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Summary

Join us for our latest interactive on-demand session aimed at the UK MLA, which covers the cardiovascular system. Presented by Daniel, a second-year medical student at the University of Buckingham, this comprehensive session will explain the intricate details of the cardiovascular system, from concentration gradient and diffusion to the anatomy and pathologies of the mediastinum. The session can be paused, rewound, and replayed as desired, facilitating a customized learning experience for all medical professionals. Active participation is encouraged, with questions welcomed in the chat during the session. Feedback forms will be available post-session, helping us enhance future learning sessions.
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Description

UKMLA Revision held by Daniel Fattouh.

The session will be 1 hour and 30mins with UKMLA style questions at the end.

Understand the structure and function of the human cardiovascular system, how it is assessed and how cardiovascular function is altered in common diseases. Also, understand the broad principles of management of cardiovascular disorders.

Learning objectives

1. Identify and explain the components of the cardiovascular system, including the heart, blood vessels, and the functions and properties of blood. 2. Understand and apply the principles of Fick's law and Darcy's law to blood flow and diffusion. 3. Demonstrate knowledge of the physical anatomy of the cardiovascular system, such as the mediastinum and the positioning of the heart within the chest. 4. Interpret the impact of changes in the cardiovascular system, recognizing common symptoms and signs of cardiovascular pathologies in imaging like chest X-rays. 5. Understand the role and structure of pericardium in the cardiovascular system and its relevance to overall heart function.
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Computer generated transcript

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The following transcript was generated automatically from the content and has not been checked or corrected manually.

Right. For those of you who are new here, we aim to host uh monthly sessions geared toward the UK MLA. In today's session, we are going over the cardiovascular system. It can be presented by Daniel who is a second year medical student at the University of Buckingham. Just so everyone is aware, the session will be recorded and will be uploaded along with these slides on the medal for students who want to watch it on demand. Uh The session is highly interactive. So if I can just ask everyone if you can keep your mics muted unless you have been asked to unmute yourself. Um If you do have a question, please don't be uh hesitant to pop it in the chat and we will read it out by uh one of our medical members. Um And however, if you do have a burning question, feel free to raise your hand and we'll ask you to unmute, unmute yourself. At the end of the session, I will send out a feedback form if everyone can fill it out as professionally as they can. So that way our presents can add it to their portfolios and that is it for me, Dan. Feel free to take over. Awesome. Um So thank you everyone for joining. Uh my name is Daniel. Uh and as Jody said, I'm a second year medical student at uh the University of Buckingham. Um and I will be taking you guys through cardiology um and all the interesting bits about that. Um So yeah, feel free to pop any questions in the chat as we go and uh yeah, let's see. Let's see how this goes. Um Great. Um So let's get started. So um I've kind of split these into kind of micro lectures. So it's, it'll be 5 to 10 slides per lecture, essentially le lectures worth of content if that makes any sense. Um So we have a lot to get through but we'll work through it quite quickly. Um But again, feel free to stop me at any point. Um And I can answer questions great. So starting off with fixed law of um diffusion. So it's essentially telling us um the relationship between er concentration gradient and diffusion. So essentially the first law split up into two laws. So the first law states that as uh the as diffusion increases, sorry, as concentration gradients increases, diffusion also increases. Um the second law er comes with an equation. Um So J equals pa multiplied by changing in concentration. So you have what um what all of those individual letters stand for. So diffusion rate uh permeability coefficient surface area and change in concentration. Um It's responsible for telling us about how concentration changes with time. Um And it's important to remember that diffusion rate is put in minimal per second. So whenever you're asked to work something out, using the second law of fixed law of diffusion, make sure you have those um units kind of sorted out in your head. Great. Um So in terms of what makes up the cardiovascular system, you have the heart, which essentially acts as a pump as I'm sure you know, um the pipes, so the blood vessels act as pipes. So they transport. So the blood is being pumped by this heart and is being transported through the blood vessels which act as pipes. And the actual thing being transported, the actual fluid being transported is of course, the blood. Um so veins are capacitance vessels and arterioles are resistance vessels. Um Yeah, I think that's pretty self-explanatory in that sense. Um So we also have two types of circulation. Um pulmonary which is responsible for oxygenating the blood and um blood. So, and back to it takes it back to the heart. So, um within blood, we have oxygenated and deoxygenated blood. Um And that depends on where we are throughout the cycle of of uh the cardiac cycle, but we'll talk about that a bit later, but the pulmonary system is responsive responsible for making sure that the blood has a high concentration of oxygen within it. Um There is also the systemic circulation, which is responsible for transporting oxygenated blood from the heart to the tissues and the organs. It's no good just having oxygenated blood kind of sitting in the center. Um It needs to reach uh all of these different tissues that are constantly contracting, that are constantly working, that need oxygen for respiration and other kind of processes to keep them functioning properly. So that explains why it has quite a high pressure cos it needs to reach all of these different tissues all across the body. Um Yeah. Now, in terms of Darcy's law flow, um generally, it's um that blood flow moves from a region of higher pressure to a region of low pressure. Um OK. So that unit of pressure would be mmhg um And there's a simple equation to remember, it makes kind of sense if you break it down. So flow exists as a change of pressure. So like we said, from high to low um and that would be divided by resistance. Cos um you have to take that into account in terms of all the different variables that would impact flow. So, as you can see because resistance is the do the nominator in this um flow is inversely proportional to resistance. Yeah. So now moving on, um we've touched a bit on some of the equations there. Um I'm going to talk a bit about anatomy and I think we're starting off with the mediastinum. Yes. Um So the medium stum is the region between the lungs. So you have the two lungs, it's that region there. So it consists of kind of the sternum to the vertebrae, to the bodies of the vertebrae. Um That's in terms of depth. So it's raining a bit. I don't know if you can hear that. It's a bit Haley. Um But um, so you have the sternum of the bodies to the bodies of the vertebrae, um the superior thoracic aperture which you can see on that diagram on the left just there um up there and then uh the diaphragm at the bottom. Um It's important to know this, er because there are certain pathologies that are associated with the mediastinum. Um and they're split up into different uh kind of subcategories within the mediastinum and there are different structures within them. So it's important to know what kind of where everything lies within the mediastinum. So let's get into that. Um So starting off with what the subdivisions kind of are broken down into um on a very basic level, let's talk about the differences between the superior and the inferior mediastinum. So how do you actually work out what the, where the superior mediastinum and the inferior mediastinum is? Does anyone know? Oh, it's, it's, it's on there anyway, actually, sorry. Um So it's the angle of lo um which is also called the sternal angle. So you can see that there um separates the superior mediastinum Um and uh the inferior mediastinum um as well as that simple kind of differentiation between superior and inferior, the inferior is broken up into three separate categories where you have the anterior, the middle and the posterior. Um and we'll get into kind of what, what goes on there. Um a bit more. So, so starting with the superior media sign because that's nice and simple. It's its own thing without any other subdivisions. So um you start off with the trachea, the esophagus, the great vessels, um the nerves, the vagus and the phrenic, which are really crucial in uh the cardiovascular system, the thymus, which is present in Children. And we'll talk a bit about, you know, some of the pathologies associated with the, with the thymus, um the thoracic duct and muscles. Um So this is kind of something you'd wanna know just to kind of gather where everything is anatomically. So, yeah, so as I said, there's um uh thymuses are quite large in Children. Um And it can lead to a thymic C sign and chest X ray. So you can see that kind of, that sail kind of looks like a, like a kind of like a cartoon picture of what a boat looks like, you know that there's, there's white sails. Um So that's what's known as the thymic sail sign if you know that it's just an, it's enlarged in Children um structures in the middle mediastinum as you would kind of expect you'd find the heart um the pericardium. So, the origins of the great vessels, as you saw the superior um mediastinum, we had the great vessels up there, but this is where they originate from. Um and also various other nerves. Um So the pericardium, I'll give you some information on that because I feel like that, that uh that kind of confused me. I feel like that was just put there without much explanation. So the pericardium is kind of like a fibrous sac. Um It, it um kind of encloses the heart in like a s keeping it in a kind of stable location. So kind of holding it down. It's a, it's a, it's a firm fibrous sac and we'll get into it a bit more later in the lecture. But that's the, the crux of it. Um structures in the posterior mediastinum um consist of the thoracic aorta, the esophagus, the thoracic duct and the azygous system of veins and sympathetic tracts. OK. So um why is this all important? Um you know, what are some pathologies that can exist around the mediastinum? So you have um an abnormal silhouette as you can kind of see in this chest X ray right here. Um kind of widening or a shift in the mediastinum can be indicative of mediastinitis. And if you know the ITIS at the end of any of these words means inflammation. Um So that's kind of what's indicated by this. Um widening and shift is the mediastinum. Goodbye. So it surfaces of the heart. It's important to kind of know how the heart actually