Join the second online webinar session of the UK MRA series presented by Dr. Milan Jacobs. This session focuses on cardiology, specifically tailored for final year medical students or those nearing the end of their medical education and who are interested in working within the NHS. The lecture includes real-life scenarios that doctors often face, providing attendees with practical knowledge and preparing them for potential challenges. This program focuses on high yield topics necessary for a foundation year doctor in the NHS, with specific emphasis on arrhythmias, heart failure, and ischemic heart diseases. Audience participation is encouraged. Attendance is certified and useful for future professional development.
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Are you a newly qualified medical professional or a medical student looking for information on how to effectively prepare for your Medical Exams? Join us for our new 4 part webinar on different aspects of medicine.

Part 1: Heamatology led by Dr. Teilmanns

Part 2 : Cardiology led by Dr. Jacobs

Part 3: AKI led by Dr. Latif

Part 4: Fluid management Dr. Latif

This series is tailored for final year medical students and newly qualified medical professionals who will sit the UKMLA, offering essential advice regarding the different aspects of medicine. Come and join us on knowledgeable guidance within medicine, covering common aspects of treatments and care for patients. Attendees will leave with invaluable insights to help improve patient care during times of crisis and help with a better understanding of the topics lectured on.

Learning objectives

1. To understand the pathophysiology and electrophysiology related to atrial fibrillation within the context of cardiology. 2. To identify the symptoms and signs associated with a patient presenting with atrial fibrillation. 3. To read and interpret ECG results to diagnose atrial fibrillation. 4. To classify and differentiate between types of atrial fibrillation, including paroxysmal, persistent, and permanent. 5. To identify and apply appropriate management and treatment strategies for a patient with atrial fibrillation.
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Computer generated transcript

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

OK. All right. Uh Hello, everyone. Uh Welcome to the second online web webinar session of the UK MRA series. Uh My name is Imron. I'm one of the medical educate educators, uh educators in Medipap. Um Today's lecture is gonna be around cardiology and it's gonna be done by Doctor Milan Jacobs who's in fy two, who's happily come in today. Uh Before we start a reminder for everyone, um feed feedback forms are gonna get sent 15 minutes after the end of the webinar. So if you can do the feedback form, that would be great. It just helps us improve for next time. And when you do the feedback form, uh we can send you out a certificate to show that you've actually come in today um to see the se the lecture today. Um And if you have any questions during the seminar, then just feel free to message in the chat. And then at the end, uh Doctor J Ks will go through the questions um and we will answer them and with that over to you, Doctor Jacobs. Um Thank you very much. Um I just wanna preface this talk by just saying that I'm in no way shape or form a cardiology expert. I'm just an fy two, I'm quite interested in cardiology. So this talk is specifically tailored for final year students or medical students coming towards the end of their unique career um wanting to um work in the NHS. So a lot of the talk is gonna be about scenarios um that are quite realistic within the NHS. So as a doctor, you'll be faced with scenarios when you're on call. Er for example, nurses believe in you to do certain things. And this is this is gonna incorporate a lot of those scenarios. So it's very specifically tailored to what your knowledge level should be like as an fy one slash fy two, but mainly fy one. So I just wanted to preface that. Um So I'm not gonna, so I've, I've picked specific topics for this talk um that will sort of be at the highest yield in terms of functioning as a doctor in the NHS, as a foundation, you doctor in the NHS. So I haven't gone into like full detail about all the all the niche conditions. I've picked a few high yield topics that I think is very useful for us to focus on. Alright, so this is the agenda for today. Uh So we're gonna have a look at arrhythmias, heart failure and then ischemic heart disease cos I think especially when your uncle. Uh those are the main sort of presentations slash pathologies that you'll be faced with and you need to know how to treat them, manage them or at least initiate treatment while you're waiting for senior help. Yeah. Uh, and throughout this talk, if you've got any questions, just pop them in the chat, I'll try my hardest to answer them. Um, as quick as I can. Ok. So the, the form of this is gonna be in the form of different scenarios, as I said. So we'll start off with the first scenario. So you are on call, you're an fy one on call, you're doing a ward cover shift. So in the NHS, er, you've got on call basically means it's out of hours and you're covering different wards where they don't have their regular team present looking after patients. Um, so you are doing a ward cover shift where you're covering multiple medical wards. Uh, and you're holding a bleep and you'll get bleep by nurses from different wards with regards to patients that they're looking after they might be worried about a particular patient and they'll bleep you and ask you for advice. So you need to obviously go and treat patients accordingly. Yeah. So the first scenario is a nurse bleeps you and she goes ok. Um, hi doctor, I've got a 72 year old gentleman that I'm really worried about. Um, so then you ask the nurse. Uh ok, what's, what's the history of what's happened? What are you worried about and she tells you, ok, I've got Mister Smith here in bed too. Uh, he's a 72 year old gentleman. He's currently be, he's currently being treated for a chest infection and he has a very fast heart rate. I'm just really worried about it. Um, and then you'll ask her what his past medical history is as he always should do. Uh, just to get a good understanding of the patient and his background, um, she tells you that he's got a history of high BP, uh type two diabetes previously had an M I. Um, and also got chronic kidney disease. Uh, you ask a bit about the social history, um And you know that he's being followed up by cardiology and renal um for his kidney disease and his heart disease. Um And then you ask the nurse, what, what the um observations are. And she tells, she tells you the temperature is 37.37 degree C. Um, he's saturating around 98% on room air not requiring any extra oxygen. His blood pressure's around 1 50/90 his heart rate is 100 and 40 BPM and his respirate is 18 breaths per minute. Ok. So that is the information that's given to you is 73 year old gentleman who's got a very fast heart rate, um, previous history of renal renal disease and cardiac disease. Um, and you've got the observations there with a heart rate of 100 and 40. Yeah. So you go and see him, um, and you examine him and I'll give you the examination findings. So on appearance, he looks quite anxious and he's a bit uncomfortable. Um, he's warm and dry. Um, he's got an irregularly irregular pulse when you palpate his radial pulse. Um, but his chest is clear. Um, and he's got his heart sounds one and two but no additional sounds. What would you guys do next? Just pop your answers in the chat. Yeah. Brilliant. Yeah. Good. ECG. Exactly. Brilliant. Anything else you guys would do other than ECG? Yeah, good out there. Yeah, so yeah, all of you guys are all saying E CG is a brilliant spot. Exactly. The first thing you would do is obviously ask the nurse, you would even tell the nurse on the phone before you even get there, tell them I'm gonna come and review the patient. Can you just get an E CG um while while, while you're waiting for me to arrive? Yeah. Um So obviously you do an E CG. Um You also wanna do some bloods actually. Um So when you get there, you wanna do some bloods. Um and in terms of other imaging, you do want to also do um a chest X ray as well. OK. So E CG comes back. Uh So they, they've done the E CG and um it looks like this. What do you guys think what's your working diagnosis at this point? Yeah, exactly. It's atrial fibrillation. Good. Very good. So, your working diagnosis at this moment is atrial fibrillation? Ok. So, and how would you treat this situation? So, I knew some people who said antico antiarrhythmics control rate depends on the clinical state. Yeah, I agree with all of that. Um ok, cool. So, before we get into the management of it, I'm gonna go through af just very quickly. Um just so that you guys have a better understanding of atrial fibrillation and that as a result, we'll help you manage it in the future. Um OK. So essentially atrial fibrillation is a condition where you have a rapid and in ineffective atrial electrical conduction and the clinical presentation of it is an irregularly irregular ventricular rate. OK. And you can diagnose it on an ECG uh we'll talk about that first says at the bottom. But basically, um if we go back to the electrophysiology of the heart, so you obviously, you've got the different nodes, you've got the sinus node, you've got the atrial ventricular node, you've got um the um bundle of his and you've got the purkinje fibers. So in a normal heart, you've got electrical impulses being generated at the sin or atrial node to the SA N and then it goes in one direction. So it's unidirectional. So it's only going in one direction and it's not meant to go the other way. So it goes from the SA N to the AVI N and then from the AVN, it goes down the bundle of his and into the purkinje fibers and causes ventricular contraction. Yeah. So it goes from the sa the impulses go across to the atria, causes the atrial atrial contraction goes to the AVN, then down the bundle of his to the purkinje fibers. So in a healthy heart, the, the, the order is always sa Atria Avian bundle of the fibers, SAA and B of the fibers. It should always be in that order. It should never be, it should never deviate from that. Yeah. So if you get that into your head, you understand what's normal. Yeah. In atrial fibrillation, if you look at that diagram on the bottom, right, you can see you've got random electrical activity being generated from various different places in the Atria. So it's not just originating from the SA N but you've got all these little impulses, all these little electrical activity being generated from all over the Atria. OK. And because it's all happening randomly and it's very uncoordinated as a result, what you get is a very uncoordinated contraction and you get on the ECG, you can see it's very, it's irregularly irregular. So what that means is it's an irregular rate but there is no consistency with the irregularity. It just happens. It's almost, it's just completely random. And that's all because if you look at that diagram, you've got all these random little impulses being generated from all over the Atria. OK. So that's what atrial fibrillation is. And in an ecg