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As I said before, welcome to everyone who's joined. Uh We're gonna give it two more minutes. Um And then she'll start the talk. Hi, Rosie. Sorry to interrupt. Um It looks like your audio is not working. Your mic might not be working, the audience can't hear you, but I can see that you've unmutated. So it might be a mic issue maybe with your earphones. Hi. Can you hear me now? Yes, we can. Ok. Sorry about that. I'm not sure what was wrong. Um So le let's start that again. Um Sorry, I couldn't um I didn't see the chart. Um But yeah, if there is anything, um just let me know. So, um as what I was saying before, um didn't miss anything. So I was just saying we're gonna do um a bit of a brief introduction to cardiology. Um So these are the things that we're gonna be covering. So we're gonna start off by looking at the basic anatomy and physiology. So this will be a bit of a recap. Um And then we're gonna go into the cardiac cycle and heart sounds and kind of link all of that anatomy together and then at the time, uh at the end, if we have a bit of time, we'll do an introduction to EC GS and look at some abnormal ECG S. So, um let's start with the basic anatomy. So we'll look at some of the main structures um that we need to be familiar with uh to understand the cardiac cycle a bit better. And we'll just get a picture of the general flow of blood around the body. So when we're looking at these images, the uh image on the left is the anterior view of the heart. So we're looking front on and the right hand side is a posterior view. So we can see we've got our Vena Kvi. So we've got the S VC and the IVC. So the S VC is bringing blood from the head and upper limbs and the IVC is bringing blood from everywhere else. And then we've got the pulmonary trunk and the pulmonary arteries. So these are bringing deoxygenated blood from the heart to the lungs. And then we've got our pulmonary veins and this is oxygenated blood um from the lungs to the heart. So we could also see the aorta um which we'll go on to uh as well. So the aorta arises from the top of the heart and that goes from being the ascending aorta, we hit the aortic arch and that goes to the descending thoracic aorta. So the major vessels um and the atria. So let's look at the atria now. So we have two types of chambers. We know this, we've got our atria and ventricles. So if we focus at the atria, which are at the top of the heart, so the atria, we know have thinner walls and they are receiving blood. So the right atrium is getting our venous blood coming back um into the heart from our SBC and IVC which we saw on the previous slide. Um and on the left for the left atrium, it's a confluence of all of our pulmonary veins. So we're bringing deoxygenated blood um from the lungs, uh and then the carotid sinus. So this is there to drain deoxygenated blood from heart tissue into the right atrium. And that's located on the posterior side of the heart. And there are other main chambers which are the ventricles. So compared to the atria, these have a lot of muscle. So these are helping to push blood out um of the heart. So the right ventricle is connected to the pulmonary trunk. So that's helping to move blood out of the heart to the lungs. And then the left ventricle is connected to the aorta. So it's there to pump blood into the body. So we know that our two ventricles are separated by a sulcus and this is called our interventricular septum. So a little bit more about the aorta. Um So if we just focus on these main vessels, so we'll talk about the aorta and then our vena cava. So the aorta is a major vessel and this supplies all the blood to our body. So, we've got, as I mentioned before, we've got this ascending aorta, we've got the aortic arch and then we've got our descending or thoracic aorta. And so there are three branches of the aortic arch. So this is asymmetrical. First, we've got the brachiocephalic trunk and this then splits off into the right common carotid artery and the right subclavian. And then we've also got the other two branches of this aortic arch. So this is the left subclavian and the left common carotid artery. Um And so this is slightly more medial. Um and this takes blood um into the neck, into the head. And then we've got our dissembling aorta and we've got lots and lots of branches coming off. We can see these here. Um So we've got the posterior intercostal branches and our mediastinal and esophageal branches. But we don't need to know much about those in too much depth. It's just more um it's a good idea to have a rough idea about what's going on down there and then going on to our Vena cava. So we saw, we've got the IVC and the SPC. So these are responsible for bringing blood back into our systemic circulation um to bring from systemic circulation back to the heart. So this is the deoxygenated blood being dumped back into the right atrium, which you mentioned before. And on the aorta, we had these intercostal um mediastinal and esophageal branches and these all took oxygenated blood to different places. So they're branching off the aorta and taking blood away from the