sits in your chest. Um cos it's not straight on as you might expect, it's slightly rotated. So anteriorly you have your right ventricle, we'll go into specifically what, you know, the atria, the ventricles, all these different kind of spaces do and some of their features. But for now, just understand the ventricle is kind of ventricles are the bottom two parts and the uh atria are the top two parts of the heart. So it splits up into four sections, imagine like a cube, uh split up into four sections. You have your atria and your ventricles. Um So your right ventricle is anterior, so sternocostal. So on your sternum kind of here on your ribs, um posteriorly, you have the base of the pyramid. So your left atrium inferiorly, you have the left and right ventricles a bit there. Um You have your right pulmonary out of the arteries in your right atrium and the left palmary to your left ventricle. Great. Um Again, this kind of follows suit. It's not too important, it's just understanding the positioning of how it sits in your heart in your chest. Um Great. So we talked a bit about the pericardium. Um So it's supplied uh by the phrenic nerve. Um and it can be split up into both either the sis or the fibrous. Um So we talked about the role of fibrous sac, it holds it in a stable location, uh the serous membrane. Um So that's visceral a adheres to the heart uh allows it pers kind of a cavity which contains a small amount of fluid. And it also has a peral layer which is the inner surface of the fibrous pericardium. So just so you understand the visceral bit. So what they mean by visceral, it's kind of the outer layer. Um and the peral is the inner surface. Um So, yeah. So I imagine if you look at this bottle here, the outside bit would be the visceral layer and the inside is the peral. Um Yeah. OK. So the transverse pericardial sinus um uh yeah. So that is um essentially a passageway between the arterial output and the venous input. You can see it right here in this diagram. Uh it's posterior to the um ascending aorta which you can see right there and um posterior, sorry, it's posterior to the ascending aorta and the pulmonary trunk um which is also right there. And uh it's anterior to the superior vena cava, which you can just kind of see right there. You can see that finger is kind of going anterior to the S VC. Um Why is this important? Just a gap? No, it does have a um a use. Um It's used to identify the arteries of the heart during coronary artery bypass grafting. So I'm sure many of you have heard of grafting. It's when you kind of take a vessel from one part of the body and put it somewhere else. So this is, it's a key identifier basically in that particular procedure. Um Lovely. Um So now we'll talk a bit about heart valves. Um So we have atrioventricular valves kind of in the name um exists between the atria and the corresponding ventricle. So the left atria connecting to the left ventricle has an atrioventricular valve between them. Um Those are split up into tricuspid and mitral or bicuspid. I find it more helpful to remember it as Tricuspid and Bicuspid cos again in the name, you'll, when you see the structure of them, it makes a lot of sense. So the tricuspid has kind of three openings, three barriers almost, whereas the mitral or the bicuspid has two. Um So they're what separates the atria and the ventricular, sorry, the atria, the um the atrium and the ventricles. Um the semilunar valves are between the ventricles and their corresponding artery. Um So you have to understand. So the um blood moves from the atria into the ventricles and it can go up through uh the uh various vessels there. And the valve that separates the ventricle from the vessels are um semilunar valves. Uh So the pulmonary is on the right side up through the pulmonary trunk. Uh and the right ventricle and the aortic is uh from the left side and the ascending aorta. Um ok. Uh So yeah, so here you have it a bit more clearer. This is kind of the, the structure I was talking a bit about here. So you have your right atrium, left atrium, right ventricle, left ventricle. Um As you can see here, those are the tricuspid valves. So that's on the right side and the mitral valve or the bicuspid valve on the left side. Um You also have the aortic valve. Um So that's one of the uh the uh semilunar valves we were talking about between the ventricles and the vessels. Um And yeah, that's the pulmonary valve there. Um So the flaps are kind of like cusps that are anchored to the wall of the ventricles through chordae tendinae, they're your heartstrings, right. So that's what you um talk about when you hear heartstrings. Um uh They're attached to something called papillary muscles, which you can kind of see at the bottom there. So there's your papillary muscles and your chord tendinae. Um They're kind of attached directly to the um to the valves uh and they prevent them from blowing into the atrium. So, preventing them from flipping upwards and that's just gonna lose all control of, of blood flow in the heart. Um So, yeah, it leads to valve incompetence. So it's not working and that can in turn lead to a cardiac murmur which you can hear. Ok. Um There's also the fibro skeleton, which is also known as the annulus fibrosis sits between the atria and ventricles, I'll go back to the previous slide. So you can kind of see that um it prevents the free conduction of electrical signal from the signaling from the atria to the ventricle. So, um I'll just go back a slide so you can kind of see the fibro skeleton kind of not very clearly here, but it's there kind of separating it um from the fibro skeleton. Um And I'll talk a bit about why it's important that we prevent the free conduction of electrical signaling from the atria to the ventricle because the conduction of electrical signaling throughout the heart is very important. And um we'll talk about that a bit uh in later slides. Ok. Um So where do the coronary arteries originate from? So, first of all coronary arteries, main function is to supply blood to the heart. Um It arises from aortic sinuses above the cusps of the aortic valve. Um the left posterior cusp and the left coronary artery and the anterior cusp is the right coronary artery. Um Yeah. So we're talking about how the right coronary artery kind of branches outward. So you have your um coronary artery which splits off into your sinal, your right coronary artery, which splits up into your sinal sinoatrial node, artery and your sa node, which is very important in terms of the conduction of the heart. And we'll talk a bit about that later. Um uh get into the right and left atria, um marginal artery through the right ventricle and um the posterior interventricular artery and the posterior third of the septum is the A V node. The AV node is also important for the conduction. We'll talk about that a bit later as well. Um Left coronary artery kind of branches off into the circumflex artery to the left atrium and the le and ventricle and continues as the P I VA which will come up again very shortly. Ii realize these these but it it all connects together. Um But it is the posterior interventricular artery. We'll talk about what that does a bit later. Um Also to the left, anterior, descending to the right and left ventricles. Um the anterior two thirds of the septum and marginal arteries like the left ventricle. Um lovely. So going into the posterior uh intraventricular artery, uh it supplies the posterior third of the septum and the septum is, if we go back here, you can see the intraventricular septum there. So its supplies the posterior third of it. Um It's a 60% chance that this might arise from right coronary and a 40% chance that it arises in the left Coron coronary artery as a continuation of the left c of the circumflex artery. Great. Um talking a bit now about cardiac uh veins. So we've got the great and small cardiac veins which produces the coronary sinus which empties into the right atrium. Lovely. Um Right. So now we're gonna talk about some surface anatomy. So in terms of it's really important to know this because um it's um so it's really indicative of where you would put your stethoscope when you're listening, when you're auscultating the chest to kind of listen to all of the individual valves. So you can tell precisely where the murmur is occurring, giving you more of an indication to where that pathology might be. Um So the um we use the phrase all patients take medicine. So it goes all patient. So yeah, all patients take medicine. So the second is referring to the second intercostal space. So you can count that down. So you start on, you know, your first intercostal space moving downward and on your right side, that would be your aortic valve, your left would be the pulmonary in between the fourth or fifth, could be on the left side would be your tricuspid and fifth, more kind of midclavicular. So in the middle of your clavicle and downward, the fifth intercostal space, that would be your mitral. So all patients take medicine very simple, you know, lovely. Um Now, um we're gonna talk a bit about the internal features of all the different kind of uh openings in the heart. So the both the both atria and both ventricles. Um So as you can see here, the inferior vena cava and the superior vena cava kind of both pull into this um um uh into the right atria. So that's bringing um oxygenated blood into the uh right atrium. Um You have the fossa ovalis here, which is the um you know, in uh it formally the the Foramina Valley um as the heart is developing in the embryo, but closes up to form the fossa ovalis. Um that's really important as we go into congenital heart defects later on in the lecture. So, keep that in mind, I understand that it was previously opened during development of the heart, but it now closes up um and uh kind of encloses that uh right atrium. Um You also have the sinoatrial node really, really important for the uh conductivity of the heart. We'll talk a bit about how that comes into uh it a bit later. But it's, it's important in terms of producing that electrical impulse that causes the heart to contract, causes your ventricles to contract and causes the heart to pump. Um your tricuspid valve we've talked about already um attached to the Cordy Tendinae which is attached to the papillary muscles causes that contraction, making sure that um the valves stay um stay vigilant and stay strong, um lovely um the left atrium's internal features. So that's the other side of the fossa ovalis. So the fossa ovalis is kind of like. Um so once it was in its position as um the foramen ovale, it connected the right atrium to the left atrium, but that closes up. So you kind of have this closed off tunnel on both sides and on the right side, you have that bit that's closed up on the fossa ovalis. And um on the left side, you also have that closed up in the faucet of valis. Um and the mitral valves there as we talked about before pulmonary veins. And uh yeah, that's pretty much it. Uh that takes it to the rest of the lovely. So the left ventricle internal features, um the mitral valve again, papillary muscles, again, Chitina again. Um And yeah, Trabecula car. Um Yeah, so just kind of dips in there in the, in the, in the walls of the uh or the ventricles. Um Yeah. So a similar kind of set up in the um right ventricle where you have the Conus arteriosis Trabecula carne. Um this