what you see is you see an irregularly irregular tachycardia with no discernible P waves. And the reason why you don't see any P waves is because like I said, that you don't get the, what's the word? The contraction is not stimulated by the contraction is not stimulated by A, the, the SA N. If that makes sense, it doesn't, it's not coordinated in the sense that it doesn't go from SA N to A VN down the bundle of this, it's just completely random. So it's not dependent on the P wave. OK. So um the key thing to note is that on an ECG uh you don't see any er discern but you don't see any P waves and you see an irregular rhythm. OK. So that's very important to know and which we saw in this patient. OK. So as soon as you see that patient, you can see that the heart rate is very fast and you have a look at this ECG and you can see the no discernible P waves and the, the rhythm is irregular, you know, straight away, it's atrial fibrillation. OK. Cool. Um So there are different types of atrial fibrillation. So you've got parox is more persistent and permanent. OK. Um In, in an on call setting. Um This is not so relevant. Er this is more so, more so for like the chronic management of atrial fibrillation, but it's still useful to know. So, paroxysmal is just another way of saying temporary. Um So it's when you have more than two episodes of atrial fibrillation, when we say it's an episode of atrial fibrillation, it's an episode where they've got a very irregular heart rate and it's not, it's not sinus rhythm. Ok? Um So you've got more than two episodes of atrial fibrillation which lasts less than seven days and it terminates on its own. So you don't need to intervene. You don't need to give any medication. It just terminates and goes back into regular rhythm on its own. So if you imagine all these random little impulses happening across the atria, that happens for more than that, there's more than two episodes of that happening, which lasts less than seven days. So for example, let's say um those random electrical impulses are happening and you've got an irregular rate or irregular rhythm, sorry for three days. But then on the third day, randomly, without you giving any medication, it just goes back into a coordinated rhythm of sa and, and bundle of his, the fibers and it's coordinated again in a sinus rhythm. So whenever we say sinus rhythm, it means there's ap wave before every single QR S. Yes. And uh and that means that the electrical impulse is going from the sa into the Avian in the regimented in an in an organized manner. Ok. So that's what character was. It's self terminating, it lasts less than seven days. Persistent is when you got this, when you've got more than two episodes which last more than seven days. Ok. So it's not less than seven, it's more than seven days and it's not self terminating. So you need to intervene, you need to give medication or do any type of intervention, a specific type of intervention, sorry to terminate the atrial fibrillation and bring it back into sinus rhythm. Ok. So, paroxysmal is self terminating, persistent, is not self terminating and it's longer. Ok. Permanent is when a patient is in continuous atrial fibrillation and they either cannot, they cannot be cardioverted or like previous previous attempts of cardioversion have been unsuccessful. Does that make sense? So, those are three types of atrial fibrillation that you need to be aware of? Ok. Um And then in terms of causes, um there are a few um sort of triggers slash insults to the body that can stimulate and cause or send a patient into atrial fibrillation. Um So the way I split it up is cardiac respiratory and systemic. Yeah. So cardiac causes, obviously ischemic heart disease um is a cause. So if you have a previous um M I where the tissue of the myocardium is damaged, you could, you're prone to having scar tissue develop. Um So the scar tissue in the myocardium predisposes patients to um having uncoordinated irregular electrical impulses because the tissue is not healthy, it's scar tissue. Yeah. So, ischemic heart disease is one, the next one is valvular pathology. So, in particular, um issues with the mitral valve. So specifically mitral stenosis can lead to atrial fibrillation. Um then we move on to respiratory. So, lung causes so and pneumonia and pulmonary embolism are both insults that can happen to the body. Ok, causing a patient to flip into air. I've had a few patients where, um, they've obviously obviously presented with tachycardia and you're trying to find out exactly what to cause them. And then you figure out that their white cells and their CRP is going up and, um, that infection that they're developing or probably a pneumonia that's flipped them into atrial fibrillation and that's caused them to present in this way. Yeah. Uh, and then moving on to systemic causes, um, hyperthyroidism. So everything speeds up. Um, it can cause tachycardia, um, alcohol sepsis, which is linked to the pneumonia. So pneumonia can obviously lead to sepsis. Um, that's a massive insult to the body leading to um, atrial fibrillation and obviously hypertension as well. Um, in terms of what you would do for investigations, your investigations should be tailored to finding the cause. First, you're obviously diagnosing atrial fibrillation that's done by an ECG. But in terms of further investigations like blood tests, imaging things like that, that should be tailored towards, um, finding out what the cause is because if, because if you know what the cause is, then obviously you can treat the cause and you can resolve the atrial fibrillation. Yeah. Yeah, I can see some of you guys have spoken about um different types of um medications that we would do. So obviously, as you said before, um we were doing ECG and things. So I'll get on to that in the next slide. So in terms of clinical features, so if you think back to the patient that we were presented with um on the on call shift, um he was actually asymptomatic. I mean, he was a bit anxious, but he wasn't really complaining of any particular symptoms. The clinical feature that you noticed was that he had an irregularly irregular pulse and he was very tachycardic. Um And in, in the hospital, a lot of these patients will just have that you'll just notice it on the observations and they will be symptomatically, they'll be fine, but it will just be the nurse telling you, oh, you know what my patient's got a really fast heart rate. Um What do I do? Um So yeah, so they are likely to be asymptomatic. Uh So you just need to be very tuned in on their observations. Some of them can however present with palpitations, they'll come to you and say, are doctor I'm just feeling a bit of discomfort in my chest. I just feel like my heart is beating really, really fast. Um, in my chest. Um, and as a result, they'll get some chest pain discomfort. Like I said, they might get some syncope. Um, er, they, as I now and as I said, they have an irregular, irregular pulse. Um, and also the other thing to remember is they might display symptoms of the cause of e so if you think back to some of the causes pneumonia, pulmonary embolism, uh, they might present with a chest pain, they might have a fever bringing up green sputum, um indicative of a, of a pneumonia or if they're very septic, they will just, their body will just completely shut down, just be very unwell. Y you can definitely tell who's obviously got an underlying infection by just looking at how sick they are from the end of the bed. Yeah. So these are the clinical features to look out for um investigations, like I said, we have gone through a few of these before. So, ecg um does anyone know why you would obviously on that moment, you do a, you do an E CG immediately, but in terms of long term slash in a less urgent slash acute scenario, does, does anyone want to put into the chart? Why you would do a 24 to 72 hour tape or E CG as opposed to just an on the spot E CG? No. So, um as I said, there are three different types of atrial fibrillation. So you've got paroxysmal persistent and you've got permanent doing an on the spot E CG is not always helpful because remember what we spoke about with paroxy or atrial fibrillation slash with persistent, the, the, the patient might only be in atrial fibrillation or af only momentarily if that makes sense. So they might be in af just for a, just for a certain amount of time and then go back into sinus rhythm. So, doing an on the spot E CG is not always helpful because you might do an E CG where they're in sinus rhythm. Yeah. So, yeah, exactly. Exactly. Exactly. To know exactly what type of af that's the reason why you do a tape. So let's say over a course of 24 hours, they're in atrial fibrillation for three hours and then the rest of the day, they're in sinus rhythm. If you do an ECG for the rest of the day, you won't be able to diagnose the atrial fibrillation because it's at a period where it's sinus rhythm. But if you do it all the way across 24 hours, you'll pick up the few hours of which they're in atrial fibrillation and then they go into um sinus rhythm. Yeah. And that is all recorded. Then you have a look at the system. Obviously, you upload everything to like an uh get the electronic image and you have a look on the computer and you can see at what points they were in sinus rhythm versus what points they were in atrial fibrillation. Ok. Um So that's why it's good. It's good because it's more sensitive to picking up um atrial fibrillation. Yeah. Moving on to bloods. Uh full blood count using CRP is very good because sometimes electrolyte derangement can cause patients to go into arrhythmias. So, magnesium, in particular is very important to have a look at calcium as well. Um You also want to have a look at full blood count, like I said, for white cell count, see if there's any signs of infection CRP as well. Just to see if they basically um have any insult to their body, which kind of tips them into atrial fibrillation, thyroid function test. Yes, you want to do that because obviously, if they're hyperthyroid, that can be the cause of atrial fibrillation troponin to rule out ischemic heart disease. And as I mentioned, calcium and magnesium. So all of these blood tests you are doing to find out the cause of the atrial fibrillation. Yeah. And then in terms of radiology, you'd wanna do a chest X ray. Um So chest X ray, obviously, you can diagnose a pneumonia if that is what's triggering the atrial fibrillation. Um You can also um do an echocardiogram. So once again, you wanna do an echo with an echo, you have a lot of information. So you can obviously see if there's any element of heart failure and you can see if there are any valvular pathologies. So, obviously, we were looking at what I was talking about mitral stenosis being a cause of atrial fibrillation. So when you do the echo, you can see if there's anything wrong with the mitral valve, um you can also have a look at the overall movement of the heart and see if there's any hypokinetic areas, any regional wall motion abnormalities, which is indicative of ischemic heart disease, which is once again a cause of atrial fibrillation. Yeah. So with the echo, you get a whole whole variety of information that is very useful um on with your ongoing management. Ok, good. So those are the