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Summary

This teaching session will give medical professionals a comprehensive overview of cardiac physiology, diving deep into the topics of hemodynamics, cardiac electrophysics, and ECG analysis. Led by Dr. David EK, this session will cover topics related to diagnosis and treatment of cardiac physiology and will include CPR and pacing in cardiac surgery. Participants will also gain an understanding of how to assess a patient's ECG in the pre and post op phases, as well as learn about the causes and management of various cardiac disorders. The session will be interactive, giving the attendees the opportunity to ask questions and learn from both the presenter and each other.
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Description

Fourth session in the teaching series, Basics of Cardio-thoracic Surgery.

Topic: Cardiac Physiology 2

Speaker: Dr David Ikenna, Cardiothoracic trainee, Royal Papworth Hospital, Cambridge, UK.

Time: 6pm

Learning objectives

Learning Objectives: 1. Identify and differentiate between the waves of the ECG, including P-wave, PR interval, QRS complex, QT interval, and ST segment. 2. Describe the importance of the various waves of the ECG in diagnosing cardiac conditions. 3. Explain the impact of the ECG on pre-operative and post-operative care of cardiothoracic patients. 4. Describe the implications of a prolonged QT interval. 5. Analyze and interpret ECG data to identify trends in patient health.
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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.

Good evening everyone. Um Apologies for the delay. Thank you. Yeah, no problem when you wifi, I switched to my phone out spot and brilliant. Could you tell me which hospitals wifi were you using? Um Royal Hospital in? So we'll contact them and we'll try and get them to disable that um for us because we're a safe website. But thank you so much. That's perfect that it's worked for you. Thank you very much. I'm just in the background. So if you need any help at all, just let me know. Um and then I'll help you out. No problem. Thank you. Thank you everyone for joining and um apologies for the delay in starting the meeting. Um We are 10 minutes delayed. Um So a bit of technical error, but we are um starting now. Um I can see that um about nine people are on the meeting so just start and others can join us um as as the meeting progresses. Um So, um this is the teaching series Basics of cardiothoracic surgery and today is the fourth session on the series. Um and it's on the topic, cardiac physiology. So, um two weeks ago, um the first, um the first part of the um cardiac physiology lecture was taken by doctor David Ek who has joined, kindly joined us today for the second part. Um So we will continue from there um Just to a brief recap on all these sessions we've done so far. So the fourth session about a month ago was on cardiopulmonary bypass. The second session on um the first part of the cardiac physiology, the third session on um aortic disease and aortic surgeries. And today we'll be doing the fourth session which is the second part of the cardiac physiology. Um Later on this week on Saturday, we'll be doing the fifth session which is on um arrhythmias and cardiac pacing ins uh and pacing in cardiac surgery. Um So if you are yet to sign up for that session, please do soon. So not to waste much of our time. I will introduce doctor David. I who is the um cardio training at Park Hospital and he will be taking us on this session. Thank you David for joining us. And yeah, thank you. Yeah, thank you. So I I need to share my screen, don't I? Um That's good. Ok. Uh Family. Can you see my street? Yes. Um Yes, I OK. And you can see the slides here. Yes. Ok, perfect, great. Um Good evening. Um Thank you for joining us today again. Um Last week, no, two weeks ago we went through, I'll just go all the way to the start. So, um I'll introduce myself a day to day meet, you know, me, I'm uh uh David EK. I'm a train Kio Kio Thoracic Surgery at Rotor Hospital and also the cof cof founder of the London School of Kio Thoracic. The School of Ky Thoracic is a surgical teaching center based here in London and connected to ST BA Hospital. Please just look, have a look at the website. We have lots of courses that we are doing if you're within the United Kingdom and soon we should be taking this out of the country. Um Moving on from that, um, last week, we decided to tackle cardia physiology. And as I said to the family, the important thing for me was not to regurgitate the things that we could learn by picking up a textbook or at the same time, none of us can compete with a cardiologist with regards to um having any sort of discussion on cardiac physiology. But then I thought that we could approach the topic looking at it from the perspective of a surgeons, er, need for information and er, cardiac surgeons are probable cardiac surgery is one of the few specialties that needs a very strong medical foundation and medical knowledge. And therefore, what we've been trying to do with these sessions is to think about cardiac physiology while we are looking at our patients in the pre op stage and then the POSTOP phase as well. And so we were tackling each aspect of this with regards to disease physiology, operative physiology, POSTOP and complications. So at every stage, as I have shown in this slide, we are always thinking at the back of our minds, what is the heart doing? And if we know what the heart is doing, then we can intervene appropriately. Right? And so brief summary, we went through hemodynamics and uh related all of this to disease and um vela disorders and so on. And um I think if I'm not mistaken, and if only we stopped somewhere at during the cardiac electrophysiology slides. Um and I believe that I started to rush through um the slides because I was hoping to finish the lecture on time. However, if family was kind to say that we could have another week to finish these full slides before we even attempt to go into mole two. So um what I will do is to go through the slides again um very briefly and at the same time, um starting from the um from here, summary of cardiac electrophysiology. And I can then um proceed towards the discussion in terms of applying this to disease physiology, applying this to pre op POSTOP phase and also complications as well. And see if we can have a useful discussion on this. I'll be asking lots of questions during the lecture because I believe that we should be having a discussion. And um we're not, um you know that no one is er, repository of knowledge. So I'd also want to be learning from you as you're learning from what I have to say in these slides this evening. Um Is that OK in for me? Are you happy with this? Yes, because I'll be proceeding to start now. OK. So we definitely covered the hemodynamics in great detail, but I do remember I started to rush and I've just gone through this. So I'll start again from