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Summary

In this teaching session, medical professionals will learn how to approach the subject of cardiac physiology in surgery by discussing various topics alongside a discussion. Participants will cover important topics like hemodynamics, action potentials, ECG, cardiac electrophysiology, cardiac disease, pre-op and post-op phases, and complications. The trainer, Doctor David Ek, who is a cardio training at the hospital and the co-founder of The London School of Cardiothoracic, will guide the lecture and help participants have an engaging and productive discussion. Join this session now to get the most up-to-date and pertinent information to enhance your medical practice!

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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. Understand the components of a standard ECG and their importance in analysing cardiac physiology.
  2. Identify and describe the processes of cardiac depolarization and repolarization.
  3. Analyse the significance of prolonged PR, QR, QT intervals on ECG.
  4. Assess ECG changes during pre-operative, intra-operative and post-operative stages of cardiac surgery.
  5. Recognize and understand the implications of myocardial ischemia, STEMI and NTEY on cardiac physiology.
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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 hospital's wi fi 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 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 just 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 uh 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 up 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 in uh and pacing in cardiac surgery. Um So if you are yet to sign up for that session, please do so. So not to waste much of our time. I will introduce doctor David Ek who is a um cardio training at hospital and he will be taking us on this session. Thank you David for joining us. And yeah, I think you can. Yeah, thank you. So I presume I need to share my screen, don't I? Um That's good. Ok. Uh Can you see my street? Yes. Um Yes, I can. Ok. And you can see the slight here. Yes. Thank you. Bye bye, great. Um Good evening. Do 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 for those who don't meet, you know, me, I'm, uh, uh David EK, I'm a trainer of surgery at hospital and also co co founder of the London School of Cardiothoracic. Uh London School of Cardio Thoracic is a surgical teaching center, um, based here in London, um, and connected to S hospital. Please just look, have a look at the website. We have lot of course 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 cardio physiology. And as I said to the family, the important thing for me was not to um 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 cardio physiology. But then I thought that we could approach the topic looking at it from the perspective of uh surgeons uh need for information and uh cardiac surgeons are uh 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 um is to think about cardio physiology while we are looking at our patients in the pre op stage and in the POSTOP phase as well. And so we were tackling each aspect of this with regards to disease physiology, operating 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 a brief summary, we went through hemodynamics and uh related all of this to disease and um var disorders and so on. And um I think if I'm not mistaken uh in the family, we stopped somewhere at, during the cardiac electrophysiology slides. Um And I believe that I started to rush through um these slides because I was hoping to finish the lecture on time. However, in November was trying to say that we could have another week to finish these er full slides before we even attempt to go into module 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 electrophys. And um I can then proceed towards the um discussion in terms of applying this to disease physiology, applying this to uh pre op POSTOP um 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, you know, no one is uh repository of knowledge. So I would 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 family 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 this slide. And um I'll go on to talk about uh when we're thinking about cardic and the control physiology, we're thinking about the current, what's going on with the, the heart is the um uh is it works. The foundation of how the heart works is action potential, isn't it? So, uh how has, 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 EC GS if I'm not 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 ATRA and we have the pr interval which will show the initial depolarization of the ventricle. OK. And we'll then look into the QR S complex which shows the depolarization of the ventricles itself. OK. So the pr interval is showing us the um A V no 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 I can someone post here on the chat? What is the first sign of an A V uh a heart, a heart block of the first degree? Does anyone know what will be the sign on an E CG your family? I presume this is working, right? The chat system perfect, prolonged a pure interval. And can you tell me please how long that will be all? No, that will be 0.2. OK. So that would 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 pr interval, which is greater than 0.2 then we know that that patient has a problem with the conduction system and that will be the no conduction system. Now, the QR S complex um shows a depolarization of the fles A widened Q Rx 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 E CG. 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 QR S to come this QR S to hit a maximum of three boxes if it starts to go wider than that. And we thinking about uh widened QR s widened QR S start 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 all lead to, 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 depolarization and equalization of uh um across the ventricle. So we're talking about your heart has depolarized in the phase for systole and now is going into diastole and is repolarise at the same time. 