investigations that you would do. Um And remember this is all like in the acute setting. So obviously with the, let me go back to the slide. So with these investigators like chest X ray and echocardiogram, uh but more so with the echocardiogram, it's not something that you would do immediately, that's something that you would do in the next couple of days. But in that immediate setting, when you, when you're in front of a patient who has atrial fibrillation and they've got a heart rate of 100 and 50. Um and you've done an ECG you've diagnosed the atrial fibrillation, you want to quickly just do some bloods, send it off. Um I mean, depending on that, what you're thinking the cause could be. If you're thinking more of an infected picture, you can get a portable chest X ray where the, where the radio bring the chest or the X ray machine and they quickly just scan the chest just to see if there is any sign of infection. Um But even before you even consider an echocardiogram, you want to start treating the patient. Yeah, cos you cos obviously atrial fibrillation is very dangerous. If you use this left very fast, it can lead to serious complications. Ok. So in terms of management, um I think you guys mentioned it before. You were talking about rate control. You're talking about cardioversion, you're talking about anticoagulation. So you bring all of that into one. The way you treat atrial fibrillation is three things. You rate control. So you control the rate you control the rhythm and you anticoagulate. OK? Um Rate control. Obviously, the first one that we use are beta blockers. Um Other medications that we use are calcium channel blockers and also we can use inotropes. So um just a question to you guys give me an example of a calcium channel blocker that you would use for controlling. Give me an example of a beta blocker and also give me an example of a calcium channel blocker that you would use to control the rate. Yeah. Spot on. Exactly good. So yeah, yeah, brilliant. So examples of calcium channel blockers that you use? Oh sorry. Um uh dilTIAZem and ARAP. I'm glad no one said uh so yeah, so you wouldn't use Nifedipine because so with calcium channel blockers, you've got two different types, you've got dihydropyridines and you've got non dihydropyridines. Ok. So the calcium channel blockers that we use for high BP, examples are amLODIPine, Nifedipine, those are dihydropyridines and they act specifically on the smooth muscles of blood vessels. Ok? Um So what, what that does is it stops the vasoconstriction. Ok. So it, it relaxes the smooth muscles. So causing a reduction in BP. Ok. So that's very selective for smooth muscles. Whereas in, if you give amLODIPine in tachycardia, it's not going to be effective because it only targets the smooth muscles. It doesn't target the calcium channel receptors in the heart if that makes sense. So to reduce a heart rate, you use different type of um calcium channel blockers. So you use non dihydropyridines, which obviously target the receptors in your heart and slow down the heart rate. Ok. So it's very important that when you are treating a patient and you're considering calcium channel blockers, you don't go to amLODIPine cos that's for, for BP management, you go to verapamil or dilTIAZem. Yeah, good. Um Examples of beta blockers is uh um mesoprion is the first one that you use. Um You can start off at 1.51 0.25 mg and titrate upwards um of a max of 10 mg once a day. Um And this is all sort of based on how the patient responds. Um examples of inotropes are basically um digoxin. So what digoxin does is it slows down the heart rate, but it also improves contractility. So, if you're worried about patients dropping their cardiac out, but you can give digoxin because it helps maintain the contractility. So you have a good stroke volume. OK? Um And you for digoxin, you usually give her 500 mcg as a loading stat dose and then you give 1 mg over 24 hours. Um So a total of um 1.5 mg. OK? Um In terms of um what was I gonna ask you guys? I was gonna ask you a question. Um We're talking about beta blockers, calcium channel blockers. So that, that's the rate control part done. Yeah. So when, when you're in a, in an acute situation, when you've got that patient in fast af your number one priority is to control the rate you need to control it and you, you roughly aim for around below 100 BPM. Um And you obviously wanna do repeat EC GS or once there, uh You either want to do repeat EC GS or obviously when you're on your own, you've got the patient, they're in af you start rate control, you start them on bisoprolol. Um You obviously, the first thing to do is straight away, escalate to your senior call, your medical registrar, tell them to come and see, tell them to come and see the patient. Um and then what you do is you tell the nurse, can you please complete the site manager? Site manager is the person who organizes beds and everything. And can you please organize a cardiac monitor bed for the patient? Because you need the patient to be on a continuous cardiac monitor because they're in an arrhythmia. You don't know what could happen. You need to know exactly what the rhythm is at all times. So you move them to a cardiac monitored bed. OK. So break control escalate to see your cardiac monitored bed. Cool. So you've done that. And then what you do is in terms of the other management of rhythm or other management of atrial fibrillation, other things that you can do is controlling the rhythm. So as you guys are saying perfectly, um you would cardio, there's two different types of cardioversion. There is pharmacological and there's also electrical. So electrical is obviously given electrical shock. Um So you do synchronized cardioversion. So make sure you um reestablish sinus rhythm for the patient. OK. And in terms of pharmacological cardioversion, there are different medications that you can use, which would fix the irregular rhythm and flip them back into sinus. So, examples of flecainide and amiodarone, OK. Um Now, in terms of the cardio version, you wouldn't do it for every single patient. OK? Um For reasons that I'll explain in the next slide. But one thing to really, really, really understand and make sure that you cover is basically know exactly how long they have been in atrial fibrillation. And think about stroke risk and clotting and the risk of emboli forming and think about the need to anticoagulate patients before you cardiovert them. Ok? And as a rule, if they have been in atrial fibrillation for longer than 48 hours, you're not going to cardiovert them straight away because you basically assume that because they've been in atrial fibrillation for that long, there is a higher risk that they would have already formed a blood clot and you cardioverting them and sending them back from atrial fibrillation to sinus. There's a high risk that the blood clot that's formed can be pumped to your brain and cause a stroke. Ok. Now, my next question is why do patients in af have a higher risk of blood clots forming slash stroke? What is it about atrial fibrillation that increase the risk of blood clots? Yeah. Spot on exactly blood stasis. Yeah. So if you imagine the mechanism of atrial fibrillation. So if you imagine this, my hand here is the atria because of the random electrical impulses, you don't really have proper effective atrial contraction. So in a normal heart, your atrial is meant to contract like this. Yeah, to pump the extra blood into the ventricles. Ok. But in atrial fibrillation, the electrical impulses cause the atrial to do this. So it's not effective contraction. So, because usually the heart is actually doing this. But because in atrial fibrillation, the heart is doing that the blood here is not moving properly and that causes blood stasis and blood stasis is part of work of triad um which increase the risk of blood clotting. Yeah, good. So that's why you need to think about anticoagulation for all patients in atrial fibrillation. And you consider it for all the patients, you don't do it for every single patient. Um but yeah, that moves us on to anticoagulation. So first line is a Doac so example is it Apixaban and Doxy um Rivaroxaban. Um in the past, you would use Warfarin. Um but now the guidelines are not to use Warfarin because it's quite tedious for patients to have weekly blood tests. Cos if you're on Warfarin, you have to have weekly blood tests to check your I NR and your clotting function. But um in with Apixaban and like Dox in general, you don't need to have regular monitoring. So it's a bit easier for patients to manage. Yeah. So when you're deciding if a patient needs to do an anticoagulation to reduce the risks of blood clots and strokes, you do two scoring systems, you do a chads scoring system and you do an orbit scoring system to calculate the clotting risk or stroke risk versus the bleeding risk because obviously when you're giving them anticoagulation, there's an increased risk of bleeding. Yeah, so it's all a balance for these patients. So patients are either put on anticoagulation based on the balance between a stroke risk and bleeding risk. Yeah, if the bleeding risk is higher than the stroke risk, you wouldn't put them on anticoagulation. But if the stroke risk is significant and it's higher than the bleeding risk, then you would put them, put them on anticoagulation. Ok. So just to recap, you control the rate you escalate to your senior, move them onto a cardiac monitored bed and then you obviously your senior will help a lot, but you obviously discuss with your senior with regards to rhythm control and obviously anticoagulant patient based on the chad vs and orbit score. Yeah. Um OK. Cool. Um Moving on to when to cardiovert. So obviously, as I said, cardioversion is an option, but you wouldn't do it for every single patient. So you would do urgent DC cardioversion. Obviously, after you've spoken to cardiology, after you've spoken to your seniors, if they are hemodynamically unstable. So, if their blood pressure's dropping because of this very fast heart rate, this heart rate is very, very fast to the point where you don't get adequate ventricular filling and you're not getting good cardiac output and your blood pressure's dropping as a result. Um obviously, that can lead to lack of brain perfusion and things that's gonna be very detrimental. Secondly, if they're complaining of chest pain. Um So there's, if they're showing signs of myocardial ischemia. Um and thirdly, they've got signs of acute heart failure. So if they're having difficulty breathing, they've got bilateral crackles, they've got signs of pulmonary edema. You notice that on chest X ray. So those are three situations in which you do urgent DC cardioversion because it's detrimental to the patient if you just don't cardiovert them. OK. So if, when they, when we say a patient is unstable, those three things are what we need. OK. So that's when you do do DC cardioversion. The next situation you do, you would consider um cardioversion in, in these four scenarios. So if there is a clear and reversible cause, OK, of the atrial fibrillation. So for example, if it's caused by a pulmonary embolism or a pneumonia, and you're confident that treating the cause will resolve the atrial fibrillation, then once you treat the cause, you