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So welcome everyone. Um So today, we'll be learning about cardiac physiology from David, um who is a trainee at hospital, a cardiothoracic trainer at hospital. And um this is going to be in two sessions, cardiac physiology. So it will be taking us about 30 minutes to about 40 minutes you about today. Um And then we will schedule another session for the second model on cardiac physiology. Um If you have any questions during the course of decision, feel free to put it on the chat and it will get through to answering its own sometimes during the time, I guess. Yeah. So I'll leave it to you, David. Um OK. Uh Yeah. Thank you and your family. Me. Uh Good evening everyone. Um My name is uh David KK. I'm a cardiothoracic trainee, as the family said. Um I'd also shamelessly talk about our endeavor, which is called the London School of Cardiothoracic, um which we set up about 3.5 years ago in with uh a couple of my colleagues and a couple of consultants here in the UK. And this is why we set it up because we would like to improve surgical training specifically cardiothoracic surgical training. Uh not only in the UK but abroad as well with specific should, should I say a specific focus on creating an a, a sort of equitable provision of cardiothoracic training for everyone who's interested in this wonderful specialty. Uh So, uh thank you the femi for having me today and we are going to be talking about cardiac physiology. Um Now, when the femi asked me to uh present on cardiac physiology, the first thing I thought is this should be a cardiologist. Um uh what's the why, why should the cardiac surgeon be talking about cardiac physiology? Um And that's because the first, I was looking at it from a, a very bookish point of view. Um what are the values? What are, what are the timings, cardiac action potentials, things like that. And I thought to myself, we never really think about this um as cardiac surgeons. However, I was wrong because if you cardiac surgery is one of the few surgical specialties that cause its surgeons to be not only surgeons and good with their hands, but also good with your brain. In terms of your clinical approach to the management of your patients at every stage of your journey of the patient's journey, you are managing the patient clinically with robust input of their physiology, anatomy, pathophysiology, and all of these things will come together through your various investigations and tests to determine how you'll proceed with the treatment of the patient. And so with that in mind and having corrected my initial error, I, I started to think about how I could talk about cardio cardiac physiology to cardiothoracic surgeons. Um junior surgeons, as I've been told, um uh as I'm a junior surgeon as well, and I think about uh the application of cardio physiology to our day to day practice. And therefore I decided that I wasn't going to come here and the wax lyrical on these special numbers um because you can read that from a textbook, I'd rather want us to have a discussion on how cardiology impacts our clinical decision making. We started by just an overview and remind ourselves of key concepts and then start to tackle the the preoperative and postoperative period of our patients. And unfortunately, we can't go into depth in terms of dividing the patients into um ischemic heart disease, valvular pathologies, uh arrhythmias and so on. But what we can do is we can have a sort of overview of the cardiac patient. Um and where necessary I will be specific and um where we can't for the benefit of time, I'll just uh talk about the patient, uh the cardiac patient as a holistic in a holistic view. And so moving on from that, we dividing this session into a pre op and POSTOP. We're looking at disease physiology, operating physiology, POSTOP physiology and complications. So we're looking at cardiac physiology and then we're thinking about how does this affect our clinical decision making? When we are looking at the pathway of the journey of the patient starting from presentation of the disease to um the operative period, the post operative management and find any complications that may arise going ahead and tackling it this way means that we, I wouldn't have time. I do not believe multiple studies have shown that the maximum attention span for anyone is about 40 minutes. And given that we've had a bit of a late start, I've created this slide so that I can hit 30 minutes. I'm hoping to finish this in 30 to 35 minutes. I would like this to be an interactive session. So I've kindly asked and you feel me uh to, I will be asking questions and I'll be uh I will appreciate if um there can be some sort of response on the chat system. And so in order to test this, I'll start by saying, can everyone hear me and can just random people post yes or no. So that I, because I haven't used me all before. So I'd like to know if people are actually there listening um in terms of using the chat function. So can someone just post a random yes or no on the chat? Oh, brilliant. Thank you. OK. Um So moving on, uh we'll start off from uh cardiovascular anatomy and this is, thank you, everyone. Thank you, everyone. I can see that brilliant. Ok. So we'll start off from cardiovascular anatomy because we can't start talking about physiology without talking about the heart itself. Um You will definitely know the anatomy of the heart. So we'll move on to um why I am talking about cardiovascular anatomy at this moment. And my next slide will make things clearer