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amazing. Thank you. Is so nice to see so many of us here today on dust. Reset. It is one of our favorite topics. Cardiology. Today. This is lined up with the card if curriculum case to cardiology. And so these are the things that I'm gonna be covering today. So let's get right into that. Staying off with cardiac anatomy. I am going to start the session, start each topic with a bit of a few questions. If USDA is just to get your mind rolling, just make sure everyone's listening in s so we'll get right into it. The first question and during auscultation of the heart valves, What is the physiology behind the sound off love. So that's the S one. Thank you. And the girls up, Guys, I love participation from everybody. It shows me that you guys are in tune with me as well, so please just gain as many answer you can. It doesn't matter if you get it wrong. That's why the sessions for gonna look through it. So just get everybody's answer. Doesn't matter. I can see if you it who's on strength. So to get maximum participation, please. It's good. Give it a few more seconds. Um, amazing on. We'll end it there. Thank you. S Oh, yes. So you guys have just d and the answer is D And we got to look more into that coming up. I've got one more. Um, the coronary circulation. The heart is responsible for the supply and drainage of blood to the my cardio cardiac veins are responsible for the draining. Draining into the right atrium by a which opening of the right atrium do that. Do they drain into again almost really quickly and said it just many answers as we can. As much space. And you get to be amazing somebody a bit quicker. Close in a second. Amazing. As a reading from the pool for this one. Love it on will end it there. Thank you. Hopefully guess and see that. Um amazing. So it is the coronary Sinus. So cardiac anatomy. Where do we start? I'm looking at the mediastinum. What is the media style? Um, here's the division of the thoracic cavity. That house is a lot of the vital organs. And so this includes the lungs, the heart, and the great vessels that come off it and we'll look more into that little bit coming up. Can anybody in the chat So hopefully we're gonna get participation here can really tell me what the divisions of the mediastinum are. So there's 22 initial divisions. Me can't see the shop people saying yes, so superior, inferior that is right on. Then the inferior is split into anterior middle and posterior. So the important things to know about the mediastinum or for a year one at least, are the boundaries on the contents. So, as you can see, I put it quite knees quite neatly out here for us to see. So the boundaries for the superior mediastinum being anteriorly manubrium off the sternum. Posteriorly t one t four superior the we have the thoracic inland. And so the rasagiline. It's just this on an anatomical junction that runs between the neck and the floor accident is connect those two structures and includes the first rib on in fairly. We have this turtle angle of Louis. This is just an imaginary line produced by that stone Langella, and it lives between the manubrium on the body of the standard. So just a quick know about the stone language Louis. Just the clinical relevance of this is that I love important structures like at that level and near near that level on the way to remember this is wrapped blunt. And so it just, um you know, a new monitor for you guys to read. But that's how you would remember certain language is really important to know how to how to feel for it. So you'd find the second rib come in to sternum, and that's where the sun language and for the contents I always love these new Monix. And the problem is, you just learn. Oh yeah, contents. So the contents, it's bats intense for superior mediastinum. Just remember that you do need to know these little like few exceptions and stuff. So yes, back surgeons and I'll let you guys read that. And I know that you'll let it through that. But a few things I want to know is, and just just bring to your attention the famous I've put in Children. They're the finest, actually, was your reach puberty that So you start to shrink and it becomes replaced by fat on By the age of what 75 the pharmacist just looked a little bit more than just fatty tissue. But thankfully, it produces a lot the T cells that we need before then and so, so sorry. Bye bye. Puberty. So that's the first thing today. Think the intense esophagus unfortunately spelt Sorry about that. Unfortunately, spelled in the American way on then nerves. It's good to know that end is the nerves. But you need to know that it's the vagus phrenic and recurrent laryngeal. We look about a little bit more with the information, a sign of a little bit more simpler boundaries being the next compartment down on the contents being dates, eso it once again just to bring to your attention eating a soft goose on the sympathetic drunk on the sympathetic chain in dates. I'll let you guys be through that. I know you guys don't get these slides, but these are just the easiest way that I felt like a teacher. But the important thing to know is the contents and just just generally where they're placed in the mediastinum. But moving forward, we're gonna look at the blood flow through the heart. So I'm not going. I'm not gonna talk down to you like Children. I know this is being covered in Jesus'. He's a levels and all, but I think we're going to live a passion. Probably just kind of get you guys thinking. I'm gonna ask you a few questions about the valves. So starting from the right atrium, the right side, the blood contracts, it goes into the right ventricle. Through what about does it go through? So again, you have a eye on the chat. What bowel? So right atrium to right ventricle. It goes through the the try custody battles. Yes, amazing guys. Then the right ventricle contracts and it pumps blood through the palm tree trunk, goes the lungs of fixing to move the oxygen and returns. The left atrium contracts goes into the left ventricle. Sorry. Before that, from the right ventricle contracts. What does do they go through yet? The pulmonary valves, or this? Probably 17 about it gets to the right atrium, and it goes through the mitral valve right atrium into the right ventricle. Mitral valve on the right. The left atrium contracts goes through mitral valve into the left ventricle. The left ventricle contracts pumps blood through the aorta. On that passes the aortic valve semilunar aortic bowels. So it is a very simple concept. It's, I think, the valves that will be looked. But just do remember where they are. Where they're placed is especially important pathology, and I know she is going to cover this very well coming up. But I've I've put the diagram there for you guys to look through another concept that because you know the heart layers, so start from the most external layer. Can anybody tell me what that external layer is cold on the chat again? So we get epicardium. So yes is the pericardium as well. That's the external layer. This extent was explaining to to it's the fibrous. So the fibrosis layer onda we have the seriously the fibrillator is this tough loose fitting in a in elastic layer on the seriously is split into two. It's the parietal and the visceral. Um, uh came up in the other way. So the brighter layer lines that lines that fibrous pericardium and the visceral pericardium lines the outside of the heart. And as you made it may have, you may know there's this face in between the pericardium cavity. This is filled with fluid on the function of this is to allow the heart contract in a coordinator and smooth way, and it to stops friction between these two pericardial layers. So allows the heart to contract, as well as protecting the heart encasing it in that pericardial there. Then we have the myocardium. We have the fat think muscular layer on, then the endocardium on. Remember that the left side is thicker the left side of my card in a sticker just because asked pump blood around the body that very easy concept. So yesterday, looking at the surface and ask me now eso the important things to know about the surface and ask me is where the heart is placed on the area that the heart takes within the rib cage on also oscal three sites for the bowels. So obviously everybody should know there are 12 lbs of ribs, 24 ribs and total. The boundaries off the heart are as follows. It's the right 3rd and 6th rib on, then the left 2nd and 5th room on what this produces is this called regular space. And that's what you guys sees. No, this quadrangular space that the heart occupies in the thoracic cavity. And then So the way to remember that is our our 36 l 25 moving on to the US and tell to ask her to take three sites. These are this is where you put your stethoscope to here for the valves. Can anybody tell me what that first left sided valve is to see? Everybody knows is the aortic valve very well done. So we have the aortic on the second intercostal space of the left side. And this is just off the standard of the sternal body. We have the pulmonary on s, so it is on the right side. Um, sorry about that. So else sick on the right side. Pulmonary on the left side, in the second intercostal space in the fourth intercostal space, we have their try caspit on in the fifth intercostal space at the midclavicular line. We have the mitral, so but that really they're so again when you when you get the opportunity, do like, try and listen to these mountains on yourself. It's just learning anatomy. It on yourself is the best way of learning and asked me, in my opinion, But these are the, uh, surgery sites, and it's very important that you can feel for the ribs and fill be listened to right valve using a stethoscope Moving forward. We have the arterial venous strange of the heart. So there are two main coronary arteries up supplies the heart. We have the right coronary artery on the left coronary artery. So just remember that the cornea arteries perfused with blood. Does anyone know we are gonna look at this further on in cardiac cycle? But is it in systole that the coronary artery perfused or is in diastole? Anybody tell me Well, you're very rapid response is very well done. Is that a little confusing? But it should make sense. So when the left ventricle in tracks, blood is pumped in the aorta on when the a little out, whether eventually relax. The blood kind of flows back on that where the cloni artists Corey Sinuses are on. So when the heart is contracted, the the colon arteries or it's it's hard to refuse or you can't refuse because of my partners contracted. And so the coronary arteries, they just can't be refused. But when the heart starts to relax during diastole the corner right is then confused. Blood flows from the aortic trunk down into the Sinuses, Sinus on into the coronary arteries. So looking at the branches off each artery with the right coronary artery. So I bear with me here that it's not on this diagram, but the first branch is the sign of atrial brunch on, So you can kind of kind of imagine where this is. It supplies that the right the top right atrium on that. Sign it on vitamins with sinoatrial. No displaced. And so that's a sign. A jewel branch. We have the right marginal branch supplying the left. Sorry, the right ventricle on, then coming further down it. It goes down the left down the right side and reflects Posteriorly. We have the posterior descending brunch on then the branches of the left coronary artery. We have the left circumplex. It supplies that left left atrium, and it kind of coats brown to the posterior side. If the left anterior descending coming directly down on in the diagnosis lunch. And so they So the important thing to note here, it's just haven't idea of where these branches what what area of the heart they supply on dime. I'm gonna leave it a she because she got some lovely sides of the CDs and I know that's what mercy are here for today, but just don't know where I just have an idea of anatomy and then where where they supply as well. So put into this diagrammatic kind of representation of each of the branches the a way that I remember It's not the best way, but the best way to better think about it is just am Sep for the right coronary branches, marginal sinoatrial and posterior and then see mad for the