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And hello everybody. Uh Thank you everybody for coming. I'm just here to moderate and give it a little bit of an introduction. I'm Donovan Campbell, I'm the treasure cardio. So, but I'm here just to welcome uh t this evening, um K is our social media officer and he has taken us through cardiac physiology this evening. Uh If there's any questions at any point during the chat, just fire into the uh messages section there on the side or yeah, we can address them at the end or so. There is a few questions as well. So I'll be out in a few polls in for you to get stuck in and we can't see who's answering. So there's no right or wrong answers in this case. So if I further day I'll pass over the tur and somebody can say, well, you can see here t to see the slides, OK, as well. And the job that would be great. So, thank you. Um Well, hello there everybody. My name is Steve. I'm a second year medical student at Queens and I'll be leading the session for cardiac physiology. If you guys could just go ahead and let me know if, if I'm audible as well as my screen, uh as, as well as my slides, if they're visible to send a text in the chart. Perfect. Ok. Thank you, Emily. Um Again, first of all, this presentation is made by James who is um also a part of the County Society. Um I, if I'm not wrong, I think he is the secretary. But yeah, so here's thanks to him for, for sharing his slides with me. Um We're gonna be talking about cardiac physiology and these are the things that we're gonna go over. So there's the cardiac elective physiology, the cardiac cycle, the output control of BP and the control of region of blood flow. Um Before we start, I think it's important to preface this, that understanding the physiology is quite important. But I don't want you guys to get uh but I don't want you guys to get too caught up with understanding the nitty gritty of this physiology because I think the best way to study um a system is by studying the pathology first, then coming down to the path of physiology and then finally, the physiology and that just helps. It's, it's like a backwards system, but that helps set a frame. And that's a strategy strategy that I use. Uh but just starting on, on the physiology. When we talk about the heart, there's two main types of cells. We've got the cardiac pacemaker cells and then we've got the cardiac nonpacemaker cells. The difference is that these cardiac pacemaker cells, they've got the ability to intrinsically generate action potentials. The cardiac pacemaker cells by their names, uh by their name, uh represents that they are the ones responsible for initiating and maintaining um the rate of uh the rate of the heartbeat. So what we know as 60 to 100 beats that is regulated by these cardiac pacemaker cells, the average pace is around 72 BPM. So these specialized pacemaker cells then again are located in the SA N and the AVN uh that stands for the sinoatrial node and the atrioventricular node. And you guys might have covered this in the previous anatomy lecture. But just as a quick recap, the sino atrial node is located in the superior wall of the right atrium just beneath the superior vena cava, the opening of the superior vena cava and the A V node is present at the tip of the interventricular septum. Um And both of these are then uh capable of generating their own action potentials. Just um as I ta here again, just remember that s dominates a basically the action potential generated by the sinoatrial node is what determines the base of the heart. It's not the one generated by the AVN cause that happens as well in certain pathologies. So the sinoatrial node controls the number of heartbeats. Uh and now just looking at the action potential of these cardiac pacemaker cells, they're different to the cardiac myocytes of the non pacemaker cells. Uh These ones have got 12 and 33 phases, but they're numbered in a very weird manner. So it so it starts off with phase four, phase zero, phase three. If you before actually diving into the electrophysiology, there is a few terms I need to know. Um there is depolarization, depolarization, hyperpolarization. So, depolarization basically means making anything positive and that leads to contraction. Uh repolarization is making anything negative and that leads to relaxation. And then finally, hyperpolarization is taking it to a very negative state. It's like repolarization but much, much more intense if that makes sense. So the resting membrane potential is what is what potential these cardiac pacemaker cells are at uh continuously or as a normal. And it's from this minus 60 millivolts uh is where the action action potential starts generating. And we get these action potentials then. So we start off with the phase with the fourth phase, which is as written here, slow diastolic depolarization. And what happens in this case is you get, you get sodium influx, it's a slow sodium influx. So because it says depolarization, we're moving from a, we're moving from ne negative 60 up to negative 40 that negative 40 is known as the threshold potential. So as sodium moves into the cell, we have it moving from uh minus 60 to minus 40 reaching the threshold. And what happens at threshold is we get rapid influx, rapid influx of calcium, um calcium ions. So at the threshold potential, we get voltage gated calcium channels opening up and that leads to rapid influx and that pushes the overall potential to a positive that is above zero. Here, once we reach that positive phase, we enter repolarization because these cells can't be depolarized always. So in the repolarization phase, what happens is the calcium channels are inactivated and potassium channels open up potassium has a tendency of moving from within the cell to outside the cell because that's how the concentration gradient is. So potassium then moves outside the cell and potassium being a positive ion leaving the cell would then make it fall to a lower potential so quickly, just to summarize everything. Again, we've got massive sodium in well slow sodium influx in the beginning to push it from resting membrane potential to threshold potential. Following that, we've got, we've got the calcium channels which open up, which further intensifies calcium influx, bring it up to a positive potential. The calcium channels, close potassium channels, open up potassium efflux. Therefore, we get the drop and then finally, we go back into going into phase four. Now, there is the autonomic nervous system control here. Uh that says that the heart rate is affected by the PNS and the S NS. Now, the PNS stands for the parasympathetic nervous system. S NS stands for the