the slide and um I'll go on to talk about when we're thinking about card and the physiology. We're thinking about the current, what's going on with the, the heart is the um is it works, the foundation of how the heart works is action potential, isn't it? So how have we, as humans decided to observe what the heart is doing? And so we'll start off with the ECG and I think there is going to be a lecture on ECG if I'm not mis mistaken. So we wouldn't um waste too much time on this. But this is a summary of both phases of the heart. So, depolarization and repolarization. And we see that the, if we're looking at, I'm just going to pull my cursor. If we're looking at that, we have the P wave which usually is um denotes depolarization across the ARA and we have the pr interval which will show the initial depolarization of the ventricle. OK. And we'll then look into the Curis complex which shows the depolarization of the ventricles itself. OK. So the pr interval is showing us the um a V normal conduction. Um And this is important because if we do remember, what is the, can someone tell me what is the sign on an ecg of a first degree heart block? And hardly can someone post here on the chat? What is the first sign of an av uh a heart, a heart block of the first degree? Does anyone know what will be the sign on an ECG you fe me? I presume this is working, right? The chat system? Perfect, prolonged apr interval. And can you tell me please how long that will be? Not, no, that will be 0.2. OK. So that will be 0.2. OK. Not 0.12 was 0.2. OK, great. So, um well done everyone. Um So that's, that's, that tells us so on an ECG if we see a long P interval, which is greater than 0.2 then we know that that patient has a problem with their conduction system and that will be the AV nodal conduction system. Now, the QRS complex um shows a depolarization of the ventricles. A widened QRS complex tells us that there is a problem as well, right? And so, um usually we would say that um and this is where um you have the 0.12 that you were talking about. But that will be in terms of the number of boxes that you will take on the normal ECG. So if you remember each ECG box on the 15 millimeter ECG machine slide print out is 0.04 seconds. And so you're always expecting your QRS to come, this QRS to hit a maximum of three boxes. If it starts to go wider than that, then we're thinking about a widened QRS, a widened QRS fast to let us know that there's a, there's a problem with the depolarization across the ventricles. It could be that we have hypertrophy. It could, it could lead to um a lot of questions, it could tell us that we've got a bundle branch block as well. Um And so moving on the QT interval is the entire period of de and ization of um across the ventricle. So we're talking about your heart is depolarized in the phase for systo and now is going to die and is repolarization at the same type. So in, in the QT interval is giving us AAA good. Look at that whole process. Now, we know that if we have a prolonged QT interval, then that could be dangerous. And you'll also see that very, a lot of medications that we give come with a lot of warnings about QT intervals. Why? Because if we have, and I think I mentioned this last time, so I'm not going to do too much about it. That qt interval that is prolonged could cause us to have to side the point. And usually the uh to correct this will be given a magnesium infusion. Now, the part of that we are most concerned about in um our surgeons is the ST segment. All right. Um Now, the ST segment would always be something that we're looking at on an ECG if we've got an is patient. Now in the pu stage, obviously, if you have a stem, which is an elevated ST segment that telling you that you're having myocardial infarction going on, or you could have an NSTEMI, which, which is also myocardial, in fact, that does not um portray this elevation of the segment, but could also show us things like a depressed ST segment or a peaked T wave. And obviously, with the clinical signs of chest pain or shortness of breath or fainting or syncope and then having your troponin, which is higher than normal, depending on which troponin you're using. If you're using Troponin, I or Troponin T that gives you an idea of whether or not your patient is um having an ischemic event. So an ST segment is something that we pay close attention to. Now in the postoperative period, if you look at an EG so you have a patient who has come in and you've done a nice uh um you know, graft to, to the um the Lima to lad, you've done another graft to the second flex and maybe one more to the diagonal, the right coronary was fine. So you didn't touch it and you're really happy with your case and you, you're really happy with your case and you decide that you are um now going to um your patient is in ICU, you've extubated um day one, you appear and you open the, you ask for the ECG in the morning and then you then see that this patient who had come in previously with an NS sty. And so there was no elevated ST segment. But now you see that as global SD segmented ra are you taking this patient back to theater? What's your concern? So every single um need of the ECG is showing an elevated ST segment. Can someone tell me what they'll be thinking when they see this? Anyone and anyone answer the question I've asked. So now you've got uh an elevated SD segment across all leads. What would you be thinking about possibly on day one, usually day two, you, you see this sometimes. So this is a patient. You've done a beautiful triple graft on any ideas. Would you be taking that patient back to theater? No. OK. Why not? Sure kids? OK. If you have global SD elevation, um you're thinking of pericarditis. OK. So you wouldn't be taking your patient back to theater because a global ST elevation will be um pericarditis. OK. So which is quite normal after surgery. However, if you have new ST segment elevation in any other lead that was not present in the pre OP BCG, then you're sending your patient to a Cath Lab because you want to check if you've had graft failure. And we know there are many reasons for graft failure in a CBG patient. But you have to, you have to have this at the back of your mind. So this is you as a registrar, seeing your patients in the morning, you pick up the ECG. It's always very important to look at that ECG and compare it to the pre op ECG. So you'd always request for both ECG S and then you have to look and see where's the dynamic. OK? If you see a an ST elevation in one or two leads, that was not there in the pre op ECG, you have to look at your patient and think very carefully. Maybe I need to send this patient to the cat lab. We need to have a look and see what's going on if you and especially also if the patient is still a lot of infusions and struggling to be weaned off the A and re know and so on and so forth. But if you see global ST segment innervation, you're not concerned anymore. OK. That is pericarditis and that usually