left. Um, on regarding the venous strain is you just need to know where the blood is drained where the blood is collected from. So first we have the small cardiac pain coming off the marginal branch. We have the middle cardiac pain coming off the posterior descending, and then we have the great cardiac vein they're saying directly empties into right atrium on Go into that coronary science that we talked about of the right atrium way. You look at where that is coming up now, so hope you have a better idea of the branches again. I hate to be like, Oh, you don't have to know it, but the best way to learn it is just revising it over and over on. I hope that these kind of this kind of gives you an idea what you need to know specifically. But these are the branches that you need to keep an eye out for. A said you got a link it to the E C gs coming up looking at the key features of heart chambers. So you need to be able to look at on something hard on, be able to differentiate them, so starting all So it's starting off with the right atrium. What we have first are the clings to the vena cava. So I'm going to go through all of these, but I'll let you read through them. But I'm just highlight the specific ones we have the fossil Vallis, which is the Revenant off the form and overly the formula of Allah is this intercept a lot like whole. Almost on before birth, the form of a body allows blood to pass, basically bypassed the lungs. So, rather than being rather than the right ventricle, contracted blood into the lungs, it allows it to go to the left side and be pumped around the body and then, um, to the placenta. So the fetus in in the room, it doesn't actually get an oxygen. It gets it from the placenta on. So the lungs we don't actually need the lungs when we're in the room. And so this Obama allows the blood the bypass it effectively. When we When you don't take their first breath, it soon closes on. Then it becomes this remnant so known as the faucet off are less, you know, the opening, the quarry Sinuses we saw on. Quite importantly, the crystal terminal is and the pectus pectin eight muscles. So the Christian terminology is this, um I guess just connection or kind, of course, is between the vena cava. And it separates the atrium pot atrium proper from the Sinus of the vena cava Onda coming off the crystallize of the pack in a muscles on these air, just ruffling in the right atrium and it allows you to differently, right from left, a z can see the left atrium has smoother in the walls on then, looking at the right and left ventricle little bit different what we have, obviously, the opening to the pulmonary and aortic trunk. We have trabecular Carney again, these rough lings in the cardiamin in the wall. We have the court attending on the pap your muscles. Eso again important know the function's probably muscles. They pull on the so they contract and they pull on the quarter 10 today on they allow the custom open and allows intricate feeling when in the relax, relax, Asian stage. We're gonna look at that little bit more coming up on the court. Attending effectively prevents inversion off the bicuspid tricuspid valves on Botox blood from this leaking backwards. So on just a little note on the nurse here is well, so the important thing to know is the recurrent laryngeal nerves where they wind around as you can see the left one's around the art theatre and right, but one's around the subclavian artery. So again, I hope you can see that there are some key features that you know in each of the heart. So if you ever saw an image you able to like kind of different sheet and again, remember that thing I said right and left, how you write in left ventricle had a different rate than the left is thicker, said Move forward, the great vessels of the heart. I'm not going to focus on this and love it too much. I know you guys probably have your own ways of remembering yet, but I've got it here in the diaphragmatic representation. Um, you so you should know that cup branching off the aorta are three main stem, so we have a break. Alec Trunk, the left common carotids on the left, subclavian on the right common carotid. That's a play been coming off the brake is cephalic trunk brick. With regards to the superior vena cava, it's a little bit easier to see. It's just the veins coming together. Subclavian, internal jugular. Coming together to make the break is cephalic on Dim Port. Thing to know is the azygos pain, and he's into the right break a cephalic. And so, just just for your note there put it in on that joins together the right and the left, going to the other to make the superior vena cava again. I hate to just put on you, but this is just there's no better way of learning it right there looking at images, revising it over and over and just being comfortable. The idea how the blood circulation works and the's anatomical structures look. Eso put a little note that is just coming up receptors, so there are some receptors located. Lt. Art from character Sinus on the aortic virus except ER sends impulses by the vagus nerve on the character fire. They've lost a friend deal. They are similar ated by arterial stretch, so their mechanical receptors that can detect stretch changes on. So when the pressure increases, when there's a lot of love volume, they they can send impulses to effective account track down. We're going to see that a little bit more coming up with regards to the rast system on the kidneys. But moving forward, that was the cardiac and after me and those are the key points again. This is the full extent of cardiac can ask me, but I hope those are the key things that you could take away, and the key things that you need to record be able to recognize moving forward to cardiac cycles a little bit more interesting, livable. What I'm here for side of the question so it's just really could get the pole up. Please. Eso This question is, during the cardiac cycle, when did the a V valves open? So please don't click. He There's only four options. Here's hours. My bad eye sure made at the option. But you should know there are only four stages in the kind of cycle four main stages of the cardiac cycle. So we got a mixed response here again, please. Full participation. I want to make sure everyone still this thing. You had everyone still in here. Okay, Again. Bit more months. He coming? Guys, get a few seconds on. We'll close it there. Thank you. Um, so you guys have gone for a and the answer is a But we had a bit more of a Ms mixed response for this one. So we'll look at that thing up on. I think I have one more question yet. So it is a true fall, so there's only a little B. So, please, um, really click. It'll be draw a false with regards to ventricular feeling. Most blood is pumped from the atria to the ventricles during atrial systole. True, awful. They will be love somebody over. Okay, level mixed. Okay, More leaning towards one side. Get a few more seconds or maximum participation, please. On will close it there. Thank you. And so, but mostly for be, but a little bit mixed. And the answer is beat. I'm going to look at why that is coming up. So the cardiac cycle gave you a low T Is the trailer there? Cardiac cycle. So I've copied this diagram in It looks like a lot, but we're gonna break it down. Bear with me. I think the first thing I want to know is you get you going to see this diagram quite a bit on. But I just need you guys to be able to rest for a bit. Be able to know what we're looking at here. So that that blue line that the light blue line is the ventricular pressure, That red line it's ventricular boiled you on. So just just for you know, this is the left side, but looking at because the left side has greater pressure changes and greater volume. So that's what we're looking at the left side. But this is in regards to the heart in general. And you can see how we relate this to the e c g. I didn't know that the bottom that top black line is the aorta Aorta pressure on. So keep that ahead. We'll look at why that is on Ben. That bottom. It's just the atrial pressure. Most importantly, just remember the ventricle pressure involved. You were gonna look about another more specifically. So the four stages off Cardiac cycle, Intricate feeling or notice. Diastole have eyes a volumetric contracture in systole or early. Cicely, we have injection the injection phase systole again on isovolumetric relaxation, which is early diastole. So you break it down into those parts. I'm gonna look at what each other's entail. So ventricle fitting. Uh, diastolic, um, as you can see, the the diagram. I've got it on the side so you can follow it up. Hopefully, you guys and see my cursor as well. So we'll work through it. But that is what diastole is on that on the diagram. So start enough. We have the Atria Andre Trickles. Relax. That's what I asked the means. It means just relaxed. We're going to get is blood filling the atria So through the vena cava on the right side of the pony reins of the left side. From this feeling we get past before this filling, we get passive filling into the ventricles. So this happens until there's a neutral bet. Trickle, a volume that's reached and eso is you can see. That's when the venous pressure on the ventricle pressure's equal. It's all about making personally equal in the cart exactly received how that works so again to review and that eventually relax a lot of blood to fill the atria. You get this passive fitting into the ventricles on this happens until the venous pressure, the ventricle pressure match and at the end of diastole the atria contract. So this is atrial, sisterly and injects the small last amount of volume of blood into the ventricles so you can see that how you can see my cursor. But that red line you see there's in Diastole. There's passive Ben trick your feeling on, then, when you can see the P wave and she's going to talk to you about the CD side. But when the atria contract, you get that last bit of blood flowing into the ventricles. Okay, so it's and then just a note there. Volume in the ventricles at the end of diastole is known as the end diastolic. Well, you should know that it's quite straightforward, but so that that's been tricky feeling. Then you get this really cool small stage called eyes, a volumetric small face, very isovolumetric contraction. So what happens here is the vengeful start contract, Um, with the ventricle contracts and they contract from the bottom up we get, we see that the A V valves close closing on cells, and this just prevents blood flow back it. Atria, the started sister, You see this sharp rising precious you can Now we're looking at a blue light again, that light blue line of lesions about cancer. So this really sharp increase. But what happens is there's no change in volume on that's effectively. It's quite straightforward. Eyes of all the metric contraction eyes. Oh, same volumetric, same volume, contraction. So in contraction with this that we see this massive pressure rise. But there's no change in body. So this last around 50 milliseconds before the pressure in the ventricles on the arteries match. So I hope you can see that crossover that end of that isovolumetric you can see. Remember that top black line was the aortic pressure. So those two pressures cross, and that's that's that isovolumetric contraction stage. So keep that in your head. The same amount of volume, the ventricles contracting but bloodiest blood is the volume of blood isn't changing. The pressure is just increasing. So and even even you can see that red line is just It's just this is a flat like a The volumes are changing. Then what you get is this injection stage the ventricles, it matter. Ventricle pressure matches that aortic pressure, but then what you get, it exceeds the artery pressure on D effectively Ajax blood from the ventricles of light is then pumped out from the aorta on the comedy trunk on this is that injection phase. This would last around 330 milliseconds on. This is this is known as end of Cicely, and that's the end of Cicely. The ventricles start to relax again so you can see the There's a sharp rise and pressure peaks, and then the pressure starts to relax again. Um, you can see that all the blood well, most of land, so I won't go into that is injected on, we'll see why that is and what that is. Um, on when the ventricles relaxed, there's