but the flow blood. So um the flow blood, it's chicken and the egg situation. Some people like to start from the lungs. Some people like to start from the aorta. Some people like to and, and so it, it, it really depends on your preference. I think that's if we're talking about blood flow, we should really be starting from the point of oxygenated blood. And that's when blood has left the lungs through the pulmonary veins, going into the left atrium, going past the mitral valve into the left ventricle, in diastole, going into the aortic valve, going into the aorta in systole, then going around the blood, the the the human body branching off into major arteries which become materials capillaries and then finally going into the venous system and uh going into the superior inferior vena cava uh and coming back as mixed venous blood into the right atrium through the tricuspid valve, into the right ventricle, finally into the pulmonary valve and back into the lungs for oxygenation and to repeat the process quite a simple flow and quite beautifully designed. Um Now, the question is, how does that affect our discussion for today. So we'll start by talking about cardiac hemodynamics. Uh This is quite an interesting aspect of uh um cardi physiology because those who really like physics uh will enjoy the talk on cardiac hemodynamics. It's all about flow. The body is made up of arteries, veins and these are all pipes. They, they're not different from a plumbing system. And the key concepts that we normally look at when we're talking about cardiac hemodynamics are velocity of blood flow, blood flow itself, resistance, laminal valent blood flow, compliance and pressures. So what I'll do right now because I'll just take you back to the slide above where I talked about disease physiology or preop physiology. And POSTOP physiology is I'll run through um these concepts to remind you because all I'm doing here is reminding you of the themes that you, you, you studied um in medical school. And then finally, we'll talk about its application into um our, our practice. So what is the velocity of blood flow? It's basically the uh speed at which blood flows through the arteries and veins. And basically the vascular system and V stands for velocity Q stands for blood flow and the A stands for a cross section or area. So we can see that velocity is directly proportional to um the blood flow. And uh this is also proportional to the cross sectional area of the um vess in question, which then makes you think OK. What is, which blood flow is fasting? What arteries, arterials? So Bluffer is, will be faster in the aorta rather than the smaller arterials. And why is that? And that's because you have a smaller cross sectional area because remember your arterials and capillaries, they are small but they are in no, they the many of them, right? So if you think about cross sectional area, we're talking about the total uh um area that they cover. If you were to pull out your capillaries and lay them down, you would see that they constitute a larger cross sectional area than the IOR. And therefore, it's only um uh proceeds from that concept that the blood flow will be faster than AORTA. Now, how does this have clinical correlation for us as surgeons? It means that just very simply when we're going on bypass the due to the speed of the blood flow in the AORTA, you, it, it takes very a lot of technical skill when cannulated the AORTA in the first place as anyone who has watched um or has observed or has done it themselves. And when we can, we can be thinking about this blood flow is the velocity of blood flow in the aorta. We'll talk about pressure, it's much higher than in other aspects of the um of the um system. And therefore you will be, you will be thinking to yourself like, well, when I'm putting my speeches, I've got to be very careful. I've got to be very careful when I'm proceeding with this because this is quite a difficult technical skill to obtain. Then we also think about in terms of just uh generally the um from the preoperative aspect is when we move on to what the, the pressures in the different uh vessels in the body. We're thinking about things like the cause of ischemic heart disease, a patient with hypertension, for example, high BP or we're thinking about patients with narrowing arteries and so on and so forth. Well, why don't I just move on and then we'll talk about blood flow in terms of um uh output, cardiac output. So cardiac output is as you move up to number two is a function of pressure, pressure gradient and resistance. Now, the question I want to ask is what is pressure, pressure gradient and what is resistance, pressure gradient? Does anyone know very quickly? Can you post and say and, and tell me what you, what the pressure gradients we are talking about in, in this particular um uh formula? Does anyone remember? Yeah. OK. Um So it doesn't seem like anyone is posting this. So the pressure gradient we're talking about will be uh the difference between um mean arterial pressure. Yes, difference in blood pressure very good. But in this case, if we're being specific, we're talking about the difference in mean arterial pressure and the pressure in the right atrium, right? That's the pressure gradient that we're talking about because that's what facilitates the flow of blood, the cardiac output through the system. And when we're talking about resistance, what are we talking about? We're talking about the um properties of the various vessels. So, um where do you think resistance is