resolves after a couple of days or weeks. So, um this is why the, the knowledge, this knowledge is very important you know, to, to have that in mind. And finally, the T wave ventricular repolarization, I always say T wave is very important because um you can, it, it gives you insight into multiple things. If you've got a peaked T wave and you have chest pain, that is a sign of angina. You want to be um checking that patient very carefully. If you've got a peaked, very peaked T wave with a flattened pe uh wave as well. You're thinking electrolyte disturbance. So you're thinking high potassium, OK. And this is something you would want to be care. You know, if you think you have a patient who has gone through surgery who may or may not have or most likely has renal um chronic kidney disease. Um So they are quite susceptible to having um electrolytes disturbances. Now, usually we want to keep the potassium between 4 to 5 for our patients. However, we don't want you to start going above five, right? So the ECG is also apart from your multiple um investigations, your bloods, your abgs and so on. The ECG is also another way to look at um whether or not you have a problem um with regards to your electrolyte disturbances and that a PT wave would give you that idea in the post operative period in the preoperative period. It gives you an idea of whether or not you have ischemia going on. Ok. And negative T as well is another um uh that is when the T wave is still being positive flips down is negative, that also gives you some insight into um ischemia as well that should be investigated. OK. So this is the, we're not going to spend too much time on ECG because I'm sure there's another lecture for it, but this is an overview. OK. And there's a method to my madness today. You'll see why all this information will come to play as we go further in the slides. OK. Finally, um secondly, we'll go into action potential. Now, most people um hated this in, I hated this when I was in medical school. I hated to remember all of this. And so I have been very kind to just list it out and not start questioning everyone on what phase 01234 is. Um I know some of you do remember. I know some of us don't remember. Um But I will take my time to explain this, but there is only one question. I want to ask this picture that I've shown. Is this for a normal cell, cardiac cell or is this for a pacemaker cell? So this um picture graph I've shown for cut it potential have a look at the answers. Anyone know I'll show you the picture again one more time. OK? So the normal cardiac cell in the ventricles. Perfect. OK. So this is that is what I'm showing to you. OK. And so that means that the pacemaker should have a different picture. And I'll show you that. So we'll start off by talking about this, what is going on in when a cardiac action potential? So we know that festival across the membrane at equilibrium, which is the equilibrium of potassium, the potassium channel, this is a minus 96 millivolts. OK. So that is, we're starting off from here. Now, when you, it receives the impulse you have what you have is you have sodium channels that start to open. OK. OK. And there's an inward current of sodium channels to make the membrane more positive. OK. Now, it is important that this is happening at minus 96 because sodium channels will not open if it's not this negative. So if this was at minus 50 you will not have sodium channels opening up and the influx of sodium irons across the cellular membrane. So at this value at minus 90 they are activated. And then what you have is a very quick. Um and in this case, de delation, right? And you get to the membrane becomes positive at 52. And again, this is a sort of an average value across all the cardiac cells that you look at in the ventricle. Now, at this point, you move on to phase one. What we then have is the potassium ions um starting to flow out of the um membrane which is the brief period of repolarization. OK. Now what is happening is that the cell is now trying to reverse back to normal. OK. But remember this is the ventricle, we're talking about the ventricle needs to contract for quite a long time. So, um and that is because it needs to push out all that blood that is receiving, it has received endosy, he needs to push our old up the um the systemic circulation. OK. And so biology then thought, OK, what can we do to prolong that phase? OK. We don't want to go back into, we don't want the heart to repo immediately. And so you then have calcium margins now coming in because he wants to keep this potential going. OK? And so this is phase two. OK? And that's why we have this plateau. So that is the logic behind it. It wants to keep the calcium ions are coming in to keep the membrane more positive to continue that action potential. OK. And then finally, in phase three, we then have multiple potassium channels um opening, you have the slow, delayed ones, you have the rapid, delayed ones. And, and that's all fancy stuff for the cardiac electrophysiologist. What we care about is that we know that potassium is now leaving um and this is in order for the um cell to revert back to its negative um the negative potential across the cell of the membrane. OK. And so there's an in for that phase three, what you realize is that the calcium channels stop, start to slow. OK. And nothing ever happens in the heart immediately. So no, nothing's ever happening like that in a cell. It's all relative movement. So the the the conduction of calcium decreases, the output current of potassium increases. And then you have that uh the resting membrane potential across that membrane. Now reverting back to normal which is minus 96. Now, it is very important, as I've said, for you to go all the way back to minus 90 because once it hits minus 90 then it allows the sodium channels um open up again so that they can repeat another action potential. Ok. So this is a summary, a short summary on this aspect of the cardiac electrophysiology. Now we're going to talk about why every aspect of this is important and why this knowledge is important. Why? Because all the medications we use in cardiac surgery or in the post operative in the preoperative intraoperative postoperative period for different forms of treatments all have used, they act at different sites, right? So it's either you have heard of, you know, medications called sodium channel blockers, you go head of calcium channel blockers, you have head of potassium channel blockers as well. And that is the whole idea. So if you have the knowledge of the action potential, you're thinking about it from the point of view of what it's doing to the ventricles and the heart, how the ventricles are responding um, physiologically, you then have a better idea of why you're giving certain things and why you're giving certain medications or what is the right medication to choose in you at the appropriate time? Ok. And we'll quickly talk about that. But before we do that, um, I decided to then test