a decrease in pressure, as we said, and this decrease and pressure causes thie semilunar valve. So that's that aortic and pulmonary valves to close in on itself to prevent blood from blood flowing back on a Z. See when blood doesn't flow back, it contributes to the closure. So the seminal you know valves prevent any kind of leaking. Um, so that's the injection phase. Moving forward, we have eyes, a volumetric relaxation so the realization side occur, so the blood blood is being injected. The ventricles start to relax. Then you get the small period of time where there's no change in volume. So at the end of Cicely, both sets of ours a closed the ventricles continue to relax, and there's a decrease in pressure as you can see that the dip. But then, for a period of time, there's there's no change in volume, and so again, I've ordered metric same body. Relax a shin a Z conceive there. There's a, um, line, and there's a decrease in pressure. And so now we've reached the start of our cycle again the atria and then trickle relaxed. The valves are closed. You get this passive feeling and then the a V vials allow past filling into ventricles. And the cycle started all over again, as you can see. So I hope that's broken down that cardiac cycle A cardiac cycle a little bit better for you guys. So when we are talking about kind of cycle, talk about the consistency and I asleep, we're talking about Ben Trickles. But to be more specific, you say atrial, atrial systole in, in, in diastole. But I hope you realize that these four stages and how the physiology work, so it's not too complicated, but it's all to do with pressure changes on the pressure changes. Uh, but what causes the vast open? And I hope you can see that, so to see it a little bit better, and I don't know how everything feels about this. I know we get mixed responses with TV loops, but it is a concept that you need to go regards to pee pee. That's okay. I'm gonna is gonna be a bit of you guys helping me out, because now we've gone through cardiac cycle. I'm gonna ask you to help me out here, so we'll start at that bottom. That bottom point they're on gonna give you is a little bit of tip. The red boxes are valves, great cardiac cycle, stages and green. A key terms that you too low. So starting off of us, that starting point. Can anybody tell me so? Okay, please. Quick note PV loops. We're looking at the left ventricular body against left pressure. So we're talking about left ventricle. Remember? Bowels were talking about. So the start, we have this set volume, and the volume starts to rise on a slight rise in pressure as well. So to allow the left ventricle volume to increase what bowels have to open. Anybody tell me the chapped there are I don't want to do. Amazing is a valid, but bit more specifically is the mitral valve. The mitral valve opens allows this passive feeling off the ventricles, the left ventricle, and that's what you can see this rise in volume and then at the end off Theo, end off the passive feeling a certain contraction starts certain valve closes. And that's the mitral valve. Again, I'll get I'll give you this one, but we're gonna help me out with an excellent So my trip so you can see there's passive feeling. Mitral valve closes. So this stage want to be called a stage, you know? You tell me the shot. Yeah. Initial stage. That gray box. Uh huh. Anybody tell me So remember, guys, it's the passive feeling. Nothing's contracted yet so that that red line is diastolic feeling. But you got to take it a step. Well, very well. So I would go more on his coming in now. So at the end, off enough, given, you know, the end of diastole we have the set volumes 120. I should see a matter after this is known as the end. I saw that value. So then, at this point, the ventral start to contract. And this is what you guys were talking about before eventually start to contract. And there's a sharp rising pressure but no change in volume. That is. Anyone Tell me the chance. That is isovolumetric contractor. Very well done. So the eventually pressure rises and rises, and then it reaches the aortic pressure and then exceeds the aortic pressure. And so when it does exceed what valves open the aortic valve. And you get that just now is a little valve opens. We get this injection phase and I've given you the phase. It's ventricle ejection and then the practice. Then you get this injection phase. The pressure starts to decrease on Ben. Something happens. The aortic valve closes very well done. And then you get this AYSO volumetric. Relax. A shin give you the sun as well. So we have this. We have this change. We have this decrease in pressure with no change in body. So you can see the sharp rises and sharp changes of pressures Is the eyes of volumetric side that the contract with the contraction relaxation Onda. At each stage you you get it's just a cycle. Do you just get a cycle of filling and injection? So I gave you that The there at the end of Diastole you have the end diastolic value. Can you tell me what we get the end off Systole? Yes, we get the end systolic volume. I hope you can see the bottom there and so on. Before we get into that, we have to pressures that we need to know as well. One is the diastolic BP. And that is when that that the pressure when the before the aortic valve opens, and then we have the systolic BP. That's when the LDL actually uses. And so those two pressures are are systolic BP, diastolic BP that you read on when we take something that somebody's BP on, then the next key term that you need that we're gonna look at this more. Coming up with the math side is the difference. So when I weigh, have set, we have set volume of blood that is injected, and so can anybody today wouldn't know what that said. Volume is called in one heartbeat. Yes, very well done. It's stroke volume lost myself there. Start for you and it's gonna see from that. A graph The end of the stroke volume is end diastolic value minus the end systolic volume. So it's the volume off blood once after filling and then minus the value applied after it after, but volume of blood after blood has been injected. So those two volume see if you that stroke one you the total amount of blood that has been injected. Okay, so I hope you can kind of relate this locally. A cycle? You kind of understand what people Lupus showing. It is just clearly showing that there's this isovolumetric stage. I's a volumetric. Relax. A shin contraction on you just need to know. Specifically went about open where they close. Done moving forward looking. We're going allow. Look at starlings law. So this is just a concept that I know some people find hard, but we're going to break it down a little bit. Just give you guys better. Better idea of what? What? What you need to know more you to apply. So for stylings, law, stroke volume. So we're talking about it. It's a difference between the end diastolic and systolic volumes. So it's that difference between the volume of blood in the heart, the end of diastolic. So once the blood is filled in the left ventricle, and then whatever minus whatever is left in the blood after the injection face so you can kind of see that is directly related to the amount of the heart, fills by on the ability of the heart to pump out blood. So there are two fat. So they're few factors that affect stroke volume one being central venous pressure. So why is this being this pressure? We talked about central venous pressure. Is the BP in the Venus Cavor near the right tree? Um and it It's basically a reflection off how much blood is returning to the heart and effectively the ability of the heart to pump blood back into the arteries. The changes in the CVP result in a change in the diastolic feeling pressure. Then we have total peripheral resistance or arterial resistance. And this Just detect this. This is just how easy is for the heart. Expel blood out off the heart. So how How easy it is hard are easiest, exposed blood out of the heart. And then why importantly, what we got, guys preload and pre load is the volume of Venus blood that stretches the resting cardiac muscle. And this is what starlings was all about. So they're the idea songs, or is that the energy released during contraction depends on its initial fiber like so I'm sure you guys want to upon your physiology of people know about how the muscle and act in mice in this cross recycling. So for there to be maximum contraction, you need, uh, you need to reach this, um, you need You need the fibers to be stretched a certain length. So the more you stretch the fibers, the greater the energy that is released during a contraction. But obviously, this up to a certain point. After a certain point, you can't form those bridges on. So obviously, too much of a good thing can be a bad thing. So as you can see, the more heart more the heart chambers of stretched, the stronger the ventricular contraction and greater the stroke call you so you can almost see there's a rise in central venous pressure automatically means a rise in strict Well, um, so the more blood returning to heart increase stretching more plus expelled, our more returning. And it's it's this is cycle almost on. This phenomenon is due to the stretch dependent sensitivity off myocardial contractor proteins, toe calcium. And this is no no starlings law. So you can see I told you, um, that it is to do with the feeling and to increase feeling means increased stretch so well with the styling or we get this curve s. So I put the diagram there for you to see on the curve relates stroke volume to let at the venous pressure on go, you might be asking venous pressure should be. In the end, I start them on you. But basically end-diastolic volume and, uh, started pressure is there's almost linear relationship between them two on so just pressure is easier to measure the curve on that. The a slope of the curve defy is the contract I'll force. So if there's an increased or steeper slope, that's increased contraction, it has decreased. There's decreased contraction. So although the initials so yes, so yes, sir, not myself a little bit. The right illustrates the relationship between that stroke volume. On that end, I start pressure that end diastolic value on, as you can see as you increase end-diastolic Morelia mule and increased stroke volume on there's there's almost linear relationship, obviously up to a certain point, but that's the important part. And then the slope is that contract, the contraction force. We'll see how that links with the gas, and that's coming up. But that's the basics of starlings law. I hope I ramble on too much about that. I'm trying to keep up quite simple again. Just the basic concept is the further you stretched the heart muscle. The the increased contraction that you can get from it is the increased potential energy that have you apogee. Stay as of that starlings law, Move on to rust the raw system. I'm trying to check time. I think I'm gonna have to speed up a little bit the wrong system. Sorry I am. I'm going to be through this one a little bit. Don't. Don't fret, though, because she is going to cover this a little bit better with the gas of pharmacology side and I will discover the main bits. Start with one quick question. What electrolyte changes Does aldosterone coat aldosterone? Cause if we get the polar one more time, Thank you again, does. Even if you get it wrong. You're right. It's one C max. Um, participation for everybody. Please. Your few seconds and okay. Good. It's finally ended there. So everybody is going for B. The ant is be increased serum sodium at reduced syrup. A task way I look at why that is so with regards to the nephron in the system. What you need to know is that within the kidneys you have f one and you have the glomerulus. Uh, this, um, blood is sent to the kidneys to be filtered to filter out waste products. And I owns and molecule that we don't need or that we will need on there's this Very fine. There's a very fine negative negative feedback system that allows for a specific concentrated off specific, uh, sorry for a specific blood concentrations daycare. So just to cover their from quite quickly, we have the after Afrin arterial blood coming in in SoCal Merrill. A capsule. You get the blood, get it filled out. Eso you get s o not Glad filter out you get um so everything's a passing real