high, is resistance high in the aorta or is resistance higher in the capillaries? Where do you think resistance is higher? Is this quite an easy one? Right? Because the answer, yes. Well, with the season three, it's right there staring at you very good news for me because um in we have the yes, resistance is high in the cap is why? Because we if we look at the um par equation and if you're a French speaker, don't come after me for pronouncing it that way I do not speak French. Um So the resistance is directly is the resistance in any um in any vessel will be directly proportional to the viscosity, the length of the blood vessels, but will be inversely proportional to the radius. So that means you're going to have high resistance in smaller vessels, right? And so if you have high resistance in smaller vessels, then you then move on back to number two. When we're talking about blood flow, it just means that blood will flow um faster in a vessel that has a um larger diameter or larger radius as opposed to a vessel that has a small diameter, smaller radius. And So what um from a preoperative context? Again, going back to our clinical correlation. What does this mean? It means that a lot of our diseases stem from this actual fact. So we talk about ischemic heart disease. The reason why once you have some sort of stenosis or narrowing of the um uh of the arteries in the heart that feed the heart, you already have a situation where blood flow through the heart itself. As through the heart, the muscles becomes not reduced. And um now it's good that capillaries have a slower blood flow because then you are able to have um good perfusion and oxygenation of your tissues. However, if you get to a point where the resistance is further reduced, then you have a situation where that blood flow that was optimal, even drops and becomes sub optimal. And therefore, you don't have perfusion, you don't have exchange of oxygen. And this is where we then get ischemic heart disease because then the muscles uh are overworked, the oxygen demand. Um when that goes up, the blood vessels are not able to feed um and meet their demand. And therefore you get cellular death, which needs to um occur infarction, which obviously leads to death of muscle and finally the heart failure and decompensation. And then you have uh pressure in the system in the pulmonary veins. Uh and you uh uh go into either acute or um uh chronic heart failure and in some cases, if the infection is really great and covers a, a large area, for example, if it's uh major um uh left lad at anterior descending artery, then you have a, a significant infarction of the left ventricle, which could lead to in a lot of cases sudden cardiac death. So um when you start to, this is what I'm trying to achieve today to remind you of these principles, but then bring our clinical what we face clinically so that we can start thinking about why we do what we do. And therefore, when the resistance goes up in, in, in a narrowed um uh artery or vessel in the heart, what do we then do we go ahead and do a cardiac bypass uh operation which was pioneered in 19 seventies if I'm not 19 sixties and seventies, if I'm not mistaken by an Argenti surgeon. And so, um this is why we do that because now we're going to bypass that narrow the narrowed um artery. Now, obviously, the cardiologists are able to stent, but today, we're not talking about the um difference between PCI and CABG and uh which is better on what the latest evidence um is. And now moving on to four, we're talking about laminar versus Vallin blood flow. This is also an interesting concept, right? Because blood flow should usually be laminar if it's lamina it uh your um flow gets to your blood and uh the um oxygen oxygenation that it carries, gets to all your uh relevant um uh areas in the body. So your organs and uh your, your brain, your um uh kidneys and so on and so forth. However, if you have a narrowing of your vessels, again, you may have trouble in blood flow. If you have anemia, if you have uh reduced hematocrit, you may have trouble in blood flow, which does not bode well for um oxygenation and perfusion of these uh um end organs. Now, moving on to compliance, um compliance as a concept of uh hemodynamics, I have written C equals to V of A P and I'm sure I've done this uh on purpose. I'm wondering if anyone knows what the V is and what the P is. Can anyone um I wouldn't say guess because I'm trying to remind you of all the things that we studied when were in medical school. Um But does everyone remember what uh this equation is about and talking about hemodynamics and compliance? Ok. So I, I'm not seeing any answers. So compliance and maybe if I started by saying what compliance is, it may juggle your memory. And so compliance is basically the or in some situations we say capacitance is the ability for a vessel to dilate, right? OK. And I've written a cheat there by saying greater for veins than arteries. Why? Because arteries are more muscular than veins and therefore are stiffer, right? And so if, if I've said that then you can uh deduce that we are talking about volume and pressure, right? So this is a response of the vessel in terms of their volume, they able to carry based on the pressure in the system. And so veins do have greater compliance because they're able to dilate once the volume increases, arteries do not do have some sort of compliance. However, that's restricted and that stiffens as we grow older, this is why the older you get, the more likely you are to suffer from high BP as