sympathetic nervous system the way these work is the parasympathetic nervous system. When stimulated releases a neurotransmitter, uh which we in short called ach or acetylcholine. This acetylcholine then goes and acts on mt tousin receptors within the sinoatrial node to reduce the heart rate because these cells are the ones that regulate the heart rate. So when, when the PNS acts on it, they act specifically on the musculin receptors. Conversely, we've got the sympathetic nervous system, sympathetic nervous system is your fight or flight system. So it tends to increase your heart rate to improve blood circulation. So what they do is upon stimulation release, not adeno, this no adrenaline then goes and acts on beta one Adreno receptors which then increase the heart rate. Um Donovan, if you can just put up a poll, uh This is our first question for the night guys, which of these locations is normally the natural pacemaker site of cardiac muscles. A is the sign of atrial node. B is your atrioventricular node. C is your coronary sinus T is ventricular myocytes and E is for KG fibers. So I'm not too sure as to how many people we've got live on call today, but there is a few responses there. And as I think most of them have selected the correct answer, I think in fact, all of you have selected the correct answer. So I think you can just go ahead then and stop the pull. It is indeed the sinoatrial node which is the natural pacemaker site of the cardiac muscle. The atrioventricular node is also a pacemaker site. But then we know that s dominates a. So whatever the sinoatrial node decides is what's going to happen to the heart. We've got a second question here. Again, it don if you just mind releasing this one as well, when the parasympathetic nervous system releases ac or acetylcholine to act to decrease the heart rate. What receptor does it act on? A is beta one adrenoreceptor. Second is new opioid receptor. So is alpha alpha one, a adrenoceptor. And the last one is the muscarinic two second receptor or the two receptor. Now, just to quickly remind you guys, we had the parasympathetic nervous system, which is your rest and digest. If you wanna, if you wanna have it, check to remember it pa ra. So it's called R and parasympathetic R stands for rest and digest. So this is when the heart rate is reduced. We've got different neurotransmitters for the parasympathetic and we've got different neurotransmitters for the sympathetic system, sympathetic is fight, fight or flight. So there is a bit of a mixed answer. Uh Well, there's, there's two main options that people are selected. It's the beta one adrenoceptor and the second is the muscarinic receptor. So the beta one adrenoceptor is acted upon by your noradrenaline, which comes from your sympathetic nervous system. So, if it was to increase the heart rate, yes, beta, one adrenoceptor is the correct answer. But in this case, the actual correct answer is musculin two receptors because they are stimulated by acetylcholine, which is then released, which is actually released by the parasympathetic nervous system. So, we've got a proper split here, 55% answering Musc musculin receptor and 44% answering beta one receptor. Uh I think you should be good to stop the pole. Now, uh then we've called the electrophysiology of uh of ventricular myocytes. So if you guys remember in the beginning, I mentioned that we've got two types of cardiac cells. One is your pacemaker cells that have um a national potential including phase 40 and three. And the second one is your ventricular myocytes or the cardiac nonpacemaker cells. Now, these cardiac myocytes are connected to the pacemaker cells via gap junctions. That's what you have to take away from all of this here basically. And they're different from the normal or they're different from the pacemaker cells in the sense that they've got five phases, that's phase zero, phase 123 and four. the main channels that act, I mean the main channels involved in this in this mechanism. Excuse me is the sodium potassium and the calcium channels. So just moving on here, now you'll see that this action potential is very much different from the action potential that we had in the the cardiac pacemaker cells where it just went up and down in a simple wave here. This um this particular one is very important because if you look at phase two, there, you'll see that it's a bit of a plateau and that is related to, well, whenever you're starting your pathology, you will talk about that phase two quite a lot. So just again to put this into context, this these cells are the cells that contract, they do not have the ability to generate their own action potentials. So they are stimulated by the action potentials generated by the N and the AVN, the cardiac pacemaker cells. Um They for, for the cardiac myocytes, the non pacemaker cells, they've got phase 0123 and four. Phase four is the resting membrane potential, which it says minus 85 here. But you'll find multiple books getting different values. It's usually around minus 90 millivolts. So what happens here is in the zero phase, there is a rapid influx uh of sodium. So when they're at the resting membrane potential at around minus 90 millivolt, they are slowly stimulated by the SA N and AVN uh via calcium. So there is, there is just a tiny influx of calcium initially to push it from minus 90 to around minus 70. Uh and when it reaches minus 70 that's its threshold potential. As you can see here, phase zero shoots up. Uh and that is just when you reach threshold potential, your calcium channels, sorry, your sodium channels open up and there's a rapid influx of sodium causing it to go from minus 70 to a positive action potential to a positive voltage. Uh And what happens at the end of your phase zero? Once it's reached that positive potential, uh your sodium channel closes and your potassium channels open up. Uh If you remember, I mentioned that potassium has a tendency to leave cells. So whenever your potas potassium channels open up, they leave uh and a positive atom or a positive ion leaving will make you lose that the positive voltage within the cells. So you tend to fall down. As you can see, there's a droop in phase one. Again, phase zero, rapid influx of sodium. Phase one is slow leaking of of potassium. And something interesting happens in the second phase here. The phase two where it's there's there's there's slow influx of sorry, there's slow efflux of potassium. So potassium is still leaving here in the second phase. Following from the first one, it slowly leaves here. But to counter that there is uh a similar influx of calcium which is why there's a battle between the positive ions because