This on-demand teaching session dives into the specifics of epicardial pacing, a form of medical pacing specific to cardiac surgery. Led by a cardiothoracic junior doctor at Papworth Hospital, Dy, the session will discuss why we pace, different pacing modes, the three letter acronyms used, causes of heart block, and more. Medical professionals will gain an understanding of why pacing wires are placed intraoperatively, how the heart rate equation works, and other core concepts necessary for successful patient care.
Generated by MedBot


The fifth session in the teaching series Basics of Cardiothoracic Surgery

Topic: Arrhythmia and Pacing in Cardiac Surgery

Date: Saturday, 29th July, 2023

Time: 6pm

Speaker: Dr Fadi Al-Zubaidi, Clinical Fellow in Cardiothoracic Surgery, Royal Papworth Hospital, Cambridge, UK.

Learning objectives

1. Understand when pacing is necessary and why it is beneficial for cardiac surgery patients. 2. Identify the different types of cardiac pacing, including epicardial, endocardial, and transcutaneous pacing. 3. Describe the importance of heart rate in mean arterial pressure equation. 4. Recognize the context and likelihood for needing ventricular and/or atrial pacing wires in different types of cardiac surgery. 5. Analyze the risks and benefits of pacing wires intraoperatively.
Generated by MedBot


Related content

Similar communities

View all

Similar events and on demand videos

Computer generated transcript

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

Uh hello. Can you hear me? If someone could just drop me a message and me or anyone just to say that you can hear me, then we can get started. Ok. You can't hear me. No. Oh, excellent. Excellent, good, good, good, good, good, excellent. Sorry about that. I don't know why this always happens when I uh when I try to do this. Um Great. I'm just gonna load my slides up. Um and I've managed to get my camera working as well. So if you'll bear with me for a second. Yeah. Ok, great. Can you guys see my slides? Yes. Yes, you can. All right, great. Uh Good afternoon or good afternoon, morning or evening everyone. Thank you for attending this uh talk. Uh My name is Dy, I'm giving uh I, I work as a cardiothoracic junior doctor at Papworth Hospital and this is a quick overview of epicardial pacing, which is specific to cardiac surgery. So this is slightly different to the kinds of pacing that you may hear about or be aware of. So far. For example, the subcutaneous implants in cardiology, this is different. This is specifically surgical and I'll go over that during the talk. So as an overview, I'm going to discuss why we pace, I'll go over the different kinds of pacing and then focus it on epicardial pacing and then we'll talk about different causes of heart block and then help you understand the different pacing modes. So these are the three letter acronyms that you hear as well as different issues that you can have with pacing wires. So I assume that the audience is somewhat familiar with er broadly familiar with cardiac surgery. And uh so based on that, we'll we'll proceed. So what is pacing? So pacing essentially is when we talk about pacing, it's 22 processes taking place essentially simultaneously. On the one hand, you have the continuous measurement of the cardiac rhythm and then the second function of pacing is to intervene and amend the heart rate according to the inputs that we put into the pacing device. So in the context of epicardial pacing, that would be a pacing box, er we put certain settings into the box and that box through the wires that are attached to the heart could constantly read an ECG and then it will intervene when their heart rate drops too low. That's the essential, the essential concept. So this begs the question, why do we pace? What's the purpose of this whole thing? Now, in order to understand why we pace, you have to go back to the basics and consider the role of the heart, which is to perfuse tissues and organs and to perfuse them, blood circulating blood blood needs to be circulating at the appropriate pressure, which is determined by this equation. Mean arterial pressure equals cardiac output multiplied by systemic vascular resistance. And if we isolate cardiac output and break that down, we see that the heart rate is one of the key components, heart rate multiplied by stroke volume. So we can break the whole of the mean arterial pressure equation down into three components, stroke, volume, heart rate and systemic vascular resistance. Um And so for the purposes of this talk, the key component is heart rate. The reason that we pace a patient is because they may develop or they essentially it is to prevent bradycardia. It's to prevent the patient's heart rate dropping too low. And the reason we care about the heart rate is because the heart rate, if it does drop too low, will impair the heart's ability to perfuse tissues appropriately. So that's the bottom line. If we could tolerate a heart rate of 40 blood pressures were fine, then we probably wouldn't pace. But because of the BP and specifically