can think about cardioverting the patient because obviously you've gotten rid of the trigger that's put them into atrial fibrillation. Second is if the patient is unlikely to slip back into atrial fibrillation following a cardioversion. Thirdly, if the symptoms are still persisting, um despite controlling the rate, then you would cardio cos that basically just means you're still probably at risk of becoming unstable and deteriorating. Um And then lastly, if the rate control is not successful and they're just still very unstable and you're not able to manage the situation, then you would think about cardioverting. Ok. So those are situations in which you would cardiovert, but just the main things for you to know are the first three. So you'd have to consider urgent DC cardioversion in the first three. But remember as an F one, when you're treating the patient, you will help, you will ha have help sorry around you once you escalate to a senior and they will help guide the decision. OK. Good. Um I'm gonna move. I hope that hopefully that was, that makes that a that makes sense. So I should say, um I'm gonna just do a very quick brief talk on um, arrhythmias. Once again, you don't need to know this in a lot of detail. Um I've just included information that I think is very helpful to know. Um, because I think as a student, I didn't fully understand arrhythmias and I found it very complicated, but the reality is when you start working, you don't really need to understand all the ins and outs of arrhythmias. You just need to know why it's why broadly, you just need to understand roughly what's happening and what your rationale is for choosing certain medications. Ok. Um, so arrhythmias basically very quickly, just quick run through, you split it up into too slow or too fast. Ok, bradyarrhythmia, it's too slow. Tachyarrhythmia is too fast. Ok. So bradyarrhythmias, there are three main types. You've got sinus, bradycardia, junctional, bradycardia, and you've got heart block, ok, tachyarrhythmia, you've got, you split it up into two sections. So you've got a narrow QR S OK. Um So a narrow QRS means that the ventricular depolarization or the QRS complex is less than 0.12 seconds or three small squares. OK. And broad QRS is the opposite. It's greater than 0.12 seconds or three squares, three small squares. OK. So in terms of brady arrhythmias, so a sinus, brady arrhythmia is basically, it can be physiological. So if you've got very fit athletes, so a good example is, I don't know, just Usain bolt. Um in his prime, he would have had a very slow heart rate just because he's a very fit and healthy individual and he's an athlete. OK. So it's normal for patients or people who are a very healthy to have a slow heart rate. Um and this is normal because it's sinus rhythm. So it's very coordinated. The impulse is from the SA NAV and bundle of the king fibers. It's in that regimented manner. OK. Good. Um junctional bradycardia basically just means that there's basically, it just means that the electrical impulse starts from the junction. Uh So in other words, it starts from the AV node um and it doesn't start from the SA node. So in an ECG the P waves will be absent um or it will come after the QR S complex because the ventricular depolarization is not dependent on the SA node. It starts from the AV node and goes down. OK. It's the bundle of his and the pin fibers. So that's what Johnson and Brady Cardia is. Um, heart block essentially just means um there is a miscommunication or problem with the wiring in the, in the electrical conduction system between the SA Nan and everything. Ok. So it's a problem with the electrical activity communication from the SA node to the AV node. And there are three types which we'll get into later. But one thing I want to keep it very broad um because I don't think you need to know in too much detail when you're managing these patients in an acute situation. So you've got first degree, second degree, which is split up into Mobitz one and Mobitz two. And then you've got third degree heart block. OK? Um And then on the flip side, tachycardia, you've got a narrow QR S which basically narrow QR s just remember just memorize this narrow QR S means supraventricular tachycardia and broad QR S means a ventricular tachycardia. And what we mean by that is in a narrow complex ie supraventricular tachycardia or svt. The reason for the fast heart rate originates from above the ventricles, OK. And in ventricular tachycardia or what the broad complex tachycardia, the reason for the fast heart rate originates from the ventricles. Ok. So, supraventricular tachycardia is above the ventricles and it means a narrow complex um ventricular tachycardia is from the ventricles and it means broad complex tachycardia. OK. So that's, that's basically the broad overview of what you need to know with regards to arrhythmias. Ok. And now this slide is quite important because, like I said, when I was a student, I didn't really fully understand why certain medications were used. Um, I didn't really understand the rationale behind it and I found it very difficult to memorize it. But I think when you start working, like I said, you just realize you need to pick out different, different bits of information that is useful for you to know, to justify what you're doing. So if you understand it more than try to memorize random medications, you will find yourself just remembering it a bit easier because you understand the rationale behind it. So the the reason behind tachycardias and bradycardias and all that stuff, the arrhythmias in general, it's, it's largely because of if you think back to the cardiac action potential. Well, in general, the cardiac action potential or electrical impulses are stimulated or it's generated due to or was generated by the movement of ions or charged ions going into and out of the cells. If that makes sense. So into and out of the myocytes, you've got movement of the ions and the movement of the ions is what causes the electrical impulse to be generated, the electrical activity to be generated. Ok. So in arrhythmias, there is an inappropriate influx and efflux of ions across the myocytes. Ok? And that's what causes the arrhythmia. So when you're treating, when you're treating patients. Yeah, when you're treating patients with arrhythmia, what you're doing is in your, in your, in the back of your head. You're thinking, ok, it's probably because of an issue with the electrolytes or it's, it's, it's due to an issue with the receptors or an issue with the movement of the electrolytes across the, the channels in the myocytes. So therefore the medications that I'm going to give, even if you don't remember the specific medication, just think in your head, the medications that you are going to give are going to target these channels broadly. And you're basically going to try and normalize the movement of the ions across the myocytes or the cardiac cells. Does that make sense? Yeah. So just remember electrolytes are moving across the myocytes and as a result when you're treating, you are basically trying to normalize the movement of the ions. Ok. So I'll go through the 4 may or very broadly, I'll go through. So the four main anti arithmetic agents that you use for patients. Obviously, you've got sodium channel blockers. So obviously, that's an electrolyte beta blockers, uh Bisoprolol that you would use potassium channel blockers and calcium channel blockers. Ok. So if you think back to atrial fibrillation and things we talked about controlling the rate by giving them beta blockers and calcium channel blockers. This is why. So you think you're basically thinking of the electrolytes moving randomly in a, in a, in a in an abnormal manner in terms of how fast they're moving and like all that stuff. But just think back to these four types of medications, see exactly what it's doing and you don't have to when you're working. Like I said, you don't have to know all the specific details, like all the different ions or whatever, but just remember this is how it works. Yeah. Um, so now you know exactly why you're giving flecainide cos a sodium channel blocker because there's too much sodium influx or efflux or whatever it is. Yeah. And then now you know why you're using amiodarone co a potassium channel blocker. Yeah, good. So that's why you would probably use anti arithmetic agents for the treatment of arrhythmias. OK? Cool. So going quickly, just going very quickly back to heart block. Um like I said, um you've got first degree, second degree and third degree. So first degree is defined as a pro. So you've got a prolonged conduction from the SA to the AV node. So essentially you've got a very long pr but it's consistent. OK. So it's a long pr which is longer than naught 0.2 seconds. OK. So it's longer than um naught 0.2 seconds and it's consistent and it's regular. OK. So you still, it's still sinus. So you've still got po before QR S but it's prolonged. So it's a bit of a delay. It's a bit of a lag between the conduction from the Atria to the ventricles. OK. So that's what first degree is second degree. Like I said, there's two types, there's Mobitz one and Mobitz two. Yeah. So Mobitz one, the way I remember it is, I think you guys probably remember this phrase. It's going, going gone. So essentially you've got progressive prolongation of conduction through the A V node. Um and then eventually you get a miss beat. So you get a failed conduction. So you get the, the conduction is prolonged. So through the AV node. So going the electrical impulse is going from the atria to the ventricles. It's prolonged, meaning it's delayed and it keeps getting more and more and more delayed to the point where it reaches a point where it just misses a beat. So there is basically um a missed missed electrical impulse going from the atria to the ventricles. OK. So that's going going on. So the Pr gets longer, longer, longer, longer, then it's gone. So you get AP wave Q RSP wave QR S was longer P wave QR S was even longer. Then you have P wave, then a missed beat, then you get P wave again and then a QR S Yeah, I shouldn't have said Mr. So it's P wave Q RSP wave QR S is a bit longer. P wave QR S is a bit longer. Then you get P wave, no QR S then P wave again, then QR S Yeah. And you keep repeating that cycle. So that's, er, Mobitz type one, Mobitz type two. there's, there isn't, it's not progressively getting longer, the conduction is not getting delayed, progressively. It's more that, um, basically you get, um, what's, what's, it's, it's an intermittent failure of conduction of an impulse. So some beats are conducted, some beats. Also, some impulses are conducted from the atria to the ventricles. Some are not, um, so typical examples are like you have 2 to 1 block. So 2 to 1 block is basically when you get two. So two sets of P waves being conducted to QR S, but then you get AP wave that's not conducted to a QR S. Um And then you, then you get another two P waves conducted to a QR S and then you get AP wave that's not conducted to QR S. So it's 2 to 1. So for every two conducted impulses, you get one non conducted electrical impulse. Does that make sense? Hopefully? Um So that's Mobitz type two. And then you've got a third degree heart block which is there's a complete