America capsule that you conceived water, glucose and other things on. But what you have is this this'll secretion but also reabsorption system. So, yeah, you have to speak up a little bit. So I just checked the time regard regarding psoriasis. Is the rain in on your attention to aldosterone system? So I took these slides from my peace history session, so I know you all got it here, but focusing on the most important things. The Renan. Ready. An angiotensin two aldosterone system allows for a fine BP control. And how that is is done is through this We get an angiotensin on. So effectively get angiotensinogen released from the liver that's converted to understand in one vial, Renan. And this is released by the kidneys. The kidneys. How did checked changes in our blood? It can. It can detect changes in salt concentrations, and it could be simulated sympathetically on it can also detect changes in blood pressure as well. On with regards today. Say it. Then it s a relation to this. It releases Renan. Reading converts creates Oh, convert understands indigent. Angiotensin one on angiotensin one converts eso eighths converts angiotensin one into angiotensin two. So leaving us up there and attention to is it is important that we're looking at here. It causes the's, uh, reactions in the body. It causes specific a control in the body allows effectively for the BP increase on. It does this through different ways. It can increase sympathetic activity. It can increase the blood volume so increasing blood volume increases the BP and then increase is increasing the BP effectively. There's also a lot of secretion that causes salt retention on disinterested BP as well Have 80 80 secretion allowing water resorbtions increase water resorption in the net front as well. So the important thing to know about this system is that a negative feedback loop the two books to blow blow Merrill a feedback loop. So what we have here is, um, Brennan is released when there is a decrease in blood pressure or they detect a decrease of lab Russia on it causes angiotensin to exert all these effects BP, them rises, and then this is detected by the atrium. So remember we talked about those barrel receptors. There's also this one reflex that you need to go, and it's called the Bainbridge Reflex. This is the effectively where the atria can detect, uh, BP changes like it can detect the stretch in the atria. And so when there's increased stretch, it releases a M. P on MP directly inhibits Renan on so that that's where this feedback. So there's increased BP. A trip to check this and then Atria inhibit Renan on Brennan and goes is to probably go back down. So this is very fine Control of BP by the raw system in the kidneys and a little note I just want to put areas as well understands into causes Atrial, uh, arteriolar basic constriction and specifically if front arterial phase of constriction and the glomerulus on. So if you remember how the Damaris a structured, if you can If you constrict the different arterial, you can increase the pressure in the gut Marylise by effectively causing more blood or blood to spend more time in little Marylise on increases that the g f r that that pressure that we weigh know about this allows for further filtration on further control off blood. So, as I said, that's a quick from from it's really sorry, but I really I know you guys gonna have this these slides on you, But again, as I said, she's gonna link it very beautifully to the pharmacology side. And then that's what that's what it's gonna allow you to, um, understand a little bit better there. But I know you guys go look through these slides afterwards, I'm gonna have to speed up a little bit. So cardio activist action potential gonna break this down quite nicely because this is another really important concept that you have to know. So quick question for you guys again. Uh, really? The pool again. Sorry. Thank you. And the conductive system of the highest responsible for synchronize contraction of the myocardium. Different parts of conductor system. Very in conjunction velocity. Which of the following has the fastest conduction velocity? So again, a mixed response here. Okay, end it there. So the fastest conduction velocity is through the back injury fibers a lot of, um first the sign. A jewel node. We'll get a look at that. We can look that coming up. One more question. Sorry. Um, we'll see why that is a swell. The ventricle actual potential represents the electrical activity of the ventricles. Which of the following is responsible for the rapid depolarizations feeds off the ventricle action potential. Just again. So don't worry if you don't know the answer, as I said, like we're going to see you see why this is coming up. Uh, just everybody give give a good, good time a few more seconds, but that, um, we'll send it there. Thank you. You've gone for a and The answer is the rapid sodium in flux, and we'll see why that is now. So Oh, we have one more question. My back. What specific channel? Of course. His face to play. So in cardiac, actually. Attentional. So which channel is it? Just to see if you guys see if you're still with me to see if you guys haven't idea If No, no problem. So we gotta look through now. Few more seconds. This one, um on did their bedroom extra ones. But generally everyone's got the right idea. It is the l type calcium, two channels. So the electrical conduction of the heart I'm I was going to review the electric conduction, but I know she's gonna look through this. So I'm going to skip through this. I know you guys have a general idea of this, but this is the physical. We're gonna look at the physiology side. So we're looking at two actions, two types of action potential. We have the pacemaker on the note last potential, and then you have ventricular actual attentional, so you can see right there. I've also completed this diagram to start give you an idea of what it looks like on the C g of the century will cover this. So we're going to look at what they contain specifically what? Thistle tail. Specifically, starting off with a pacemaker, actually. Attentional stages of the note. Alaska Attentional. First off, we're gonna start with this face full this slow up stroke and this is the pacemaker potential. What's happening here is slow depolarizations or it's known as the funny. This effectively allows. It was just a slow depolarizations until it reaches. I remember a potential. Remember how the conduction works in the heart we have with the node, especially it it sends actual attentional and the whole heart needs to contract on then than it is. This is regular rhythm that it this is regular rhythm that propagates. And so the faithful allows for this slow up stroke and allows for the whole heart contract. This is actually achieved by the hate seein channels, which allows a slow interest sodium sodium ions into the my side. So pacemaker. So I put a little note there. Pacemaker cells spread throughout my cardio on it. Just this just allows a coordinator contraction, but they're mostly found in the side of a truckload the slow entry of potassium ions allows this slow upstroke this allows increased. It's a slow, deep organization allows a slow entry of potassium. Sorry, it's low entry of positive ions into the cell on. So just a little note the hatred channels are activated around minus 50. So that bottom line, you're not the doctor line, but the bottom of face for is around minus 50. Then we have phase a row this quick upstroke, a fast, deep organization. So the memory potential for a pacemaker Southern around minus 40. And this is this is around the potential when where the action potential is propagated. This is when s o there's a quick depolarizations and this is caused by the opening off the voltage gated calcium channels. So we have a slow entry of sodium ions, causing a slow rise and potential. But then the this this opening off many of altered gait, a calcium channel allow this quick depolarizations so quickly peaks and then it quickly falls again. So at the peak, the calcium channels, clothes or inactivates, and then the potassium channels open. And that's a start of phase three. You get this down stroke a report or is a shin. So again, we're gonna look at again. We have sodium ions coming in. This is so a positive positive island. Positive. I don't enter my sight. And then we have a rapid report or the rapid depressurization when the council channels enter on. So the cell quickly the opponent rises on, then the inactivate and then potassium. Potassium channel opens on allows. But ask him. I owns two reflux out of the cell, so positive islands leaving the cell and it causes it causes. That report is a shin sorry. And so this report, either until those hate seein channels open on, allows another action potential to be generated. So as we can see that this is a little bit more simple, but there's a few. There's fewer steps for this one, but the important things to know that that faithful that slow upstroke, the and watch handles open our specific time. So face for the potassium whatsoever. Haiti internals open on the sodium ions or coming in, and then in phase zero, the up straight. The fasting polarization calcium channel is open and calcium irons movement on that causes that deep organization on the face three the potassium channels open, allowing the flux so allows potassium ions to leave on That causes the report or is a shin the ventricle action potential Go through a little bit more step by step. Hope you guys gonna bear with me with this face for again So there's a few more phases in this But I got I break it down, Make it a little bit more simpler Faithful is the baseline to conceive just a straight line There's potassium channels open oppressed on. So at this stage, the myocyte the cardiac My sight is very probable. Two potassium on So the member of potential is actually close to that equilibrium potential of potassium. And what was equilibrium? Attentional? It's when, if effectively, it's when. If so, if the memory was parable just a Passy, um, it would have this equilibrium potential on. That is why the at the baseline, the cardiac. My sight is permissible Potassium, very bottom, able to do the potassium. And it's very close to that minus 90 to memory but equal, even potential of potassium. Then what you get is a propagation. So the impulse comes in from the nodal cells On what we get is this phase there? Obstruct a really quick, fast depressurization at this stage, the voltage gators sodium channels open from depolarizations Onda when one opens, many open on this causes that sudden, steep depolarizations. So the voltage gated the vulva, gated sodium channels open allows the sodium entry. The cardiac myocyte becomes a lot more positive on that cause that depressurization and they're almost instantly. It will activate it and or clothes on. But this will then only open and negative memory potential when the cell has report arised. So again, uh, go looking back face for a taxi. Um, my own's are moving I/O of the cell on this causes that baseline, and then we get a propagation. We get actual potential generated. That's when the sodium ions into the cell. Phase one is this notch. So what happens here is the borders gator sodium channels close. But then you have this transient opening off assassin channels on, so there's a momentary reported ization when we see, um, I was actually leaving, but this just happens for a small amount time before phase to the plateau stage in the plateau stage. What we have is else? Absolutely Mostly correctly recognized. It's the l type calcium. Two channels open. So again, I'm gonna I'm gonna ask you to remember, Remind yourself of their kind of physiology. Cardiac, how the muscles work on, um what Calcium is useful. So we get Is calcium entering the myocyte What this allows is for calcium induced calcium release, so count of enters on it binds to allows. The PSA has been particularly to release more calcium on this is for two things. It causes a plateau it causes. It causes that like a base almost a plateau stage it also it also causes contraction of the cardiac myocyte. Remember, this is for the ventricles allows the ventricle contracts and it allows the ventricles contract for enough amount of times that all the blood could be injected and so that my eyesight is depolarizing