potassium is trying to leave calcium is entering. So it it goes ahead and then forms a plateau here. And eventually, I think at, at around 10 millivolts is when, if I just go on here to the next slide, you'll see phase three here at 10 millivolts around around that voltage. After phase two is when the calcium channels close and potassium channels are open and then there is a rapid efflux of potassium which causes this drop down in the third phase again, just now, quickly put everything together because I know I've said quite, quite a lot of things. So phase zero is your rapid sodium influx. Phase zero pushes it from minus 70 to a positive potential. After that, after attaining that positive potential, we move on from, we move on from the phase zero to phase one. Phase one is when potassium channels open up, potassium has a tendency to leave. So there's an efflux that efflux leaves the cell a bit more negative but it is still positive, meaning it's still above zero, the act the the actual voltage of it. So that's what phase one, that's what happens in phase one, potassium leaves phase three, you've got potassium leaving, but calcium coming in. And then finally, phase three is when calcium, calcium stops coming in. And we've got massive or rapid potassium efflux, which brings it down again to your uh to your resting membrane potential. And within the resting membrane potential, it is your sodium potassium pumps which ensure that it stays uh effectively at your resting membrane potential. So these action potentials continue to happen over time. Uh And you see that we've mentioned 200 milliseconds there, I think that's called the refractory period. It is. And within during this period, you cannot give another stimulus to excite the cardiac myocytes again. So it will complete this entire action potential. And only then can another stimulus from the sinus atrial? No, the atrioventricular node stimulate the cardiac myocyte to, to contract again. Right. We've got another question here. Then just keep in mind, I did talk about the second phase. That's when we've got two ions battling each other. Both of them are positive, one's leaving the other one's entering if you could just go ahead and put the pull up. Perfect. So the question is what ion in phase two V action potential maintains the phase, preventing rapid depolarization. OK. So I see that there's mixed answers so far, but it's between the two, but it's between the two actual ions. So we're still on the right track. Well, someone's just gone ahead and selected completely. So, so something very different, but that's alright. We'll speak about this in a bit. So I see a lot of the answers are pointing towards potassium. Uh and that could be one of the answers but to, to prevent the rapid repolarization. Uh if you guys remember, repolarization is the negative charge. So calcium tends to come in to bring in the positive charge. So realistically, the answer in this case should be the calcium because again, just to quickly summarize the plato bit, which is the phase two potassium channels open up. Uh calcium channels are also open. So potassium efflux, it's a positive ion leaving the cell and as a result, it be much more negative the cell, the interior of the cell. But we've got calcium that comes in keeping it, keeping it positive. So in this particular case, the answer is calcium, this is just a better representation of the ventricular action potential or the action potential of just the normal cardiac myocytes, the nonpacemaker cells. Um Again, here, phase four, phase zero, we've got the rapid sodium influx. Phase one is when we've got potassium leaving slowly trickling out is what we call it. Uh And then the second phase, we've got potassium leaving calcium coming in. And the third phase calcium, sorry, potassium leaves. The fourth is then maintained by the sodium potassium box here. Oh Also the finger on the left here, I think uh you'll come across it uh in our lectures as well when you guys start PCR, if you guys are your one students and that'll help summarize uh everything appropriately. Now, moving on to the cardiac conduction system. So, unfortunately, I'm not able to use a pointer here. So I'm just gonna have to walk you guys through through what's on the screen here. The conduction system uh of the heart has two main components. The SA and the AVN the sinoatrial node, which if you look here is located superiorly in the right atria just underneath the opening of the superior vena cava. So the sinoatrial node generates electrical impulses and transmits them to the node within the right atrium via the internodal pathways and to the left atrium. If you see, there's a particular bundle here called the Bachman's bundle, that's how it, that's how it transmits the electrical impulses to the left atrium. So once the electrical impulse has been transport, transported from the SA N to the VN, the N is uh is specialized in a way that it holds onto the colon for a bit. Because if you know the heart pumps, atria, ventricle, atria ventricle. So if in case, there was no, if, if in case the Avian did not hold on to this current A ta and the ventricles would bump together and that would render the heart in insufficient or maybe it was just, it'll, it'll lead to heart failure because it's not filling up well enough and it's not contracting effectively. So the AVN is specialized in order to hold on to that colon for a bit and then pass it down to your left, your bundle of left and right bundle of his and then finally your pre K fibers. So if you guys just want to go ahead and have a look at the, at the actual heart diagram here, we've got the essay node, top uh top right corner uh in the heart. So superior border on the superior wall of the right atrium node is just at the in the interventricular septum. And then we've got the bundles the, the bundle of his splitting into the right bundle branch, the left bundle branch. And then finally, we've got tiny fibers coming off of it referred to as the burn fibers. The the Burkin fibers are responsible for causing ventricular systole. So electrical impulse from the bur perkin fibers then cause the ventricles to contract. Ok. So, well, we'll, we'll come back here for a second actually. Um I forgot to explain as to why the AVN holds onto this current or how it does. So, so the electrical impulses are transmitted mainly via gap junctions. And the more gap junctions you have the quicker the transmission of elect uh the quicker the transmission of the electrical signals is occurs. Uh in the AVN particularly, we've got less gap junctions. So whenever there's less gap junctions, the current, the flow of the current is