heart. So, obviously, with the vena cava, um it's a vein, so it's bringing blood back to the heart. So it's a reverse where the brachiocephalic veins work um in an opposite pattern and they kind of anastomose back on to the SPC. Um So just be aware that the right um brachiocephalic vein is longer than the left brachiocephalic vein just because um simply the location um because the vena cava is on the right hand side of our body, but just to be aware of the slight difference. So let's go on to more um of the stuff leading up to our cardiac cycle. So talking about action potentials and excitation coupling. This is something that will probably come up a little bit in exams. So it's good to have a picture of what's going on here. So the coordination of the heart really depends on a specialized um electrical conduction system. Um So it makes sure that our heart is beating rhythmically and efficiently. So cardiac action potentials are generated by specialized cells. And this refers to the sequential flow of electrons across ion channels um in cardiac cell membranes. And this causes the activation of myocardial cells. So the myocytes. So these are our cells in the heart. So these receive signals from our pacemaker cells. Um And this causes them to contract so they're able to depolarize spread these action potentials. Um And so let's just talk a little bit more about the different phases of the action potential. And what's happening at a cell at the cell level. And myocytes also are quite unique because they don't require stimulation from the nervous system. That's what makes them a specialized cell. The heart is able to generate its own action potentials. So they're connected by gap junctions. So what these do is they form channel ions. So it allows the flow of ions between myocytes. And this means that we can get the electrical co uh electrical coupling of neighboring cells. So if an action potential is generated in one cell, it then triggers the generation of action potentials in neighboring cells. So it's much faster. Um So the pathway that we need to know about is going from the sa node to the A V node. Um and then we go to the bundle of his the purkinje fibers and then our ventricular myocytes. And so let's just discuss these in a little bit more depth. But first of all, let's just get our head around polarization, which is something that um people often find quite difficult. So cells are polarized. So there's an electrical voltage across the cell membrane at rest. So in a resting cell, we call this our resting membrane potential, right So this is usually negative um around minus 90 millivolts in a normal myocyte. Um So if we think back to our a level and G CSE movement of ions that will kind of help us think about the flow of the various ions by active transport. So, more sodium and calcium are outside of the cell, but there's more potassium naturally inside of the cell. So this is maintained um by different concentration gradients. So the action potential essentially is the brief reversal of the normal electral polarity of the cell membrane. Um And so we regulate this through um voltage gated ion channels. So the two main movements that we want to consider are depolarization and just normal polarization. So, depolarization that is the c movement into the cells. So we're producing a positive cell charge compared to the outside of the cell. So the membrane potential is increasing to become less positive. So we become less polarized. And that means that we are depolarized and then polarization. So that's when the anion, that's the anion movement um into cells. So we're producing an overall negative cell charge compared to the outside. So the membrane potential becomes more negative. So um when the when the membrane potential becomes more negative, we are repolarise. So in the heart, we have two action potentials that we want to consider. So one is for pacemaker cells and one is for the myocytes. So you might have seen these grafts or remember these these types of grafts. So pacemaker cells, this is an important thing to remember that pacemaker cells don't have a true resting membrane potential. So if we go through the different phases of this graph, so starting with phase four over here. Um so that's our slow oh sorry, slow depolarization. So the pacemaker cell basically is undergoing depolarization due to the action of these things called funny currents um which are only present in our pacemaker cells. So the sodium channels, they only open when the membrane voltage is less than minus 40 millivolts. So this causes the slow influx of sodium and then we reach this thing called the pacemaker potential. So then once we've hit this pacemaker potential, we hit phase zero and this is our rapid depolarization. So um during our rapid depolarization, once we've reached this threshold, the calcium channels can then enter and we get further rapid depolarization. So this is our rising phase of this action potential. In other word, and then phase three, which is our repolarisation. So once we've hit the peak of the action potential, the potassium channels open and then our calcium channels inactivate. So that means that we get