moderator band, which I wouldn't say is too important to remember that. Um And the cord di tendinae, you should always be able to tell uh the papillary muscles as well and the Tricuspid valve. So these kind of things are just important to kind of look through. You have to kind of get these in your head what they look like. So you can recognize them if they were to ever come up just easy marks if you can learn them. Yeah. Um So let's talk a bit about the great vessels. Um Again, this is a lot of anatomy. So you kind of just need to know it. Um So you have the carotid on. So let's, let's start off the way I like to do this diagram on the right is really, really easy to get your, your head around. Um If you kind of remember the order on one side, it's the same on the other side, mostly until you're getting a little bit lower, but we'll talk about that later. So, um we're starting up here and if you move one across, you have the common carotid artery. So that's first, then the left internal, the internal jugular in the subclavian artery and then subclavian vein. So it's really easy artery vein, artery vein. Um And that's the same across on the, on the right side as well. Um As you go down here, you have, oh, sorry, you have the um uh uh right brachial phallic vein and that can be palpated ki kind of superficially by finding the sternoclavicular joint. Um So right up here, um you can, that would lead you to find the, the ligamentum arteriosum. Uh Yes. And uh you have your superior vena cava, kind of just here. Uh So yeah, kind of just getting familiar with the diagrams getting familiar of like the anatomical locations of all these um different bits and Bobs. Um But it just takes some time in writing them out a couple of times. Now we're moving onto the conduction system, which is really cool and really interesting how it works. So let's break it down really simply. So we're starting off with the sinoatrial node, which we said was in the right atrium if you remember. Um So it's referred to as the natural pace pacemaker because it generates electrical impulses. Um These electrical impulses are cause kind of spread across the, the myocardial cells of the atria causing them to contract. Um And that pushes the blood through that atrioventricular uh sorry through the um through the um tricuspid valve um uh into the uh ventricle. Um Yes. So uh the that electrical impulse then spreads around going to the atrioventricular node. Um once it reaches the atrioventricular node, uh it stops briefly uh to allow a ventricular filling. So, imagine a so atrial node produces that electricity. All that blood goes to the ventricles past the valve. It needs time to do that before we start contracting the ventricles. So we give it a minute, it gives it a second. Um I mean less than a second. Um And um that allows the ventricles to fill with blood. Um then it spreads down the bundle of hiss. So as you can see, there's two bundle branches, the left and right bundle branches. This is kind of just carrying that electrical charge down um down the, the ventricular septum. Um the right and left bundle branches uh transmit the electric down the septum towards the apex of the heart. Uh You also have these perky fibers at the bottom Um So they um distribute the electrical impulses throughout the ventricle. So that's what causes that contraction uh in the ventricles. Uh Yes. So those that, once that ventricle contracts, it pushes the blood from the heart to the lungs, through the pulmonary vessels um that we've seen there. Yeah. Um So the cardiac plexus. Um so it's important to understand what parts are innervated by what specifically. So, um in terms of the parasympathetic uh supply, you have the vagus nerve which reduces the heart rate. Um And then you have the sympathetic supply, which is a arises from T one to T four. So that's t one th thoracic spine, T 1 to 4. Um and that increases the heart rate. Um So, yes, a referred cardiac pain occurs in the medial upper limb and supralateral thoracic wall. Um Yes. Um So, in terms of congenital heart abnormalities, um it's important to kind of understand the differences between cyanotic and acyanotic um kind of uh abnormalities. But it's first of all important to understand the flow of blood uh through the heart. So we're starting off with um think of it as kind of like a journey that the blood needs to go on. So it's going from the inferior and superior vena cava into the right atrium at this point, it's oxygenated, it's just come from the lungs. Um the the blood from the right atrium then passes through the right ventricle. We've just talked about how the electrical impulse causes that contraction of the atria causes the blood to move into the right ventricle. At that point, the ventricles contract, uh this pushes all of the blood up through the um pulmonary arteries um into the lungs and then back up through the pulmonary veins, the pulmonary vein that then goes to the left atrium, which passes through the um valve to the left ventricle and up through the aorta to be um to be transported around the body. Um ok. So now we're gonna talk about the difference between acyanotic and cyanotic defects within congenital heart abnormalities. You have these two kind of subcategories and the main difference is um acyanotic refers to defects that involve abnormal pumping of blood throughout the body. Um uh but the blood tends to contain enough oxygen. It's just the blood isn't reaching it as, as well as it should be. Cyanotic defects consist of um uh the, you know, heart defects that will reduce the amount of oxygen that is delivered to the rest of the body. Uh Blood contains m So what you know, kind of like an arbitrary number is 5 g per deciliter of, of reduced hemoglobin um in blood. Lovely. So let's start talking about them. So, starting off with acyanotic, we'll talk about um atrial septal defect. Um So atrial septal defect is an opening between the septum of the atria. Um So, as you can see here, that's kind of that opening between the left atria and the right atria um right atria. Um So that continues to stay open, postnatally. So, if you remember we were saying the um the uh fossa ovalis closes up during the development of the heart. Um sorry, the um gosh, it's, it's left me now, but the the fossa ovalis um is stays open essentially. So you have that kind of mixing of oxygenated and deoxygenated blood in the heart. Um uh So, since the left ventricular pressure is generally higher than the right ventricular pressure, the oxygen uh oxygenated blood will flow back into the right ventricle through this opening. Um So, yeah, generally, the shunt goes from uh from um uh uh right to left, sorry, not enough pressure, it's higher than the right ventricular. So, yeah, so the left pressure will move from left to right, sorry. Um So, oxygenated blood oxygenated blood flows back into the right ventricle. Um The abnormal flow results uh from the left ventricle to the right ventricle changes the flow cycle. So you have your inferior vena cava and superior vena cava and the left ventricle because that's become involved in that system, uh then goes to the pulmonary artery. So you're left with kind of a mixture of oxygenated and deoxygenated blood going to the lungs, getting re oxygenated, coming back in through the pulmonary veins, going into the left atrium, the left ventricle and the aorta. Um So it's not, it's just, there's a lot of mixed blood. So it's not very efficient because you're, you're sending partially oxygenated and partially deoxygenated blood back to the lungs through the pulmonary veins, sorry for the pulmonary arteries, um to get it re oxygenated again, even though it doesn't need it. Great. Um So these are the different anatomical variations of ventricular septal defects. I've put this here. So you're aware of it. Um It's just different types. Um just so you can kind of look at that and understand how that works. Um But it's not too important. It's mainly just understanding how that opening affects uh affects him. Yeah. Um So some clinical features and complications of ventricular septal defect. So, um you have um a small ventricular septal defect can be asymptomatic. Um moderate ventricular septal defect can be uh can result in tachy uh just fast breathing, um fatigue when um feeding excess sweating and poor weight gain. Um So large VSD is um all of the above plus you'd be able to hear a murmur. Um There'll be some central cyanosis or some blueing kind of blueing of the skin or paleness, almost the pallor or just discoloration because there's not enough oxygenated blood going through. So, um um that's causing kind of a blowing of the skin and exertional syncope, which I believe is um passing out um or losing consciousness uh when exerted. Um So some complications. Um So there's more mixed and more blood in the right ventricle So there's a higher pressure in pulmonary arteries which uh causes an increase in pulmonary vascular resistance and that causes the shunt to reverse, which is called Eisenmenger Syndrome, um which is quite uh important to take into account, cos that completely changes the whole system. Um This causes right ventricular hypertrophy. So, because of this increased pressure, the muscles sur the myoc the myocardial cells of the um right ventricle are working much harder, so they're getting stronger. So it becomes hypertrophic. Um So yeah, so there's more unmixed blood in the right ventricle uh which causes a aortic valve prolapse resulting in aortic regurgitation. Um So yeah, there's mixed and more blood in the right ventricle, which can also lead to infective endocarditis, which is uh infection of the endocardium of the heart. Ok. So then you have patent Foramina Valley. So if you remember that, um So it's more probably more clinically relevant here than it is an atrial septal defect. But um the Foramina Valley, it was that gap between the two atria again, that was kept open post um postnatally. So it it's it stays open basically which causes the uh blood in the atria, both atria to kind of mix together and combine uh usually generally the left atrial pressure is greater than the right atrial pressure which maintains the closure of that flap. So it's not really a big deal until that changes, which we'll talk about in a bit. Um So um Yes. So the left atria generally bigger. So it won't um kind of open, it's keeping it kind of separated, which is quite good. Um It's asymptomatic in about 20% of the population. Um The issue arises when right atrial pressure becomes higher than left atrial pressure because that, that now closed, uh Foramina Valley becomes open. Um because it's a one way open valve. So it, it opens when it's going from, when the pressure's going from right to left. Um And that can be quite serious um because now you have the inferior vena cava and superior vena cava going to the right atrium, which then goes straight to the left atrium, then to the left ventricle and out through the aorta which produces this kind of mixed blood again, which we don't want cos it just makes it a bit uh inefficient. Um Possible complications can be paradoxical embolisms, which is when an embolism kind of goes through this whole process. Um and it follows kind of a similar pathology to DVT. Um And an ASD cos atrial septal defect has that same, the, the pathology between um PPF O and ASD are quite similar other than the