dissociation and complete loss of conduction from the atria to the ventricles. Ok. So um the atria is not responsible or the, the sa node uh causing impulses, electrical impulses going across to the atria via the A V node. It's not properly working. So the ventricles, what they do is the ventricles actually have this very clever system where they have pacemaker cells within the ventricles. So even though the ventricles are not receiving impulses, electrical activity from the Atria, telling it, telling the ventricles to contract the ventricles. Just realize, oh, wait, hang on, I'm not getting any impulses. So I'm going to contracting on my own. So they generate their own impulses. And that's why there's a complete dissociation between the atria and the ventricles. So when you have a look at the ECG, there's no relationship between P waves and QR S complexes, the P waves go at a certain rate and you get QRS complexes going at a certain rate, there's no relationship between the two. Yeah. So those are the three main types of heart block and I hope that's helpful. Um In terms of what you would do for treatment of this, you would, they type two, Mobitz two and third degree heart block need a pacemaker because otherwise they can't, it's not sustainable. OK. Um OK. So I'm very quickly go through this. Um So management of bradycardia. So obviously, if you're uh face and the patient's got a very slow heart rate, like let's say less than 30 whatever. Um And you're on the ward and you're treating the patient once again, always revert back to your ABCD E approach. So, airway breathing circulation, disability and exposure always do a systematic approach. Every single patient with a slow heart rate or a fast heart rate needs an ECG um I say every single patient but remember back to the situation where I said the patient is very fit and healthy sometimes, you know, when it's normal for a patient, for example, if they're like 40 or 50 BPM and they're an athlete, then you're probably are, it's completely fine. Um But yeah, other than that as a broad rule, uh well, that's like a main rule. Every patient needs an ECG um you do their basic observations and then obviously, like I said, you have a look at the bloods. Um You wanna specifically have a look at the electrolytes, like I said, it's because of an influx and efflux of ions across the the um myocytes. So you want to fully have a look and see if their calcium is off, if their magnesium off is off, their sodium is off, the potassium is up. You want to know exactly what the cause is. Um thyroid function tests to have a look and see if the hyperthyroid or hypothyroid. And obviously you want to do troponin because obviously a complication of arrhythmias can be myocardial infarction. Um OK. Um And then the next thing you do, you escalate to your senior. So you immediately get, you get on the phone and you call your medical registrar and you get them to come and review the patient and then eventually you will refer to cardiology who can give you some good advice. OK. So that's what you do immediately. Then once you've discussed with your registrar, you can give atropine um then what you do is in terms of the um the algorithm, you give 500 mcg and you can give it six times to for a total of 3 mg IV. OK. And what that does is that basically speeds up the heart rate in patients that have a very slow heart rate. OK. Cos the problem with a slow heart rate is if you think back to the cardiac output equation is stroke volume multiplied by heart rate is equal to cardiac output. So if you have a very slow heart rate and they're not able to compensate with their stroke volume being higher, um you have a reduction in their cardiac output and having a reduction in their cardiac output. Obviously, that leads to perfusion issues, problems with perfusion of end organs, for example, brain other organs, it's very, very important that you correct this. Yeah, so obviously you give atropine which is a muscarinic. So it's a muscarinic antagonist. Um so that speeds up the heart. Um if atropine is not effective, you can consider an isopro infusion but realistically from number four onwards, you will have seen your help anyway. Um but this is very useful for you to know. Um just so then er you understand exactly what's going on. I mean as an F one F everything from five onwards will be done with a senior anyway. So don't worry about that. But obviously as you progress later in your career, you need to be able to initiate management as you're a regis when you become a registrar and things like that. Yeah. Um, other things that you can use other n of Preline, you can use a violin. Dopamine Glucon. Um, I'm not gonna get into how that all works. Er, cos I'll be honest. II don't, I don't even know how it properly works in terms of the mechanism of action. But the thing is you don't really need to know it or as an F one F two, you don't really need to know it. Um And then obviously, after you've discussed the cardiology, if the pacing attempts that you've given like medically are not working, then you need, they need to take them into the Cath lab and consider transcutaneous pacing. So that's basically when you're controlling the heart rhythm and you're pacing at a, at a, at a safe rates at the moment. The issue is their SA N or their pacemaker, their natural pacemaker in the SA N is not properly firing um at a sustainable, fast enough rate, seem to pace it properly at a safe rate. Yeah. Um and like I said, er, Mobitz two and third degree heart block need a permanent pacemaker. Um type three heart block needs a pacemaker because obviously there's a complete association, there's a complete disconnect between the atria and the ventricles. So you need a pacemaker to coordinate everything properly to go from SA N A node bundle of his pin FRS um Mobitz two. There's an increased risk of it going into um uh a third degree heart block. So that is why you would, uh that's why you would um do a PP PM pacemaker for that. Sorry. Um OK, I know we're coming up to the one hour mark, but this talk is gonna go later, but if you guys need to leave, that's completely fine. It's gonna be recorded anyway. Um but I'm just gonna keep talking until um I can get to the end. Um cos I think er the other topics are quite useful as well. I think um management of tachycardia. Um like I said, um before we kind of touched on it with regards to atrial fibrillation but obviously like very similar to the bradycardia segment A A to E approach ABCD E ECG basic observations, bloods routine, you do routine bloods, thyroid function tests, electrolytes, escalate to see you refer to cardiology. It's the same regimented pattern. OK. Um In terms of if, if there are life threatening issues, like we mentioned before, if they're he un unstable, showing signs of heart failure, showing signs of ischemic heart disease, you do a synchronized DC shock up to three times. If the third attempt is also unsuccessful, you would give amiodarone. Um And then what you do is um basically, when you initially do the ECG, you will have a good idea of whether it's a narrow complex or if it's a broad complex and then from that, you treat them both differently. So if it's a narrow complex, it's a supraventricular tachycardia. If it's a broad complex, it's a ventricular tachycardia. In the situation of a ventricular tachycardia, you would treat with amiodarone 300 mgs as you can see on that diagram there. Um If you, if you're faced with a supraventricular tachycardia or a narrow complex tachycardia and it's regular. Um You would start with the vagal maneuvers. So you do a carotid sinus massage. Um I had a patient the other day on the wards who went into SVT. So we started doing carotid sinus massage and you also try and do valsalva. So you get a syringe to get the patient to blow very hard into the syringe, lift their legs up and do a repeat ecg to see if their heart rate is controlled and the rhythm is OK. Um If that doesn't, if the vagal maneuvers don't work, you, then what you do is you give adenosine, so you start off with 6 mg, then you give 12, then you give 18. Um And then obviously, you can consider wrap or beta blockers and then you can give a DC cardio version, administer a shock atrial fibrillation. We already went through rate control, rhythm control, anticoagulant. Um Quick question, not question, sorry, quick to quickly just to clarify. Um So S VT basically is different to atrial fibrillation because SVT is regular but atrial fibrillation is irregular. OK. So that's just important for you to know. And even though both of them have no P waves, you just differentiate between them by seeing that SVT is regular and atrial fibrillation is irregular. OK. So the treatment for both of those would be different. Um OK. Cool. So um the next, the next case that I'm going to do is, um, so you're on, on call, take shift. Ok. So take shift is basically when you are the medical doctor who's gonna go and see patients who have just presented to hospital for the first time and you're just basically doing a full clock and if you're taking a history, you're examining and then you are treating accordingly to what your findings are. So essentially a lot of the times you are the first doctor that the patient has seen in the hospital. Um, so this is what happens in your take shift. So you go and see Mrs Johnson who arrives in the emergency department, um, complaining of increased shortness of breath over the past week. Um, she said that her swelling in her legs is worsening, um, has been getting worse over the past week or so and it's especially worse around the ankles. Um, she also notices a persistent cough that's been, um, worse during this week period. Um, so she's come in with shortness of breath and cough and some swelling in terms of past medical history. She's got a history of hypertension. She takes amLODIPine for that. She's got type two diabetes. She, she's on Metformin well controlled. Um, she's got a previous history of, um, myocardial infarction. She had a stent put in five years ago. She's also got a, she's also got chronic kidney disease. Um, and you also, she also has a history of heart failure with a reduced ejection fraction, which was diagnosed three years ago. Um, and she's on uh Carbo and Furs. Ok. So you go and examine her and you find out that her BP is 100 and 60/90 heart rate is 100 and 10 BPM. Respirate is a bit up. Uh Was, it was quite significantly elevated actually. Um, and her oxygen saturation is at 92% of air. Um, she's working very hard to breathe. Um, when you examine her and her peripheries show, well, her, she has a regular pulse but she's got bilateral pitting edema up until the midst and she's got an elevated JVP. And when you listen to her chest, she's got bilateral crackles at the base. It heart sounds are normal. Ok? So what would you do next? I can see you guys have put in some differential diagnosis. Um, what would you do next in terms of, uh, we've already examined her. What would you do next in terms of investigations? Good, good, good, good, good. Very good, very good. So I can see a lot of you said the ECG chest X ray echo. Perfect, brilliant. So ECG shows a normal sinus rhythm and she's actually rate controlled. Now, her heart rate is not too fast. Um You do some