the efflux or calcium leaves the cell and the voltage then returned back to 60 millivolts. So this is our falling phase. So just to recap, we've had our slow depolarization, we hit that threshold, we then reached the rising phase of the action potential where calcium um channels open and calcium enters. Um then we have the repolarisation where the calcium channels are inactivated, we see the efflux of potassium through these potassium channels. And that's our falling phase of the action potential. Yeah. So once all of this has happened, we are kind of back at our original ionic balance. So this is restored and then this repeats. Um So just uh when comparing it to our myocyte action potentials, the reason why pacemaker cells slightly differ is they don't have that phase one and two, which we'll go on to talk about. So once we've done this action potential in our pacemaker cells, this then goes on to our myocytes which have a different set of ion channels. Um And the myocytes, let's go look, look at this action potential. Now, so as we said, they receive the signal from our pacemaker cells and they can only contract through electrical coupling coupling. So this is when we get the firing of an action potential from a neighboring cell. So the action potential of myocytes is what makes them unique in their firing capabilities. So if we start from the start here, so we've got phase zero, which is our depolarization. Um So we get a rapid influx of sodium into the cell. So it's an inward current which is responsible for our rapid depolarization. So once we've depolarized, we have more sodium and calcium into the cell. And this can leak into the gap junctions which you mentioned before, which is um in between cells. So we've got the gap junctions and this leaks into the adjacent cells and then we hit our membrane potential of minus 17 millivolts. So we can see that there and then as we hit phase one. So this is when we reach our uh the action potential reaches its peak, the sodium channels close and then the voltage gated potassium channels open and then we get a small decrease um in membrane potential. So this is our early repolarisation. Yeah. So it's not complete repolarisation. It's just a slight decrease. And once the sodium current stops, we get potassium going out of the cell depolarization stops and then our repolarization stops. So I know this is quite a lot um at once to kind of go through. But hopefully, you can see how this is slightly different compared to our pacemaker cells. Now focusing on phase two which is our repolarization. So we've got these L type slow potas um calcium channels, sorry. Um And these open once we hit minus 40 millivolts and we see the slow influx of calcium into the cell. So calcium channels open and once these calcium uh calcium moves into the cell, we get potassium efflux. Um and this kind of balances out. So we've got the influx of calcium and the efflux of potassium. So it means that we're relatively stable and this is our plateau phase. Um This is what makes the action potential of myocytes um very unique and it's characteristic of it. So we can see that this, there's this plateau phase in phase two. Um So calcium is very important in um coupling electrical excitation with physical muscle muscle contraction because um if there's not enough influx of calcium, then there isn't gonna be um enough energy for contraction. So, calcium causes uh contraction. And if we think back to our sliding filament theory, like in skeletal muscle, um that's why it's very important, calcium is really important in this balance. So um the charge, as we said, just to recap that the charge balance between the inside and outside of the cell is what creates this plateau phase. So hopefully this is all making sense so far. Um And then let's go on to our phase three. So this is our repolarization. So as the calcium channels slowly close potassium efflux is what's more predominant. So before we had the potassium and calcium kind of balancing each other, but now, as these calcium channels close, the main thing leaving the cell is potassium. So as this uh continues to move out of the cells, the membrane voltage returns to the resting value. Um So the sodium potassium pump, which you probably are familiar with, this is what helps to restore ionic balance across the membrane. And this allows repolarization to continue and then phase four, it's potassium current moving out of the cell. Um And this uh as this approaches equilibrium between the inside and outside of the cell, um we can see the sodium sorry calcium current moving into the cell to balance this outward potassium current. So then we reach our resting membrane potential. So I know that's all quite a lot of information to digest at once. But hopefully, once you look back uh over the graph, it will kind of help um make sense of things. So the one thing, if you were to look at any of these grafts, the thing that is most characteristic or the thing that should stand out to you is this plateau phase um which is a lot longer than the contraction of skeletal muscle. Um And we need this kind of longer plateau phase to help um with the expulsion of blood