since you all know that that was not the graph for, um, for the pacemaker. I have now included one for the cardiac pacemaker cell. OK? But I have put no markings. So can anyone now that I've jiggled your memory? Can anyone tell me what are the phases for cardiac pacemaker cells? So here you have phase 01234. OK. For cardiac pacemaker cell, what is it? How many phases do we have? Just post quickly? You don't need to tell me about it. Just tell me how many phases we have and that's all OK. I'm waiting for an answer guys. OK. Three. Well done. Can you list them out for me? Yeah, that to up here. OK. Crista. Yes. OK. What else? OK. We always know that there's a depolarization and uh uh repolarization but well done. We we you have done really well. So I'll go back to this. OK. So what is different about a cardiac pacemaker cell is that you only have three phases. So while we're here, we talked about having um 01234 in the pacemaker cell, you only have phase zero. You have phase three and you have phase four. OK. And the idea for this is because, and I'll go back to Z that if you look at that, this is a slope, right? This is the fourth phase. And the reason why we have that in the cardiac pacemaker cell is that remember that it's constantly depolarizing. So instead of having a trigger like the ventricle, right? Because the ventricle has to contract and then relax Indy to receive blood and then insisted they contract again to push that blood out and then rep polarize and rest. OK? So that's what the ventricles will be doing. But the pacemaker cells, they need to constantly be providing impulse, OK? You need to be providing impulse to the heart to say, OK, this is the, this is um we at rest, we need to maintain 60 to 70 to 80 BPM depending on your how physiologically fit you are. And so you need to go, we are sending an impulse now and then another impulse, then another impulse. OK. Right. And then if you are having some sort of um in, in increased activity exercise or whatever it is, the pacemaker has to then go faster. So you need to um carry out that impulse faster. Therefore, it has to have a different physiological mechanism. And so the summary of uh cardio pacemaker cell is that the action potentials are generated spontaneously within the cells. OK? Um They have a constant resting potential that is steady depolarizing. So, and that is what you can see in this um in here, right? OK. You can see that here. And then finally, what we want to see is that they are also the fastest pacemaker cells will normally be the si atrial node. Now, can anyone tell me which other two aspects of the heart will have um has the ability to perform pacemaker pacemaker function, which of the two sides? So I've talked about the se node, the se node is the one I've just talked about. So where else the A V node? And you're right, pa the AV node is one. Yes, the broken system perfect, broken five is excellent. So they also have pacemaker potential and why they have that is because if you have a problem with the se node, then they will take um they can also have a steady depolarization potential which then takes over the pacemaker function of the heart. Which is why when you have a patient who you've brought out from theater and you've put a pacing box. And then you said to your um registrar, the consultant says to you um I want you to leave this box on a backup mode. OK? And then you have the heart rate of the patient at 80 or 90 BPM. And then suddenly you get a call from the nurses. Oh, my patient was was, you know, the the heart rate was at 90 but now it's at 50 or it's at 40 right. At that moment, you're running back to have a look at the pacing box and to make sure that the, the pacing box is working. And um at this moment, what you know is that there's a, an A V conduction system, um has, has take, has had a problem. So there's an AV block, right? So the normal pacemaker activity of the heart, which is a sign the atrial node should not be giving you a heartbeat of 40 or 50 right? That is something that you'll find if the A V node has taken over that um uh job. OK. And that is obviously not enough to maintain adequate cardiac output. So then you are then fiddling around with the pacing box to make sure that you have um that now if you apart from this, if you have other drugs, you know, something like beta blockers can obviously suppress the rate of the um action potential of the pacemaker cells. So, in the S A node that is possible. Um but the doses that we give, you should not be seeing that go below 55 to 60 right? If you are giving your patient beta blockers to the point that they're reducing their a suppressing the S A node to 40 BPM, then you're doing something very wrong. OK. And very quickly, what we're talking about here is that the resting potential is at 60 you have a slowly steady depolarizing potential that goes in here. And then here you have the I furry channels just in this upstroke, they open up and in the same way that in the ventricular cells, they have an inward current. That's the same thing that you'll have. Here, there's an obss stroke of activity and then immediately after that upstroke of activity, then you have the potassium channels also doing their bit with um moving out of the potassium current increasing quite much more faster than you would have had in um in er in the ventricular cells. Why? Because you don't have phase one and phase two anymore. So you don't have calcium channel, the calcium inward current going on to elongate that potential. So you'll have that reach a post of 10 and then finding you have potassium um leaving the cells to then repo this membrane and get it back to minus 60. And that's really simply how this is um how this occurs. OK. So this is a brief anatomical picture of the heart showing the sign the atrial node, showing the AV node showing the right bundle branch, showing the left bundle branch and then the two divisions, um the left anterior and left posterior divisions. OK. Now, um talking about cardio regulatory centers and chemo receptors in the middle of it. This is uh one other thing to think about why because our sympathetic and parasympathetic nervous systems will do impact um the heart, right? And, and if we're anxious, we do find that our hearts are beating really quickly when we're at rest and we're very calm and, or we're meditating, you know, we find that our hearts um rate also slows down. So it's important to remember that um you have, you can have not just a subconscious or well not subconscious and unconscious control of the heart. That is when you're just not you, you're not doing anything about it, but you can also have a conscious control of your heart as well. You can get yourself into panic and increase your heart rate or you can make yourself calm and reduce your heart rate. Now, how is the heart doing? How's the brain and the heart doing this? How, how are they connected? So we, we have baroreceptors in the internal walls of our carotid arteries and we