well because the stiffer your arteries are the less compliance they are. Which means that if there's a volume increase, your arteries are not able to respond as quickly as they normally would do when you're younger. And because of that, the pressure in the system becomes greater, which means that the end organ perfusion pressure is greater than what it should normally be, right? So if you're thinking about an organ that is very sensitive, you're thinking about the kidneys, for example, if there's an increase in the systemic BP that automatically starts to affect the kidneys as well. And this is why high BP um is uh quite dangerous for uh kidney health. And there's a direct uh correlation between um high BP and um chronic kidney disease. So you have that keeping that, that keeping that in mind is very important. Uh and, and also we can talk about the clinical correlations for compliance, we can talk, talk about the use of uh volume to improve pressure and we can and in this case, what will I be talking about? I'll be talking about um uh you fluid resuscitation um in patients when they've got low BP. However, we also have to remember that if you have a very dilated vessel, the more volume you put in, you will need more volume to achieve a set in pressure. And these, this is why when we think about things like the postoperative period, when a patient um in some cases, in some cases, um when we have a massive uh uh release of cytokines and um inflammatory markers that cause dilation of our vessels. What do we do? We in order to improve that, we try to vasoconstrict and we vasoconstrict because if we can vasoconstrict that we reduce the compliance, which means that by reducing that compliance, we can improve the pressure as we concede. It's an inverse relationship. OK. So this is something that I'd like you all to just keep in mind. Finally, we're talking about mean pressures. So we have gone through the basic summary of cardiac hemodynamics. We've talked about velocity of blood flow. We've talked about cardiac output in itself, that's blood flow itself. We've talked about resistance of our vessels. We've talked about how the blood flows. We've talked about the compliance of the vessels in um and, and this is based on the property of the vessels that we find it's different for veins, it's different for arteries, it's different for vessels, different for arterials. And then finally, we come to uh pressures because we've been talking about pressures. We've not actually um uh spoken or elaborated on that mean pressures. So, um which is important when thinking about uh your patient's end organ perfusion, uh systolic diastolic pressure or mean arterial pressure, anyone with an answer, which is more important. So your surgeon, you've uh finished your case, you've done a triple bypass, you've sent your patient up to ICU. Um You have all the monitoring kits installed for your patient and you walk in and you, your, your uh junior calls you and says I have a problem with this patient. Um His BP is not really doing well. Excellent. Mean material pressure. Mean arterial pressure is the most important concept. So um I haven't written how you calculate that. But then the question is why, why is mean arterial pressure, the the most important pressure or the most important information that you're looking for? Does anyone know just very quickly if you can write a short answer? Yes, perfect. OK. Excellent. Thank you. So I will um just uh go on and say that um uh Dain, you are on the right on the money. And um what we are looking at is uh something that I've not actually put in in this at the moment is called uh pulse pressure. So, pulse pressure obviously is the difference between your systolic and diastolic uh BP, which you've rightly pointed out da And so, um when we take pulse pressure, the question is what is pulse pressure? And maybe I can quickly add that here. Uh So pulse pressure. And so, um that is the difference between systolic and diastolic pressure, which is based on stroke volume. Now, stroke volume is what is what you um the amount of blood that is being pushed out in N systole? OK. And um why do we then focus on mean material pressure? Why someone would ask me why are we not taking uh pulse pressure, pulse pressure is reflective of stroke volume and stroke volume is the most important concept. Why? Because we want to know how that patient is doing over time. We don't just want a snapshot, right? You've done a four hour, 3 to 4 hour procedure. The patient is in ICU and you're thinking about how long that patient is um has been doing. So what you want is not just a pressure. Um uh at one time, you want a pressure over time and this is what mean arterial pressure gives you because it's uh uh it's, it's the idea that you are looking at the pressures over a period of time. And for those who are very good at um mathematics, if you remember what you will see on the arterial line, it's the area of the curve. And if you remember um calculus, you'll know that we'll have to um calculate the area of the curve to get uh mean material pressure. And that is what the monitor is doing automatically for you. And that gives you an idea of um how well your patient is doing. Ok. Finally, I uh and not only how well your patient is doing, it gives you an idea of the and uh the fusion um and that helps you regulate um with other factors and values including your central venous pressure, your uh pulmonary we pressure, which I'll talk about uh and um uh the overall volume state of your patient that can