the mean arterial pressure drops, we have to pace. So there are different ways to pace. And these are, these are different ways that are implemented according to the different clinical contexts. There's epicardial pacing, endocardial pacing also known as transvenous pacing and transcutaneous pacing. Now, because we're talking from the perspective of cardiac surgery. We're talking about epicardial pacing, but I'll just give a brief overview of the concept. So you have something to orient yourselves with in the future. Epicardial pacing is as it sounds. So on the surface of the heart, the epicardium during surgery in theater, we place uh pacing wires onto the surface of the heart. You usually have one ventricular wire and one atrial wire. Uh And so these are wires in direct contact with the outer surface of the heart that are attached that are brought out through the chest wall and attached to a pacing box. And we can use that pacing box to deliver electrical stimuli to the heart in order to try and achieve pacing. That's what we do following cardiac surgery and every cardiac surgical patient, each and every cardiac surgical patient has pacing wires placed. And this is because the nature of cardiac surgery is that it can predispose patients to bradycardia in the immediate postoperative period. And so it acts as a safety net because we know that the patient's heart rate might drop in the first few days after surgery. We put a pacing, we put pacing wires into the epicardium so that if it does, we can manually bring the heart rate up by delivering direct electrical stimulation. So that's epicardial pacing. Uh the second one, endocardial pacing. So this is what cardiologists will do. So, um this is more done in the case, for example, of a patient that develops, you know, a heart block in the community, they may develop type two or type three heart block. Uh And in that, in that situation, uh it will be a cardiologist via an endovascular approach, can place the pacing wires uh into the chambers of the heart and achieve pacing that way and finally, transcutaneous pacing. This is something that we do in the emergency setting. This isn't just a cardiac surgical thing. You could find this on a medical ward. Um A&E and really this is if a patient has a very low heart rate, you just put pads on the chest, attach it to the defibrillator. And usually there's a pacing mode that pacing mode. When you set it to the pacing mode and set a specific heart rate, the defibrillator will deliver shocks what we call synchronized shocks uh at a specific rate in order to stimulate the heart into beating at a set rate. And so that's the purpose of transcutaneous pacing. And you would do that if the patient in the acute setting had a heart rate of, let's say 30 or 40 it was compromising their BP. And of course, as with all these things, this is something that you'd always do under senior guidance, you know, you'd never do something like this really on your own as a junior doctor. So bringing it back to epicardial pacing, which is the purpose of our talk er for the majority, the majority of cases when we talk about pacing leads, we talk about a bipolar lead. So that means that each pacing wire actually, even though it's one wire, if you were to zoom in and look at the end, it's got two small ends. And that's so that there's a potential difference between the two between the two leads is what creates the electrical stimulation at the chamber of the heart that it's stitched into. So broadly speaking, we always talk about bipolar leads. So if we talk about a ventricular wire and an atrial wire, each one of those is bipolar. And again, so that there can be a potential difference between the two. So here you can see an image which kind of in a gross way demonstrates that. So here we can see the bipolar epicardial pacing on the left. You can see that the there's two wires that will be in the stitched onto the surface of the heart, there'll be a cathode and an ano. Er and again, it's the difference between the two note on this diagram. It looks like the two leads are far apart, but in reality, they're so close together, you can barely see the difference. Er So this is just a diagram to help illustrate the concept of the of the completion of the circuit. So you understand, hopefully now the concept of pacing, why we pace in in the context of physiologically why we pace now it begs the question, how do we achieve pacing? And so the first question in the context of cardiac surgery is where are we going to put the pacing wires? This is quite important. And if you are a junior doctor working on a cardiac surgical ward, um you know, you'd be expected to understand the difference between just atrial pacing or um dual chamber pacing or just ventricular pacing. And so this all comes back to theater. So if you take your mind back to the operating room, you imagine the surgeon has finished the, the the main part of the operation, they're about to put the pacing wires in. They can either put pacing wires just in the ventricles, just in the atria