and report arising actively at the same time on that's what causes that baseline and around the stage. We also have potassium. We have specific potassium channel called the slow delayed Rectify a channel open as well, so well, first for a period of time, the potential it will be a plateau stage. But then we get reported is a shin, and that's face three again, the name quite nicely similar to the noodle actual tension as well. In Phase three, what we get is the calcium channel closed, and now it's just the potassium channels open, allowing potassium ions to leave the cell on. So the card it my second report, arise, and these are the delayed, rectify tunnels that we talked about. So then we get the baseline and the accidental sound like it's that it's cycles again it the ventricular active attention was only propagated when a impulses sent from the nodal cells to remember that's a sign of actual know. Do you have the Aviane node on then? The pacemaker's every we have Deep Benfica was in the cardiomyocyte. The important things to know again, so bring to attention is it's good to know that what channels open at what time on what? What? I was moving in what way? So when positive. Just a general for general knowledge. When I positive ions moving into the cardiac, my sight, we get depolarizations, as you know, but it's the lead. It's the e flux of potassium ions that cause the report rising of each stage. So that is the ventricular action potential. So, again, I know you guys gonna have these slides on you? I move to this quite quickly, but I hope I have made it clear enough that I step by step and that you know what? You guys know now what you need to look out for what you eat. Er, learn specifically very, very greatly. The math in cardio. Quick crescents. Again we get a hold up. What is the definition of cardiac output? Get no problems. You guys don't know it. You guys have been on the ball is in time. I've got Give it to you Hands down to you guys. Um, cardiac. But again, some mixed responses. Yeah, your few more seconds. Close that few seconds. Maximum participation. Lovely. Amazing. So we've the answer is actually see so mostly you have a That's not a problem. It is the volume of blood ejected in one minute. It's a cardiac output Stroke volume is the volume of blood ejected in one ventricular contraction. And we're gonna look at that now that this was a mass question. I'm going to skip over it, but that's not a problem. We're going to see what? Why it is. But just to have an idea. So if you're if you were measuring mean arterial pressure using systolic and diastolic, it would be okay. The whole is up. If you guys want to send this, I make it really quick. Guess, King, just give it a good skill. Good guess. Or a lot of you guys got around, sir. Okay, a few seconds. I'll let you guys aren't this one for a few seconds and then on close. It's that most of you guys have got the right answer. It is. See, we'll see how you calculate that Now, coming up so quick. Definitions on concepts. So put this out quickly for you guys to work through again. Cardiac output is the volume of blood ejected by the ventricle of one ventricle in one minute. But stroke volume is jet. Is the blood ejected in one ventricular contraction? Um, we talked about total peripheral resistance. Is that resistance? The blood flow in the whole system through the arteries? Um, mean arterial pressure is Theo average pressure and put patient arteries during one cardiac cycle. And then ejection fraction is a percentage of blood that is reacted in from the left ventricle after sisterly. So it's important to know these definitions because, uh, lecturers, every anyone will use these words expecting, you know what they mean. So just remember that there are these slight differences, but they're all here noted for you guys. Just a quick note to things that directly affect cardiac output is the end. I solid problem with the right heart and then the resistance, the outflow. We don't see why that is. You see what that is now? So the important formulas that you need to have noted them out for you guys, I'm gonna just show you all of them. So there's again no better way to learn it than putting them into practice. Just do as many questions he can call them. As we said, cardiac output Is that stroke for you? Times by heart rate a stroke while you again. Remember, it was the volume of blood ejected of one ventricular contraction on the heart rate. Being like your heart rate BPM. And that's what the cardiac output is. It's the amount of blood, uh, ejected in effectively. Uh uh um and really in relation to your heart, so see kind of help. It is a stroke volume type of harboring. So following. We've looked at this and I started volume I nece and systolic volume ejection fraction is the Remember we said it was the eyes. A percentage of blood ejected in one contraction. So it would be strict, William, over the end diastolic volume. So how much? How much volume, how much volume of blood is left in the heart attack? End of diastolic And then how much is it jacked in relation? How much it's injected mean arterial pressure. There's multiple ways. So, uh, calculate this, but this is the one way that kind of covers it all Diastolic pressure, plus a third of your pulse pressure pulse pressure being the difference between your systolic and diastolic on, then total peripheral resistance being mean arterial pressure over cardiac output. So I've left these for you guys to look through, and I'm I'm sorry that I had to speed up, but she's got some lovely content. Mind up for you linking all of these concepts together. I know you guys going at the slides on you afterwards, but as I said, this was just This is just most of the vision from PCs, in my opinion. And I hope you guys, I've got the really important concepts, but I'm gonna hand it to she now. Tow, take over on the cover. The pharmacology. Andi pathaphysiology side. Thank you so much. Just in. Um um that was a really good and comprehensive presentation. A lot of high yield concepts covered. I think before I start, we'll just take a five minute break so that you guys can sort of get a drink. Girl goes to the toilet or whatever. And then we'll come back at, um, 8. 17. And I will be covering the CGs because I know that's a really daunting, um, concept as the first year. So I'll be going through the very basics and hopefully simplifying it for you guys. I'll be going through a cardiac cath pathophysiology Onda, um, cardiac pharmacology as well, So yeah, we'll meet back in five minutes. Great. So I think we'll get started with it now that we've given enough time for everyone. Right. So, um hi, guys. I'm Shree. Um and today I'll be doing the HCG section. That's gonna be the bulk of my session, really? Just delving into the basics. Um, and then we'll be going through a few pathologies and then finally, cardiac pharmacology. Great. So to start off with, let's talk about the actual needs. So I'm going to start off with a unipolar limb leads. So these are the ones where it has just one electrode attach to each arm or leg, so the first one will start off with is a VR So are for right. So our positive electorate is gonna be on our right arm that are negative. Electrodes are going to be on our left arm and are left leg. Now, notice how there is a arrow sort of pointing away from the negative electrodes on that sort of shows the axis in which the action potential is traveling. But at your stage, that's a very important. The main thing you need to be able to pick up is what area is this lead actually picking up electrical activity from? So that's what I'm going to try and explain to you guys. So the easiest way of sort of remembering which areas picked up by which lead is by imagining that you're standing on the positive electric. So imagine you're standing on the right arm over here and you're looking down at the heart. The part that you'd be seeing of the heart is the right side, Uh, probably superior early. So the area from which the electrical activity is being picked up by a VR is the right side of the heart superior. Really great. So I just put an eyeball on here Just for you to do is for you guys to visualize It's gonna be the same concept for the next few leads. So for a V l again l for left. So are positive. Electric is gonna be on her left arm this time. Um, and then we're gonna have are negative electrodes on our right arm and are left leg. So again, if we imagine that were standing on the positive electrode. So for standing on the left arm on looking at the heart, we would be looking at the left lateral side of the heart. So this lead a V l would be picking up electrical activity from the left lateral aspect of the heart. And then finally, we have a B F. So f 4 ft. So are positive Electric is gonna be on her left leg this time and then are negative Electrodes are going to be on our right arm on our left arm. So again, if we imagine that were standing on the positive electrode here looking up, the heart would be looking at the inferior aspect of the heart. So now this is gonna be really important. When we talk about territories, I'm going to have a few slides on that as well, so don't worry. But, um, it's just at this stage, it's really important to know which lead picks up electrical activity from what territory of the heart. So yeah, um, in a normal e c g, you're a VR would usually be inverted. Sorry. It's always inverted in a normal EKG on. The reason for that is because you would be looking at the heart Superior Lee, whereas for all the other leads, you sort of pick up electrical activity from the positive electrode down. So everything looks inverted in a B are on. Sometimes a way to know that you've put on your SED leads correctly is looking at a VR and seeing that it's inverted on, do yeah, this is my main sip. Imagine you're standing on the positive electrode and looking at the heart. That's the territory that is associated with the particularly good, right? So that's our unipolar limits. Let's talk about our bipolar limits. So this has two electrodes attached to one area on. That's why you have a 12 lead, SCG, but only nine way forms produced. So if we talk about our first lead, which is lead one, we have our positive electrode on the left arm and then are negative electrode on the, uh, right arm. Right? So imagine that we're looking at it from the positive electrodes, same as the previous slides imagine were stood on our left arm. And we're looking at the heart lead. One would be picking up electrical activity from the lateral aspect of the heart. Um, and that's because imagine you're just stood on the left arm and you're looking at the heart right? So now let's talk about lead to. So for lead to our positive electrode is on our left leg and are negative. Electrode is on our right arm. So again, same premise. I know this sounds monotonous, but it's the easiest way of learning your stood on the positive electrode and you're looking up in the heart and soul eat. Who would be picking up electrical activity from the inferior aspect of the heart? Amazing. And then finally, we have our lead. Three. Where, UM, there is a positive electric on the left leg and a negative electric on the left arm, and it's it's the same as the two. So we're standing on the left, were standing on the positive electric on her left leg, looking up with the heart. So would be looking at the inferior aspect of the heart, So it will be picking up electrical activity from the inferior aspect of the heart. Right? So I do have, ah, kind of silly memory. Eight. Taking insurance from Beyonce's So it's to the left to the left, Everything positive in the box to the left. What I mean by that is usually when we have a left arm or left leg, it's usually a positive electrode. The only exception for this would be really three, where both of them are on the left, but our left arm would be negative on the left leg would be positive, so it's quite complicated sometimes to remember which arm or which leg has a positive or negative elected. So this is the memory eight, I sort of used to remember. Great. So now we're finding going on to our chest leads. Um, it's very high yield to sort of remember where you place these chest needs. It's tested a lot in this keys and even in your s one exams for Carter students. So for the one, we would be