tell you what you need to do. Do I need to give more fluid? Do I need to constrict my patient? Do I need to dilate my patient? This is you, you start thinking about how to manage um your patient based on this. I mean, arterial pressure is definitely the one of the most important concepts in. So now I can um I can write it there because I wanted to ask you all that question. Now, moving on pulmonary we pressure. Now what is pulmonary we pressure. Um and, and has uh if, if, well, I, I I'll quickly move on because I think we are running out of time. Uh Someone has posted a question, ok. In doctor Addy, some of the questions you're asking may not be uh um topical today. But I'm def I, I'm definitely interested in discussing um some of the questions that you've posted and finally pulmonary, we pressure is a way of looking at the pressure in the left atrium. And um this gives us an idea of the pressure within the pulmonary vasculature as well. Normally, how we uh assess this is by putting the catheter um through um the IDV all the way down through the right atrium and into the right ventricle and up the pulmonary through the pulmonary valves. And we try to wedge that into um uh a pulmonary artery to get the corresponding pressure of what it is because that the pressure in your system usually in should be equal across um uh the board. And that will give us an idea of what the pressure is in the left atrium. And this is important because it tells us what our feeling pressures are. Um And knowing what our feeling pressures are, we can then start to understand um whether our pa patient is um uh well filled on the field or if there's a lot of dilation that's going on, if there's a lot of pressure in the per uh uh vasculature, um uh if we need to, in some cases, diurese our patient or in some cases, do we need to give more volume? So, you know, these are the overall concepts of cardiac hemodynamics. OK. And so um having done that and reminded you all of this then I'll just quickly go. This is I'll move on to the next slide, which will just give you a quick overview of what we're talking about with regards to ischemic heart disease and just pointing out what I said about um in, in uh you can ignore all the fancy stuff. Um If you're into ischemic heart disease research, um you can take note of that if you're not, what's most important is we talked about narrowing of arteries. So we talked about resistance. So, ischemic heart disease, we're talking, looking at vasospasm in some patients who um uh there's some patients who have this, there's uh pre metal um there's syndrome X uh and um also a reaction to um stenosis as well. You can have vasospasm as well. Uh And in some cases, drugs as well. There are lots of patients who ha have taken uh cocaine overdose end up with an acute uh myocardial infact. And why does that happen? Because it does cause vasoconstriction. Um an acute vasospasm which can then lead to a myocardial myocardial infarction. We talked about atherosclerosis, again, narrowing of the arteries as per hemodynamics. And again, going back to this increases the resistance increases the tur of blood flow. It reduces the ability of the um vessels, the coronary arteries to um properly perfuse the heart muscle, which then leads to settle to death. Ok. Um And then we have uh choon microvascular dysfunction, which is, which is, which is and this is a chore in the very small um uh microvasculature. Uh And as we've seen, we've talked about this and the very small microvasculature resistance is really, really high and blood flow is um much lower. And if you remember in this s equation, I've not written it, it's eight times um length over pi radius, uh times radius to the power po therefore, if you have any uh reduction um uh in, in, in this, your resistance is increasing um by factor of uh four. Um So, so this was just to give you an overall uh summary of what we've been talking about. Now, moving on to something that I haven't really focused on while we're talking about cardiac hemodynamics, valve disorders. We have aortic stenosis, uh aortic regurgitation, mitral stenosis, my mitral. So I'll just quickly put down here uh a quick overview of the valve of the pathologies that one could have and very quickly, we'll look at this and quickly go back to four. So, in aortic stenosis, when we have a narrowed um uh aortic valve, while we expecting, we're expecting. So, if this valve over here, you can see my point of that is then we're expecting that the blood flow here is going to be more turbulent and coming out at a higher pressure as well, right? And if that's uh happening, then what we will also expect is that the pressure in the um it takes more pressure in the left ventricle to push um blood out into the aorta um for the same stroke volume. So if you have a narrowed aortic valve for the same stroke volume that you're going to be pushing out of the aortic valve, you'll need a higher pressure to achieve that higher pressure. The left ventricle itself has to i it is basically like going to the gym for the left ventricle. But in this case, it's not very beneficial to the system because then you get um hypertrophy of the left ventricle and then subsequently you get dilatation of the left re cord. Ok. And um uh when that um occurs and has progressed for quite a long time, we then finally get the symptoms that we've talked about. We get dyspnea, uh we get angina and we get um syncope in some cases and we have heart failure if this is not treated. Um by way of aortic valve replacement, these