blood as well. Pardon me? Um The full blood count is normal white cell count is completely fine. CRP is 10. Her electrolytes shows some derangement which is a little bit low potassium because he's on genetics. Anyway. Um You also do a BNP level um which is quite important. We'll talk about B and P in a little while. Um Essentially long story short, BNP is a good marker of how much stress the myocardium is under. So how much strain the, the, the, the heart muscle is under. It's a good sign. Um So the higher the BNP is the more indicative of the, what's the word of the strain on the heart if that makes sense? Um They notice in terms of radiology, you wanna do an echocardiogram. Um And you also want to do a chest X ray. Um So in this situation, we assume that she's, we've done a bedside echo and she's got a left ventricular ejection fraction of 33% um which is obviously reduced. Um And you have a look at this chest x-ray, what do, what do you guys think? What does the chest X ray show? One person said cardiomegaly potentially the reason why I'm not gonna give you that the reason why I'm not gonna accept that. It's a good thought. It's very good thought. Um The reason why I'm not gonna accept that is because you don't know if this film is AP or PA. Um So AP versus PA is basically a direction in which the X rays travel through the body. So PA is from posterior to anterior AP is anterior to posterior in a chest X ray where it's ap you cannot interpret the heart or the size of the heart. Ok. Only in pa films can you interpret the size of the heart? So, without knowing if this is AP or PA, you were, you're not allowed to say that it's cardiomegaly. Um If it specifically said it was apa radiograph, then yeah, I would have accepted cardiomegaly. Um But it should be more than 50% of the overall uh width of the um the lung fields. OK. So that was a good thought. So cardiomegaly would, would be one um pulmonary edema. Very good. So if you, I'm not gonna go through all the different little signs of cardio like of um pulmonary edema. But if you have a look um or have a look at the lungs, one, you can see it's very fluffy, fluffy is the word that we it's very fluffy. It's not area is meant to be black. So it's not the lung feels you can see that there's something uh in between the X rays and obviously the, the air. So that's essentially fluid, that's fluid that's accumulating around the lungs. And that's why it looks, it has that whitish type of picture and it's not very opaque. Ok? Not opaque, it's not very lucent or like very you you can't properly see it. Um So, and that's because of all the fluid and this is a classic chest X ray which shows cardiogenic pulmonary edema. Ok. Good. So I think you guys have already said you guys have said heart failure. So the working diagnosis is decompensated, heart failure. Ok. So how would you guys treat Mrs Johnson? Just put a few things in the chat and then before I go through the management, I'm just, I I'm gonna go through heart failure and talk about a few things that um that I think is very important to know as an F one which I didn't fully understand before I started working. Theresa might very good. Very, very good. So, yeah, I think you guys are on the right line so you can get oxygen therapy. Very good. So, flusemide oxygen therapy. Good. So we're gonna go through heart failures very quickly and like I said, very similar to the other stuff, other topics that we went through. Um it, it, it's very important for you to understand the pathophysiology slash the, the broad concept of heart failure just because then you understand why you're doing certain things when you're treating patients with heart failure. OK. So to define heart failure, so basically, it's if you look at the bottom right corner, that diagram, it's a mismatch in the supply and demand. OK? That's broadly speaking, what heart failure is. So if you go back to basics, your organs or your tissues need oxygen to survive what delivers oxygen to your body or to your tissues, it's blood. OK? So as a result because they need oxygen, they need a good blood supply. They need good blood supply. Yeah, good, good, good perfusion. Ok. In order to function properly. Ok. So heart failure is when there is not enough supply of oxygen or blood going to the tissues to meet the demands of of to meet the oxygen demands of the tissues. Does that make sense? So the blood or the oxygen demand of the tissues is too high and the the oxygen supply by the heart pumping the blood to the tissues, it's not, it's not enough for it to meet the demand. Ok. So like I said, the cardiac output is not enough to meet your oxygen demand of the tissues. And if you think back to your equation, cardiac output is equal to stroke volume multiplied by heart rate. Ok? And your classification of heart failure is based on ejection fraction. So you ejection fraction is essentially um so the equation is stroke volume divided by end diastolic volume multiply by 100 and the best way I can describe it is if you think back to your cardiac cycle where the blood fills, blood fills into the ventricles and the. So if you split it up into diastole and systole, yeah, diastole is when blood is filling into the ventricles, it's relaxing. Ventricles are relaxing and then systole is when the blood is being pumped out because the ventricle is pumping out at the end of diastole. So, at the end of the filling phase where the atrial ventricular valves, the tricuspid and the mitral valves shut, you've got a certain amount of blood inside the ventricles inside the right and left ventricles. Ok. So let's say you've got about um what's the word, let's say you've got 100% just for, just for argument's sake, we've got um X amounts of blood in the ventricles at the end of diastole or the filling phase. Ok? When you then pump blood out from the ventricles during systole, not, not all of that X amount of blood is gonna get pumped out with systole. Does that make sense? It would only be a certain percentage of that X amount that is in the ventricles at the end of diastole in a normal healthy individual. That percentage is above 60%. Ok. So, in probably like myself, my ejection fraction would be above 60%. So 60% of the blood that is left in the ventricles at the end of the filling phase is pumped out with every heartbeat. Ok. So the stroke volume is probably stroke volume will probably be above 60% in a healthy individual of the end diastolic volume. Ok? Cool. So, um just to make it a bit more clearer, if you imagine the end, if you look at this equation and the end diastolic volume, let's say very just, you know, just to keep it simple numbers, it's not the right number at all, but it's just to keep it simple numbers. The end diastolic volume, let's say is 100 100 mL and the stroke volume with every pump is 70 mL. If we do 70 divided by 100 times by 100 obviously, that's 70% ejection fraction, ok? So that's basically what you classify heart failure on. All right. So heart failure is a mismatch between the supply and demand of oxygen slash blood through the tissues, ok? And that's all to do with your cardiac output. Now, in terms of pathophysiology, like I said, you've got preserved ejection fraction and reduced ejection fraction. So, reduced ejection fraction is a bit easy to understand. The issue is the pumping. So not so less than 50% or less than 40% sorry of all of the blood that is at the that is inside the ventricles at the end of the filling phase is pumped out with every single heartbeat. And that's not good enough because less than 40% means that not enough blood is gonna get pumped out with every single heartbeat to the peripheries or to the tissues. Ok. Um And basically you get a good filling phase. So, diastole is normal, but systole is abnormal with reduced ejection fraction. Ok? And examples of that is ischemic heart disease, valvular disease and hypertension. So, if you imagine with ischemic heart disease, you've got a problem with one of the areas where the coronary arteries are supplying. That myocardium is not gonna be able to pop properly. So therefore, you get a reduced ejection fraction, preserved ejection fraction is when you have normal normal ejection fraction. But the issue is the problem with the filling face. So you might get X amount of blood going into your ventricles at the end of what's it called? Um um at the end of the filling phase. But when you're pumping, you're pumping a good proportion of the blood. But the initial amount of blood that's staying in your ventricles at the end of diastole is not enough. Does that make sense? And examples of that? Obviously, once again, ischemic heart disease, obesity, hypertension diabetes. Ok. I hope that sort of makes sense. Ok. Um So those are the two ways in which you classify um heart failure right? So now you've got uh I think we've already spoken about this. Well, I'm not gonna get into this because we've already spoken about the different causes of heart failure, reduced ejection fraction, preserved ejection fraction. Ok. So this is, this is probably one of the most important slides for you to know when you're working as a foundation year one doctor in the NHS. So II didn't really fully appreciate this when I was a student. So I think it's very important for you guys to know cos I don't really taught me this properly when I was a student. So I think this is very important to understand when you started working. So there's a clear difference between acute heart failure and chronic heart failure. Ok. So chronic heart failure is basically, if you read that first sentence of people with chronic heart failure, let's say their pumping function is not good. Their ejection fraction is not good. They have heart failure by definition because their cardiac output is not good enough to meet the demands of the tissues. But patients are still, it can be asymptomatic because they are managing well with the maintenance dose of medications that they're on. So the genetics that they take the bisoprolol that they take. Um, the, um, what's it called? The, um, prognostic medications that they take? They are well controlled in symptomatically because of the medications that I take. Because if we go back to uh that diagram here, this mismatch at the bottom here is not present. It's more of a balanced scale. Yeah, cos you could be in chronic heart failure but the medications tip the balance like this. Ok. So you won't be symptomatic because your heart is just about functioning at the right level for it to meet the for the demand to meet the supply, ok, or supply to meet the demand, sorry. So chronic heart failure is when patients are managing well with their medications. Ok? But acute heart failure is also known as decompensated heart failure. Ok? And what we mean by that is there is for example, there could be an insult or something to the body, which basically if you go back to that scale, it suddenly tips the scale to the point where the supply is not meeting the demand and that can be an infection that causes it. It can be non compliance with medication that causes it. But long story short, the cardiac output is not enough to meet the demands of the tissues peripherally and that causes symptoms. Ok. So that's the key distinction between acute heart failure and