placing it in the right fourth intercostal space Paris sternly, which means on either side of the part of the sternum. So in this case, it would be on the right side of the sternum. Then we have our V two, which would be placed just opposite. That would be the left fourth intercostal space, Um, Paris Turney's on the left side of the sternum. Then we have the three now, obviously is usually placed after be two and before, because it sort of just slots in between. So the three you just remembered as between be two and before and then we have before, which would be in the left Fifth intercostal states in the midclavicular line. So if you sort of draw a lot and imaginary line down the middle of the clavicle. That's sort of where your fourth four chest lead should come in the fifth intercostal space. Then we have the five. So the five would be in the fifth intercostal space, but in the anterior axillary line. So that's sort of just before your Axler just before your armpit area. So if you sort of draw a line from there, it will come the left fifth intercostal space. And then finally, we have b six, which is the left 15 hostile space of the midaxillary line. So that's just drawing. Um, it's sort of the most lateral chest leave. That there is great. So now that we've looked at the leads, let's just quickly do it on SPF. We could get the pole launched parent. Yeah, So if I could get you guys to participate as much as he can Great. Just for the sake of time, I'm going to stop it there. You guys do have the questions. You do have the slides so you can look at it in your own time. Um, but yeah, most of you did get it right. It would be the left anterior descending artery. And I'll go on to explain why in these slides, right? So the CT territories, we've looked at the leads on we sort of look at which, um, sort of leads supply which area? So let's just look at that in more depth so our anteroseptal territory is going to be covered by firstly, we'll talk about the anterior territory, which is covered by leads V three and before. So if you want a refresher of where that is RV three slots in between RV two and before on our before sort of occurs in the left fifth intercostal space in the midclavicular line, right? So if you can just imagine the heart behind these leads, you can sort of imagine that V three and before would cover the anterior aspect of the heart, which is why it picks up electrical activity from the anterior aspect of the heart. So any sort of occlusions ischemia infarction any damage to the left anterior descending artery, which supplies the anterior wall, would then be reflected in vitro and before as ST elevations ST depressions. So yeah, leads V three and before correspond to the anterior territory of the heart. Now the one and the two can sort of sometimes also be clubbed in with the anterior territory. But that, like, more specifically, it does pick up activity from the septal area. So if you guys remember our intervention, your septum sort of running in between the heart, Um v one and be to, if you remember, would be placed in the right fourth intercostal space and the left fourth intercostal space Paris Turnley. So if you can imagine just the heart behind it would sort of be covering the area around the septum. So will be picking up electrical activity from the septum. So again, theseventies area is, um uh it's supplied by the left anterior descending artery. So if there's in fortune, is Kenya any damage to the lady? Then that would be reflected in needs. V one B two uneven, be three. And before so usually the anteroseptal area is club together. Ah, but in specificity, septal area is picked up by V one B two on the anterior wall by the three before. Great. So I'm moving on to the lateral territory. Um, it's going to be picked up by leads. One a v e L V five b six. Now let's break that down again into the location of the leads. Um, if we start off with a B l where we're where we have our I situated where the positive electrode is. So for a positive electric is on the left arm and we're looking at it. Stood from the left arm would be looking at the left lateral aspect. Same with a lead one. So if we're stood on the positive electric, which is on the left arm, we're picking up electrical activity from the lateral aspect. Um and then finally the five and B six. So if you guys remember, the five is in the left fifth intercostal space of the anterior axillary line, and then the six is in the left fifth intercostal space of the mid exhilarate line. So again, those are placed Christ quite actually as well. So if you could just imagine the heart behind it would sort of be covering the lateral aspect of the heart. It's another lateral aspect of the heart is supplied by the left circumplex artery. So if you remember, the circumplex sort of curves behind the heart. And so if there is an occlusion or any damage to the left circumflex artery. It would be reflected in these leads one A v, e l t five and t six. Great. And then, lastly, we have our inferior territory, So this would be leads to three and a V f. So if you guys remember our leads to and leads three, both have the positive electrode placed on the left leg. So that would be that we're standing on the positive electorate on the left leg, looking up with the heart, and so it would be looking at the inferior aspect. So these two and three would be picking up electrical activity from the inferior aspect of the heart. And then, um, finally, we also have a B F, which is a similar premise. It has a positive electrode on the left leg. Now the inferior aspect of the heart is supplied by the right coronary artery. So if you guys remember, the right coronary artery sort of curls under the heart, and it has a bunch of these branches that, um, supply the inferior aspect of the heart. And so if there's any occlusions are damaged to any of these branches, or the R C itself. That's gonna be reflected in needs to three Avia. Now, some people use this memory eight to remember which, uh, leads are inferior on that's that on an E C G usually leads to three a Be a form a boot shape on. So if you imagine you put your boots on your legs so you put your boots inferior, least so leads to three a V f word supply the inferior aspect of the heart. Great. So that was, um, a quick run through, uh, VCG ease, uh, sug leads and the CT territories. Now let's look at the CD waves, which is probably the bulk of the session before we actually talk about the waves. You know, the P Q. R S T. Let's talk about a few golden rules. So if we have an action potential moving towards the positive electrode that's going to form a positive deflection on our way form. That's gonna make more sense when I go through it in the actual slides, Um, and it's the same for the opposite. So if in action potential travelled away from the positive electrode on negative deflection like this would occur And now, just recapping from Justin slides the pathway of conduction. We have an action potential emanating from the S A n or the sinoatrial node on. That's going to reach the avian on now at the Aviane, there's gonna be a 0.1 2nd delay. Can anyone in the chat put why there'd be a delay at the avian? What does it allow for? Just to make sure you guys are still there. So why would there be a delay in the ab in great amazing? Yes. So, um, you want your ventricles to fill before they actually contract so that more blood is going to be pumped out of the heart? So that's 0.1 2nd delay accommodates for ventricular feeling before bed regular systole actually occurs. Great. So now we've reached our ABN, and then our action potential is going to travel down the bundle of hiss on. Then finally, it's going to travel up the pricking your fibers. Um and that's gonna depolarizing the heart from the apex, which is the bottom upwards. Right? So that's our pathway of conduction. Now, let's just talk about the actual STDs, so I'm gonna go through each one on. I want you guys to tell me what it signifies. So, what does the P wave actually show? We have our first wave here. P wave. What does that actually show? Is that atrial depolarizations? Amazing. Yeah. Atrial contracting or atrial depolarizations. Great. So now what about this QRS complex here? What does that show enteric you a report? Or is a shin Depolarizations amazing on? Then? Finally, what is our T wave show centric? You learn repolarization Great. Yeah, And then we have a few intervals that we also need to be aware of. First are PR Interval that signifies the AB and delay. Like we mentioned the previous slide. Um, the ab and delay allows for rent regular feeling before then. Trick your systole. Um, we also have the ST set segment, which is the time between the ventricular depolarizations on repolarization on. Then finally, we have the q t interval, which is time between the start of the ventricular depolarizations and the end of intricate every polarization. Right. So remember, how is talking about if and action potential moves towards a positive electrode that's gonna cause a positive deflection. Well, that's what's gonna happen initially So like we mentioned the previous slide are P waves signifies atrial depolarizations. So in action potential is going to be generated from the sinoatrial node and it's going to move down to the avian. Now, notice how this action potential is moving towards the positive electrode. Since it's moving towards the positive electrode, it's gonna cause this positive deflection. Now there's also gonna be a slight negative deflection. And the reason for that is because some of the action potentials reaching the Abyan go back up to depolarizing rest of the Atria. And since it's moving away from the positive electrode, it's gonna cause that negative deflection. So, yeah, overall, it causes this positive deflection because the action potential is moving towards the positive electrode and the P wave signifies atrial depolarizations. Great. So then let's talk about the PR interval, which signifies hour delay at the avian. So what happens here is an ice electrical line actually form, so it's just a stationary line Now. The reason for that is because, like we mentioned, there's gonna be a delay at the avian. Um, there is no action potential either moving towards or away from the positive elected, so it's just gonna form this straight Isolette trick line. So yeah, the direction of the action potential is neither here nor there. So a nice electric blind is produced. Amazing. Then we have our Q wave, which is this slight negative deflection here. So for acuity, what happens is it signifies intraventricular septal depolarizations. So we know that our QRS signifies ventricular depolarizations all together. But this qh signifies intraventricular septal depolarizations. Now, how that happens is there's a left bundle branch or structure known as a left bundle branch, which actually depolarizing the septum from the left to the right on. So you can kind of see that the waves of action potential are sort of moving away from the positive electrode, which is why there's that slight negative deflection. Great. So then next week move on to our our way, which is this huge positive deflection, and it signifies the depolarizations of the apex of the ventricles. Now, the reason for this positive deflection again is because these action potentials are moving towards the positive electrodes on the reason it's such a huge positive deflection is because the left ventricular mass is actually really high. As you guys remember, Um, the left ventricle is really thick because it needs to sort of compensate for the systemic circulation so needs to pump blood at a really high pressure. So due to this huge left ventricular mass on the action potential moving towards supposed to electrode, that's gonna cause this huge positive deflection for the our way. And then we have our s way, which is just a huge negative deflection on the S wave is going to signify the depolarizations of the base of the ventricles. So a Z concede here the wave of action potential is now moving away from the positive electro to sort of depolarizing a base of the ventricles. And since the action potential is moving away from the positive electrode, it's going to cause this negative deflection Great. And then after that, we have our ST segment, which is like we mentioned the time between