patients have quite poor outcomes. Now, if we're talking about aortic regurgitation, it's the opposite of that. What is it? It's in, in this case, this valve has for one reason or the other become um does not close appropriately. And therefore, um post C you get regurgitation of blood blood back into the left ventricle which increases the overall end the study volume in the left ventricle. And when that happens, you start to get dilatation of the left ventricle which then increases the pressure in left atrium increases the pressure in pulmonary vasculature. In some cases, the patients have because of stimulation of the J receptors in the uh pulmonary vasculature, then that stimulates your medulla and Bogata tells you that you have to breathe. That's why patients have dyspnea. Um And then also because of the increased pressure, you have increased uh feeling pressures in your right ventricle in your right atrium. Uh And uh what does that lead to, that also leads to uh pulmonary edema and um worsens the um oxygenation of the patient. And therefore, we have the symptoms that we have written here in terms of uh dyspnea, angina or severe heart failure symptoms, mitral stenosis is very much the same thing as we've said. Um when you've got AAA narrowed mitral valve, you have the same situation where um you find it, the left atrium finds it's much more difficult in daly to feel the left ventricle. And therefore you have an increase in left atrial size. And that leads to all the, the, the sort of physiological changes that I've talked about going into the pulmonary vasculature as well. And then you have uh decreased exercise tolerance, exertional dyspnea over probably a longer period than you do for aortic stenosis and aortic regurgitation. And we can go on and on and on um with all these uh different disorders and symptoms. But there you can finally see how the uh uh an overview of cardiac hemodynamics helps us to understand better the um pathologies that we deal with on uh a daily basis. OK. So we're going to move to the last um physiological con concept, I believe I have only uh 15 more minutes. Um And this is uh cardiac electrophysiology. So again, just to go back to overview of what I've done, we've talked about hemodynamics. I'm talking about my electrophysiology now and again, I'll relate this to our clinical uh practice. Um And in module two, we'll be moving on into things like cardio because I'm sure people are going to ask me um uh questions about uh um you know, uh cardiac output and uh the autonomic effects on the cardiac system and, and deeper physiological um physiology questions. Um But I will follow this um model that is we, we'll talk about uh a key area and then I'll link that to all we do in terms of clinical correlation. OK. So summary of cardiac electrophysiology, we we're going to be looking at the electrocardiogram which a lot of surgeons hate cardiac action, potential conduction velocity, excitability, autonomic action and heart rate and conduction velocity. Uh this will, I'll say form the core um concept of cardiac electrophysiology. And if we then move on, um we're talking about this now, I think I've made a mistake by actually putting what they are here because you'll have been good to just quickly um refresh our memory on what these are. But um in the interest of time I wouldn't ask any questions, I'll just move on and uh uh provide the answers. So we have the classic P QR ST uh uh image here. And we can see that in starting off from P is, is, is our atrial depolarization. And uh it's that, which will be the P wave. And so what do we see on an ECG, why is the P wave important? Now in any left atrial enlargement, we do see an increase in the size of the P wave. Um And so this is something to just keep in mind. And then we talk about the pr interval, which is the initial declaration of the ventricle that tells us uh the tells us about av nodal conduction. And so if we're thinking about pr intervals, we know that the normal pr interval is anywhere between um uh 0.12 to 0.2. And so the question is if you have uh if it's much longer while we were concerned about, then we're concerned about some sort of A B block going on. Um We know that if we're then going deeper into that, if it's of the first order, then we are thinking about just a lengthened pr interval. And then if we're going into things like type two, then we're looking at whether or not the interval is lengthened and there's a drop in Q beat or whether or not we have um uh uh just drops in the QR beat without a lengthening in the pr interval and, uh so on and so forth, or if we just have a complete, um, uh, there's no association between the P wave and the QRS wave, then we're looking at, uh, at ventricle, uh, block of the third order as well. And so if we move into, uh, cure the QR complex, that tells us what the de, that, that's the depolarization of the ventricles. And um the uh it's quite interesting when we think about the, the size of it, the wider the Q uh complex, then we start to think about bundle branch block because uh widened QRS is telling us that the conduction is being delayed through the uh protein fibers. OK. And um we can then start thinking about what uh why we have either a left or a right bundle branch block. Um And if we have both of them in a patient, then we have a full atrioventricular block. And the question is, what are we going to be doing with our patient? And in that case, there's that will be when we're calling for pacemaker, put in a, a pacing system to help with, with, with