reduced, the speed is reduced. Therefore, the A BN tends to hold on to this current. If anyone was just curious as to why that happens. Now, moving on to the question here. Uh The fourth question don, if you can just put it, put up the pole here, uh at what cardiac structure is the electrical action potential delayed by around 120 milliseconds. Is it a the sino atrial node? B the atrioventricular node C the breaking fibers, D bundle of phase or E ma membranous intraventricular septum? No. So this one's yeah, everyone's gone for the correct answers here. It's stage of ventricular node. Perfect. Yeah. Moving on now. To the E CG. So this one's, this is basically the fun bit. This is what all cardiology sweats want to know artery and ECG. We're not gonna dive too much into depth. But at the bottom there, we've got a really interesting piece of information. The bottom left corner, I'll just walk you through what we're looking at right now. Um I think we're all aware of the different waves that we see within an ecg uh the P wave, the QR S complex, the T wave. Uh And then there's also au wave that I'm not aware of. But uh we're not going to talk about that. The B wave represents the atrial depolarization. Again, depolarization, making it positive leads to contraction, atrial depolarization basically means atrial contraction. We've got the P wave, we've got the PR segment uh which is basically the time between the atrial systole and the ventricular systole. So the QRS complex is the ventricular systole is when the ventricles, is, is when the ventricles contract basically. And following that, we've got the ST segment and then we've got the T wave, the T wave is ventricular repolarization, which is ventricular relaxation, the PR segment and the ST segment. Uh they're quite important when it comes to pathologies because you'll be looking at uh I think if we've all heard of terms such as sties and these are basically myocardial infarctions uh that have ST elevation or ST depress, that's following the G point it may be either if you can just look at that the G point after the S wave or if it is a semi, which is an ST segment elevated myocardial infarction, the line following the J point will not be straight, it will be elevated. Uh And I think we've further gone here and broken down the QR S complex into Q wave R and S wave, Q wave is the initial ventricular depolarization R wave is when the bulk of the ventricular depolarization take takes place. And then finally, the ventricular S wave represents the depolarization from the apex of the base. So when we talk about the heart, the tip of the heart, the bottommost part of the heart is referred to as the apex and your contraction happens in an opposite direction. So it starts from the apex and then goes up. Uh and then the interesting bit that I was talking about uh at the bottom left corner here, we've got the ECG cardiac the. So if you guys, I mean, I don't know if you guys have heard of terms such as an inferior wall, mi a lateral wall M I anterior wall M I uh you often tend to come to such conclusions, often looking at an ECG uh and if you ever looked at an ECG strip, we've got lead, one leads, 123. And then we've got a VL A VR aVF and then we've got B1 to B6. Now, placing of these um electrodes, uh you guys will learn that eventually if you guys are in your one, they're, they're located all around your heart and a few on your uh on, on your list as well. Uh Whenever you look at the ECG strip, you tend to focus on your second lead, which is the longest one, the one that you get at the bottom. Uh And if there is any, well, if we just look over here, so it says inferior do three and aVF signify the inferior wall. So any changes in your ECG within your strips or, or within the, the 2nd 3rd of the AV F lead is uh representing a pathology in the inner wall of the heart. And the inferior wall of the heart is supplied by the right coronary artery. Then we've got the lateral wall of the heart. Uh and uh and pathology related to the lateral wall of the heart can be, can be seen in the ECG strip pertaining to leads one aVL, AVR B5 and B6. And these are supplied by the left circumflex artery. So if someone was to have a lateral wall, mi, that probably means that their left circumference artery is occluded. And as a result, there's ischemia. So blood isn't being supplied to the heart and then that causes death of the heart wall, which is known as an M, we've got the anterior leads that, that's, that includes B3 and B four, the interior wall is supplied by the L ad the left anterior descending. You would have come across that in your previous lectures uh talking about cardiac anatomy. And then finally, we've got the septal uh septal lead, which is we one and we do now this bit. Uh I'm not gonna go too in depth with this because it's really, I don't think it's that important when it comes to when it comes to cardiac physiology. I'm just gonna give you a brief overview. So in the diagram here, it says can induce calcium release. So what happens is um cardiac muscles they contract using the sliding filament theory. Uh And that is important when it comes to physiology because it is a particular theory by which your actin myosin et cetera, your your proteins found within the non pacemaker cells they interact to, to contract. So what happens is whenever the pacemaker cells they send out so some, some amount of calcium into the pacemaker cells that helps them get off uh and start the ration potentials. So whenever that happens, whenever there is somewhat of calcium within your non pacemaker cells, this calcium in the system stimulates further release of calcium. Uh So that's what it means by calcium induced calcium release. So then again, inside your cell, the calcium that has, that has been acquired from the pacemaker cells stimulates for the calcium release from the sarcoplasm reticulum and the t tubules. These are both structures that help increase acellular calcium levels. Uh When you have that le when uh when you attain a particular concentration of calcium within the cell, uh within cardiac cells, it's, it then causes you to form cross bridges and then leads to contraction. So we're gonna move on now to the cardiac cycle. Uh on the right. What we have is a very interesting figure because um it basically talks about different things with whilst, well, it it goes into the cardiac cycle but focuses on different aspects of the heart. So, we've got the heart sounds, we've got the ventricular volume, we've got the right atrial pressure. We've got the JVP here as well, which is uh which is the right atrial pressure actually. So the cardiac cycle has four main stages. We've got