matricular depolarizations and before ventricular repolarization actually commence is so this is another is electric blind because it's just a delay is just wait thing for, um the action is just waiting for repolorization to occur. So there is neither a a potential moving towards or away from the positive electrode, which is why it's gonna form. This is electric line. And then finally, we have our T wave. Now the T wave can kind of be a little confusing for people to get their head around, but it signifies ventricular repolarization. Now, as you can see, the action potential is moving away from the positive electrode so immediately your question should be okay, then shouldn't form a negative deflection. Because if in action potential is moving away from a positive electrode, it should form a negative deflection. Well, the reason that it forms of positive deflection is because the waves of repolarization are negatively charged. And if a negatively charged wave is moving from the positive electrode, that's going to form a positive deflection. So basically two negatives are going to make a positive. That's the easiest way of remembering it. So a negatively charged wave is moving away from the positive electrode. So these two negatives are going to make a positive deflection. Great. So we've covered RSCG is we know what the normal should look like. Let's talk about a few abnormalities. So, um, before that, just a small SP a pap, if we could launch the pools. Great. I think just for the sake of time will end it there. Um and the other is a mix of answers, but I think most of you did get it. It is Thean Fear ears. It's an inferior stemi. And I'll talk through that in the next life. Right? So we know are normally see gi. We've gone through just now. We need Peewee Aves on. We need a cure complex. We need T waves and we need regular our interval. So that's just the space between our our waves. So now instead measles That means is it's an ST elevation myocardial infarction. So in the case of an inferior ist, I mean you're going to see an ST elevation so the ST segment is gonna be elevated in leads to three a V f. So if you remember from the from when I was talking about the CD territories, our inferiors are inferior. Leads are 23 and a V f. So an inferior stemi What? What artery do you think would be included? Included in an inferior stunned me. You guys put that in the chat. So what artery is going to be included for unfair e er sent me to occur. Amazing. Yeah, it's gonna be the right coronary artery. Because if you remember, the right coronary artery sort of curls under the heart and has a few branches that supply the inferior aspect of the heart. Great. So then if we move on to a few others, we have anterior stomach is so this is just going to be ST Elevation in the anterior leads. Um, so the B B one b two B three before you can sometimes find a semi in be five and b six. So this would be turned on anterolaterally stemi. Um so for an anterior stemi, which artery would be included? You guys for that in the chat? Yeah, Amazing on then, for a lateral stemi. Which artery would be included? Just testing you guys to see for a week. Great. Amazing. Well done, guys. Yeah. Um, so, yeah, that's the basis of stem ease. I've done a, uh, a few slides on tachyarrhythmia Zinbryta arrhythmias as first years. You're not expected to know this at your level. I just wanted to add it in for a bit of clinical relevance. So, in your own time, you can go through these sort of put the main SCG findings for each sort of pathology. Great. So the EKGs, the bulk of the session is now done. Um, let's talk about pathologies. So a C s. And after sclerosis. Before we do that, let's have a quick SBA so that the pole launched again. Great. I think most of you have got it. So I'm just gonna end the pole there. Um, Yep. The right answer was stable. Angina. So before we talk about that, let's just talk about the process of atherosclerosis, which is basically, um, the formation of a plaque inside blood vessels that end up narrowing the lumen. So what happens initially is there can be sort of damage to the endothelial cells that could be due to high blood flow. Sorry. High blood flow velocity that could be due to another ambulance, sort of moving really fast. And then that's going to cause maybe a rupture or a care in the end of the little cells of the blood vessels. Um, and what that's going to allow is LDL's or, um, low density lipoproteins just sort of feel infiltrate into the space, and then white blood cells from the immune system are going to bind to the addition molecules that are flagged up by the infiltration of the LDL's on. That's going to cause more white blood cells to be coming in and moving into the space of the LDL's have occupied. Then what's gonna happen is these white blood cells are going to engulf the Sorry. The macrophage is a rowing to engulf LDL's and form something known as foam cells. And the reason they're called phone cells is because they look quite foamy on micrograph. So right, So now these phone sells this process going to repeat over and over, and these phone cells are going to start accumulating in the actual damaged endothelial cells. And then what that's going to do is it's going to form something known as a fatty street. Now this process is gonna happen over and over again until a lipid bridge core plaque, forms and calcium will also start binding to it in order to count. If I and hard in it now, if you have a thrombus, which is what it's called or o'clock, that sort of forms in the Lumen of the blood vessel, it's gonna narrow the Lumen of the blood vessel on. That's going to increase the BP, which is obviously a very bad thing. Um, sometimes people use the term strong Ms and embolism interchangeably, but they're two different words. A promise is a clot that's actually attached the plaque. So what we just talked about on an ambulance is when this thrombus sort of breaks off and flows into the blood stream and goes to other places in the body. So it's just gonna be a free floating from this, um, and then acute coronary syndrome. So that's usually broken down into, um sorry. Yeah. Um, so that's usually broken down into three main topics. Unstable angina, end stem ease and stem ease. But before we start before we talk about that, let's talk about are stable angina. So if you remember from the question the patient presented with a crushing chest pain, so more often than not, patients will talk about this crushing chest pain that might even say, Oh, it's like an elephant is standing on my chest. Um, so this chest pain usually only occurs when they're doing physical activity, but it's relieved by rest. So if they if they don't do any physical activity. If they just rest, that chest pain is going to go now. That's going to be a little different in unstable angina. So they're gonna present with the same crushing chest pain. Except this occurs at rest and on exertion rather than just on exertion on. You're going to have abnormal SED findings as well, so you can have ST Depression or inverted T waves. However, your troponin levels would be normal then, if we move on to end stemi and stemi so far and stemi, this is when our plaque are athletes. Lot of plaque has actually ruptured. It's going to cause a sub endocardial inform. So if you guys remember from Justin's talk about cardiac and at me, we have our endocardium or myocardium and then our epicardium. So in this case, are some end of our sub endocardium, or endocardium is no longer receiving oxygen supply, which is why there's an infarct on down in the E. C. G. It would present similarly to unstable angina and that there would be ST Depression and inverted T waves. However, you'd also find elevated proponents in instead, me and then finally are stemi. So we looked at, um, a few ECD abnormalities. We look that interior, inferior entre lateral step means, but in a stem, you'd have a transmittal in front. So what that means is, it's it's gonna be across the wall on it's going to present with ST Elevation and elevated proponents amazing. And now, finally, for my final section before we let you guys go is cardiac pharmacology. So just another SBA. If we could get that launched, please, can I think I'll end it there just for the sake of time? Right? So let's go through this question. The answer is be apixaban. Let's go through the mechanism of action for each of these sort of drugs, right? So Apixaban is an anti coagulant drug on, and places in which anti platelets on anticoagulants air used is when there is an increased risk of clot formation on for been elliptic drugs would be used when there's a clot that's already been formed, and you want to sort of break up the club. So like we've seen in the previous slides, clot formation is not really good because it's going to increase your BP because it narrows the blood vessel, Um, in. So the first one we'll talk about sorry is, um warfarin, which is an anti coagulant. Now, the way warfarin works is it inhibits vitamin K hypox. I'd reductase, which is an enzyme, um, and this is a really high yield fact as well. Um, little man k, the factors that they sent the size is factors to 79 and 10. So if you see the clotting cascade here, I've sort of striked out, um, all the causing packers that would be synthesized by warfrin. So if warfarin is used and these clotting factors are no longer synthesized, that means it's gonna be harder for a clot to form, which reduces the risk of clot formation, which will then thereby reduce, um, you know, increase BP or hypertension. Now, apixaban is also an anticoagulant, but it has a slightly different mechanism of action. So the way it works is it inhibits factor 10 A, which is responsible for the conversion of prothrombin so thrombin on, and that that would lead to fibrinogen to fibrin. And then finally, the cross linked fibrin clock. So if a factor 10 a.m. inhibited, uh, that means that prothrombin cannot be converted to throw me in. And so again, that's going to prevent clot formation. So that's going to reduce your risk off, um, clots from occurring. Um, the way I like to remember Apixaban is that it's a factor. 10 80 Hib. It's, er so X A is literally in the name of picks a band, so it's quite uneasily to remember that Apixaban is a factor. 10 inhibitor, right? And now we have to pick a girl. So political is slightly different in that it's an anti platelet rather than an anticoagulant. So on anti platelet is different on anticoagulant because it inhibits platelet aggregation rather than clot formation on platelet aggregation is the first step that's required before confirmation can even occur. So it sort of inhibits, um, confirmation before the cast. The clotting cascade can even occur the way in which this works. Is it inhibits? Um, it inhibits the binding of ATP to pee, too. Why 12 receptors, whatever. But, um, the main thing you need to know is that it inhibits platelet aggregation, which means that it's gonna prevent the clots and cascade from even occurring on. Then finally we have all the place, which is a few. Bring elliptic drugs like I mentioned before, um, for being allergic. Drugs are used when a clot is already formed and you want to break down that clot because you don't want the clock narrowing the blood vessel, um, in Great. So now let's talk about a few drugs that are used to tackle hypertension. The first one we have is blister Ultram and I trade, or DTN. So usually the way gee 10 works is it's sprayed under the tongue, and that's going to increase the concentration of new trick nitric oxide night. Nitric oxide is also known as a vasodilator on the way in which that happens is it's going to stimulate this casket. So what is going to do is it's going to stimulate guano cycle is which is going to stimulate the CGM Pee cascade. Now the CMP cascade has a multitude of of of effects, but the main one that we want to focus on for this mechanism of action is that it's going to increase potassium flux. Now if we remember from our box under action potential graph, we know that an increase potassium reflux is gonna cause hyper polarization on that's going to decrease calcium influx. Now if you guys remember, calcium is a very important player in muscle contraction. And so if there's a decreased calcium concentration, that's going to decrease the amount of a muscle