from the chambers. So as we said, it's about 250 milliseconds or 200 milliseconds. Um But in scleral muscle, it's only about one millisecond. So we need to make sure that the muscle has relaxed before reacting to a new stimulus. Um So this prevents things like summation and tetanus. So let's talk about the electrical conduction system. Um So as I said, this is all gonna be a bit of a recap and hopefully, you have come across this before. So if this does feel like a lot of in um information, we can go over bit again. Um But uh actually let me just pause to see if anybody has any questions at the minute at the moment. If not. Ok, cool. Let's carry on. Um If you do have any questions, I'll kind of stop periodically between each section. Um Just to see if that's all um, digested. Ok. So, um going on to the electrical conduction system. So starting off with our sinoatrial node. So this um helps with the spontaneous firing of action potentials and this is what forms a heartbeat. So it's located, as we can see here in the wall of the right atrium, um near where the SPC enters and it's deep to the epicardium and it's compo uh composed of nervous tissue and cardiac muscle fibers um and connective tissue. Um So it's our natural pacemaker and it sets a normal rhythm which is about 60 to 100 BPM and it helps to spread electrical impulses via myogenic con conduction. So, this is sending signals um through cardiac muscle. Um And then if we carry on down the pathway to our A V node, which is over here. So this is located at the junction of the right atrium and the right ventricle. So it's near the opening of the coronary sinus. Um It's smaller than RSA node, but it almost acts as a relay station to help delay this impulse. Um So this allows the atria to contract fully before the ventricles can contract. So it's kind of delaying that signal and it helps to distribute the signal from the sa node to the ventricles via the A B bundle and bundle of HS. So, um it goes to the tissue of the heart and it tells the cells when the myocardium has to contract basically, and then a bundle of hiss. So this is here. So it's located in the interventricular septum. Um So this is used to transmit signals from the AV node to the ventricles. And there are two bundles. So we've got our left bundle and our right bundle. Um So the left bundle travels through the IV septum through the ventricle walls and into our papillary muscles. And then we've got the right bundle which goes again through the septum, but it goes uh to our septum marginal trabecular or uh moderator band. Um but don't worry about that too much kind of just know the pathway if you can. Um So this helps to transmit signals across the width of our right ventricle. And then the last bit of this pathway going down to our purkinje fibers. So these are the terminal fibers that help spread across the entirety of the ventricle wall. So this stimulates the ventricular myocardium. And so we get this coordinated and powerful contraction of the ventricles. So, between our um about uh between our chambers um and in our blood vessels, we also need to understand how these electrical signals can translate into effective blood circulation. So the blood um flow within the cardiac cycle is very important. And so I'm sure we all know the basic function of a valve. It's there to ensure that blood only flows in one direction. And in the cardiac cycle, they are very important because they mark the beginning and end of systole and diastole, which we'll talk about in a bit more detail. Um So we have four main valves in the heart which can be grouped into our V valves and our semilunar valves. So the V valves are mainly there to help us prevent regurgitation. So the backflow of blood. So we've got our tricuspid and mitral valves. Um So the tricuspid is here between our right atrium and ventricle, um mitral or you might have had it as bicuspid. Um That kind of helps you to remember that this is the only valve which has two leaflets as we can see here. So we've got pulmonary aortic and tricusp cuspid will have these three leaflets, whereas a mitral valve or bicuspid only has these two leaflets or two cusps. Um So the semilunar valves, these help prevent outflow from the ventricle. So we've got our pulmonary and aortic valves. So pulmonary is the right between the right ventricle and pulmonary trunk and then the aortic is between the left ventricle and the aorta. So these valves very uh become very important. We start to think about murmurs and heart sounds in the clinical setting. Um and trying to figure out where exactly the problem might be. So this now brings us all, uh we can bring this all together and think about the cardiac cycle. So we can put all this information about the action potentials, excitation coupling. Um and this anatomy altogether. And we want to be thinking about the two main phases of our cardiac cycle, which are systole and diastole. So you've probably seen this diagram and I think this is a really nice one to kind of help sum up what's going on. Um So systole, this is when we have contraction of the ventricle. So they squeeze, they shorten and they help empty and shoot blood