also have chemo receptors in the carotid body. OK? And the sensory fibers that, that are there that measure things like output. So if your cardiac output is not sufficient, so let's let's imagine the hypothalamic patient. Ok. The hyperkalemic patient does not have enough cardiac output going into the aorta. So the um the baroreceptors in the internal carotid artery find that the pressure that he is going through is just not the normal pressure that the body is used to. And then that sends an information to the brain and the brain, you really is feeding that back to the heart and saying, OK, look, I want you now through the sympathetic level fibers, I want you now to what I want you to stop pumping faster. OK. And uh the same with the and so you have the sympathetic fibers and the sympathetic fibers all feeding the S A node and feeding the heart as well as you can see, the sympathetic nervous system is not only just feeding the S A node, in terms, it's also feeding the, the heart as well, the heart muscle, which is also trying to give, which is um uh an important concept. So you're not only asking the heart to, you're asking the pacemaker cells to do their job faster or to slow down depending on if we're in our flight mode or flight or fight mode or if we are in our rest mode. Ok. And finally, we also have some level um fibers that go to the adrenal glands and the adrenal glands will release um epinephrine and norepinephrine. And what is the adrenal medulla doing this for? Well, if you have a situation where you have uh hypovolemia, uh what is the point of releasing epinephrine and norepinephrine because you want the heart to beat faster? Because again, you're trying to maintain cardiac output. Cardiac output is a function of heart rate times stroke volume if you remember that. So how do I improve cardiac output? If there's any problem with the heart, I can either increase the heart rate or I can increase my stroke volume. Now, what is my stroke volume dependent on my stroke volume is dependent on the preload or the afterload. So if I, if I decide to and what is my preload? That is the volume that is coming into the heart? And what is my afterload is the resistance that the heart is going to face when pushing out that volume into the second atrial system. So what my heart is thinking about and then also at the same time, there's also Frank Sta forces that is the contract contractivity of the heart. And, and, and if you remember it's all about stretch, the more you stretch your muscle fibers of the heart, the more you're getting a a stronger contraction. However, there's always a limit to how much that stretch will go and that stretch will lead to a proportional um increase in the force of contraction. Ok. So if you have that in mind, you automatically understand why the brain and the heart are connected in this way. So I give you a patient patient is hypovolemic um uh bleeding on the table while, while you're doing the operation, while you're closing. So you finished the patient is off bypass now and immediately you realize that you've come off bypass and then the BP started to return. And one of your grafts, unfortunately, it was done by maybe a junior member and these patients have started to bleed profusely. And while you're doing that, you're asking to give blood products wide. Because at that time, you're going to realize that even though you're coming off a rest, you're going to see that the heart rate of that bleeding patient is going to go up. So the brain itself is going to start doing things for you um that you um uh you can, you as a surgeon can control, right? So the and it it starts beating faster. Why? Because the heart is trying to compensate for that fall in cardiac output. Ok. The same thing with a patient who is um POSTOP and is on um ICU if they're bleeding, you're going to see that they become tachycardic. And that's because the brain is asking the heart to beat faster. Because why in that equation if I increase my heart rate, I can increase my um cardiac output. Now, what else can epinephrine and norepinephrine do if we're looking at the afterload, if I can squeeze vasoconstrict um around the body, then I can ask the heart to pump more, right? Ok. I can increase the BP and if I can increase the BP in the system, I can increase the perfusion pressure across the different organs. Ok? And that is why we have epinephrine and our epinephrine being released into the system. And then if I can ask the heart to fill more in preload, then I can ask the heart to pump more as well. Ok. So these are some of the ideas of why the brain and, and um has um is connected to the heart in this way. Ok. So now that we've learned all of this, um we'll now talk about the useful, why is this useful to, to us? So, drugs affecting cardiac action potential for sodium channel blockers. The most important drug here is for the kind, a lot of the medications here we did not use. Um again, so we don't use quiNIDine as we used to proin is um is uh has sort of been reduced in terms of its, its use. Lidocaine is rather used as uh um is rather used as an an anesthetic, a local anesthetic aesthetic. This is why also when you're given local anesthetics that is lidocaine as a local anesthetic to reduce pain for any um procedure that you may be conducting. So this could be putting in a central line or putting in an arterial line depending on the pain threshold of the patient. There's a certain amount of lidocaine per kilo that an anesthetist must give. Why? Because if you start going above that amount, then you're more, you're very likely to suppress the sodium channel and you can actually cause a cardiac arrest and this is why. So this is why it's very important to keep that in mind. And if I'm not mistaken, it's about five mgs per um kilo, that's the um maximum lidocaine amount that you can give for a local anesthetic. And if you, um, and that can slowly go up to seven mgs, if you use the uh the medication, the lidocaine that has a bit of um adrenaline infused into it. So there's a mixture of very weak. So that, that helps um negate some of the suppression activity on the sodium channel. Um So this is just to keep that in mind. Um the going need to be used as a pill in the pocket. And we normally use that in patients who have got paroxy or af. Um and if a patient who has got paroxysmal af and maybe has a F and goes into atrial fibrillation every now and again. Uh then you can, and you can give them the pin in the pocket. So they hold that and when they start to feel that the palpitations they take it. Um And its method of action is um is a sodium channel blocker. OK. So we move on to class four, the class fours are the calcium channel blockers. So we have verapamil dilTIAZem. Uh these are mostly BP drugs. However, dilTIAZem is also used for vasodilation um in so I'll first of all focus on it as a channel blocker for BP and I'll focus on it also uh as a um me mechanism for vasodilation. So in as a channel blocker for a lot