contraction that can occur. So if in this case there's decreased muscle muscle contraction in the vascular smooth muscle. So in the muscles of the heart, that means there's gonna be vasodilation of the arteries on beans. That's going to reduce the BP, because now the Lumen is a more dilated no, no Grand A works in a suit a similar way, except it works in the coronary artery. So if there's any occlusions or any atherosclerosis, plaques in the coronary arteries obviously are. Coronary arteries are really important because they are what supply our heart with the blood. So they have a similar mechanism action. They're going to raise a dilate these coronary arteries, and that's how it's going to reduce BP in the coronary arteries. Great. So then moving on to our beta blockers are calcium channel blockers. Um, so I sort of split it up into a negative control pick and negative I know Tropic effects because I find that easier to remember you. Can anyone in the chat? But what a kronur trope is And what angina trope is anyone still listening? So what is a kronur trope? What does that mean? What's an inotropes? What does that mean? Yep. So corn a trope determines the rate of contraction. That's correct. And then an in a truck. I know Trump is a force of contraction. Amazing. Um right. So if you want something as so these actors anti hypertensives, right. So you want them to be negative control. So you want to reduce the rate of contraction, and you also want them to be negative. I know trips. So you want to reduce the force of contraction is, well, eso that it reduces BP. So for Beatles blockers, the way it works is it's negative. Chronotropic effect is going to inhibit the visa to adrenal receptors in the sinoatrial node. And if you guys remember, the sinoatrial node is what emanates the action potential so that the contraction can actually occur. So if these Byetta two adrenal receptors are blocked, that means there's gonna be a ah reduced rates of contraction. So that's how it exerts. It's negative chronotropic effect now, for it's a negative. I know tropic effect. What it does is it's going to prevent, um, calcium influx. And if you guys remember, calcium is important for our muscle contractions. So that means with less calcium, there's gonna be less contraction of my sights. So that's going to reduce the force of contraction. So that's how it it exerts. It's negative. I know Tropic Effect. So examples of this would be the common side effects Olaude So bisoprolol, atenolol and metoprolol great. So then, for our calcium channel blockers again, I split it up into negative chronotropic nine a trip. It's negative. Chronotropic effect is, as it says on the tin, it's going to block the scalp. Him channels thie l type gated voltage gated calcium channels. And if there's less calcium being in trafficking through these channels, that means there's going to be of reduced rates of contraction, especially in the notes. So if you're a sign Rachel Node has fewer calcium, my own's. That means it's going to be able to, um, stimulate fewer action potentials, so that's going to reduce the rate of contraction on then it's also going to stop the calcium iron trafficking in the cardiomyocyte, which is which is like the muscular layer of the heart. So there's less calcium in this muscular layer of the heart. That means there's gonna be a produced force of of contraction, so that's gonna cause and negative. I know tropic effect so I can mention calcium. It's going to sort of blockage or inhibits healthy calcium trafficking in the cardio, my sights and then is going to exert either negative corn a trocar in a trump. In effect, I have a bad gene is quite similar in that it's a great limiters, so it's a negative chronotropic drug. Um, I won't talk about this too much because it's not very high yield, but it limits the phase for funding currents in the notes that Justin talked about. So that's how it sort of exerts. It's negative chronotropic effect and then write. So a senators and, uh, angiotensin two receptor blockers. Let's briefly talk about the rast system, so I know just in sort of touched on it. Um, so what happens when there is a reduced BP is that a molecule is angiotensinogen is released by the liver that's gonna be converted into angiotensin one via an enzyme known as Brendan, which is secreted by the kidneys. Then, angiotensin one is gonna be converted into angiotensin two by an enzyme known as angiotensive. One converting enzyme, which is released by the lungs and then finally under attention to is going to buy into the angiotensin two block receptors on is going to cause all these effects. But the main one for this drug that we need to be aware of is aldosterone secretion. So what happens is one angiotensin two binds to angiotensin two receptors. It's going to increase aldosterone secretion, which is gonna increase sodium reabsorption in the collecting ducts of the nephron, which means water. Reabsorption is also increased on that overall is going to cause an increased blood volume, which will then go on to increase BP. Great. So we prescribe is inhibitors and a to Arby's for people who already have a high BP. So the weighing that in which they work is for the first one is inhibitors. They're going to inhibit a PSA on. So what that means is angiotensin. One cannot be converted to angiotensin two. What that means is there's gonna be a decreased aldosterone suppression, which means sodium reabsorption is gonna be decreased, which will then cause, um, a decrease in water reabsorption. Now, if water is not being reabsorbed, us going to decrease our blood volume, which is I'm going to go on to decrease BP, which is ultimately what we want. Um, so the common sevens for Suffolk's for a centimeters is Prilosec on a common side effect. And this is really high yield. Is that a sin? Him bitters cause dry cough because it it inhibits the breakdown of body kind and in the lungs. But and then we also have our under two receptor blockers, which are usually used when a sin hip bitters are either contact contra indicated or not tolerated. The way in which they work is like this and the tin they're going to block your angiotensin two receptors, which means less angiotensin two is gonna bind to your under tens and two receptors, which which is going to decrease aldosterone secretion, decreased sodium reabsorption and water reabsorption. That's going to decrease blood volume, which is then gonna go on to decrease BP. I hope that makes sense. Um, and then our final s p A If the polls could be launched again, Yeah, I think I'll just end the pole there because, um, I'm sure everyone just wants to coat this point. Um, so, yeah, the right answer for that would be furosemide. And I'll talk about why in the next slide, So diarrhetics again, diabetics are used in hypertension as well. Um, so the first one is our loop diuretic. So this is going to inhibit the sodium calcium chloride pump on the think ascending limb. Okay. And the way in which this works is since this pump is inhibited, that means less sodium is going to be re absorbed into the blood or into the nephron. On that means since sodium is osmotic, be active like I've been talking about for the past few slides. Since less sodium is reabsorbed, less water is gonna be re absorbed. That's going to decrease your blood volume, which will then go on to decrease BP. Now, the reason is the most potent diuretic. And in that question, the reason why it caused diabetes is or an increased urine output is because this pump is actually responsible for 25% of sodium reabsorption on there by 25% of water reabsorption. So if less water is being reabsorbed, that means more water is gonna be trapped in the urine, which, which will cause the patient to urinate more often because they're gonna want to expel this urine out of their bladder. So, yeah, like I mentioned, um, the some of the adverse drug reactions include very recess, um, and naturally, sisters. Well, because that's gonna, um, sodium is also trapped in the urine along with the water. Because of the pumping inhibits it now, it also causes hypokalemia on hypokalemia means have reduced potassium concentration in the blood on. The reason for that is because since this pump is being inhibited, more approximately so sodium reabsorption is being inhibited More approximately, that means there's gonna be more sodium trapped in the urine around the collecting ducts, which is where our principal cells alive. So our principal cells, if there's more sodium, that means more sodium is gonna be re absorbed by these principles cells in the collecting ducts and by definition, if more sodium is reabsorbed, that means more potassium is gonna be secreted some more potassium is gonna leave the blood and go into the urine, which will then cause ever do serum, potassium concentration or hypokalemia on an example of this would be for us. Um, I like in the SBA we just discussed. So then our thighs, I diabetics. So, um, the way in which they work is they inhibit the sodium chloride pump on the early distal, convoluted tube. You, um and it's a similar concept. So it's gonna inhibit sodium reabsorption, which has been a inhibit water reabsorption, which then decreases blood volume, which will then go on to decrease BP. Um, it's going to be less potent than furosemide, and the reason for that is because it's not responsible for as much sodium and water be absorption as in the thick of sending limbs. Only about 5% of sodium is reabsorbed in this area. Um, and then some of the eyebrows. Drug reactions include irises, hyper clena and, in some cases, hypercalcemia as well, because it's going to inhibit calcium. Sorry, it's going up. Regulate calcium reabsorption into the blood. Um, like I mentioned in the previous slide, why hypokalemia occurs. It's the same sort of concept on an example of this would be bendroflumethiazide and a common side effects for thighs. I did recticare would be thiazide. And then finally, we have our potassium sparing diuretic. So what this means is that it's going to cause hyperkalemic and sort of hypokalemia. And I'll talk a bit about that, um, in the slide. So what happens is this is also termed as an aldosterone and tag a NIST because how it works is that it down regulates thes in AC and sodium potassium ATPase channels. Ah, by inhibiting aldosterone. So if you guys remember, aldosterone is responsible for sodium re absorption on. So if aldosterone is out computer or inhibited, that means less sodium is gonna be a reabsorbed. And so last water is gonna be re absorbed, which will decrease blood volume and then BP. Um, so some of the eight years include gynecomastia and hyper clena. The reason it causes gynecomastia is because gynecomastia is basically when a breast tissue in men are enlarged on. The reason for this is it also inhibits sex hormone binding globulin, which means it is going to increase the breakdown of testosterone and also upregulation concentration of estrogen, which is what's gonna cause this enlargement in breast tissue. Now, the reason it causes hyperkalemic a ride that, rather than hypokalemia is because over here, since aldosterone, um, since the aldosterone concentration is drop, that means less sodium is being reabsorbed by the actual principal cells of the collecting. The on, if less sodium, is reabsorbed. By definition, that means less potassium is being secreted out of the blood into the urine, which means more of that potassium is gonna be retained by the blood that's going to increase our serum potassium levels, which is what's going to cause the hyperkalemic on an example of this would be spironolactone. Right? So that is the end of my presentation. These are just a few useful videos I found when learning these concepts when I was doing case to a swell Ah, please do fill in the feedback form. And we're so sorry that we overrun um and yeah, thank you so much for attending. Thank you guys. Thank you so much. Also, if you guys have any questions, you can put it in the chat, but yeah. Thank you so much for attending. Right. Sorry. Was that now, I think there's just a question in the tell you your, um Right. So I think Freddie kind of is responsible for a sort of, um, um, moistening the lungs so that things like dry cough doesn't occur. So inhibiting the breakdown of body kind of hold in result in dry cough.