fact that P FO would require um a shunt reversal from right to left to create that opening. Um Next, you have patent ductus arteriosus um which is a persistent opening between the two main blood vessels. Um So that leaves the heart, um the aorta and the right and left pulmonary arteries kind of o open to uh kind of coming up through. So, the essentially, um there's an opening between the aorta and the pulmonary arteries, essentially, which uh it occurs in, it's, it's occurs in 5 to 10% of congenital heart defects. Um is associated with Down Syndrome. Um um rubella infection, uh birth at high altitude, I guess due to low oxygen tension. Yeah. Um there's an abnormal flow from the aorta into the pulmonary arteries. Uh it affects the cycle. So, inferior vena cava and supra vena cava through to the right atrium. Um I don't know if you can see my mouse but this is essentially its passage. So the inferior vena cava and supra vena cava goes to the right atrium um which then goes to the right ventricle um and in through the aorta um to the pulmonary arteries because of that gap right there. Yeah. Um and left atrium, left ventricle and like like a lot of this uh the uh cyotic defects, it produces this kind of mixed blood um situation. Uh So, some clinical features and complications of PDA. Um A small PDA is asymptomatic. Um the moderate and large PDA S uh result in tachy, which we talked about already fatigue and feeding excess sweating, poor weight gain and a murmur. Um it can cause respiratory distress syndrome, pulmonary hypertension, right ventricular hy hypertrophy, which eventually leads to congestive heart failure. Um lovely. Um So now we have coaction of the aorta. So it's pretty clear what's going on in there from the diagram. Um There's a narrowing of the, of the aorta near the ductus arteriosus, um commonly associated with bicuspid aortic valve, ventricular septal defect turner syndrome and bar aneurysms. There are uh three different types. There's a ductal coaction which happens exactly on the ducts, arteriosis. There's preductal um coaction which happens before the ducts arteriosis and post ductal coaction, which happens after the duct's arteriosis. And you can see it kind of has a different effect. So it's more clear between the preductal and the post ductal where you can see that. Um OK, it's kind of being splitt off before the ducts, arteriosis has a chance to kind of uh attach itself to the uh to the aorta. Um And that's only performed. Um So the clinical features and complications of co of the AORTA. It's um a lot of similarities here. Uh tachy e fatigue when feeding dizziness, chest pain, intermittent leg claudication. That's a unique one today. Sorry. Um hypertension difference in BP between upper and lower limb. So that's a way you can, you can keep an eye on it. So you can do a BP cuff on the the legs. And also the arms, you can also check for radio radial delay. So you measure the radial pulse on both arms measure to see if there's any delay between that. Um Also checking the pulses, the difference in pulses between um the lower limbs and the upper limbs. Um as a general failure to thrive, you'll be able to see m hear murmurs, um some complications that result in hypertension and rec coaction after repair as well as right and left ventricular hypertrophy because the heart's kind of trying to have to kind of having to work a lot harder to push past that kind of coaction that closing it, it needs more force to get past it, causing it to become hypertrophic, which then can lead to congestive heart failure. Great. So now moving on to cyanotic defects. Um so you have tetralogy of palate tricuspid arteria, transposition of great arteries and hyperplastic left heart. Um So the way to remember tetralogy of fallot number one tetra. So there's four things that you need to remember and you need to remember prove. So p pulmonary stenosis narrowing of the pulmonary valve uh right there. You can see that uh right ventricular hypertrophy, you can see that slightly thicker, more hypertrophic overriding aorta. Um So that's right there. So there's kind of like not really a gap between the septum of the right ventricle and the left ventricle. So there's kind of a mixed blood reaching the aorta and a ventricular septal defect which is causing a right to left um shunt. So all of this is commonly associated with trisomy 1318 and 21 as well as the George syndrome syndrome. So, that's Patau Edwards and downs um as well as fetal alcohol syndrome. So, risk factors are, are alcoholism, alcoholism or phenylketonuria in the mother, um, as well as pregnancies uh over the age of 40 diabetes. Um So in terms of um how this is affected, there's an abnormal flow now, tetralogy of fate. So, um it comes from both ventricles due to that ventricular septal defect, it empties into both semilunar valves um due to that kind of overriding aorta that we talked about over there. Um uh So you have your um inferior, inferior vena cava and superior vena cava going to the right atrium, then to the right ventricle, uh then that right ventricle and left ventricle kind of come together over here, get pushed up through the um um pulmonary arteries into the lungs where they're oxygenated to come back through the pulmonary veins, go in through the left atrium and the left ventricle and then into the right ventricle and aorta. So it's quite a long process. Um and due to the abnormal flow of the pulmonary arteries, both ventricles and aorta will have mixed blood. Um So talking a bit about the clinical features generally can be asymptomatic dysnea. So um struggle, breathing, struggle, breathing, and then uh fatigue when feeding, squatting to rest during exercise. Uh So that's something you might notice to try and kind of bend the vessels um to get blood flow, kind of more, more easier. Uh cyanosis hypoxic spells low birth weight, finger clubbing. So you can do um the scout window test clinically to see if there's uh any clubbing in the digits. Um complications, uh aortic root dilation, sustained ventricular tachycardia, paradoxical embolus, uh progressive pulmonary regurgitation, right ventricular failure and congestive cardiac failure as well as sudden cardiac death. Um So now moving on to tricuspid arteria, um as you can see that that right ventricle is tiny compared to the left ventricle and that's where the main point of this defect lies. So, um it's a heart defect in which a tricuspid valve that is meant to separate the right atrium and the right ventricle just doesn't form. Um The heart defect often includes undeveloped right ventricle as well as a hole between the atria um and or a hole between the ventricles. So it can come with ASD or VSD. Um the disconnect between the right atrium and the right ventricle um changes the cycle, the flow of the cycle. So, uh infra vena cava to the right atrium, uh then go to the left atrium um where I can go through the common ventricle cos the right ventricle is so small and so uh malformed that it just has a shared ventricle where it kind of has that mixed blood. Uh it then goes up through the pulmonary arteries and the aorta, um then through the left ventricle and the aorta again. So, again, due to abnormal flow like most of the other ones uh on the common ventricle, uh there is mixed blood dyspnea, fatigue when feeding, progressive cyanosis murmurs hypoxaemia. Um So, transposition of great arteries, um a heart defect in which the two main arteries carrying blood away from the heart to the aorta and the pulmonary artery are switched in position or transposed. Um So it creates kind of two parallel circuits. So it's not, it's not one kind of nice flow like it would be normally or like in any of the other one, this has two separate cycles. Um And it's, I don't think you can sustain life yet. It's not compatible with life. Um unless a shunt is maintained after birth. So, uh that can be through atrial septal defect, patient, ductus, arteriosus ventricular septal defect. Uh And that's typically what it's commonly associated with. So, yeah, this is talking about the two circuits. So um I'll just show you what that looks like here. So you have right. Uh let's say you have your left atria there, left ventricle there and um goes up right through the um pulmonary arteries and systemic circulation to the right atrium into the right ventricle into the aorta. Um It just doesn't allow for the flow of um uh oxygenated blood throughout the body. And it would only cycle in circuit two, whereas deoxygenated blood would only cycle in circuit one. Um Yeah. So there's a lot of a lot of common things here across congenital heart defects. So you kind of get the gist of, of what they're looking like. So you're looking for cyanosis fatigue when feeding tachy ea generally, if they're small, they can be asymptomatic. But um you know, tachycardia poor weight gain is a common one. A lot of it leads to congestive cardiac failure, especially with ventricular um hypertrophy as well as respiratory disease. Um And it can also result in metabolic acidosis due to the build up of carbon dioxide in the tissues and the lack of oxygenation reaching the tissues. Um great. And now we have hypoplastic left heart. Um that's a defect in which the left side of the heart is underdeveloped, meaning that it doesn't pump very well. So the right heart right side of the heart has to pump really hard to get the blood to the lungs. Um This causes underdevelopment of the left heart which changes the flow cycle again. So IVC and S VC to the right atrium, right ventricle pulmonary arteries, lungs and AORTA through the patent ductus arteriosis, which goes to the pulmonary veins, the left atrium, the left ventricle and the right atrium in through the aorta due to the abnormal flow. Again, mixed blood, common ventricle, same story, different day. Um Yeah, uh clinical features again, asymptomatic dyspnea, cyanosis murmur, right ventricular issues and aortic valve leakage cool. So now let's talk a bit about the heart as a pump. So that was a long one on the congenital heart defects, but it's important to know. Um So spend some time kind of understanding how um the circuits work. And first of all, understand how blood flows through the heart normally and then understand how that's affected by um by the different abnormalities that take place. Great. So um in order for the heart to function, it needs to contract um the contraction generates a force which pumps blood, which produces the pressure gradient. The contractions need to be coordinated and synchronous. Um And the flow must be erection also. So it must be working. You know how we said it would move from the sa node to the A V node down the bundle of his through the pine fibers, moving down through the kind of bundle downward through the heart. Um And this is achieved by or by the order of contraction and then followed by flow. So um talking about the different uh the heart muscle and the cells in general, um cardiac muscle cells are known as myocytes. So 99% of myocytes are contractile. So they're actually producing the force that causes the blood flow and the remaining 1% are conducted, meaning that they uh produce uh an action potential. Um I've realized there are some kind of uh white text there. So all that I'll read it out to you. Um The remaining 1% are conductive and the meaning that they conduct a cardiac action potential. And we'll