of hypertensive patients we use um verapamil and dilTIAZem. Um And the idea is that if you won relax the, the, the, the, the you can slow down the heart rate. That's number one and number two, you can also relax the um the force of contraction. Um And this is the idea of blocking, you know, having channel block. Um calcium channel blockers, you also have amLODIPine, which is also a calcium channel blocker as well. Um being used in hypertensive patients. Um and dilTIAZem has also found use in radial artery grafts. So, radial artery grafts, as you all know, um smaller diameter can still give you the same benefit of a Lima but is very prone to vasoconstriction. And so um these patients then end up having dilTIAZem um 90 mg BD. Um if you've done a full arterial revascularization and then using a radial artery graft. Um And so that's another use for that uh potassium channel blockers. We've got amiodarone, a sotalol. Everyone knows about amiodarone. It's the thing that we love when we have patients in A F, especially if this is a patient who has had new postoperative. Um af you're starting them on amiodarone infusion, you start them off with um between the 300 mg stat and then you continue a 900 mg over one hour and you continue with a 900 mg infusion over 23 hours. So they get a maximum of 1200 mg of amar on over 24 hours. And you're hoping that when you give this to them, they revert back to sinus rhythm. And now when you think about it, you know that the reason why this is happening is because you are giving them a potassium channel blocker which should sort of um help uh flip the heart back into sinus rhythm. OK? And then finally, we have uh a class two drugs which are beta blockers. And we can see that um propranolol metoprolol beta blockers have a huge range of au not only are they acting on potassium channels and they're called potassium channel rectifiers, please ask the cardiologist why they name it that way. Um but then also they affect the the nervous system, right. So the beta blockers also affect the nervous system and they help reduce symp sympathetic um activity or modulate parasympathetic activity as signals to the heart, which um usually ends up with um controlling the heart rate, suppressing um the pacemaking potential of the heart and also reducing force of contraction. And this affects things like BP. Ok. So if you're hypertensive relaxes the heart and enables the heart to feel better in the study. Now, when you the heart is feeling better in das study, because there's more of a prolonged heart rate, what's happening is that you are also feeding the coronaries as well because the heart feeds itself. So the coronary arteries gets um are perfused during dias study, right? So the longer your dias occurs, the longer your coronary perfusion occurs, which means that the myocardial oxygen demand is met. And this is how you affect ischemia. Ok. So, by improving coronary perfusion in our study, by allowing the heart to relax and feel properly, you allow the heart muscles get the oxygen demand or the the oxygen demands, you ensure the oxygen demands are met. And this is how you enable the heart to work appropriately. Ok. So, as you can see, knowledge of all of these that we've talked about then gives you a clearer picture of what the drugs we give are actually doing. And now we go into my favorite aspect and I've just realized that it seven o'clock um cardiopulmonary bypass. Ok? I really wanted to play a video but I know that your family has told me there's going to be electron on cardiopulmonary bypass. So we're not going to talk about cardiopulmonary bypass, the circuit and so on. But the most important thing that I want to peak out here is you all have um for those of you who have done surgery, you know that, so we cannulate, you have venous cannulation. Um There's a venous reservoir and by gravity, blood is um sucked out of the um body into this venous reservoir. It goes through all the heat exchanges oxygenator and it goes, which the oxygenator acts as the lungs of the artificial lungs. And you, you then feed that back into the arterial field, back into, into the system, back into the aorta and into the systemic circulation. So you can perfuse all the other end organs in the brain. While the heart, you have a blood less and mua less field. So the idea of cardiopulmonary bypass is to ensure that you can work on the heart and still perfuse the rest of the body. But while you're working on the heart, the heart is um not moving and the heart is there's no blood in that um in that field. OK. So the, the most important thing here that I want to talk about is cardioplegia. OK? So card diplegia is the way that we stop the heart. And um the, so thinking about cardioplegia and I've brought that back again. So if you know your knowledge of what we've talked about, give you an idea of actually why, how cardioplegia works, the cardioplegia has a high potassium concentration. OK? And so when we give cardioplegia in surgery, we are causing an increase in the extra cellular potassium. OK? Which means that you still have depolarization go on and you have repolarization go and but when you start trying to rep polarize the heart, so you have this plateau here in phase two. But when, which you remember is calcium coming into the um cells, OK? And trying to elongate that depolarization. But when you get into DATO, which is repolarization, what you then have is because the cellular membrane potential is much less negative, right? Because you have all this positive potassium ions in the extracellular matrix. The heart then arrests here in DATO. OK. So they how to arrest endosy and it cannot rep reporter. Why? Because you cannot, it does not reach the minus 90 mini volts that should instigate sodium channels to open again. OK. And the key thing here is because you're arresting the heart in dy, you're not using A P. So then you don't, there's no oxygen demand, the heart stops and then you can work on the and sodium channels are inactivated and then you can work on your heart um for as long as you can. Now, this is obviously, as you're performing surgery, it will wash out of the system and you would have to give it antegrade or grade as the case may be, but you'll have to keep giving um Caia and um at various points intermittently during your um surgery. OK. And uh the other thing to do is you are cardio is normally given cold. Most people prefer to give it cold. Why? Because if you give it cold, a hypothermia means that there's a reduced metabolic rate of the tissues involved. OK. Pacemakers. Now, you, we've talked about, remember when we talked about the um uh the anatomy of the pacemaking, the S A nodes, the AV node, what does the pacemaker do? The pacemaker is only substituting the function of the um of the pacemaker cells. So if your sign atrial node has a dysfunction, then your your pacemaker can uh come in and do the job for you. OK. Now again, you feel me has let me know that there's going to be a lecture on