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 draw too much about it. That QT interval that is prolonged could cause us to have to decide 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, right? Um Now, the ST segment would always be uh something that we're looking at on an ECG if we've got an ischemic patient. Now, in the P stage, obviously, if you have a stemi, which is an elevated ST segment that telling you that you're having myocardial infarction going on or you could have an TEY, which does, which is also myocardial infarct that does not um uh portray this elevation of the segment, but could also show us things like a depressed ST segment or a peak T wave and obviously, with the clinical signs of chest pain, um 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 ECG. 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 lemur 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 Anstey. And so there was no elevated ST segment. But now you see that as global ST segment elevation, are you taking this patient back to theater? What's your concern? So every single um need of the E CG is showing an elevated ST segment. Can someone tell me what they will be thinking when they see this? Anyone? Can anyone answer the question I've asked? So now you've got uh an elevated ST 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 you can 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 PCG, 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 AC A G 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 E CG. It's always very important to look at that E CG and compare it to the pre op E CG. So you'd always request for both EC GS and then you have to look and see where is the dynamic. OK. If you see uh uh uh an ST elevation in one or two leads that was not there in the pre op E CG, 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 if also if the patient is still a lot of infusions and struggling to um be weaned off noradrenaline and Milone and so on. And so forth. But if you see global ST segment and evasion, you're not concerned anymore. OK. That's his 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, t wave ventricular polarization, I would say T wave is very important because um you can, it, it, it gives you insight into multiple things. If you've got uh peak 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 P uh wave as well, you're thinking electrolytes 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 ABG S 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 postoperative 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 instead of 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 that I've shown for the cardio 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 ventricle is perfect. OK? So this is that is what I am 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 the cardiac action potential? So we know that first of all across the membrane at equilibrium, which is the equilibrium of potassium, the potassium channel, this is a minus 96 mini volts. OK. So that's it. 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 would not have sodium channels opening up and the the influx of sodium ions OK across the cell cellular membrane. So at this value at minus 90 they are activated. And then what you have is a very quick um uh and in this case, depo depo right? And you get to the membrane becomes positive at 52. And again, this is a sort of an average value across all those 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 irons um starting to flow out of the um cellar membrane, which is the briefer period of repolarization. OK. Now, what is happening is that the cell is now trying to revert 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 he needs to push out all that blood that is receiving, it has received in d he needs to push out all up to 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 it. We don't want the heart to repolarise immediately. And so you then have calcium iron 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, 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 cardi um electrophysiologists, 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 uh the negative potential across the cellular membrane. OK. And so there's an in 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 conductance of calcium decreases, the output current of potassium increases. And then you have that um uh the resting membrane potential across Nasar 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 postoperative, 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 I've heard of, you know, medications called sur channel blockers, you the head of calcium channel blockers, you the head of, uh, 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 know, 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 a cardiac pacemaker cell, what is it, how many phases do we have? Just post quickly? You don't even 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. To pa OK, Christel. 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 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 cardio pacemaker cell is that you remember that it is constantly depolarizing. So instead of having a trigger like the ventricle, right? Because the ventricle has to contract and then relax endo to receive blood and then insisted contract again to push that blood out and then repolarise 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 have to rest, we need to maintain 60 to 70 to 80 BPM depending on your how physiologically fit you are. And so he needs to go, we are setting 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 he needs to um carry out the impulse faster. Therefore, he has to have a different physiological mechanism. And so the summary of uh cardiac pacemaker cell is that the action potentials are generated spontaneously within the cells. OK. Um The they have a constant resting potential um 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 signal node. Now, can anyone tell me which other two aspects of the heart will have them has the ability to perform pacemaker pacemaker function, which other two sides. So I've talked about the SA node, the SA node is the one I've just talked about. So where