the filling stage, the filling stage uh comprises of both an active and a passive um of an active and a passive stage. So your, your heart, it the blood flows to your left and right ventricles from your left and right atria from your pulmonary veins and superior vena cava, inferior vena cava respectively. Uh When the blood comes, let's just talk about the right heart in particular, just to make it easy for us to understand blood comes in from the superior vena cava into the right atrium and then to the right ventricle during this whole time, this is known as the filling phase. Your atrioventricular valves are open. So the blood just passively flows from your right atria to your right ventricle because it is the filling phase. We also have the atrial contraction. The atrial contraction helps give an extra push to increase your ventricular filling. So we've got the when, whenever the A ta contract it pushes blood into the ventricles and that's the final ventricular volume that we have that needs to be pumped out. That is the, that marks the end of the failing stage, the filling the filling phase uh ends when the ati contract, the ati contracts and then the, the, the atrium, the right atrium contracts and pushes down into the right ventricle. Following that, we have got the isovolumetric contraction. Isovolumetric means just the whole heart in general. Uh but here we talking specifically with the ventricles. So the ventricles contract and because the ventricles contract, they push out blood to because we're talking about the right heart here, it pushes out blood to the pulmonary artery. Um Sorry, give me a second here, pulmonary artery. And when it does that, your atrioventricular valves close, because whenever the heart contracts, but the ventricles contract to push out blood to your create vessels. Uh if the, if the a valves are open, it will cause backflow and we don't want that. So whenever the ventricles contract your atrioventricular node, the atrioventricular valves close, uh that is followed by the outflow phase. Uh that's basically your ventricular systole. And then once the ventricular system happens, you go into the isovolumetric relaxation because the heart has pumped out the blood that it needs to pump out and now it's going back into the failing stage. So the isoval isovolumetric relaxation is post ventricular contraction and just before failing or the inflow phase. And then if we look here to the f at the right, we uh I think we can focus on the heart sounds for a bit. Uh We've all heard of the, the common, the way we describe heart sounds, lopped up, lump signifies the closure of the atrioventricular walls. So, in the atrioventricular valves and that happens uh post is or that happen during isovolumetric inion. So whenever the ventricles contract, they're trying to push blood into the great vessels. And so the atrioventricular valves close, that is signified by S one S two, is your closure of your semilunar valves. Uh At the end here during the isovolumetric relaxation, that's when your semilunar valves close. And then we've got ST and S 4 S3 usually occurs when there's rapid filling of the atria. So that's so these two sounds S four and S3 are not always heard, they can be heard in certain individuals. Uh It could be physiological, that is, it could be normal or it could also signify a pathology. So S3 is the rapid failing of the atria and S four is then your atrial systole. That's when the at contrast to push blood into the ventricles, that is still in the filling of the inflow face. But what we need to take away from the heart sounds here is as well. And as, as what happens during the isovolumetric contraction to prevent backflow of blood into the atria. And then s two happens during isovolumetric relaxation. Uh We've got a question here again. Then at what phase of the cardiac cycle may s one be heard, we've got the inflow phase, isovolumetric contraction, outflow phase or isovolumetric relaxation. Nice. OK. So we've got, we've got two main answers here. Just gonna give you guys a few more minutes if you guys want still attempt it. Uh I think enough people have, have attempted this question. So the correct answer is isovolumetric contraction again. S one is lb which is your atrioventricular valves closing. So that is your mitral and your tricuspid valves. Someone has also gone ahead and selected inflow phase, your it during your inflow phase. If you wanna come back here, we've got S3. Sorry S four. Yeah, no apologies for, for what I just said, your inflow phase, all of your valves are open. So there's no, there's, there's no, well, your AV valves are open and your semi valves are closed, but there is no closing that happens within that moment. So therefore, you don't hear a sound in that particular case. Um Someone, someone has asked a question, I didn't get the point of isovolumetric. OK. So your isovolumetric inion is your contraction of the heart. Whenever we say contraction of the heart, what we basically mean is contractions of your ventricles because that's when the blood pumps out to the rest of the system, right, the rest of your body and that goes from your left ventricle to, to your aorta and then the rest of the body and then from your right ventricle, it gets pumped in the heart. What happens in the isovolumetric contraction here uh on the points that I've mentioned here is your B and sl so your atrial ventricular and semi valves are closed, your ventricular pressure builds up. So because we had the atrial contraction before your isovolumetric contraction, it leads to an increase in pressure in your ventricles because there's so much blood in it at this moment that it needs to contract to push out this blood, there's an increase in pressure within your ventricles. And that is when your isovolumetric contraction takes place, when the pressure increases, the action potential transmits down to your ventricles, causing it to contract. And then when it contracts your atrioventricular nodes, that is your mitral and tricuspid valves close to prevent any backflow and then your semilunar valves are open. Does that make sense? If you've got any specific questions, please go ahead and put them in the chat right now because I do see that you've lost the isovolumetric, but there's not, there's not a question associated with it. So I don't know if I've done a good enough job explaining it or not. All right. Uh Well, we're gonna move on now to the, did I miss anything? You know? I haven't. Ok. So this is the cardiac cyclin and auscultation. This is just emphasizing on the, on the, on the points that I was making earlier, your heart sounds. So if you guys didn't get it, then