talk about how they do that through a process called automaticity in a later slide. Um So myocytes are generally quite small. Um They're between 20 micrometers and have a length of um 100 micrometers generally have a single nucleus and can be found um coupled to other myocytes. Uh They typically are striated on histology sites. So you can kind of see the stria uh the stria there and the indicated discs. Um there's kind of a, a functional sium is what it's called um which makes, which is composed of desmosomes, fascia, adherent and gap junctions and they permit communication and connection. We'll talk about them specifically what like uh the desmosomes and the fascia adherents do and the gap junctions do shortly. So, here we are um branching coupling. That's their main role. Um smooth muscle causes the contraction. Uh the individual cells work as a to work to produce kind of a coordinated action of contraction flow. Um The rapid transmission of electrical impulses can transfer between cells and trigger that's that simultaneous contraction of the heart. Um Yeah. OK. Cool. So let's talk about the the features of the functional sync and what make actually makes this kind of complex up. Um So you have um fascia adherences which are ribbon like structures that kind of help to provide stability to the tissue. Uh So that keeps it nice and strong. Um And the desmosomes kind of act as the glue providing cell to cell adhesion Um Yeah. So this is the pathway of the action potential. We've talked about this a bit already. Um So the um sinoatrial node produces that electrical conduction which moves causes the uh myocytes and the sorry, the myocardial cells in the atria to contract um allowing the blood to flow from the atria to the ventricle that conduct that uh wave of conduction then flows to the ATRIO ventricular node which moves down the bundle of his uh to the left and right bundle branches um into the pine fibers causing the contraction of the myocytes of the ventricle. OK. So we talked about this again already. Um So I'm not gonna explain a bit about why. I mean an important factor of this, we talked about depolarizing a essay. Not so there's not really a point of me repeating myself. Um But there is a fibrous skeleton that allows for the filling of the ventricles. If you remember, we said that it would be after the um uh the myocardial cells of the atria contract. Uh And the blood moves into the ventricles. We give that moment. That's where the fibro skeleton comes in. It delays and allows for atrial emptying as well as ventricular filling. Um It's a kind of a bridge across the fibrous skeleton. So it's a bridge across the fiber SKM that be that begins at the A V node and slowly conducts the wave of depolarization um through the A AV node. Um the action potential then passes through the bundle of his, the right and left bundle bundle going down kind of the the ventricular septum. Um once it reaches the contra the perky fibers which causes the contractile myocytes of the ventricle to well contract. And uh the ventricular myocytes allow for rapid transmission of the action potential. Um and it takes 100 milliseconds to complete the whole excitation of the ventricle. So it's a very, very, very quick process. Um Yeah. So I mean, this is just terms. So relaxation can go by the term polarization when referring to a ps. Uh and during that relaxation chambers filled with blood. So as we said, um that fibro skeleton slows the kind of transmission from the sa node to the A V node allowing for other ventricles to fill the ventricle to fill with blood. Um contraction can also go by the term depolarisation when referring to action potential. Um And during contraction, uh the given chambers will squeeze and eject blood. OK. Um So we have Wiggers diagram here. It's a graphical representation of the cardiac cycle. So I'm gonna try and speed it up a bit because II know I'm finishing at 330 but I have quite a lot more slides to go through. Um Yes. So, II forgive me if I go a bit quick, quickly. Now. Um So there's a graphical representation the cardiac cycle. Um So you have the mitral valve closures, you can kind of see all the different opening and closures of different valves. Um The most important thing to see here is the PQ RST waves. So um P is representative atrial depolarization. Um The QR S wave is representative of ventricular depolarization and the T is repolarisation. So, if you remember depolarization literally back here is the contraction of the different parts. So atrial contraction, ventricular contraction, ventricular were kind of regaining of the of the the the irons that basically caused that contraction. Um important to know that diastole means relaxation of the ventricles and systole is contraction of the ventricles. Um We've talked a bit about ventricular filling. All chambers are relaxed. It's kind of that that um all the valves are open. Um isovolumetric contraction. So, atrial cysto leads to ventricular systole. Um the mitral valve closes as the pressure of the ventricles is higher than the atria. Um The ventricles become a closed chamber temporarily. Uh So then there's also some ejection. So when the ventricular pressure is higher than that of the aortic valve, that's when ejection begins, and there's also isovolumetric relaxation. So you have your aortic and pulmonary valve closing each valve ventricle becomes a closed chamber and there's generally a relaxation of the walls of the the muscle cells of the ventricular walls. Uh kind of like the ventricle. It's about causing the ventricular pressure to fall below the atrial pressure so that the ae valve can then open and it can be pushed up um towards uh the um ventricle. Yeah, lovely. Um So this is, I'm just gonna cut through this a bit. So the um uh the JVP in the right atria. So there's no, there's no uh valves separating the um uh internal jugular and the right atrium and this can be used clinically. Um So when you're doing, you know, a a cardiovascular examination, you can kind of press down on, on the, on the upward of the stomach, get the patient to face away. And as you press down a raised JVP um can be uh indicative of pathology. Um Yes, it's a, it's a, it's a good proxy of right atrial pressure. Um I'm gonna miss this one out. Um So now we're gonna talk about a bit about uh heart sounds. So when you're actually using your stethoscope to listen, uh the beats that you're hearing are the valves opening and closing. Um So that sh is what should be heard in a healthy heart, uh the tensing of the heart cups to prevent blood flow and setting up a vibration that is transmitted through tissue. So there are two heart sounds or there should be two heart sounds per cardiac cycle. The first heart sound is the uh closure of the mitral and tricuspid valves. Um The second heart sound is the closure of the pulmonary and aortic valves. Um and it's more difficult to hear, but there's also an S3 an S four, but I, I've, I'm yet to ever hear them ever. Um But I'm sure I'll get there one day. Um So, auscultation is when pathologies can be heard. Um So there's incompetence, which is the failure of the valve to close stenosis, which is the narrowing of the valve and murmurs, which is blood flows through dysfunctional valves as a turbulent jet kind of produces this high frequency vibration. It's, it's hard to describe what that sounds like. But you, you, you'd know it if you heard it, I think um is, is how I describe that. But keeping in mind that stenosis is narrowing and incompetence is failure of the valves to closure. Lovely. Um um OK. And now we're gonna talk about the cellular and molecular events in the heart. Um So we're talking about automaticity, I believe we're starting off with. So um auto auto automaticity refers to the intrinsic ability of the pacemaker cells of the heart allowing them to spontaneously depolarize and trigger action potentials. So kind of think about it as a sno atrial node, being able to produce an electrical impulses on its own without much help. It's just doing it on its own, triggering the action potential on its own. This happens specifically in um noncontractile nodal cells which make up only 1% of cardiac cells. Um So they create an er iron dependent electrical event and regular intervals. So 60 to 85 minutes, that's what causes the heart to beat. Um The other 99% of the cardiomyocytes uh consist of contractile cells. Um So iron dependent impulses that started the sa node moved at the A V node down the bundle of his causing that contraction in the ventricles. We know that one by now. Um So it starts with the noncontractile nodal cells and moves into the contractile cardiomyocytes. Um and it spreads through the myocardium to produce this coordinated heartbeat, taking into account, you know, the various isovolumetric relaxation and contraction to get that pressure right, as well as giving it time for ventricular and atrial filling. Um but that's all done through the delay caused by the fibro skeleton. Um OK. Um Yes. So forces generated by a contractile mark apparatus made up of actin and myosin myosin. Um this apparatus generates. So there's tension with intracellular calcium concentrations. So, calcium ions are kind of what carries that um um electrical impulse and that explains its relationship with tension. So, the higher the concentration of intracellular calcium ions, the higher the tension. Um Yeah. So it rises to allow cardiomyocyte contraction during systole, which we said was ventricular contraction and it falls to allow um cardiomyocyte relaxation during diastole calcium channels. Um We've just talked about the importance of calcium mines um and how they can carry the charge in uh the noncontractile myocardial cells. Um And um the reason they're there is for the influx and efflux mechanisms of cardiac myocytes. So, calcium channels um are open um causing kind of like an efflux of calcium irons produces this um nice kind of um uh electrical impulse, which we've talked about that route already. Um So there's various different types of uh calcium channels. Um So you have voltage gated calcium channels, BG CCS uh probably the most common um they allow the influx of calcium ions into cells across the plasma membrane by opening in response to an increase in membrane potential. So, depolarization. So kind of voltage um and uh electricity causes that uh opening, rapidly reducible uh sarcoendoplasmic reticulum. So, SARC pumps um you know, rapidly releasable calcium induced calcium release channels. So all these kind of things that are responsible for the movement of calcium channels. I'll let you read through that on your own. Um But it's, it's understanding different things. It's more of a membranes and receptors kind of set up. But understanding that there is an efflux an influx of calcium that is that is causing this um electrical conductivity basically. Um So, uh yes. So this is a quite nice diagram that kind of explains what that looks like. So you have your action potential from the adjacent cell spreading down, causing the VGCC to open the line for the influx of calcium into the cell. Um the calcium that causes more calcium release uh through the calcium influx through these ryanodine receptive channels. So it causes the calcium spark which is just a rapid efflux of calcium. Um This um creates a calcium signal when we go down here. Um The calcium ions didn't