else? The A B node? And you're right, the, the node is one. Yes, the broken system perfect broken fibers. Excellent. So they also have pacemaker potential. And why they have that is because if you have a problem with the SA node, then they will take um um they can also have a steady depolarization uh 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 you 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, has had a problem. So there's an AV block, right? So the normal pacemaker activity of the heart, which is a sign of atrial node should not be giving you a heartbeat of 40 or 50 right? That is something that you'll find if the 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 essay 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 the essay, suppressing the essay 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 minus 60 you have a slowly steady depolarizing potential that goes in here and then here you have the if surgery on channels just in this obstruct, they open up and in the same way that in the ventricle cells, they have an inward current. That's the the same thing that you'll have. Here, there's an ob stroke of activity and then immediately after that ob stroke 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 uh in the ventricular cells. Why? Because you don't have phase one and phase two more. So you don't have calcium channel, the cal calcium uh inward current going on to that potential. So you'll have that richer possible of 10 mits and then finding that you have potassium um leaving the cells to then repolarise this membrane and getting back to minus 60. And that's really simply how this is um how this occurs. Ok. So there is a brief anatomical picture of the heart showing the sign of the atrial node showing the A V 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 cardioregulatory centers and chemo receptors in the bladder, it in this is uh one other thing to think about why because our sympathetic and prosthetic nervous systems will do impact um the heart, right. And, and if we're anxious, we do find that our heart starts beating really quickly when we're at rest and we're very calm and or we're meditating, you know, we find that our heart's um rate also slows down. So it's important to remember that um you have uh uh you can have not just a subconscious um oh well, not subconscious and unconscious control of the heart. That is when you are just not, you can, 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 a panic and increase your heart rate or you can make yourself calm and reduce your heart rate. Now, how's the heart doing? How's the brain and the heart doing this? How, how are they connected? So we, we have b receptors 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 hypophonic patient, OK. The hypovolemic patient does not have enough cardiac output going into the aorta. So the um uh the bio receptors in the internal carotid artery find that the pressure that it is going through is just not the normal pressure that the body is used to. And then that sends er an information to the brain. And the brain really is feeling that back of the heart and saying, OK, look, I want you now through the sympathetic nervous uh fibers, I want you now to what I want you to start pumping faster. Ok. And uh the same with the, and so you have the sympathetic fibers and the sympathetic fibers, all feeding the essay node and feeding the heart as well as you can see, the sympathetic nervous system is not only just feeding the essay 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 arrest mode. Ok. And finally, we also have sympathetic 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 and 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 circulatory system. So what my heart is thinking about and then also at the same time, there's also Frank Sta forces that is the contractility 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 um will go and that stretch will lead to a proportional 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, but um uh bleeding on the table uh while you're doing your operation, while you're closing. So you finished the patient is off bypass now. And um immediately you realize that you've come a bypass and then um the BP started to return and one of your grafts, unfortunately, you, it was done by maybe a, a junior member and these patients that started to bleed profusely. And while you're doing that, you're asking to give blood products. Why? Because at that time, you're going to realize that even though you're coming off, uh rest, you're going to see that the heart rate of that bleeding, um 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 are looking at the afterload, if I can squeeze uh vasoconstrict um a 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, I know PHR being released into the system. And then if I can ask the heart to fill more in preload, then I can ask her how 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 Carni a lot of the medications here we do not use. Um again, so we don't use cloNIDine as we used to procainamide as 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. This is why also when you're given local anesthetics that is lidocaine as a local anesthetic to um reduce pain for any um procedure that you may be conducting. So this could be putting in a central line or putting in an material 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 are 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 5 mg 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 M GS, 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 for the Gyne to be used as a pill in the pocket. And we normally use that in patients who have got paroxysmal af. Um and if uh a patient who has got off par seasonal af and maybe has af er, and it goes into atrial fibrillation every now and again, er, then you can, and you can give them the pill in the pocket. So they hold that and when they start to feel that the, the p palpitations they take it. Um and its method of action is um it's a sodium channel blocker. OK. So we move on to class four. The class fours are the calcium channel blockers. So we have Verapramil 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 