or both in the atria and ventricles. And the choice regarding whether or not to do just atria, just ventricles or both is uh is really down to the surgeon's preference and is largely influenced by the type of the operation the patient is having, is having the key point here is it is to think about the concept and understand the concept. Normally the conduction system of the heart, you have your sinoatrial node conducts to the AV node which then transmits that depolarization through the bundle of his packin fibers into the ventricles. So if there is reason to suspect that that transmission of a normal depolarization from the atria to the ventricles may be interrupted, then you would almost definitely want to at least make sure the ventricles have a, have a pacing wi in them, if not both. And this is determined by where on the heart you're operating, right. So if the operation is likely or is more likely to involve parts of the heart that are close to the conduction system, then you would place, then they would place ventricular wise almost certainly. Um, on the other hand, if it's an operation where they're just, they're operating outside of the area that the conduction system is found in, so that that would usually be in the context of coronary artery bypass grafting, then some surgeons would opt just to place atrial wires. And again, the concept there is that any disruption to the heart's rate shouldn't be caused by damage to the conduction system. And so if we pace the atria, we are by default, pacing the ventricles as well. And, and the reason you may ask, why don't you just always do both to be safe? I suppose the answer is as with anything in medicine, do no harm. First, there's always risks associated with everything. When you put pacing wires in 345 days later, you have to take them out. And there's always a risk that when you take the pace and wear out that there could be a small amount of bleeding from the area which could build up and, and cause some compression on the heart. This does happen sometimes. So, you know, everything you have to weigh up the the risks and benefits. Uh and so the intraoperative causes of bradycardia. So here I'm trying to get at why, what is it about the operation that might predispose a patient to bradycardia postoperatively? Um So this is really most common in terms of your, if you think about cardiac surgery in terms of just your simple isolated procedures. So coronary artery bypass graft aortic valve surgery, mitral valve surgery. And then most commonly after the common operations, you, you would say that aortic valve replacement has the the higher incidence of uh of patients requiring a pacemaker because the annulus of the aortic valve is in a very similar plane to the atrioventricular node, the AV node. And therefore, if you were to catch the A V node or just generally the conduction system, when putting stitches into the annulus, then you would risk damaging the conduction pathway. Also just the act of manipulating and handling the heart and surgery, which you have to do. Um This brings edema, this causes edema and swelling in the heart. And that swelling can temporarily disrupt the conduction system. But in that case, you would expect it to resolve in the coming days. Whereas if you had put some stitches through and actually caught the conduction system, then that's usually irrecoverable. Um And we'll talk about that and what happens in that case in a few slides. So this is just a diagram to try and illustrate further what um what I'm I'm getting at here. So um I don't know if you can see my mouse like the pointer of my mouse because I'm trying to point at things. But if not, I'll verbally describe it. Anyway. Um Can you guys see my mouse or not? Someone just puts a yes or no? Yes, yes. Oh, great. You can. Fantastic, good. So, uh if you, so this is the aorta uh and this is the, this is the, this plane here is the aortic annulus and these are the aortic cusps. So when you do the operation, you essentially resect these cusps out and then you place stitches through the aortic wall at the level of the annulus. Now you can see this is the conduction system, this is the AV node here. So if you take a stitch here too deeply, you could catch the conduction system here. You could even catch the A V node if you're going way too deep. And it's these kind of maneuvers during the operation that can cause permanent damage to the conduction system. And if you permanently damage the conduction system here, then you essentially are inducing heart block. Because if you go back to your basic physiology, the reason that the sinoatrial node is the pacemaker is because it has the fastest rate of depolarization amongst all the specialized conduction myocyte in in the heart. If you block the AV node, then your ventricle will the pacemaker cells for the ventricle will be cells within the ventricle itself. And the pen, the ventricles, intrinsic heart rate is around is around 40 40 to 50 but it can be even lower than 40. Um And so if you don't have that stimulation coming from above, then