hypothalamus, and the specific functions that they are responsible for. Enjoy! | 2/2/11 | Free | View In iTunes |
| 34 | Video027 The 3 Parts of the Brain Stem and their Functions | In this video, Leslie explains about the different parts of the brain stem and their respective functions. Enjoy! | 2/1/11 | Free | View In iTunes |
| 35 | Video026 The Function of the Cerebellum | In this video, Leslie describes the cerebellum and explains how it's involved in coordination of movements. Enjoy! | 1/31/11 | Free | View In iTunes |
| 36 | Video025 The 4 Lobes of the Cerebrum and their Functions | In this video, Leslie tells us about the cerebrum and the specific functions that each of its 4 lobes are responsible for. Wanna know why you are the way you are? Go ahead - watch and find out! Enjoy! | 1/28/11 | Free | View In iTunes |
| 37 | Video024 Re: nicodube23 How Myelin sheaths Speed up the Action Potential | In this video, Leslie clarifies how the myelin sheaths speed up the conduction of the action potential, in response to nicodube23's question posted on YouTube. Enjoy! | 1/27/11 | Free | View In iTunes |
| 38 | Video023 How Reflexes Work (Knee Jerk and Eye Blink) | In this video, Leslie's wife helps to demonstrate both the knee jerk and the eye blink reflexes. Watch as Leslie explains how both of these reflexes work. Enjoy! | 1/25/11 | Free | View In iTunes |
| 39 | Video022 Re: Akbar – Inactivation of V-gated Sodium Channels | This is a video answering Akbar's question regarding the difference between the inactive and closed states of voltage-gated sodium channels. Watch as Leslie explains this difference using a box. | 1/24/11 | Free | View In iTunes |
| Total: 39 Episodes |
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- LHS Biology Teachers
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- Mr. Craig's Biology Podcasts
- Jesse Craig
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- Carleton University Television - Biology 1903
- Carleton University Television
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