mechanism for vasodilation. So in as a channel blocker for a lot of hypertensive patients, we use um Vil and dilTIAZem. Um And the idea is that if you want 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, 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 uh graft, as you all know, um smaller diameter can still give you the same benefit of an leur but is very prone to vasoconstriction. And so um these patients then end up having dilTIAZem um 90 MGB D. Um If you've done a full arterial revascularization of them 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 af especially if this is a patient who has had new postoperative. Um af you are starting them on a 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 amiodarone over 24 hours. And you are hoping that when you give this to them, they revert back to sign this 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 uh class two drugs which are beta blockers and we can see that um propranolol metoprolol er beta blockers have a huge range of action. Not only are they acting on potassium channels and they're called potassium channel rectifiers, please ask the cardiologists, 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 sympathetic activity or modulate parasympathetic activity um as signals to the heart which um usually ends up with um controlling the heart rate, suppressing um the pacemaker 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 our study. Now, when you, the heart is feeling better in our study, because there's more of a uh prolonged art, what's happening is that you are also feeding the coronaries as well because the heart feeds itself. So the coronary arteries get um are perfused during the study, right? So the longer your d 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 to 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 um are actually doing. And now we go into my favorite aspect and I've just realized that it's seven o'clock um cardiopulmonary bypass. Ok? I really wanted to play a video, but I know that the M has told me there's going to be a lecture 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 peek out here is you'll have for those of you who have done surgery, you know, that 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, um, this venous reservoir. It goes through all the heat exchanges oxygen and it goes, which oxygenator acts as the lungs of the um the artificial lungs. And you, you then feed that back into the arterial filter, back into, into the system, back into the aorta and into the um systemic circulation. So you can perfuse all the other end organs and the brain. While the heart, you have a blood less and munia less filled. So the idea of uh cardiopulm bypass is to ensure that you can work on the heart and still perfuse the rest of the body. But while you work on the heart, the heart is um not moving and the heart is there's no blood in the um in that field. Ok. So the, the most important thing here that I want to talk about is cardioplegia. Ok. So cardioplegia 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. So, cardioplegia has a high potassium concentration OK. And so when we give cardioplegia in surgery, we are causing an increase in the extracellular potassium. OK? Which means that you still have depolarization go on and you have repolarization go. But when you start trying to repolarise 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 de depolarization. But when you get into the study, which is repolarization, what you then have is because the cellular membrane potential is much less negative, right? Because you have all these positive potassium ions in the extracellular matrix, the heart then arrests here in D OK. So they are hard to arrest in and it cannot repolarise. 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 resting the heart in the study, you're not using ATP. 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 retrograde as the case may be. But you'll have to keep giving um cardioplegia and um uh at various points intermittently during your um surgery. OK. And uh the other thing to do is you are, your P PJ is normally given cold or you prefer to give it cold. Why? Because if you give it cold 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 pacemaker, the sa node, the B node, what does a pacemaker do? The pacemaker is only substituting the function of the um of the pacemaker cells. So if you sign the atrial node has the dysfunction, then your, your pacemaker can come in and do the job for you. OK? Now again, N femi 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, it's a topic I like. And so I kind of wax lyrical about this for as long as possible. But I will just say that very important to remember for pacemakers. What are 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 first letter in a pacemaker mode is tells you the chamber that is being paced. The second letter tells you the chamber that is being sent. 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 the consultant has told you, I'd like you to um put this pacemaker on A I mode. What they are saying to you is they want the atrial, they want the Atria paced, they want the Atria sensed and when that is sensed, the pacemaker will inhibit its activity. OK. So when will we use an A 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 set in that the A V node will not, you've not done anything to the A V node. You have not been naughty at all. Um And so um and, and you're only pace in the patient because either they have um it will take time obviously with local information and so on and so forth or if they had the right coronary issues there. So they, they, 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 8090 BPM. And you also want to ensure that they have a good cardiac output. Remember I told you cardiac output is heart rate and drug volume, right? So in order to pace them. Um artificially, you put them on 90 BPM A A I mode. Um And this tells you that you are your Atria, is your both Atria are being paced. The um both Atria 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 that it continues its activity, when the heart has recovered its intrinsic function, you can have something called the at 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 an eye 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 make sure I adequate 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 V viv vi is the same thing, it 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 trigger delay. OK. And trigger today means that the pacemaker itself is going to pause for a while and decide whether or not it, see, see, sees that there's intrinsic activity in the heart going to be 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 D DD. 