you guys can maybe, hopefully this slide makes a bit of sense. Your s one is your lb, which is your a val shotting again. To put it into perspective, you've got the heart, your, whenever there is blood within the ventricles, it needs to contract, it needs to contract and push this blood out of the system right to the systemic circulation. So whenever it contracts, it has to close the A V valves because otherwise the blood will just flow back into the atria. So it contracts the A valves close and then you've got blood pushing through the semilunar valves, that is your aortic and your pulmonary valve. And because the A V valves are close shot when the ventricles, when the ventricles contract, it causes the lock sound, then we've called the dub sound which happens during your isovolumetric relaxation. So whenever the heart is done contracting, when it's done pumping the blood out to your systemic circulation, uh it's going to then go to relax stage. Uh but when it pumps this blood out, it pumps it via the aortic and pulmonary valves, which are your semilunar valves. So they are kept open whilst it's pumping. And once it's done with that contraction, they slowly close. And that closing is what uh we hear as the second sound or S two or top. Uh when, when you listen to the stethoscopes, then S3 is early diastole. Uh and it's normal in young people and athletes, uh, again, S four is then late diastole. It's, if you just look here, yeah. S S3 is more for filling whenever there is rapid filling of your A and then S four is whenever there is an atrial systole. Uh Now moving on a bit to the clinical aspect of this. Um when you're listening to heart sounds, you need to know where exactly to listen to them. Uh And I'm pretty sure I think uh this was covered within the cardiac anatomy. But if not, we've got your aortic valve which we listen to in the second intercostal space to the right. We've got the pulmonary valve which we listen in the second intercostal space to the left. We've got the tricuspid, which is, I think the fourth intercostal space, parasternal edge uh to the left again. And then we've got the, the mitral valve, the fifth intercostal space, midclavicular. Now there is pneumonia for this and uh that's how I remember it during my C as well. It's all physicians take money. So that's a good way to remember it. Aortic Pulmonary Tricuspid uh, mitral, all physicians take money. Uh, and then focusing a bit here on the, the pathology side, I suppose. Uh, there's things that are that we hear during auscultation, known as murmurs. So these are just basically abnormal sounds. Um, and we've got systolic murmurs and diastolic murmurs, murmurs can be classified into two main subtypes, systolic and diastolic. Uh, when we say systolic, we're talking about contraction of the, we're talking about contraction of the ventricles and there are certain murmurs that we hear during this contraction. Uh So a good way I classify it as is, let me, let me have a think about this. Give me a second. So whenever the ventricles contract, there are certain valves that are open and certain valves that are closed. Ok. There's four main valves within the heart. We've got the mitral valve which is between the left a and the left ventricle, the trichopi valve, which is between the right a and the right ventricle. We've got the pulmonary valve and we've got the aortic valve. So, during ventricular systole, you know that there's closure of your mitral and tricuspid valve to prevent back flow to the atria, right. Uh and the other two valves are open. So, systolic murmurs, systolic again, four valves, atria, uh sorry, your atrioventricular valves are closed and your seal valves are open, whichever valve is closed. They usually the murmur in that particular moment is uh the murmur of regurgitation. So this is all gonna sound very complex, but just bear with me for a second. Regurgitation is whenever there is backflow. Uh and it's hurt during particular wait again, regurgitations when there's backflow. Systolic murmurs. Four types of murmurs. Four. Ok. The reason why there's four types is because there's four valves. Uh during cysto, we've got closure of the atrioventricular valves because they're closed, there is backflow there, there's, there's potential to be backflow. That's why during cysto, we've got mitral regurgitation and tricuspid regurgitation. And because the other two valves are open, they have potential to be stenosed. So we've got aortic stenosis and pulmonary stenosis. Similarly, if you move on to diastole, uh during diastole, the two valves that are closed are the semilunar valves and the two valves that are open are the, the mitral and the tricuspid valve. So the valves that are closed always undergo regurgitation, right? Or if it's a pathological case, that's when they undergo re uh regurgitation. So, diastolic diastolic murmurs have your aortic regurgitation, uh your aortic regurgitation, pulmonary regurgitation and uh mi and stenosis. Now, that was a lot. So if in case you guys have any questions, just put them in through, I can do a better job explaining it. If in case you guys have got any questions, otherwise, we're just gonna move on, moving on then to the cardiac output. Uh I'm pretty sure all of us have heard of this cardiac output is the amount of blood that your heart pumps out in a minute. So in order to find that out, mathematically, it is stroke volume, times your heart rate, stroke volume is the volume of blood that you pump out, uh per heart rate, per heartbeat. And the heart rate is quite self explanatory. So here, actually the stroke volume as well, there is a formula to do that end diastolic volume, which is DV minus E SV and systolic volume. Uh and well, enddiastolic volume. What it means is whenever the heart has failed completely, sorry, whenever the heart pumps out the blood, whatever is remaining in the heart is known as the enddiastolic volume. Apologies. I've had a very long day guys, you guys need to bear with me. Your end diastolic volume is the the volume in the heart of. So if you remember your receive blood from the atrial and the respective vessels. So whenever it's done filling just before the contraction is what is known as the anti histo volume and it then undergoes systole, so contracts and then that is your systolic volume, whatever remains after the contraction. And when you subtract, whatever was in the in the heart before and after the contraction, you got, you get the stroke volume. So minus yes, we we're talking about two concepts here after that is the preload and the off preload basically is the extent to which the heart, the the the cells of the heart gets stretched. So