your ventricular rate is is likely to be too low to sustain a good mean arterial BP in in the long term. And so this is the key, this is the key point really. So this takes us back to the function of the pacemaker to monitor the underlying rhythm. So the pacemaker is constantly reading the kind of reading an ECG strip. And what it, what it will do is according to the settings we put in, it's looking at the heart rate. Yeah, it's looking at the heart rate. And there are different ways that we can ask the pacing box to look at the heart rate depending on whether or not the patient has atrial wires, ventricular wires or both. So we want to monitor the rate and that where necessary intervene to maintain an appropriate rate as per our setting. So that brings us to the settings that we can use. And really when it comes to the pacing box that we have in the wards, there are three main settings that we can use. There's VVI A A I and DDD, these are the three that you need to know and learn about and be aware of. Uh I'll explain what the acronym, how they generate the acronym. But essentially VV I is ventricular backup pacing A A I is atrial backup pacing and DDD is sequential dual chamber backup pacing. So when we say VVI is backup pacing, ventricular backup pacing, what that specifically means is we're asking the pacing box to track the QR S complexes. Yeah, to track the ventricular depolarizations and ensure that the ventricles are depolarized at a minimum rate. So we may set the pacing box to VV 80. If we set the pacing box to VV 80 then the pacing box will read the information. And if we found if it finds that the QR S depolarization rate, let's say 60 it will then kick in and start trying to pace the ventricles by delivering a small electrical stimulus via the pace of wires that are stitched into the ventricular wall to try and elicit a response from the ventricles because that's how pacing works. You basically give a small electrical stimulus and that prompts a depolarization. And so that's how ventricular backup pacing works. Atrial backup pacing exactly the same. But instead of tracking the QRS complex rate, it will track the P wave rate. So look at the P waves and again, if the rate at which you have P waves is less than the rate we've put into the pacing box, then the pace, the pacing box will start to stimulate the atria until it sees that the P waves are present at the rate that we want them to be, which could be a could be 90 could be 60. Any of these things. DDD requires a longer explanation and I'll get into that. But the the concept of DDD pacing is to stimulate both the atria and ventricles er in order to replicate a kind of more perfect physiological scenario. So just so you have an idea to orientate yourself about these acronyms. Uh Remember PSA psa will tell you what each letter in the acronym stands for. So the first letter pace, which chamber are we pacing? If we want, if, if we have to pace, which chamber are we pacing? That's PS is which chamber is being sensed. So almost always these two are the same because we want to read information from one chamber and then use that information to influence whether or not we're going to then paste that chamber. So that's why it's Vviaa I uh and then action is what are we asking the pacing box or the pacemaker to do? So, the reason VVI is VV I is essentially as follows. VVI 60 means pace the ventricles. But if the ventricular rate is 60 then stop pacing the ventricles. That's what it's a bit confusing, but that's, that's why it's, that's why it's inhibit. So essentially the pacing box wants to continuously pace, but then you're asking it to inhibit itself from pacing once that rate is 60. That's why it's VV I, that's why it's a A I and that's why it's a backup mode. D essentially means dual mode. So uh DDD means that we are pacing both um and a key point to mention here is that there is a pacing mode called VOO. Yeah. Uh or, or, or Doo which is where you pace both, either the ventricles or both chambers. Irrespective of information coming into the pacing box, you just deliver, you just deliver pacing stimuli at the heart, at the rate you set it to. This is actually a very dangerous mode and should not be used on the wards. Er and certainly should not be used eee even on it without very, you know, specialist consultant support. And the reason I make this point is if you ever see a pacing box set to Voo or Doo, you must immediately ask a question, is this intentional or an accident? Because it can happen by accident? And the reason it can happen by accident is because often the O and the D on the pacing dial look very similar. The consequences of the potential consequences of Voo is you try, you may, you may try and pace. In other words, try and stimulate a depolarization when the ventricle is already rep polaris and this would institute what you, what you may have heard of as an R on T phenomenon RNT from R wave and T wave, you get the R wave in the D in, in the depolarization um and the T wave in the repolarization. So it's called a RR