out into either the pulmonary artery or the aorta. And when we think about our heart sound, this is our lob. So, you know, lub dub this is the lob bit. So at the start of systole, we've got the mitral and tricuspid valve. So these are our A B valves, they are closing and this is preventing the backflow of blood into the atria. Yeah. So then we hit isometric um contraction. So this is when the ventricles begin to contract, this is generating pressure and the pressure in ventricles rises very rapidly. And so um if you remember before the papillary muscles, these um contract and they are pulling on the chorda tendo. So these are uh within our papillary muscles and they tighten to prevent the valves from prolapsing and moving back into the atria during high pressure. So we know that there's high pressure and we basically don't want the valve to collapse and allow back flow of blood. That's essentially what's happening. So remember that the papillary muscles, they don't open or close the valves, they are just there to stabilize the leaflets or the cusps of the valves um during ventric clear andion. And then we go on to ventricular ejection over here. So that's when you hit the point where the pressure in your ventricles is greater than the pressure um of the pulmonary artery or aorta. Um So the semilunar valves, which are our aortic and pulmonary valves, they open and then we get the contraction of muscle and blood uh shoots out to the body and the lungs via the aorta and then we hit the end of cyst. Um So this is where the pressure in the ventricle is now less than the pressure in the aorta and pulmonary artery. And so the semi luna valves snaps shut and that's our dub sound. So we've got the lub at the beginning when the A V valves close and then when the semi luna valves close, we've got that dot And if you've seen heart sounds before you may not have come across that you may have. So that's a S one which is our lb and A S two, which is the dot And then going on to diastole. So the opposite is kind of happening. So we've got um we've got the refilling um of blood into the ventricles. So we get the relaxation. Um the valves are opening up and the ventricles elongate so that they fill with blood. So when we start the mitral and tricuspid valves are closed, but during early diastole, you get isovolumetric relaxation. So this is now entering diastole here, we've got isometric relaxation. So the ventricles have relaxed. Now after systole and this causes a drop in ventricular pressure. So after this drop in ventricular pressure, because it's below the pressure of the aorta and pulmonary artery, we get this backflow of blood and this close uh closes the semilunar. So these are our aortic and pulmonary valves. So, during this phase, the AV valves, which are our mitral and tricuspid valves, they are closed. So that means that no blood can enter the ventricles. But then in mid diastole, this is where we get rapid ventricular filling. So this is mid diastole. Um so as the ventricles continue to relax, the atrial pressure is greater than that of the pressure inside the ventricles. Um so the V valves now open and we get this passive filling of the ventricles. Um but obviously passive filling, it doesn't sound very powerful, does it? So we have this thing called the atrial kick or late diastole. And that's when the atria contract to push and push that additional last bit of blood into our ventricles. So this atrial kick contributes to about 20 to 30% of our ventricular filling. So um our ventricles can fill up nicely. So, um as I mentioned before, we've got that lab and DBA S one S two, which is the sounds of our valves closing. So, um these produce these characteristic heart sounds, which are indicators of cardiac function and they can help us reveal if there's any underlying pathology or things that we might need to explore further in a clinical setting. So, looking at our heart, heart sounds. Um so when you're hearing that, as we said, it's when the valve is closing. And that's because there's tab and blood flow causing the vibration of that tissue. Um and they mark the start and end of systole and diastole. So as we said, s one here, that's our uh closure of the mitral and tricuspid valves. And that's the start of ventricular systole. And then our S two, which is the closure of our pulmonary and aortic valves um at the end of ventricular systole. So those are the main two heart sounds that we'll hear. You can sometimes hear an S3 and S four as we can see here. So the S3 is t uh the turbulent blood flow entering our ventricles and you can sometimes hear that in Children, pregnant women. Um but it can also be a uh pathological sign of heart failure. And then the S four is oscillate oscillations in uh blood during atrial contraction. So we can hear that immediately before S one sometimes that can be known as the atrial gallop. So that's kind of the clinical relevance um of the closing and opening of valves. Um So sometimes you might have heard of heart murmurs. So these can occur when the valves are leaky or they're not working properly. So you can get regurgitation, um which is our leakiness and you can get