bind the troponin to initiate the contraction after the calcium binds to troponin. Uh the relaxation occurs in which case, the calcium ions unbinds from the troponin. And calcium is then pumped into the sarcoplasmic reticulum for storage three sockets. Um OK. So action potentials and membrane potentials. Um action potentials are a characteristic disturbance of the membrane potential of the cells. Um There's an elevated intracellular um concentration of calcium ions due to an action potential in the cell membrane. Um membranes are charged by the movement of ions across them and some membranes are capacitors, they store electrical charge. Um The electrical current and biological system is carried by ions and not electrons. So it's important to remember that the ions actually carry the charge. Um So it's all it's important to remember there is always kind of gonna be a membrane potential but um it's generally quite resting. Um So the conce the concentration of um I mean, you know, hypothetically uh the cell membrane is only allowed to is only allowed the movement of potassium ions and the potassium irons leave the cell take their positive charge with them. Um And this allows for a negative charge intracellularly. Um at the point of equilibrium, there would be uh kind of the same, same level of intracellular potassium and extracellular potassium irons kind of kind of producing this equilibrium where there wouldn't be any movement in or out of the cell. Um And that is kind of how the resting potential is defined when you've kind of reached either all the potassium has moved out of the cell and there's kind of a balance where there's no more movement, no more carrying of the charge and it's nice and stable, hence resting. Um Yes. Um So, membrane permeability um pretty much in the name how easy it is for a molecule to pass through the cell membrane. Um Generally, ions could be um can cross membranes by channels. Uh They can either be selective or just open and close. So um you know, they can be specific to specific ions, they can be specific to specific molecules or they could just be like everything is welcome open or close them. Um There are also um ion channels that are gated. Uh So there are two types of voltage gated which we talked about already in the case of V GCC. So that's voltage gated calcium channels. Uh But there's also ligand gated. In which case, there is a, you know, a molecule binds to the um um to the to the gate and causes it to open cause kind of producing um a complex um a ligand binding complex that allows for the iron channel to open um in terms of equilibrium potential. Um you have uh the hypothetical membrane potential that would only develop if they are given the iron uh with the only iron that could cross the membrane. So in this case, we're talking about the K plus um which would move out, carrying that uh electric potential with it and producing that depolarization. Um Each iron has its own individual equilibrium potential. And uh that's seen here. So that's just worth knowing. It's very good to remember. Potassium and chloride kind of have the same um equilibrium potential. Sodium irons and calcium iron. You need to learn. Yeah. Yeah. Uh So myocardial cell membranes, we talked about voltage gated channels. So this is the different ones that exist. Uh There's three important components that allow for the contraction relaxation as the ap passes through it. Um You have the voltage gated potassium channels, voltage gated sodium channels and voltagegated calcium channels. Um The cardiac ap in diastole, the cell membrane is most permeable to potassium ions. Um The member potential that is close to the poten the uh potassium equilibrium potential. So K plus tends to be the most uh uh pamol. Uh So the so sorry, the K plus, yeah, the most probably to the cell membrane, um ventricular cells are stimulated by the cell of electrical activities. Hence why they're called voltage gated channels. Um They therefore become depolarized, causing uh the opening of the channel and the initial depolarization. Um So it starts off with uh the voltagegated sodium channels. Um membrane potential move towards the sodium equilibrium potential So remember at that point, when kind of the concentration intracellular and extracellular is equivalent. So there's no more movement of the ions into or out of the cell. Um this therefore, once it reaches that point, it opens all the remaining fast sodium channels, making the membrane potential positive on the inside. Hence why that's causing that kind of massive depolarization. Um Now fast sodium channels close just as fast as they open, which should make the memory potential repolarise quickly. But doesn't because the voltage gated calcium, calcium channels open. Um there is more calcium outside the cell than inside. So the calcium equilibrium potential is positive inside the cell and the opening of the calcium channels uh keeps the membrane potential depo keeps the membrane depolarized. Yeah. So um shortly after that, the uh calcium ions enter the cell simulating the release of more calcium from the CPS resulting in elevated calcium, which allows for cardiomyocyte contraction. Um You have those calcium channels opening for a very short period of time which happens to be the same amount of time as ventricular sly, that's not a coincidence. Um but eventually they close and allow for the membrane to be polarized at the same time, the extra potassium channels open, increasing the speed of repolarization as this is happening. So calcium channels isolated and its levels fall. So the cells relax. Um So yeah, this is kind of one of those things you have to know and understand spend some time with. It's the um kind of just the movement of irons, what channels open when they happen? Why they happen? Um Yeah. OK. So now we'll move on to pacemaker cells. Um also known as noncontractile nodal cells. They are found in essay nodes and the A V node. Uh and they spontaneously generate action potentials through the process of automaticity which we've spoke about already. Um great. So pacemaker cells have no fast sodium channels. The upstroke of their action potential uh is due to calcium channels and is slow. Uh calcium channels in pacemaker cells close quickly. So the AP is short and triangular. So you can kind of see that in this diagram over here, um no fast sodium channels up stroke of AP due to C A two plus channels is slow um and they close quickly. So that's kind of very short triangular kind of uh setup once a pacemaker action potential has ended hyperpolarisation and hyperpolarisation, activated cyclic nuclear target gated channels um open. So this turns on a slow sodium conductance. Um uh which means the membrane potential is not stable because there's still movement of ions. Um The memory potential is not stable, it depolarizes slowly due to hyperpolarization channels which are permeable to both sodium and potassium ions. Um Yeah, it creates a high polarization currents and therefore the pacemaker potential. Um So there's a slow drift of me of membrane potential membrane depolarization towards the threshold and eventually, the pacemaker potential reaches the threshold to open the V GCC. So this is now becoming quite sudden when it reaches that level, whether it opens the voltage gated calcium channel, suddenly it's gonna be a massive EFX of calcium irons. Um And a new action potential begins spontaneously. Um So the control of heart rate, um we spoke about this at the beginning of the lecture in which it is sped up by sympathetic action, which is uh if I remember from your T one to T four and slowed down by parasympathetic through the vagus nerve. Um A steep pacemaker potential is indicative of a high heart rate, whereas a shallow pacemaker potential is indicative of a low heart rate, uh cardiac action potential that this is a video, but I don't think it's working. Um but maybe watch that on your own time. I'll send out the slide. So you should have access to this video. I but it's worth looking at. Um So we'll talk now a bit about the control of cardiac output. Um So we'll talk a bit about systole and diastole. We spoke about that already. Heart muscle contracts, pumps blood from chambers to arteries, diastole, heart muscles relax chambers, filled with blood, um stroke, volume and diastolic point, uh fully relaxed at the end of diastole. Um And systolic point fully contracted at the end of cysteine. So it's considered less as you can see, there's just less area because it's all being pushed out stroke, volume SV is and, and uh diastolic versus end systolic, which kind of makes sense if you think about it. So this minus this. So in this particular case, you have about 100 and 20 mL of enddiastolic volume, um and 50 mL of end systolic volume. And that resulted in about 70 millimeters. Um and that's generally the volume of blood that's left in the ventricle ejects per heartbeat. So you can safely say after the heart muscles, after the ventricles contract, there's usually about 17 mL that's left um in the ventricle. Yeah. Um It depends completely on size um stroke volume. Um you know, bigger people need bigger stroke volumes. Uh So that OK. Um Yes. So, echocardiograms. Uh So CT S um they uh allow you to view the structure of the heart, view blood flow through dopplers, measure stroke volume and ejection fraction. It's also useful in the diagnosis of congenital abnormalities. I'm sure you can understand why. Um Given that we looked at them, you can kind of see exactly how the blood is flowing where it's flowing, where it's going wrong, um valve diseases as well as heart failure. Um So we can talk a bit about preload and afterload. So let's start with preload, which is um kind of like the stretch. So there's the volume of blood received by the heart through the IVC and the S VC, for example, um and ventricular wall tension at the end of diastole just before contraction and is approximated generally by the end diastolic volume or end diastolic pressure. So, if you remember that was about 120 mL at the beginning, um you then have um afterload, which is the resistance that must be overcome for the ventricles to inject the blood, um ventricular wall tension during contraction um and approximated by the systolic ventricular or arterial pressure. Yeah. Um So some of the factors that are affecting stroke volume, uh preload, contractivity and afterload. So I think we've talked about preload, we've talked about afterload. Let's talk a bit about contractivity raised due to sympathetic stimulation, um adrenaline, no high calcium that all makes sense. Um but decreased end systolic volume and increases the stroke volume. Um you know, is, is uh controlled by parasympathetic stimulation to lower the contractility, acetylcholine hypoxia and hyperkalemia. And it increases the end systolic volume while decreasing the stroke volume. So now it's important to understand um kind of cardiac output. Um all the factors that affect it and what it actually means. So cardiac output is about is like the total amount of blood that is um produced per um minute or so. So let's say heart rate is about 70 BPM times of stroke volume. However, many milliliters that would be um uh so let's say that's 70 you would have 70 times 70 which give you 4900 mL per minute because you have, you're doing 70 mL of BPM. Uh So that produces 4900 mL per