phenomenon. I, you're trying to induce an R wave in the middle of the T wave. This can unfortunately put the patient into ventricular fibrillation, which of course is a lifethreatening um and potentially life ending uh uh rhythm. So, be careful if you're wondering why does it exist, if it's so dangerous? It's because you can use it during the operation. So when you put the pacing wires in and you're in the safe, secure environment of theater and you're trying to get the heart pumping initially, you can just blast it with a Voo or AD OO mode. But other than that, it's not really useful good. Now, this brings me on to DDD mode. So we talked about VV, I, we've talked about A I, they're a little bit straightforward DDD uh is a little bit more, there's more to it DDD, sequential pacing. And the reason it's useful is because you maintain the atrial kick. If we zoom out for a second, when we talk about bradycardia, obviously, we're talking about uh when we talk about heart rate, bradycardia, we're always talking about ventricular rate, right? The a the atrial rate is uh you know, is, is, is not as important. Your normal cardiac output, we said is a heart rate multiplied multiplied by stroke volume. Well, the synchronization between the atria and the ventricles plays a significant role in providing cardiac output because it contributes to the stroke volume. So, in a patient where the atria and ventricles are synced, you're going to have, you know, anywhere from 15 to 20% greater cardiac output uh than if they, if they're not in sync. And an example of that would be, for example, atrial fibrillation, you lose that what we call the atrial kick. So when you maintain the atrial kick, which is the synchronized contraction of the atrium ventricles, you get a 20 to 30% boost in your cardiac output, which which can be very significant. Um And remember that ultimately cardiac output is part of the equation for mean arterial pressure. So the way DDD mode works is the, let's say you'll set your rate, your desired rate, you'll set your desired rate to 60. What the post in box will do is initially look for a P wave. So look to see do we have P waves at that rate? And if we have, if we have a P wave fine, it's not going to try and pace the atria because you have the P wave it's coming fine. The next thing is then it will then look for it QRS complex within a certain time and we set that time on the pacing box that's called the A V delay. Normally the normal PR interval is 0.12 to 0.2. However, the er 0.12 to 0.2 seconds. However, on the pacing box, we can set it. So if we set it to, let's say naught 0.3 then it's going to wait naught 0.3 before 0.3 seconds before trying to paste the ventricles. Yeah. So that's how it will. That's how DDD mode works. It tries to pace the Atria. If it doesn't see that the Atria, if it doesn't see a P wave at the necessary rate, then it will pace the atria and then it will wait to see because it's possible that after pacing, the atrium, the conduction will smoothly flow down the A V node into the ventricles. And within that A V delay, you will get a QR S complex and therefore the pacing box does not need to stimulate the ventricles. This is the concept, this is how DDD mode works. And then you can see if you, if you're aware of that, that there are a number of different scenarios that you can get. In the case of a patient paced via DDD mode, you may have that the atria paced, but the ventricle isn't paced because the conduction system is intact. You may get that both need to be paced because the intrinsic atrial rate and the intrinsic ventricular rate are both low. You may get the opposite. You may get that the atrial conduction is fine, but that not every P wave is followed by QRS complex. In which case, it will pace the ventricles after the atria uh in those cases where the ventricular depolarization doesn't come on its own. Um And yeah, really, that's how DDD mode works and we've spoken about asynchronous patient. And so you have to be careful with that. Uh And so then finally, there are some common issues that you get with the with pacing boxes on the wards. So you may find that there are issues with the pacemaker lead. In which case, you need to explore the connections and make sure that the er so there should always be er usually there will be four connections at the top in a patient that's both ventricular or atrially paced two per lead. Er However, if there's only one chamber being paced, then you'll only have two at the top of the pacing box, you can get failure to pace. Er So this can come over time as the pacing wire is stitched into the ventricle. But if you're leaving it in for four or five days, then that connection, you can get some fibrosis or maybe as the patient's moving, that lead is pulled away and it's no longer in contact with the lead. Uh In which case, it depends on the specifics of the situation. Uh If the patient's in heart block and you completely can't pae them, then they may need to get a pacemaker. Uh Sometimes you can put essentially feed both of the wires through that are