stenosis, which is the narrowing of that opening. So, murmurs can be categorized as either systolic or diastolic. And this is just a little bit of extra information. You don't have to know this in depth at this stage. Um But it, it might just be interesting to know. So the time and character of these sounds can indicate which valve is affected. Um And it can help you reach a differential diagnosis. Um if you couple this with the symptoms that the patient has. So this is just a little diagram, do not have to know this in depth. Um But just some interesting one. So as we know, stenosis is narrowing and regurgitation is that leakiness. So, we've got an ejection systolic murmur. So that's at the beginning of our systole um when uh and that can mean that there's a defect in our aortic or pulmonary valve. Um And then we've got a late systolic murmur which is at the end of our systolic phase. Um and that's a mitral valve prolapse. Um But otherwise, I wouldn't worry too much about the others, but that's just there if you want to have a look or a little bit of a read. So, um Wigger diagrams, so this kind of visualizes all of the information that we've covered so far. Um Let me just look at the chart quickly and see if there are any questions so far. OK, perfect. So this is helping us to visualize this electrical activity, the mechanical events. So the actual opening and closing of valves and things and how these heart sounds can interrelate in our cardiac cycle. Um So the four parts that we're gonna be looking at. So we've got our atrial cysto isovolumetric contraction, the ejection phase and then our diastole. So on this diagram, the X axis is our time and then the y axis is our pressure volume and then our E CG activity. So atrial cyst leave. So the atrial pressure is increasing as these atrial contract. So on our E CG, if you are familiar with these, so we've got um maybe I can go back here and this can help kind of visualize, help visualize it. So we've got AP wave, we've got a QR S complex and at wave, we're gonna talk about this in more depth. Um Don't worry. So this is where we will see our P wave on the ECG. So this is the contraction of the atria. And so our ventricular pressure is greater than our atrial pressure and that causes our AV valves to shut and this is producing our S one or L heart sound, right? We're familiar with that now then isovolumetric contraction. So the the ventricular pressure is now increasing because the ventricles are contracting. So the semilunar valves and a valves are shut. So the volume of the ventricle stays the same whilst it's contracting. But then the ventricular pressure increases to a point where it's now equal to the atrial pressure and this causes our semilunar valves to now open. So, isovolumetric meaning that it's now equal in pressure, right? And on going back to our E CG, this is where we'll see our QR S complex. Um And so this is where we'll get our ventricular depolarization and the closure of the A B valves. So then our third phase of this diagram, we can talk about the ejection phase. So um this is our ventricular systole. So, ventricular pressure is rising um as the ventricles continue to contract until they reach um a peak. And this is where our blood is ejected then from the heart. But our atrial pressure increases as blood enters the aorta from the ventricles and the aorta contracts to pump blood around the body. We know this. Um So now our ventricular and atrial pressures decrease once they've reached this peak um as blood is leaving them, and then the ventricular pressure is now falling below our atrial pressure and this causes our semi luna bowels to snap shut. So, if you remember that's our s two heart sound, which is the dub. So we've got our lub in atrial systole and then in ventricular systole, we've got that dub. So um we'll go on to this um when we look at the ECG, but just to note that a QT interval, I'll talk about this in more depth. It spans the whole of ventricular systole. So the isovolumetric contraction and the ejection phase. Um So that tells us how long ventricular systole is actually lasting. And then our T wave um which occurs at the end of systole. So just before our diastole begins is ventricular repolarisation. So that's when the ventricular are relaxed. So the final bit. So the um of our diastole, so the aortic and mitral valves are shut. So the volume of the ventricles is constant whilst they are relaxing. Yes. Um But then when the ventricular pressure now falls below the pressure um of the atria, we get the opening of the mitral valve. And so the atrial and ventricular pressures initially drop slightly, but as blood enters the atria, then the pressure starts to rise again and then we get the filling because of um due to so we get the rise of pressure, sorry due to the filling during the sleep. So hopefully, we want to put all that information together that can give us a clearer picture of what exactly is happening and what causes these changes. Um and demonstrates what's happening in one phase or one entire cardiac cycle. Um So just a few more technical bits um before we just go on to talk about the E CG in a bit more depth, you