pacemaker. So I have decided not to go in depth. It's a topic I like. And so I kind of act lyrical about this for as long as possible, But I will just say that very important to remember for pacemakers. While we thinking about, there are three positions that are important to us as surgeons, we don't really care about the 4th and 5th because that is what the cardiologists care about. But there are three positions to remember and there are three modes that are important for us. So the best letter in a pacemaker mode is tells you the chamber that is being paced. The second letter tells you the chamber that is being sensed. The third is what the pacemaker will do when it responds to that. So if you have a A I, it means if you've ever seen a mode or a consultant has told you, I'd like you to um put this pacemaker on A I mode, what they're saying to you is they want the atrium, they want the atria paced, they want the atria sensed and when that is sensed, the pacemaker will inhibit its activity. Ok. So when would we use an A I mode, we'll use an A I mode in the sense when we have a patient who has come out of a nice triple or quadruple bypass. And you are quite fairly certain that the A V node will not, you've not done anything to the AV node, you have not been naughty at all. Um And so, um and, and you're only pacing the patient because either they have um it will take time obviously with local information and so on and so forth or if they have the right coronary issues there. So they may have some sort of sinus node dysfunction. And so you would want to give them an adequate heart rate, which is anywhere between 80 90 BPM. And you also want to ensure that they have a good cardiac output. Remember I told you cardiac output, it's heart rate times stroke volume, right? So in order to pae them, um artificially, you put them on 90 BPM A I mode. Um and this tells you that you are your atrium is your both atria beam paced. The um both are also being sensed. Why are they being sensed? If, if for example, the intrinsic activity of the heart recovers after 24 hours and starts to outpace the pacemaker, you want the pacemaker to stop, right? You want the pacemaker to stop its activity. Why? Because if the pacemaker, it continues its activity when the heart has recovered its intrinsic function. You can have something called the A T pheno phenomenon where the pacemaker is given an impulse um on the T um the intrinsic activity of the heart when the heart is wants to relax and that can cause ventricular fibrillation. OK. So, just to keep that in mind. And then, um so we're using this um A I mode is normally used. When you think there's a bit of sinus node dysfunction, you want to uh make sure I ate output and you're very certain that your A B node, there's no problem with your A B node or conduction system. OK. If you, then you have VVIVV, I is the same thing. I is the same thing, but you're talking about a different chamber. So you're talking about the ventricles. So you're pacing the ventricle, you're sensing the ventricles and your response to the ventricles is either to inhibit A written T here. T also means tri guide delay. OK. And trio delay means that the pacemaker itself is going to pause for a while and decide whether or not it seems sees that there's intrinsic activity in the heart going to happening. And then it would based on that information, decide whether or not to provide some impulse or not. OK. And then you have the dual mode DDD. This means that you are pacing both chambers. So the atria and the ventricles, you are sensing the intrinsic activity in both. And then when you do your response to sensing is either to inhibit or trigger a delay in both chambers. OK. So this is the simple concept of uh pacing. All it's trying to do is replace the function of the sinoatrial node. Or in the case may be to do that um replace the AV node as well. You've. Um And so when do we use VVE, we use VVE as a back up if we think our patient is going to flip from atrial fibrillation back into normal rhythm, or we also use it in the case where we think, um, when we think that we may have a problem with our AV conduction and we want, we want the heart to be protected. So we know that I'll give you an example. Your patient has come back from theater and this is day one has gone into a AF and you start an amiodarone infusion. Now, remember you're giving them both amiodarone and beta blockers and we have just said to you that amiodarone is a potassium channel blocker. Beta blockers are also rectifier, potassium channel rectifier and can have blocking activity and suppress the pacemaking function of the heart as well. So you're given three, you're giving two medications that have those activities on the heart. So what are you going to be doing? In this case, you want to protect the, the patient? So when the in A f your problem is not the heart rate because um is, is sending about close to anywhere 300 BPM. When you get to the AV node, it slows, it's halved. And so what you see is uh the heart is, is, is, is um the, the heart rate is going at about 100 and 50 BPM. But then you give Amarone and that can now flips that back into sinus rhythm. However, because you're giving amiodarone beta blockers, you can flip it from sinus rhythm into an AV conduction block. And if you do that, if you're pacing the heart at A I, the heart, the ventricles will not receive impulse. And so what you'll do when you put it on VV R, you'll put in a backup system to say, OK, if my heart flips into a um a heart block, a complete heart block, the heart is protected and the V VR will ensure that some impulse is provided to the ventricles way to work. OK. And then DDD is a dual mode which basically helps you coordinate the function of the atria and the ventricles together. Why is it important if you're pacing the atria and the ventricles together at the same time, you are, you have the best protection possible. But also in patients who have a cardiac problem, you get that 20% atrial kick that you can give in atrial cysto. OK. And so you are improving the output and this can be very dramatic. Also, you're improving the coordination between the atria and the ventricles of the pacemaker itself of the pacing box. Why do I say that you can set AD DD mode in such a way as to ensure that if the Atria, if it gives an impulse um to the Atria to, to then push that impulse all the way into the ventricle system, you can program and delay when it gets to the A V conduction system and say, OK, you know what the pacemaker, I want you to have a prolonged um P I interval of maybe 240 or 250 milliseconds to give the heart enough time. So if the heart is starting to recover its own function, it can bring out its own intrinsic ventricle activity. And this is why we use DDD. So this is just a brief summary of uh pacemakers. What I'm talking about is because I have talked to you about cardiac electrophysiology and this is the application of it um in our work as surgeons. OK. And uh how