coming through, coming out through the chest. You can feed them through a needle and pass it through the skin and then connect it to the pacing box. As if only one of the two leads has broken, then that will create a circuit between the lead that's still attached to the heart and your skin, which is, which is perfectly fine as well. It's, it's similar to transcutaneous pacing, but it would require lower amounts of energy. Um If a patient who's in DDD mode, who has gone into a F, then you can change the pacing setting to VVI. This is important because again, if you think about it, if you're trying to track the atria and the patient's atria fibrillating at a rate of 2 to 300 then that could be a nightmare. So it's best to just switch to VVI. Uh and then you may get loss of capture, uh oversensing or in theory pacing the diaphragm, but this doesn't really happen. Um One thing I want to focus on is this loss of capture, to understand loss of capture. Firstly, we need to understand capture. I thought I had a slide on that, but I'm not sure if this is, this may be uh this may have gone. So here, if we just use this as an example slide, so if we're trying to, if we, if we're trying to, because if you set the pacing box, one of the settings on the pacing box is the voltage output. Let me just get an image of that. Just bear with me guys. This is the key points. I'm not sure why it's not come up which one does? Uh uh sorry guys just bear with me one second. So this is what the this is a common pacing box that you'll get on the wards. So if we just go through the, so this will be the last, the the last section, I'm gonna go over the the pacing set settings with the image and I'll then talk about capture, which is very important. So here you can see the different modes, it's not the best resolution, but I think you can make it out. Uh And you can see what I mean. This is DDD and this is Doo, they look very similar and you need to be careful. Er These are the two that are, that are that that people sometimes mix up and if you see on the word Doo, you need to ask questions. So here you'll set the desired rate. So if you want the rate to be 80 you'll set it there. This is the A V delay which I talked about and this is to be used when we're using DDD mode. That's when you will set the A V delay. And the reason why you may vary the delay because you may wonder, well, we have a normal pr interval of 0.2. So why would we ever have a higher A V delay? The reason is that in patients recovering, let's say just from the edema of surgery, that edema may not have permanently damaged the conduction system, but it may have impaired its function. And in order, if we set the strict physiological limit of 200 milliseconds, we may not get that in the first few days. But if we slightly extend it to, let's say 300 or 3 50 then the conduction system may be working at that may be conducting at that rate. And so by expanding the A B delay, you give the conduction system the opportunity to start kicking in. And the theory is, I think there's any papers on it, but the theory is that that will speed up the process of the heart's natural conduction pathways taking course. Uh So that's why you may use a slightly longer A B delay, um burst rate. We don't use it, forget it. And these are your four key components for determining the electrical, the ones on the right amplitude in voltage. This is the amount of energy that the pacing box is going to deliver to the heart in order to try and pace it. That is amplitude sensing, which is in Miller volt is the, is essentially think of it as how sensitively the pacing box is listening or looking at deflections from the isoelectric line on the ECG to try and pick up P waves or QR S complexes. So if you make the sensitivity too sensitive, then any little deflection in the isoelectric line may be picked up as a P wave or a QR S complex. And this may lead to under under pacing because we're overestimating the intrinsic heart rate if that makes sense. And therefore the opposite is true. If we make it not sensitive enough, it's going to miss Q complexes and P waves and then it might try to over pace because it's underestimating the intrinsic heart rate. So these things, normally you normally it's it's around, you, keep it around one or two. you know, from my experience but um sorry, no point point, no 0.10 0.2 near the bottom, neither, neither more sensitive end. Uh But you really, you use normally on the ward when you get used to these things, you'll play around with it and, and you can tell when the pacing box is, are reading appropriately. Uh And then the second input, this is the more important, this is a very important one is the amplitude. So this is a concept that I need to kind of nail. When you're trying to pace the heart, you're delivering an electrical stimulus to stimulate a depolarization. However, if that electrical stimulus is not significant enough, then you will not get a depolarization of the chamber that you're pacing. And so what this will look like on the monitor. So what the picture is