the ventricular stretch. Basically, you're filling the left, the extent to which your heart gets filled as if it to the preload. Whenever there is an increased preload, the, the strength of ventricular contraction increases. Uh and that increases the amount of blood you pump out so it increases your stroke volume. Um I think of it as a balloon, the, the more you fill it in with water, the more pressure, the more the pressure inside is. So it's just simply simply that so the greater the payload, the greater the strength of contraction and the the greater the the amount of blood pumped out that we've got afterload. Afterload basically is the amount of pressure that the heart needs to overcome in order to pump blood through the system. So afterward basically is your resistance. That's how you understand it. So, ideally, we'd like to have reduced afterload and a decent amount of preload if that makes sense because you don't want there to be that much resistance when your heart is starting to pump that out because it's gonna make it work for, it's gonna make it work harder. So this is the Starling's law. I think I spoke about that in the previous slide as well. Starling's law is just the name for the law where the greater the preload, the greater the contraction. That's basically what the law says. If you fill it, if you fill the heart with much, if you fill the heart with a greater amount of blood, the the greater will be the stretch of the cardiac myocytes and the greater uh the strength of the contraction. Uh your cardiac output is then again regulated by your autonomic nervous system. So again, this is what I mentioned earlier, your sympathetic nervous system and your parasympathetic nervous system, parasympathetic has also. So all stress in digest. So that's why your heart rate reduces sympathetic nervous system, fight or flight, heart rate increases. So your sympathetic nervous system uh stimulates increased contractility via the B2 receptors because it, so the S NS basically increases production of noradrenaline which goes and acts in B doin receptors within the heart and that leads to an increase in heart rate. So after that, we've got the PNS, which is the sympathetic nervous system. If you remember via acetylcholine, they act on muscarinic receptors and decrease the heart rate. Now, this autonomous uh nervous system control over the cardiac function and the cardiac output uh is regulated by the metal oblongata in the brain stem. There's also other mechanisms that um that keep a check on cardiac output. Uh and that is via stretch receptors present in the carotid sinus, the aortic arch and the carotid bodies. Um Again, there's also just to add on does not only act upon the speed of contraction, but it also acts on the strength of contraction. So, sympathetic nervous system, whenever you're in a fight or flight situation, you want more blood going to the rest of the body. So your uh your regulatory systems increase the speed of contraction as well as the amount of blood that is pumping. So it increases the strength of the contraction and the strength of the contraction is referred to as the inotropy. So we see a positive inotropic effect via the sympathetic nervous system. While the pa parasympathetic nervous system, because your body is not in need of, of excess blood, uh the the contraction are a bit mild. So the passing Bellary nervous system has inotropic effect. The crux of this is that it is all regulated by the metal oblongata within the brain stem. Uh And now we're talking about the heart rate, the heart rate again, I think this is all just repetition to a certain extent. But heart rate as again. Uh it's, it's, it's something that we use whilst measuring the cardiac output. If you can see the, we've got the equation here. Chronic output is heart rate and stroke. While we've already spoken about that, I also mentioned the beginning how your heart rate is established by the sinoatrial node as dominates over eight. So sa whatever it determines the rate is going to be is what is followed by the ventricles as well or the atrioventricular node as well. The normal range is 60 to 100 below 60. It is called bradycardia and above 100 it's called tachycardia. Further here, this just talks about the ac the acetylcholine binding to the musculin did the of, of, of the heart's contractions of the contraction. It's called inotropy. So it has a negative inotropic effect as well as a negative chronotropic effect. So it decreases the this of the contraction as well as decreases the heart rate. We we got the sympathetic nervous system uh that acts on the beta 100 receptors. So it has a positive chloro TRP as well as a positive inotropic effect. So it increases your rate of contraction as well as your strength of contraction. And whenever we're at rest, whenever you and I just sat down your PNS input, that's the parasympathetic nervous system. The rest and digest dominates over the sympathetic nervous system. Ok, I think. Ok. Yeah, this is the bad receptor reflex. If you guys remember, I also mentioned that there is stretch receptors that help regulate uh your BP. Uh So these stretch receptors are present are present in the carotid sinus in the aortic arch. So, if there is an increased stretch, that means the BP has increased. It um activates various pathways in order to help bring that BP down. And if in the case that there is, there is a decreased stretch of these receptors, uh that's a hypotensive stage where there is there's less BP, then we've got the alternative pathways. Uh that is your sympathetic nervous system, which is activated to then increase and regulate. And get it to a homeostatic level. So we've got the seventh question here. What structure in the brainstem regulates autonomic nervous system control, which in turn controls influence on the cardiac output. A is mid midbrain bs bones and CS me log long cut off. So I think, yeah, people are giving the correct answers. It is indeed of see Marina oblongata. I think we're nearing the end of the session here. Um Control of BP. So, again, like I mentioned earlier, uh we've got various mechanisms, various pathways through which your heart, well, your BP is maintained. Uh We've got, so whenever we take a BP reading, we've got the systolic BP as well as the diastolic BP. Uh So, uh if someone's telling you what their BP is, they tend to say 1 20/80 which is the text for BP. 120 is the systolic reading. Uh That's fresh and 80 is the diastolic reading, which is pressure elation. Your mean arterial BP is another is another tool that we use. Uh And that is calculated basically by using that formula that cardiac output times total peripheral