chronic heart failure. Chronic heart failure, patients are compensated with medications, acute heart failure, patients are decompensated and their cardiac output is not meeting the demands of the tissues. Does that make sense? Hopefully? Um So that's very important for you guys to understand and that's very important because the treatment of both of them is different. You treat acute heart failure differently in terms of the aggression of the genetics and things that you use compared to the chronic heart failure. Um Someone's asked me to go back to the previous lines. I think is it this one? So this is just a slide just going through the causes of preserved ejection fraction and reduced ejection fraction. Um Yeah, I'm not gonna go into too much detail. I think you just kind of have to know this. Um But yeah, so moving over to symptoms. Um so you've got left heart failure and right heart failure, which is another sort of way that you can cla classify it. Um The best way that I can describe it how to explain it is on the next slide. Um Just for you to remember, left heart failure, patients present with shortness of breath orthopnea, um P and D and the cough, typically, they describe it as like a pink frothy sputum, right heart failure, you get peripheral edema. So ankle swelling, you can get uh ascites. Uh You can also get a hepatic impairment as well. So if you have a look at the side, so you split the heart into um right side and left side. So the best way that I can describe it is the heart is not pumping properly. So, as a result, what happens is the blood just stagnates a little bit and it congest it, there's a lot of blood congestion. So the blood backs up. So if the blood is kind of not raining static, but it's, there's not enough fast movement of the blood because the pumping function is messed up. So what happens is the blood backs up from the left ventricle, going back up um through the pulmonary vein, um and goes back to the lungs and basically the blood just sort of stagnates and congests around the lungs and all the fluid from the blood leaks out into the lungs and causes pulmonary edema. So, the reason why you get symptoms in heart failure are just as a broad concept is because the blood is congested all over in your network of vessels because the movement of the blood is not properly good because the the heart is not pumping properly. And that's what causes symptoms and pulmonary edema, that's a sign of left heart failure, um ascites, um swelling all over your body. J BP being elevated, that's all a sign of congestion on the right side of your heart. Ok. Hopefully, that makes sense. So you, so you make sense of it by splitting it up into left and right now, clinical signs of heart failure, we kind of spoke about it, raised J BPS. Um So basically, you either see peripheral edema or you see uh a fluid around your lungs. Um So those are the main signs of heart failure you need to look out for. Um and they obviously they might have weight gain because of the heart uh because of the fluid being sort of accumulating in the in the interstitial fluid, interstitial um tissue, sorry. So the blood because it stagnates or it congests, the fluid leaks out from the blood vessels into the interstit into your tissues causing you to be very puffy. Ok. So investigations, um, I'm not gonna go into too much detail, but, yeah, E CG you do the clinical examination, um, you do the New York, um, classification, which I've actually forgotten, um, in terms of what the, um, what the different cri not criteria but the different classification is, but it goes from 1 to 5, um, if I'm not mistaken. Um but there's different, it's just all, just all ba it, it basically classifies the severity of the heart failure and depending on your symptoms. Um and then bloods we've already talked about um and then radiology, we've also spoke about um echocardiogram and um what's it called? Chest x-ray? Yeah. Um Moving on to treatment. I don't know if you guys can still hear me. Yeah, we can, we can. Oh, ok, fine. I think my camera just paused but um give me a sec. Yeah, sorry. Um ok. So um we've spoken about this, sorry. Um Moving on to management of acute heart failure. So obviously in that situation where you are a junior doctor and you've gone to see the patient and you know, the patient's in acute heart failure. Remember the difference between chronic heart failure and acute heart failure. This lady we knew she had chronic heart failure, which is being managed with um furamide and all the other medications, but she's presented with acute heart failure. So she's got acute on chronic what, what we mean by this is she's got decompensated heart failure. So her heart failure is decompensated to the point where her current supply of blood from the heart going to the peripheries is not enough to meet the demands from the tissues. Ok. So what do you do to manage heart failure? First things, first positioning, sit the patient upright. So if they're cos if they're lying flat, all the fluid in their lungs will just position in a way where it's very difficult for them to breathe. So it's almost as if they're drowning, they just find it very difficult to breathe. So you sit the patient upright, it helps them with breathing, then you give them high flow oxygen. So you start off with 15 L by non rebreathe. Um Assuming they've got not got a history of CO PD. Um You give morphine um 5 to 10 mg of that dose plus metoclopramide because metoclopramide is good for um preventing nausea. Cos morphine can make you sick. Um Then you give flusemide. Ok. Um And how does flusemide work? Just quickly put it in the chart? What's the, what's the mechanism of flusemide? Yeah, exactly. So it's a, it's a loop diuretic. Yeah. So remember if you, this is, this is why the understanding of the condition is very important in managing patients. You know that with heart failure, the problem is blood congestion and the problem is fluid leaking into the interstitial. So the issue is fluid is accumulating around their body. So you need to give them medication to get rid of the fluid. So essentially, they need to pee out all the fluid, they need to urinate out all the fluid. Ok. So that's why you give flusemide because flusemide is a diuretic. So it gets rid of the um fluid from the uh from the kidneys. OK. So it specifically acts on sodium potassium and chloride channels um in the in the loop. So it prevents reabsorption of those electrolytes. Um So the water follows all the salts in the um in the um in the collecting tubules. And as you get rid of the fluid via diuresis, like you said, yeah, it decreases pulmonary congestion, it decreases the pulmonary edema. Yeah. So that's what you do and you also give them 1.5 L fluid restriction. Um because the reason why you give 1.5 L of fluid, what the reason why you do 1.5 L of fluid restriction is because obviously the issue is fluid is accumulating everywhere. So you need to restrict the amount of fluid that you, that is going into them. OK. Um And then um obviously, and then the last thing that you need to do, you need to insert a catheter and monitor the urine output. OK? Um And that's because you need to get the nurses to accurately document how much fluid is going into them and how much fluid is coming out. Because if you're giving the reason why that's important is if you start the patient with 80 mg of fursemide and you look at their fluid balance and you realize actually they even on the 80 mg, they're still not weeing out or peeing out enough urine and their fluid balance is still in a positive ie they're drinking too much or not, not drinking too much. They're still only drinking 1.5 L, but they're peeing out not enough. So their intake is greater than that output. Then obviously, that's not gonna help with the symptoms because the, the what's it called? The fluid is not gonna get um diabetes properly. Does that make sense? Um So you want to know if you're in a, a fluid deficit or a fluid surplus and you need to aim for a fluid deficit. Ok. Um And then you need to do daily weights because you need to have a look at the trend of the weight to make sure you're doing the right thing. The weight should be coming down by a few kilograms every single day when you're doing aggressive fluid fluid um diuresis and you need to do daily blood tests specifically urea and electrolytes because remember the loop diuretic fluide acts on the um sodium potassium and chloride channels. So it can cause uh derangements in your electrolytes in your blood. So it can particularly cause um hypokalemia and it can cause weird changes in your sodium as well. Ok. If it's still, if the patient's still not improving, usually when you give them flusemide, they start peeing out all the fluid and all the, all the like all the water, what happens is the fluid goes away from their lungs because obviously you're peeing out and they'll start feeling a lot better and they'll say that their shortness of breath is improving and their swelling and everything around their body reduces as well. So that is what you do for managing heart failure. There's a quick trick that once again, I was never taught in med school that I was taught by one of the heart failure registrars um at my hospital, um which is very, very useful. Cos a lot of times you're, you're really unsure as to what dose of furamide to start. Basically at the beginning, you always, always, always, not always, but like it depends on the weight, but most times when a patient is in acute heart failure, give them a stat dose by that. We mean a one off dose of intravenous flusemide, 40 mg, ok. Catheterize the patient monitor the urine output for the next three hours. OK? So once they're given the uh 40 of flusemide monitor the urine output for three hours. And if the urine output is greater or equal to 125 mL per hour, ie in three hours, they peed out or collected in the catheter, more than 375 mL, then you continue with that dose of whatever you've given. So if you've given that 40 mg dose, you continue with a dose of 40 mg of iburia once a day because you know that's causing enough diuresis, it's causing enough uh fluid output to maintain them and sort of improve the symptoms. If the UAPA is less than 100 and 25 mL per hour or 375 mi milliliters over the three hours, then you need to increase the furamide and go up by 40 go up to 80 mg. Um then you do 80 mg once a day and you keep reassessing. Yeah. So it's all based on how much water they're losing. That's the uh broad management of acute heart failure. Um chronic heart failure. Basically, I'm not going to go into too much detail. But long story short, you need to um give medications that improve their prognosis. So, um these are all prognostic medications that are very good. So beta blockers, ace inhibitors, spironolactone and SGL T two inhibitors. So, examples of SGLT two inhibitors are topical flosin and sin. Um um um what one thing you need to know about that is basically, you don't give it to patients who are at increased risk of UTI because obviously it's also a diabetic medication as well. So S TT two in that you get increased glucose uh going out via the urine. So it increases the risk of UTI S. Um So obviously, if they're already prone of having UTI S, then you don't want to give it