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 or delay in both er chambers. OK. So this is the simple concept of er 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 A V node as well if um and so when do we use V vi we use V vi as a backup if we think our patient is going to sleep from atrial fibrillation back into normal rhythm, or we also use it in a case where we think um when we think that we may have uh a problem with our A V conduction and we want us, 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 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 medic, you're given 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 af your problem is not the heart rate because Atria um is, is sending about close to 300 BPM. When he gets the, every node, it slows, it's halves. 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 a and that can now flips that back into sinus rhythm. However, because you're giving Amy and beta blockers, you can flip it from sinus rhythm into an A V conduction block. And if you do that, if you are pacing the heart at a A I the heart, the ventricles will not receive impulse. And so what you'll do when you put it on V VR, 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 vi will ensure that some impulse is provided to the ventricles way to work. OK. And then D DD is ad 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 out problem, you get that 20% atrial kick that you can give in uh 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. OK. 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 er to, to then push that impulse all the way into the ventricle system, you can programmer 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 pr interval of maybe 240 or 250 milliseconds to give the heart enough time. So if the heart has started to recover its own function, it can bring out its own intrinsic ventricle activity. And this is why we use D DD. So this is just a brief summary of 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 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 need to focus on cardiac output, all the um lovely formulas we have. Um and that will be module two. OK. So this was just meant to sort of introduce the concept, the use of dobutamine, dopamine, epinephrine, norepinephrine in the um cardiac patient. And so we know that there are vaso constrictions, there's no adenine, there's depressin, we know that there are inotropes, inotropes, like phosphodiesterase inhibitors, Mirena. Um What do they do? They improve cardiac contractility, but they also have vasodilatory effects, adrenaline does everything. It's um it's a horse sweep 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, we go into the next aspect of our lecture next week um where I will finally talk about cardiac muscle, cardiac output and we'll that will finish off this um 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 early 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 we, you have to be thinking about when you're treating that patient in that VR in intensive care. Ok. Uh not only in the first hour intensive care, you're also thinking about when we are bringing out the patient um off, we are taking the patient off bypass. We already talked about cardio, which is an important aspect of um bypass. But what else are we thinking about when we're bringing out a patient taking patient off bypass? What are 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 uh why are we going to wean off very quickly all their um support? Why are 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 monitorings 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 ac inhibitor? Doing in, in in the physiology of not just because renal physiology is very closely tied to cardiac physiology as well. But ac inhibitors is angiotensin converting enzyme inhibitors also have direct effects on the heart. And what aspect of cardiac physiology is that uh 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're working for the rest of the week. Think about all of how cardiac physiology can help you in the routine post operative 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. Rather 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 the family, you can forward them to me. Ok? I hope this has been useful. Thank you very much for your time. Thank you very much Davy. I know. Um we started quite late so we just um about an hour in actually. Uh thank you very much for that comprehensive um teaching and um uh 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 cert of attendance after feeling the feedback at 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 minutes session of an questions and answered 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 II 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 this session, we are going to have another uh uh fifth session on the teaching series which is titled Pacing Arrhythmia and Pacing in cardiac surgery. So he has done of sort of brief introduction to pacing and arrhythmia in cardiac surgery um towards the tail end of his lecture today and uh on S 6 p.m. we'll be, we'll be continuing on that. Um Decision session is going to be taken by um another person or by David, but feel free to attend. The link is the advert for the session if on the middle page on the sig me page. So um you can check it out and sign up for it. Thank you, everyone for attending. I hope you are the uh you are the wonderful time and you were able to uh understand what was being taught. And hopefully, I will see you um on Saturday for the piecing 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 cardio 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. Ok.