stood by a patient, the patient's in bed, you're holding the pacing box and you can see the monitor that they're attached to. They've got ECG leads attached to the monitor and you can see their current heart rhythm and let's say the heart rhythm is, you know, it looks like a, like the rate's about 50 you want to pace them and you got it on VV I and you said it's a VV 80. And the threshold is if you have the, the, the sorry, the amplitude on the ventricular amplitude at the lowest level, then what you'll get is you'll see pacing spikes popping up on the monitor which indicate that the pacing box is trying to pace the ventricle, but those pacing spikes will be followed by nothing. And you'll see that the actual rate of the ventricul of the ventricles remains low. So in other words, you're delivering electricity to the heart, but you're not stimulating it into contracting or more precisely into depolarizing. So then what you would do is you'd slowly turn the dial up on the ventricular amplitude, slowly increasing the amount of energy that you're delivering each time you send that stimulus. And then what you will start to find is once you hit a certain, once you get a certain level of uh energy that you're giving each spike will be followed by a broad QR S complex. And that is defined as the ventricular threshold, the minimum amount of electrical stimulus required for every pacing spike to be followed by a QR S complex. Once you have figured out what amount of voltage results in a consistent depolarization of the ventricle after a pacing spike, then you can say you have determined the threshold. Yeah. And you say you have electrical capture, these are the two ways to describe this this number. So in practice, you'd say, OK, the threshold for this patient is three volts, the ventricular, you might say the ventricular threshold is three volts. And if the threshold is three volts, then you wouldn't want to leave the pacing box set to three volts because over time, the patient, the as the leads start to fi rose or the patient's moving or whatever that threshold may rise. So more, you know, to really picture it, it's kind of the gap between the actual electrode in the heart. If there's gunk building up around the electrode, then it's moving the electrode away from the heart a little bit like millimeters, fractions of millimeters, but those fractions of millimeters can add up and make a difference. So then you need to increase the energy to make sure that you still stimulate the heart. So that's a long winded way of saying if the threshold is three set, the voltage to five or six, that's the point there, same applies for the atrium. Um And that's basically it. So um yeah, so sorry, that slide wasn't there in the beginning, I just had to add it in. But if you guys have any questions now, I'd be happy to, to answer anything that you have to ask. Um Let's have a look what electrolytes need optimization to avoid nons shock arrhythmias. Um A G hyperkalemia follow up. Um Oh So, I mean, I I'll answer the question broadly. I'm not sure exactly what maybe the specific if you're getting at something specifically. But um post cardiac surgery, a high proportion of patients risk going into atrial fibrillation, atrial fibrillation, post cardiac surgery is common. One of the reasons for it is low potassium crucially post cardiac surgery, the threshold for low is higher. So we target all patients. We want all patients to have a potassium greater than 4.5. If the patient's potassium is less than 4.5 and they've gone into a f usually if you correct the potassium, there's a good chance that the A F will revert into sinus rhythm. Um magnesium is also something that you can give to patients who are in af postoperatively. Um As often low magnesium precipitates that as well. Any other questions about pacing or the concept or anything that I may not have explained? Uh Well, thank you very much for anyone with any questions. Um No, and there's a question is a subcutaneous defibrillator, unsuitable if there are indications that future pacing may be needed. Uh A DFIB, I believe that this is more of a cardiology question. So I'm not 100% sure. Um uh I, if I, if I understand your question correctly, I think what you're asking is you could have a subcutaneous defibrillator, which is there because we know that patients, some patients have a, you know, congenital abnormality with their conduction system. That means that they may, they may spontaneously cardiac arrest and that will shock them out of it. Can that same device also be used to pace, I'm not sure. But II, I think so, when may I in uh not to be your best longevity option? So, I mean, a DFIB device is specifically used for patients that have a rhythm that we know predisposes them to spontaneously arrest, right? Um A pacemaker is different. A pacemaker is in someone that has a heart block, a heart block is a disturbance between the atria and the ventricles usually caused by disruption to the AV node. This could be caused for a range of reasons. You know, often pharmacological agents