our um patients, uh ensure that our patients is able to have a normal cardiac cycle. And then um this is an error. It's not ot but QT uh the QT interval is the entire period of the vaporization and vaporization of the ventricles um uh that's very important from a ICAL perspective when we're thinking about the effects of certain drugs. So, you would see that um, in a lot of cases or, you know, pharmacists will tell you that your, the medication you're about to prescribe. Uh you know, for example, if you're giving a patient, um uh Ondansetron or Cyclizine, which is an antiemetic and uh the patient is already on some cardiac medication. They'll tell you things like, oh, your QT interval has been, um, uh, increased and then they'll, you know, they're very concerned and why they're concerned. Does anyone know what happens when our QT interval is lengthened? Can anyone uh, post very quickly? Well, we can have an arrhythmia point. So, so that's um, one of the, uh, reasons. Yes. Perfect Emma. Excellent. So we can have that. Do you know what the treatment for that is? Well, we're going, we're going deeper, there's no real need for that. Um, so, uh, anyone know Dr addy some of the questions you're po actually all the questions you're posting are not related to our discussion today. Um, I, I'd really appreciate it if you either focus on the topic today or you allow those who, um, would like to answer some of the questions or ask the, er, topical questions to do so. Peace. Ok. So moving on, um, we're talking about S ST segment, uh, the ST segment shows the polarized ventricles and finally the T wave shows ventricul a now what's, what's important about the ST segment? Well, we all know about uh STEMI and we all know about N STEMI. And um you know, the simple thing to say is if you have a STEMI, you have a bad, bad, bad situation. Why it means that your um the whole of your myocardial uh uh your myocardium has been affected. Thank you for your apologies, Doctor Tally. The whole of your myocardium has been affected by whatever an ischemic event you are you're having. And that has now shown in problematic depolarization of your ventricles. Usually that show will show in an elevation of the S ST segment starting from uh point J which is uh usually about 0.01. If I'm not mistaken from that uh beginning of the um uh of the sy, I'll just put my pointer and you'll see quite an increase there in your um ST segment and that tells you um and then depending on your needs uh on your ECG I have not included. Yes, you do treat us side the point with magnesium. Excellent. And obviously, if the patient goes into VF um or VT uh and becomes uh uh unstable BP wise or has then gone into a cardiac arrest, you're not going to be using magnesium anymore, you're just going to be shocking the patient uh with a defibrillator. So well done. Uh Right. So uh talking about uh the ST segment um you, if you're looking at the uh different leads, so, um, uh, either V one to V six in, um, or you're looking at um, 123 or uh a VF um, and a VL you can, a combination of these leads will tell you, um, what, where your infraction has happened. And, um, you know, iii I wish I could, I could talk a bit more about ECG but I know when you start talking about it, you have to keep going deeper into the subject to um this is greater understanding. But the most important thing to remind you about is this is the um basic uh cycle and that denotes depolarization, repolarization. And finally, uh just uh uh some clinical correlates for you to remember why this is important. OK. Um So for this, I was hoping to go through 20 slides, uh 23 slides. Actually, I'm just on number 10. Um I have a hard stop for seven o'clock. So um we will continue this um next week uh Monday. Uh Well, that's if you all think this is useful. Um uh So just you, you let me know and you let me know also in terms of the information, am I giving? Am I giving uh too easy information? Am I giving? Uh um do, do I need to explain a bit more so that I do understand uh where, where to uh focus on uh um during my next presentation? OK. Finally, um everyone knows what this is, this is uh uh an action potential. But uh this is a trick one where, which is this atrial or ventricular, this picture I've shown. So, is this of the si atrial node or is this of the cells you would find in the ventricle? Does anyone know can anyone post? OK. So this is typical uh action potential that you'll see in the ven in the ventricles? OK. Yes, perfect it, right. So this will be a typical that you and I started to be the first because before talking about um the pacemaker cells, now I'll just want to briefly um remind you all about the most important thing which is, you know, the action potentials going on the ventricles because it's, it's the um contraction of the ventricle uh that actually then pushes um or should I say is the most important part of our cardiac cycle, right? So, um uh you remember that in the um in this action potential, we have, we always start off with the membrane uh potential, which is the equilibrium, which is always based on the resting membrane potential is um very close to the potassium equilibrium. Um And that is the flow of potassium is either into or or out outside the cell. Uh And so this is usually negative right now. Depolarization occurs when they, when, when you have AAA signal from the uh pacemaker pacemaker cells and then they um uh go all the way into your ventricle. What are they actually doing? They're stimulating um a rapid depolarization of that membrane