might have come across these in your lectures before. So pressure volume loops, just some things or main things to be aware about. So the area bounded by the curve. So the area within the curve, um this is uh the amount of work that our heart is doing to eject blood during systole. And that's also known as our stroke work of the heart. So the area bounded by the curve is our stroke work. So if we just quickly recap these phases, um so going from A to B, this means we can see that there's not much of a change in pressure during the filling. So, diastole, we've got the increase of volume of our ventricles, we've got reduced resistance. Um And we've got increased pressure. So at B, this is where our mitral valve is now closing. Yeah. So B to C, this is our isovolumetric contraction. A mitral valve is closed. Um And then the pressure means as we can see from the arrow, it's rising rapidly but the volume is staying the same. So isovolumetric, same volume. And this is because our mitral and aortic valves are both closed. Yeah. Then at sea, this is where a uh the aortic valve is now opening. And so between C and D as you can see um the volume is dropping and the pressure is still increasing because the ventricles are contracting. Um And so this is where we get our ejection between C and D ventricular ejection and then between D and A as the arrow shows. So we've got our diastolic period where the B valves are closed, um or they close and then we get this fall in pressure uh in the ventricles, but the volume is constant. So again, isovolumetric, same volume, it's a constant volume. And then at the mitral valve opens and then we get the cycle restarting. So hopefully, all of this, I know it's quite a lot. Um kind of gives us a clear picture of what's happening. So just these are the main phases that we want to remember and these are some things that might come up in your exams. Um So the main equations that kind of relate to the PV loops are the things. So the distance between the two isovolumetric phases. So the isovolumetric uh contraction and relaxation, the upwards arrow and the downwards arrow, that's our stroke volume. Um And then the stroke volume that is our ventricular end diastolic volume, subtract and you subtract ventricular uh end systolic volume. And then the whole area within the loop, as we said is our stroke work. So the area bounded by the loop um and the bigger that the area is, it means that the heart is under more stress. Yeah, So it has to work harder to pump blood around the body and then ejection fraction. So this is our straight volume divided by our enddiastolic volume. So these are some things that might come up in your ques uh questions, but if not, they're just um get handy to know. So as promised, just doing a little bit of an introduction to ECG S to kind of paint a clinical picture of how we can apply all of this knowledge. So what is the ECG exactly? Well, it's a very useful technique that can help us detect heart rate, um conduction disorders, um pacemaker activity. Um and we can see if there's hypertrophy of cardiac muscles. So we saw that on the Wiggers diagram, there were the P waves, QR S complexes and the T wave. So this kind of relates to our uh cardiac action potentials that we also discussed. So, first of all, how do we perform the E CG? So this diagram is showing us where we place our leads. So we've got our chest leads or you might have had them as precordial leads. So we've got six of them. Um and they kind of go in our transverse plane. Um You can kind of see this here, we want to be six. and this kind of demarcates where they're placed and then we've got our limb leads um across our arms and legs and the positioning of the leads kind of in helps us to indicate where exactly the pathology is. You might see that the E CG isn't really done on our legs, you might see it placed on the hips in practice. Um But it does the same thing. So the normal E CG, so we have the wave of depolarization traveling towards a positive electrode and this results in a positive deflection. So if we imagine this baseline, positive deflection goes up, negative deflection goes down. So um on our ecg uh if we look at these boxes here, we can see that one small square is 0.04 seconds or 40 milliseconds and then a large square, one of these. So that's made up of five small squares that is equal to 200 milliseconds or 0.2 seconds. Um And when you look at an ECG like this strip here, this is usually a 12th strip. Now linking back to everything that we've discussed. So the P wave shows atrial depolarization. Um the QR S complex, this is when the uh ventricles depolarize. So we get ventricular depolarization spreading down into the ventricles through the bundle of his s to the purkinje fibers. And on our ECG as I mentioned, the small boxes, it shouldn't be bigger than and should be longer than three small squares. So that's less than 0.12 seconds. That's what it should be. Then our T wave, that's our ventricular repolarisation. Um And that happens at the end of systole and then we've got our pr interval and that should be no longer than five squares. So R 0.2 seconds or one big box. So the pr