resistance, total peripheral resistance is the resistance that's offered by your arterial, the smallest blood vessels. Um Here, we're talking about the factors affecting BP. We've got cardiac output. Uh If the cardiac output increases blood volume in vessels, increases vessel pressure increases. Um Basically what you need to take away from the, the last bit here is just look into the last two points, blood viscosity and the vessel length. Because if your blood tends to be viscous, it affects your BP. If it's more thick, your blood, uh it affects the BP. And if your vessels length again, I mentioned the TPR comes from the smallest vessels. Uh I think we've got a much clearer slide in the next one here. Yeah. So your regulation of the BP, short term regulation is gonna be by the autonomic system. Like I mentioned earlier. Any your BP are sensed by well here, well, particularly it says Bors, bors are the stretch receptors that I was talking about in the aortic artery in the car, in the carotid sinus. Uh when there is an increased stretch, you know that the blood, that the person is hypertensive, increased BP and that is not a safe stage to be in perpetuate. So you would want to bring that BP down. That is again via the parasympathetic nervous system, rest and digest parasympathetic so that stimulates so, so the vagus nerve is stimulated, which is one of the cranial nerves. Uh and that then leads to a decrease in your BP because it decreases the strength of the contraction. And in the long term, the regulation of BP happens via the R system. That is the renin angiotensin, the ster system for the antidiuretic hormone. The atrial uretic peptide or the A NP secreted by the, by the cardiac myocytes themselves for prostaglandins. So, the renin angiotensin system is, it is a complex system. I don't think I'll be able to covid it in this particular session. I can for the, for the second years, third years, 4th and 5th, I can just quickly have like uh do a brief review. We've got the 10 which is secreted from the juxta cells, which then converts angiotensin to angiotensin. One, angiotensin, one converted to angiotensin two via ace uh from the lungs. The angiotensin two that attacks in order to restore or in order to yeah, restore BP. But it's a very complex system. And I think the young ones are going to come across this in due time. You've got the A DH, which is released by the posterior pituitary gland. And that again has its effects in terms of reducing a hypo uh in terms of uh tackling a hypotensive stage, uh where it tends to store or save the water and sodium to prevent. Um so whenever there's, whenever we have, we're in hypotensive stage, that's low BP, ADH is secreted and then that goes and as in the kidneys and stimulates the absorption of water and the absorption of sodium. So it helps maintain that the, the, the fluid volume within your body. Similarly, a NPS and prostaglandins, prostaglandins are, are vasodilators. So if you are in a hypertensive stage, prostaglandins tend to um dilate your blood vessels and that helps reduce the pressure. Now, this is just la the last bit here. I think uh it's, this is called the flow. I don't know if I'm saying it, saying it correctly or not. Basically, there is what, what exactly flow is, is the volume of fluid passing um through a given point per unit time. R. If you look at the equation towards, towards the right, it says R which is resistance is equal to eight times viscosity times the length upon pi out to the power of four. Uh And so the resistance uh to flow offered by a, by a vessel depends on these main factors here. That's your viscosity length of the vessel, the radius of the vessel, um viscosity refers to the viscosity of the blood in this case. So the greater the viscosity of blood, the more resistance um uh the the vessel tends to offer to that blood. So uh in this particular case, I think what we need to understand uh is the radius because it is raised to the fourth power it has, it leads to drastic changes into resistance. So if in case you've it's inversely proportional. So I think the next question actually focuses on that. Yeah, what variable in in the postal slow has the greatest impact on persistence of a blood vessel because it's inversely proportional. I think uh the decrease in the radius will lead to increase in the resistance. And I think that's quite self explanatory. Yeah. Right. So everyone's giving the correct answer just again, to put it into perspective. Uh physiologically, if you, you've got blood vessels that are very narrow, so your arterioles, uh because they've, um, because they're so narrow and the right. OK. Because it's inversely proportional. If your arterioles are narrow, the resistance offered by, by the blood vessel, by the blood, by those blood vessels is gonna be very high. And conversely, if it, if you've got a vessel such as the aorta, which is so thick, it's got such a massive radius, the resistance offered by the aorta is going to be less. That's what this basically means. I think that should be the end of this then. Uh perfect. These are the references and the sources that I think James used to make this presentation. Uh Hopefully, you guys took something away from that session. I know it's, it was a lot of pain, but again, like cardiac physiology, it is, it is good to know it, but it's not quintessential to know it in order to become a cardiologist or cardiothoracic surgeon. Um As far as I know, so don't beat yourself or if you over this, if you don't understand it, it's something that he'll eventually um catch hold of. I think Donovan's popped up to say something. Go on. Donovan. I just jumping on to thank you. Thanks everybody else for enjoying this evening. Um yeah, I'll submit into the chat, the feedback and uh hopefully through there now, so be able to fill out the feedback form and you'll get your certificate for attendance. And yeah, I would say cardiac physiology is imperative. If you wanna be a cardiologist or a cardiac surgeon, we will know one for you. Um Yeah, thanks everybody for coming. So next week we were scheduled to have again, same time, but with the progress test, we're gonna postpone for a week and the following week, we'll be back to normal with the weekly sessions and, and Tuesday 6 p.m. So thanks everybody. Thanks to for leading on tonight. Thank you, everyone. Have a good night. Thank you and regarding access to side. Yes, we'll get them sorted for you afterwards. If anyone's got any questions, they can just go ahead and put them in the chart and I'll have to answer them to the, to the best of my abilities. And if not, Donovan can also assist us in answering these questions together.