potential, which occurs by moving that membrane potential from negative, which normally is an average of negative uh 90 minus 90 MNIT all the way to um uh uh the positive potential which is plus 52 usually on average. But the key thing here is that this happens quickly. That's the key thing about depolarization that it's happening quickly. It's not a slow process. That is this phase. Um And um this is caused by influx of sodium into the cell through the membrane which makes the makes it more positive. And then finally, you go into phase one, which is a transient um fight to get back into equilibrium. Uh And, and that is you have more uh positive irons which is potassium uh going out. And then what you then have is you then have calcium coming back in and saying, OK, no, even though potassium is going out, I'll come back in to maintain this potential, right? And that's where you get a phase two of your uh and that plateau. And then finally, uh we have uh depolarization, repolarization which happens when calcium stops maintaining that positive potential and starts to decrease and then the potassium current starts to increase as well afterward, current starts to increase, trying to bring that membrane back to its negative potential. And it's very important that he brings it back to phase four, which is negative potential. Because when it's repolarization, then you can have a further depolarization again, um uh of the cell. So this is how you get your action potential, which then leads to contraction of the uh myocardium. Now a very quick word on um you know, pacemaker cells. So we know that uh the pacemaker cells are fine in the S A node. And um the reason why this is the case is if you look at this and I don't know if I can um it's not very, you see that, see that now you can see that they are um constantly in um in a situation where they want to um where they, they're slight, they're less negative than your um ventricles and the cells in your ventricles. So they are that she the push to a positive potential much faster and the cells in your ventricle. However, one of the things that are very in um that's very important to, to remember is that when you have a situation where you have uh an S A node failure and where your pacemaker cells are not doing what they're meant to do. For example, any ischemic disease where you have problems with your right coronary artery, which has that small an artery that feeds the S A node just at the proximal bit. If you have proximal stenosis, then that means that you're more likely to then have problems with your sinoatrial node with your pacemaker cells. And what usually happens is you get sinus syndrome, you get bradycardia. Why? Because your sn node is no longer beating at that 70 75 80 BPM. And your action potential is now being driven by your ventricle, which is between 50 to 60 or um uh BPM. So then you have your AV node taking over um the pacemaker um uh function of the heart. So always remember that even the ventricles themselves can on their own um pace um uh uh uh be pacemaker cells in the event that there's a s sik uh sinus node. When your pacemaker, actual pacemaker cells are not um depolarizing as they should. OK. Um uh We stop here. Um And um II I, it just tells me that I will probably, we will start earlier next, next week because we will have some of the issues we had today and we'll uh just quickly go through um the last bit of uh uh uh so the last bit of uh conduction, excitability and autonomic action on the heart. And then I'll go into just discussing the clinical correlation with regards to the most important thing in surgery, which is putting our patients on a bypass, talking about drugs that affect cardiac potential. Uh I may if we have time to show a quick um uh video of a CBD circuit, we'll talk about cardioplegia which helps stop the heart during surgery and how it works by it, actions on the cardiac, uh, potential. Um, we'll talk about pacemakers, um, as well just very briefly. Um, and finally we'll talk about drugs that we use in ICU, um, and how they affect, um, uh, how they affect, uh, this, uh, prior sympathetic and sympathetic, uh, function. And, uh, finally we'll just go through a routine post operating management of the patients just, um, reviewing everything we've doc just, we've talked about in the last two slides. And then if we finish that next week and the family is kind enough or there's uh demand, then I'll move on to a module two where we'll go deeper into cards. Um Unfortunately, I can't take any questions today, but I do hope this was useful um uh for your, if you can give me some feedback. Now, I know how to tailor um uh the lecture further um next week Monday. OK. And if I me this is over to you, I'll stop sharing my uh slides. Thank you very much David. Um That was a very interesting teaching. I hope everyone um found it um insightful. And um so um as I said, the next um session, this modu two or the cardiac physiology be taking it next week, Monday. But before that, I just want to just make an announcement, there is the third session of the teaching which is already scheduled for Friday for Saturday rather which we um if you look through the C A um page, you see um you see the announcements the the session is already there, so you can sign up for that session. It's going to be on um aortic um disease and aortic surgery. So, um feel free to sign up for that. Um while we will be taking the second session of the cardiac um the second model for the cardiac physiology on Monday next week. So 15.