interval, we've got conduction through the AV node. Um So when the atria activated, we get the traction and ventricular filling. And um if that was to be immediate, the uh the ventricles would contract and we would get suboptimal cardiac output essentially. So we need that delay or that interval between atrial activation and contraction and ventricular depolarization. And as I mentioned um before the QT interval, um So that's between the Q and T QT interval. Um That's spanning of ventricular systole. So between um it's covering our isovolumetric contraction and the ejection phase. So that's our length of ventricular systole and then our T wave, as I mentioned, uh ventricular repolarization. So um just some common things that you might see um which is a semi. So let's focus on this. So that's ST elevation, myocardial infarction. So we know that the ST elevation, that's our ST segment. So going back here, we can see we've got Q RST. So with ST elevation, we've got elevation of that between that S and T uh segment and that's raised or elevated. So that indicates myocardial infarction. And that's why we see myocardial ischemia due to the complete occlusion. So, blocking of um one of the coronary arteries in the heart. So um just a little bit of pathophysiology. In simple terms, we've got a thrombus um made up of platelets that are kind of stuck together and thrombin. And this can block a coronary artery or multiple coronary arteries. And then we get reduced oxygen perfusion across the heart. And so we can see this um through E CG changes and because um you'll also match this with the blood, so we can see raised troponin and then we can diagnose ST elevation myocardial infarction. So, um the E CG kind of, as I mentioned, depending on where the leads are, that can help us figure out where exactly the problem is. Um So we can see on this diagram here, the different areas relate to different parts of the heart and the different leads. So the inferior wall of the heart. So that leads 23 and aVF that links to our right coronary artery, the anterior wall, which is leads V one to V four, which makes sense cos they place the on top of the heart, that's our left anterior descending artery and then the lateral wall which is leads one A V LV five and V six, that's our left circumflex artery. I wouldn't worry about this too much. Um But this is just a little crash course um on EC GS. Um So that's kind of everything that I thought would be relevant for a brief introduction to cardiology. Um And I won't be hearing more about the EC GS because we have already covered quite a lot. This is just um a useful diagram that helps us remember what exactly is happening where everything is traveling in terms of our impulses and how this relates. And this is kind of a nice diagram that helps show the um electrical conduction pathway. So um just to recap everything. So what we've done is we've looked at the major vessels and chambers of the heart, so we can understand how blood flows through the heart. Um We looked at the electrical conduction system, so we looked at cardiac action potentials and how the pacemakers of the heart ensure that we have coordinated and powerful contractions. Um And then we went over the different valves in the heart, their function, how they relate to the heart sounds and the different types of murmurs we can hear. And then we related all of that together. We looked at our Wiggers diagrams and the pressure volume loops to integrate all that knowledge, looking at the electrical and mechanical activity of the cardiac cycle. And then we looked at our EC GS, we covered the P wave QR S complex. Um T waves looked at ST elevation, what a normal ECG looks like and how we perform the E CG. So um that was quite a lot of information to fit in within the hour. Um But yes, if you do have any questions, please do, let me know. Um But if not, I think there will be a recording of this on the website and uh you can always look over the slides, but thank you all for joining today. Um Yeah, please do pop any questions you have in the uh chat. Um Feedback forms should automatically get sent to you. Um But I can share the form, the link to the feedback form um on the chart if you just give me one second. Um If you don't have any questions at this stage, that's completely fine. I think there will be another cardiology series which will delve into certain things in a bit more depth. Um So if you do have any questions that come up later, I'm sure you can ask them at that stage as well. Um OK, sorry. Um I know some of you are waiting for the feedback form. I think as soon as we end um this session, you will be emailed a link to fill in the feedback form. Um And uh if you don't, I mean, I think it automatically always happens. So um I don't think you necessarily need the link at the moment. Um But if you have any questions, I'm sure you can drop everyone a message. Um But yeah, if nobody has any questions, thank you all so much for joining. I hope that was useful. Um And hope to see lots of you at the cardiology teaching series. And I think we have a few more different specialty teaching series. Um which will be very, very useful. Um So.