minute, uh which you'd want to change to 4.9 L. But it's important to know that the stroke volume, which is one of the key determinants. One of the two key determinants of the cardiac output is controlled by three other things which we've just talked about contractility, preload and afterload. Um Total blood volume should be around 5 L. Um And cardiac output in pregnancy is increased by 30 to 50%. And an athlete's cardiac output is up to 25 is up to 2035 L per minute, but generally in resting, it's about uh about five. So, yeah, that's what we're talking about here. So now that you have your cardiac output, you can now work out total arterial BP. Um So you take your cardiac output that you've just worked out by, by um working out your heart rate and stroke volume. Um You get your cardiac alpa and you multiply it by total peripheral resistance. Um that allows you to work out arterial BP. Um So you have two pressures to take into account venous pressure and arterial pressure, venous pressure is determined by the cardiac output. Um the blood volume, venous constriction, arterial dilation, muscle contraction, whereas arterial pressure is determined by the cardiac output, systemic vascular resistance and central venous pressure. I'm gonna let you read this on your own because I'm a bit short on time and I want to get um a bit further through this if I can. Um Yes. Um So this is basically different factors and how they affect total peripheral resistance. Um I will send these slides out for you. They make sense if you read through them, it's kind of makes sense. Ok. Pus, pressure will fall, arterial pressure will rise. Um Yeah. So going onto ventricular thinning, um there is uh diastole which is ventricles that are isolated from arteries and connected to the veins. Uh so which fills until the wall stretch and it's enough to produce an intraventricular pressure equal to the venous pressure. Um diastole. Uh So the higher the venous pressure, the more the heart fails during diastole because there's more blood actually reaching um the heart. Uh the relationship between the venous pressure and ventricular volume is known as um ventricular compliance curve. So you can see the venous pressure and ventricular volume kind of as one increases the other increases, producing a diastole. Starling's law really important. Um So, uh basically the SV of the heart increases in response to an increase in the volume of blood and the ventricles. So think about if the ventricular muscle is stretched more, it will contract harder. Um So the more it's widely stressed out, it is, the more it can push down almost, um the more the heart fails, the harder it contracts. Um And that therefore the highest stroke volume because it's, it's really stretching, which means it can stretch really hard. Um Starling's law relates stroke volume to venous pressure. Um And uh the slope is the contractility of the ventricle. Um So there's a decrease in afterload, normal and an increase in afterload. Um ok. So how is heart rate controlled? Um Well, there are three different types of receptors uh in the medulla. So you have chemo receptors which detect an increase in carbon dioxide and a decrease in oxygen baroreceptors which which detects an increase in BP and propria receptors which detect an increase in muscle movement. So, um if you, if you um and that's all held within the medullar. So if you wanted to increase um you know, the heart rate, you would go through the sympathetic nervous system which would go through the accelerator nerve, which would produce an increase in the activity and the automaticity of the sinoatrial node producing an electric conduction, which can produce more contractions of the heart at a faster rate. On the other hand, if you wanted to decrease it based on the receptors, picking up something that's tell them. Ok, we should probably decrease the heart rate uh that goes through the parasympathetic nervous system, uh which goes through the vagus nerve, which causes a decrease in the sino atrial node, decrease in the automaticity, uh decreased in conduction and therefore, a decrease in heart rate. Um just gonna have a quick uh Yep. Ok. Lovely. Um So interpretation of EC GS. Um So I have about five minutes left for 330. Um Would you like me to continue or should I call it here? Um I don't know if, if Ellie's around, I think Dan is fine. You can continue. No problem. Ok, lovely. Um So yes, uh feel free to ask me any questions. Um I'll, I'll try and get through at least uh the interpretation of the ECG S. So, um when discussing uh ECG S, it's important to understand the difference between, first of all, understanding what they're like and then once that's done being able to interpret them. So let's start off with the understanding part. First, I'd really recommend uh the geeky Medics website for both understanding and um uh interpretation that split up into two different uh topics. Um two different pages. Um And um they're really good. So, first of all, um we've talked about this a bit already uh PQ RST. Um So, what hap what actually happens to me? So we've talked about atrial depolarization. What that means. Uh We've talked about ventricular depolarization and what that means. So that's uh atrial contraction, ventricular contraction and then kind of the movement of irons back. So we can do that again. Um But what actually happens on an ionic level um is within depolarization. There's an influx of sodium ions through the fast sodium channels. Um There's obviously the QR S duration um in which there is a um kind of uh again, depolarization. Um but there's, it's slightly slower. So there's AK plus um uh K plus um efflux and calcium influx. Um And at the third level, you have the um the um uh the K plus efflux and calcium two plus er efflux and a slow clo close on the sodium and then back on forward with that atrial depolarization, there's an influx of sodium. Um So bipolar leads. So this is quite interesting. Um So there is um let me see if I've put this in here. Yes. OK. Fine. So these leads are kind of responsible for telling you why um why these kind of lines occur. So think of it as a current kind of flowing in all of these directions. If it's gonna go that way, the E CG will spike up on the A VL. If it's going that way, it's gonna spike up on the A VR. Um But it's kind of important to understand what um these different um uh leads kind of combined to make um again with ECGS to spend some time with them. Go on the geeky medics do some questions, there's um loads of questions out there. So it's worth looking at, but there's generally what's considered uh uh the axis for the uh for an ECG. So most of the er the waves of depolarization are happening between the minus 30 to uh to 90 that's where the normal QR S axis should be. Um So if you go back here, this is a normal QR S complex. So if everything's working properly, that should be occurring like that because it's happening between minus 30 positive 90. Um If there is, um uh if it goes beyond 90 that's what we call a right axis deviation. Um And uh if it goes below minus 30 it's called the left axis deviation. So if you think about that being your axis, it makes sense, access, deviation, right and left. Um So you have your different chest leads there. Um So you have V one, V two, V three, V four, V five and V six. So the way I like to remember what they kind of represent is I write out V one, V two, V three, V four, V five and V six, I write them out like in order and then I write SSAA LL. So I don't know if you can see that. But uh so that's for that, but that's what I would do. I would take V one V two, V three, V four, V five V six, SSAA LL. So that's spelled S and therefore you can remember it as septal, septal anterior, anterior. 00 um Yes, so fine. Um So when you see a spike that's a positive complex complex and when it's, when it's actually going upwards, that's positive, that's a positive charge and negative is when it's going away from there. So kind of let's say you saw a spike in the um OK, let's say you saw a spike in, in a positive influx in lead two, right? That means it's flowing towards lead two. So you'd see a positive deflection on the ECG if you're looking at lead two. However, that goes almost kind of as you can, you see that it's going kind of opposite to the A VR um that would mean that would be a negative influx because it's going away from the VR. And I think this, this kind of um diagram that says coronal plane on it is quite um is quite um useful to kind of understand what that might look like. So you have 123 and then a VRA VL and A VF so right left and down is just a VF um great. So yeah, so you have positive complexes and negative complexes, you also have biphasic complexes. Um So yeah, as I said, if depolarization is going towards a lead, that's a positive deflection if it's away from a lead, negative deflection, so positive towards lead two, that's positive. Um And if it's away from you two, in the case of the A VR that would be a negative deflection. So now, in terms of interpretation of the ECG, this is kind of the steps you'd want to start taking to kind of interpret it. You want a systematic kind of routine I don't know. Um um if you guys do Aussies, but if you wanna do physical examinations where you're being tested on, OK, interpret this ECG and you're having to do it in front of someone, either a clinical educator or a doctor or something. Um You'd want to go through these details. Um So the main thing is you wash your hands, you turn up, you confirm the details of the patient, um confirm their name and date of birth, say that it matches the E CG. Um You check the date, not the fate. Um Hopefully the fate is ok. If they have an E CG and not dead yet, check the date and the time that the E CG was performed and also check the NHS number. Um We do here um check the calibration usually 25 millimeters per second. Um And it's very important for interpreting the E CG correctly. Usually it says it, but if it doesn't, it's fair to assume it's 25 and the rate. Um there are lots of ways you can calculate the rate. Um But you can kind of take a, a rhythm strip. Um So you can look at number of complexes and multiply that number of complexes by six. That's how I would normally do it. Um If it's normal, it'd be somewhere between 60 100. Bradycardia is less than 60 which is a slow heart rate. Tachycardia is above 100 which is a fast heart rate. Um I remember it as Bradycardia, Tommy Tom Brady, he's an American football player. He's a bit old now, so he's a bit slow. That's how I do it. Um, rhythm. So, um there are different kind of phrases used to describe heart rhythm. So you're regularly, regular, regularly, irregular and irregularly, regular, regularly, regular is like, ok, con consistently, um let's say consistently, nine small squares apart, always nine, nothing's changing there. That's nice and normal. Um Regularly irregular is a recurrent pa pattern of irregularity. So let's say it was nine, then seven, then nine, then seven, then there's a pattern to it, but it is irregular. It's not, it's not sinus rhythm, which was what we call a normal rhythm, a regular rhythm, regular, regularly, regular rhythm is referred to as sinus rhythm. However, irregularly irregular is what you can see on this kind of this kind of a small bit here where it's just kind of random nine small squares then 13, then