many slides have I got left? OK. So I'm not going to waste too much time on this. But we know um because I'm going to talk again about this when we go into cardiac output, ICU and so on and so forth uh next time. So I will jump, I'll do a deeper dive. But we know obviously that there are different receptors in different aspects of the um vasculature and um our end organs as well. And we know that there are medications that we use norepinephrine, epinephrine, dopamine vasopressin. And we'll be talking about those in terms of the infusions that we use next time because next time I'm going to focus on cardiac output, all the um lovely formulas we have. Um, and we'll, that will be module two. Ok. So this was just meant to sort of introduce um uh the concept, the use of dobutamine, dopamine, epinephrine, norepinephrine in the um cardiac patient. And so we know that their visa constrictors, there's NORAD, there's vasopressin, we know that there are inotropes, inotropes like phosphodiesterase inhibitors know um what do they do? They improve cardiac contractivity, but they also have vasodilatory effects. Adrenaline does everything. It's um it's a, a horse weep and the horse is the heart, adrenaline is the whip and it whips the heart in so many ways to ensure that it can provide output. But then it's not without significant side effects and complications. OK. Now, this was my last slide before we go into the next aspect of our lecture next week, um where I will finally talk about cardiac muscle, cardiac output and that will finish off this whole series on cardiac physiology, the routine postoperative management for a patient on day zero. You have your first eye in intensive care of your patient. Your goal is to ensure any extubation of your patient and then continue routine ICU management. You have to be thinking as a surgeon, what do I need in terms of cardiac physiology, that's going to help me provide the best care to my patient. And now we've talked about hemodynamics. We've talked about electrophysiology. Next week, we'll talk about cardiac output and we're going to be talking about all the factors that you would have to be thinking about when you're treating that patient in that r in intensive care. Ok. Uh Not only in the first hour intensive care, you're also thinking about when we're bringing out the patient um off, we're taking the patient off bypass. We already talked about cardioplegia, which is an important aspect of um bypass. But what else are we thinking about when we're bringing out the patient taking the patient off bypass while we thinking about in terms of BP, regulating BP? What are we talking thinking about in terms of reducing metabolic um activity? So we can reduce myocardial demand because the last thing we want to do is cause infection while we are taking our patient out of um bypass. Ok. Then we'll talk about day one when your patient has gone through um day zero. What are the things that you're thinking about in terms of what medications do you want to start your patient on? And what is the physiology of that that helps us know why we will start beta blockers. Why are we going to start um why are we going to wean off very quickly, all the um support while we thinking about when they tell us when the nurses tell us that there's a patient whose BP is low and they're concerned. Ok. And then day two, we start taking out a lot of wires. Why don't we need any of these monitoring anymore? Why are we taking the catheter out? Why are we taking the central lines out? Why are we disconnecting the pacing box? And if we do all of these things, what are the um why, what are the safety? What's the safety net we need for the nurses as well who are taking care of our patients? Ok. And day three, we have pacing wires out, mobilizing the patients. We're starting ac inhibitors. What is an ace inhibitor doing in, in in the physiology of not just because renal physiology is very ti um closely tied to cardiac physiology as well, but ac inhibitors, which angiotensin convert enzyme inhibitors also have direct effects on the heart. And what aspect of cardiac physiology is that related to? Ok. So I want you to have this picture to think about your daily practice. To think about when you go home today, you you're working for the rest of the week, think about all of how cardiac physiology can help you in the routine postop, routine management of the patient. And then next week when we come together, we'll finish off this module and I hope this has been useful to you. Um Again, I did not want to um talk about things that you could find in the textbook where I wanted to approach this in terms of utility. What's most useful to the junior surgeon? Ok, guys, that's the end of my lecture. And I do wish you a lovely evening. Uh I wouldn't be able to take any questions, but if you type your questions and you can forward them to me. OK? I hope this has been useful. Thank you very much for your time. Thank you very much David. Um I know um we started quite late so we just um about an hour in actually. And thank you very much for that comprehensive um ing and um our time is, is gone. So um I would just say that I've sent the feedback form on the, on the chart. So feel free to um feel free to um provide the feedback and so that you can get your feed um your um c of attendance after filling the feedback that one number two, if you have any questions for this session, I know we don't have time for questions. You can note it down and in the next um session, um you might just take a very brief 10 minute session of an question and answer before we go into the teaching um cardiac physiology for that day. So feel free to um to note down your questions if you have any questions on this session? I know a lot was said, even I, I myself have questions so um feel free to, to note it down. And um just to announce that uh I mentioned in the beginning of the session, we are going to have another uh uh fifth session on the teaching series, which is type two pacing arrhythmia and pacing in cardiac surgery. So he has done a sort of brief introduction to pacing and arrhythmia and cardiac surgery um towards the tail end of his lecture today and uh on 6 p.m. we will be, we will be continuing on that. Um Decisions are going to be taken by uh another person know by David, feel free to attend the link in the advance for the se if on the middle page on the me page. So um you can check it out and sign up for it. Thank you everyone for attending. I hope you had the um you had a wonderful time and you were able to uh understand what was being thought and hopefully, I will see you um on Saturday for the ping and arrhythmia session, please sign your feedback forms. Thank you doctor. Um If you can note your question down, um And in the next um cardia physiology session, uh we'll be able to answer that. So just note it down on your notes or in your, on your phone and um we will have a question and answer session in um the next, in the next session. Thank you.