can cause it often it it comes with aging. So as people age, they can develop nodal issues. And so if you have disruption to the AV node, then you have a significant risk that the ventricular rate will drop too low. And so in that case, you wouldn't want a defibrillator, you'd want a pacemaker and the pacemaker would, would read the ventricular rhythm in the same way that I've described here and would maintain an adequate heart rate. So that's when you'd use a pacemaker in a patient with a pathology that impairs their normal baseline heart rate. And then a patient that had a significant, a significant problem with the AV node, they, they'd never really be able to generate a heart rate of 80. Never. So, you know, that's why I put a pacemaker in to make sure that their baseline heart rate is safe and it acts as a safety net. So usually you put it in and set it to 60. So that pacemaker will sit under the skin with the wires attached to the ventricles, er endocardial. So, you know, through the like the transvenous way and, and yeah, and that's, that's the purpose of that. I hope that answers your question. And so do you any other questions? Anyone out have any other questions? Obviously, we still have a few minutes if anyone has any questions? Yeah, don't, don't hesitate guys, I'm more than happy to answer anyones if I can. Um OK, so we're waiting for WW if anyone is typing a a request, I'm just going to send the feedback form to the group now and you can fill that up. Mhm Yeah, I'd be grateful if you guys could. Um I really, I really appreciate that. Thank you. So this is the, this is the fifth session in the teaching series. Um Basically a cardiothoracic surgery that have been ongoing for the past um, I think a month and a half now and um for anyone that has attended previous sessions, um, thank you for attending. I hope you have been faithful. You've learned a lot so far. So we've talked about cardiopulmonary bypass. We've had two sessions on cardiac physiology. We've had a session on aortic surgery and aortic disease and this is the fifth session on um, pacing, um, cardio, um epithelial pacing and cardiac surgery. Um I know it, it, it, it, it's, this was very um physiology talking about voltage and all the rest, but hope it wasn't too um, too overwhelming. Um You can, the slides and the this presentation will be made available on the Me page as the on demand content. So if you just want to listen to it all over again, it will be available on the CFF on the CG page. Um So feel free to just um check, check on that. Um We will be having subsequent sessions in about two weeks. Um We are still just uh making plans to um to get to set things up and when, when that's when that session is um when plans for that session is ready. Um I would, I would, I will put up a um put up an advert on the Me on the Me page and on the group chat also, um like every other session has been so just um feel free to check it out. It should be out in. Um, hopefully sometime next week, I'm not sure sure what the topic is because I, I've tried to change around some teachers on topics due to availability of, of speakers. But, um, by early next week, hopefully we'll have, we have, it's all set up and ready and it should be on the middle page. Um, if there are no other questions, um, then, um, the session um, was a bit shorter than planned, but um very insightful. So thank you very much for the, for um for accepting the advice to speak and it's not, it's not quite easy. Um Also, just to also announce that um on also for the C Gaff, there is a teaching session from the general surgery community on appendicitis which is taking place um about 77 15. So, um you can feel fi you can join that also if you're interested in that it's not cardiac surgery. But for other, if you're a medical student or you have interest in other parts of surgery, that would be, that would be a very good session session to join. Um And that brings us to the end of today's session if you have, um please provide your feedback. Um We're very grateful if you can provide your feedback or if you have any questions, um you can, if you have any questions, do you have any questions? I don't think anyone has asked any questions. So we will bring this session to a close and um hope to see you guys in the next. Um The link is on the on, on the messages. So I have put up the put out the message for the feedback link. So um it's on, it's on the message chart. You can provide the feedback or what um Doctor Adi, what link are you talking about? Um Yes, for the other webinar. Um I have yet to yet to have a link. I'm still trying to sort out some things regarding the speaker and when it's confirmed, hopefully by beginning of next week, we will have, we will have it available. Oh, the link for the general surgery session. Yes, I can do that. Um Let me see if I can give me a second. Let me just find it. Mhm. So that's the link for the um the session taking place in, I think in about 10 minutes there about. Ok, everyone. Thank you for joining and uh hopefully see you in the next webinar.