seven, then God knows what it's, it's uh completely random. Um Now we've talked a bit about axis deviation and this kind of illustrates my point slightly. So this is normal cardiac axis, in terms of this kind of represents the direction of the action potential. You can see it's kind of near lead two kind of close towards lead two than it is towards, for example, the A VR that's the polar opposite direction. So as you can see as it's kind of closely to there's that positive deflection. Um But on the, um let's say on lead one where it's not very close, that's it's less. So and the A VR would be a negative deflection. So it would be going down. Um Yeah. Um axis deviation is commonly associated with hypertrophy. Um Solo leon criteria can be used to check for left ventricular hypertrophy, um S wave depth and V one and the tallest R wave height in VVI V five and V six, it should be greater than 35 millimeters. Um So this is just how you check for, for a deviation. Um There's also something called William Marrow. Um So, um William Marrow. So, um again, ii think ki medics would do a better job of explaining that. So if you just spend some time with that, that kind of explains it. So it's basically saying if it looks like a W, if the ECG looks like a W that's a left axis deviation. And if it looks like an uh an M, that's a right axis deviation. Um So the first things you wanna start asking yourself past that is, is there ap wave present, is there atrial depolarization is essentially what's being asked here? Is that there that initial kind of um conduction? If so is each P wave followed by a QR S complex? If it's not followed by a QR S complex, that could indicate that there isn't ventricular contraction, um which is concerning and do the P waves look normal. So if there's atrial flutter, you'll see something called a sore tooth base baseline. It's kind of quite um quite sharp and quite quick. A lot of small sharp waves that's an indica indication of atrial flutter and atrial fibrilla fibrillation is if P waves are present, there is an a rhythm and a chaotic baseline. Um So pr intervals which uh I'll go back to the uh let's see, where are we? Uh Here we are. So you see that pr interval, the distance between the start of the P wave and um kind of the, that kind of start of the Q wave there, it's called the PR interval. Um Yes. So um the P RPR interval should be between 100 and 20 to 200 milliseconds, 3 to 5 small squares. Um If the PR interval is greater than 200 milliseconds, uh there is an A V block. Um And if the pr interval is greater than naught 0.2 seconds, the P wave originates from somewhere close to the atrioventricular node. So the conduction takes less time. So if you remember, if you think about what that the structure of the heart of the, the anatomy of the heart looks like, you know, the so of atrial node is kind of in the top left of the uh atria and the ATRIO ventricular node is actually closer towards the ventricles. So it's kind of skipping the sinoatrial node bit because it's found a shorter pathway. So that's why that conduction takes less time. Um The atrial impulse is getting to the ventricle by a faster shortcut and an accessory pathway. So now we're gonna talk about heart blocks. Um There are different types of heart blocks. So we're gonna talk about first degree heart blocks. Um So that's when the pr intervals are less than 200 milliseconds. Like we've talked about um it shows the anatomical locations, the block within the conducting systems between the essay and the A V nodes. Uh There's also second degree heart block type one. Um So as you can see, it's kind of increasing pr intervals. So it keeps increasing until eventually you drop that QR S complex. So 467, no QR S. So you have that little PWA but it's not followed by a QR S complex. Um Then you have um second degree type heart block type two in which the com the, the pr interval is consistent. But there are still dropped QR S complexes and third degree heart block, you'll know it when you see it. I mean, it's a hard thing to miss very few QR S complexes um just complete heart blocked heart blockage. Um So in terms of what the QR S complex can tell you, it's um you can tell a lot by its height, it's morphology and it's width. Uh So this is the William Marrow. I was talking to you about. So on V one and V six um for a right bundle branch block, you would have an M kind of like, I don't, it's, it doesn't really look much like an M but you'll, you'll start to notice them the more you do them. There's an M kind of there um on V one and a kind of a double U there uh in V six. So that's indicative of a right bundle branch block. So do you remember if you remember in the um ventricular septum there is the right bundle bundle branch on the left bundle branch. That's what we're talking about when we say bundle branch block. So if the V one is an M um and the V six is a W, then that's indicative of right bundle branch block. Whereas on the other hand, if you have um uh V one and V six, where there's a W on the V one and an M on the um V six, in that case, you'd have a left bundle branch block. So just look at V one and V six and see if you can find those patterns. Um The height of the QR s complex um tall implies this hypertrophy. If you think about it, you'd need more conduct conduction for um uh um for an increased muscle uh cells. So it's just more muscle. Um uh Yes. Uh Just going to chat, checking us OK. Um So it implies hypertrophy, you'd need more conduction because there's just more muscle cells. Um If it's small, less than five millimeters in the limb leads and less than 10 millimeters in the chest leads that can indicate stuff like um hypokalemia and stuff like that. Um There's also delta waves. I'm just gonna take a quick look at the chat, see if there's any questions. Mhm. Lovely. OK. Um OK. Awesome. Um So, um so we have delta waves here. So you can kind of see that slurred upstroke, that kind of slow inclination um right there just after that P wave um that indicates ventricles are being activated earlier than normal. Um So what does that mean? Well, typically it indicates that there's this particular kind of very specific syndrome that you just need to be aware of that exists called Wolf Parkinson White. Um To be honest, I only heard of it from, from house, but it is a very real thing. Um And um that consists of tachyarrhythmias and delta wave. So this is the delta wave that they're referring to when they say that it's kind of mixed up the Wolf Parkinson White syndrome um situation. So, uh that slurred up stroke. Um So key waves um there are, they're normal um is just above two millimeters not seen on V one and V three. So um pathological would be 40 milliseconds. So one whole box wide, um two millimeters deep and they're seen usually in the leads V one to V three. and also in inferior QA so 23 and a VF um indicative of a previous myocardial infarction. Um There's also the QT interval um which represents the time for ventricular depolarization. So I can take us back to that. So I should have put more um kind of standard ECG S in this just so I can have them to show you. But um the um that's the QT interval over there, you see that. So from the start of that Q wave all the way to the end of the T wave, not the start of the end of the T wave right before the U. Um So let's go right back to where we want are now that we've done that. Sorry. Uh There we are. So it represents the time taken for ventricular repolarisation and depolarization. Um So normally two big boxes wide. Um There's a long QT interval. Um So that indicates hypokalemia, hypomagnesia, magnesemia. So, hypo like uh low magnesium in the blood, um low potassium in the blood, uh low calcium in the blood through hypercalcemia and hyperthermia, which is just coldness. The prolonged QT is the increased risk of ventricular arrhythmia. We also have AJ point segment uh where the S wave joins the ST segment and uh if it's elevated, the ST segment is also elevated. OK. So now we're gonna talk about ST depression and ST elevation. This indicates to us about sties and antemi. So they're both myocardial infarctions, which is a, in such, which is essentially a, uh, heart attack. Um, so a stemi is when there's ST elevation. So the ST interval is higher than the. Um, so I'll show you. Mhm. Let's see. I don't think I have a good indication of it. Give me a moment and I'll find it for you. Um, yes. So there's kind of like if you see here, that p that this kind of flatness here, if that ST segment is higher than that, that's what we call ST elevated. So that kind of distance there. Oh, sorry, that distance there between one and two, if that's higher than that wave there, that's indicative of an ST elevated myocardial infarction if it's the other way round and that's lower. That's what we call an NSTEMI, which is a non elevated uh non ST elevated myocardial infarction. Um And uh give me a second, I'll go right back to the correct slide. Um So, yeah, you can tell that, you know, that's, that's indicative of uh ST depression would be indicative of anemia, like I said, uh bundle branch block, right, or left hyperkalemia. Um A stemi could be indicative or it's greater than one small square um in limb leads and greater than two in chest leads. That's just an ST elevated myocardial infarction. So, a heart attack. Um So the T wave um represents the repolarisation of the ventricles, it's normally inverted in V one VR and three tall tented T waves are indicative of hyperkalaemia. That's right. So the T waves, the end where it says ventricular repro if they're really tall, that's hyperkalaemia. And by really tall, I mean, greater than five millimeters in limb leads and greater than 10 millimeters in the chest leads. Um The inverted T waves are to do with bundle branch blockage and general illness. Um Biphasic T waves up and down, uh can indicate ischemia and down and up can even indicate hypokalemia. Um So would you like me to stop here because I know I've gone, I've gone well over. Um and I don't want to keep anyone here. I'm sure everyone has other stuff to do. Um I'm happy to return and finish it off, but I've got another 150 odd slides to be honest with you. Um So, um whatever you'd like me, if you're happy to me, for me to continue. Um Ellie, please let me know. Um I think maybe done um what we can do, maybe we can put it as a pause and then we can start with party maybe another time. How would that sound? That sounds good. Absolutely. Yeah. Um I wanna thank everyone. I thank Ellie for, for allowing me to do this. I've had a great time. Um uh talking about this. If anyone has any questions, um, feel free to email me, I'll ask Ellie if she can send my email out. Um Yes. Um Thank you very much and thank you to medical. Thank you so much d for the talk. Does anyone have any questions right now that they want to ask Dan? Feel free to mute yourself or you could also raise your hand or pop it in the chat box below as well? So I think there's no questions. What we can do is um, I'll speak to Dan when he's available and then we can start with the part two of the cardiovascular system and then we can give it a wrap from them. But Dan, thank you so much on behalf of everyone here. I would like to just take a moment to express our sincere gratitude to Dan for his UK MLA revision series on the cardiovascular system. The lecture itself.