to those patients and you don't give it to patients who are acutely unwell because they increase their risk of developing new glycemic. OK? Which I'm not gonna go into, but you just need to know that um spirolactone is they are mineralocorticoid receptor antagonists. So essentially it stops the reabsorption of sodium stops the reabsorption of water as a result. Remember, water follows sodium. Um So as a result, it stops the fluid accumulation. So it gets rid of the fluid. Um I'm not gonna go into the um other um medications. Another thing you need to, I'm not gonna go into cos in the interest of time not to go into too much detail about cardiac resynchronization therapy. Um Just because I mean, what's important for you guys to know how to treat the patient in an acute scenario. OK. Uh So just remember genetics, oxygen um give morphine if uh if that's helpful and also metaclopramide, um reposition the patient fluid balance, monitoring all the time, um uh monitor their weights and check bloods daily. Good. Um Last case, I'm so sorry. It's gone on for a long time. But I think this this case is quite important. So the last case is you're on an on call ward cover shift. Um And you basically get bleeped by a nurse. So she calls you and she goes, um, doctor, doctor, can you please help? Um, I've got a 65 year old patient called John Duffy. He's currently being treated um, for an infective exacerbation of CO PD and he's suddenly complaining of some chest pain and it's not improving. I've given him some paracetamol, but it's not helping. I've tried to give him some morphine but he doesn't want to take any morphine. Um, I just don't know what to do. Can you come and see him? Um, so you asked them a bit a bit about the background. It's got a history of hypertension type two diabetes, high cholesterol and um, history of COPD as well. He's been a smoker for 20 years and he's still a current smoker. Um, observation wise, tachycardic, uh, respiratory rate is slightly up. Uh, saturations are good at 94% and the temperature is normal. What is your examination? So this is your examination? So he's lying in bed, he's, um, working very hard to breathe, but he appears to be very anxious. Um, his peripheries are quite clammy, actually, he's warm and well perfused, but he's got a regular pulse, but he's quite tachycardic. Um, when you have a listen to his chest, he's got mild crepitations or crackles at the bases. But the heart sounds are normal though. However, um, and his abdomen is soft and non tender and the bowel sounds are normal um calves are soft and nontender. Um There's no peripheral edema. So what would you do next for this patient? So he's got chest pain, history of CO PD. Um What else? Yeah, because someone said give nitrate, someone says stable angina, someone said X ray all valid, valid, all very valid contributions. Um Yeah. Spot on E CG. Exactly. So you wanna do an E CG. Um So you do the bloods, white cells. 40 neutrophils are raised um Using these are normal C RP is 100 and 20. So it's a bit raised. Um Troponin is 70 chest X ray. I'll put on the next slide. This is the ecg firstly, quick question. What other blood tests do you want? So, troponin 70 what other blood tests do you want? Yes, I like that. Good. Are the cause of chest pain? Good, good, good. Very good. So the other blood test you want, you wanna repeat troponin? OK. And the reason why is you wanna see dynamic changes in troponins cos because in the first the first few hours of a heart attack, which obviously you're querying here, there's going to be a rise in troponin. So if you have a single reading, more like a result of troponin, it's not really enough, you need to repeat it after an hour to see if it's going up and if it's going up, um I can't remember the exact number. I think it's more greater, greater than five or something. But if it keeps going up, then you know that this is probably a sign of an ischemic event. Ok? So a single troponin level is not good enough. You need to have at least two and then you keep doing serial levels. Ok? Um E CG as someone interpret this for me, what can you see? I think someone's already said it very good. Someone's said the right answer and this is a chest X ray. I'm gonna quickly skip over that. And your working diagnosis. I think a lot of you have said the right answer. So this is a semi in particularly it's a, it's an inferior semi like you guys said because uh 23 and aVF were the were the areas where you had um ST elevation good, inferior stemi. Very good. So now how would you treat this patient? So you're a doctor, you've been caught to the ward, they've got chest pain. You've done an E CG. It shows an inferior Mr what do you do to treat the patient? Someone said move in some of the morphine. Some A players. Good. Very good, good. OK. So um I'm gonna go into the quick definition of ischemic heart disease. I wanna rush through this because um I don't think it's too relevant for you to know as opposed to the management. So basically, ischemic heart disease is an umbrella term. Um And the reason why you get the symptoms that you do is because you've got a reduced blood supply to the myocardium. So the heart muscle is not receiving enough blood supply because remember, in order for movement or any contractions and everything you need respiration to happen. In order for respiration to happen, you need oxygen. Oxygen is delivered via blood. Ok? And if you've got a lack of blood supply, you're gonna get pain because the contractions aren't gonna happen properly. Ok? Um It is like I said, it, like it says here, it's a spectrum of disease. Um and it goes from stable angina to acute coronary syndrome. Stable angina essentially is when you've got chest pain that occurs when you are exercising or you're moving around or on exertion, but it's relieved by rest and very similar to heart failure. It's the mismatch between the supply and demand of oxygen via the blood. Ok? So if your coronary arteries are kind of narrowed, you have a reduced blood supply because there's less blood flow going through the myocardium. Um So when your heart, when you're like trying to run around and your heart rate goes up, there's not enough blood supply to supply the myocardium with a good enough level of oxygen to allow enough respiration for your heart to function at that fast rate. Yeah. Um So in stable Angina, it's not like an irreversible. It's not, it's not an infarction that happens. It, it can be some narrowing of the blood vessels of the coronary arteries, which can be relieved with GTN, which dilates it. And that narrowing basically causes I like to think of the pain that you get as your heart muscle screaming because they're screaming because they're not receiving enough oxygen. Ok? But once you settle down and you relax and your heart rate goes down and your demand for oxygen reduces, then your, there's no more mismatch, the supplier meets the demand and your pain goes away and that's stable angina. OK. Acute Coronary syndrome, you've got three types, you've got unstable angina and semi and stemi. Um So unstable angina, you've got chest pain that's at rest um from a narrowed coronary artery. But there's no, there, there is some tissue ischemia but there's no infarction. Ok? Um In the end stemi you've got some tissue death. Um but there's no ST elevation on the ECG and for stemi there is tissue death and there is ST elevation. OK? So that's the broad definition when you're in a stressful situation and you're seeing a patient, it can be very easy to get everything muddled up. And you're trying to think about, ok, what this is at rest or you're trying to understand what everything is. Keep it very simple. Yeah, just keep it in terms of a biochemical definition for everything. Yeah. So just remember the four types of ischemic heart disease. You've got stable angina, unstable angina and semi stemi. OK. So, oh, so just remember, understand me and understand me, you've got actual infarction. So you've got actual tissue death, you've got myocardial death, the other Angina, you don't actually have tissue death. You just got ischemia. OK? So the difference between M I myocardial infarction and angina is that you've got in death of myocardium versus ischemia. OK. So stable angina. So when you're seeing a patient, just think back to these definitions, stable angina, they've got chest pain that improves when they're resting. Ok. And biochemically, there's no rise in troponin and there are no ecg changes. So that stable angina unstable angina, the chest pain is at rest. It's not just on exertion, it's there at rest, there is still no rise in troponin and there are no ecg changes. So the difference between unstable angina and angina, stable Angina is simply the clinical features at rest versus not at rest. OK. Temi is when you have chest pain at rest, you have a rise in troponin. So there's a sign that your heart muscles are damaged because troponin is released by cells when the cells die. Ok. So if troponin is increasing, it means that some of the myocardial cells have died and they're releasing troponin the enzymes into the bloodstream. So in end semi where you've got myocardial infarction, ie myocardial death, you have um chest pain, you've got a rise in troponin. You've got also got some changes, but there is no ST elevation. There's ST depression and T wave inversion OK. And then stemi you've got chest pain at rest, a rise in troponin and specifically, you have ST elevation on the ECG. So those are the four different types of angina slash ischemic heart disease. And that's how you remember and you classify every single one of them when you're with a patient and you look at the results. Yeah. Um when you start working, the more, more and more you start working, you, you realize that it's less important to remember all these little meticulous, little changes on an E CG. But in the context of heart failure, you kind of just mainly just have a look at the ST segment and you kind of see if there's anything abnormal because in, in infarction slash ischemia or infarction in general will cause an abnormality in the electrical activity. And that's gonna be shown in the ST segment. And if there is either depression or t inversion or whatever um or elevation, that's a sign that something is wrong. And that's a sign that um there's infarction that's happened. OK. So just, I think this is a very important slide for you to know when you're with a patient who has ischemia. OK. So that's very important. So now you've classified it. Uh I'm not. Yeah. So I think you guys have a good idea of um the different territories, but basically in terms of coronary arteries, there's three main branches you need to know you've got the right coronary artery, you've got the left coronary artery which splits up into the left anterior descending and the left circumflex. And basically, when you have a look at the ECG, you can determine where the infarction is based on which leads are affected. So this is a very good slide uh showing you on the, on the top, right, you can see all of the different leads and you can see how each of the different leads are positioned in relation to the area of the heart. So if you look at the three, green leads the 32 and aVF, it's on the bottom side of the heart, isn't it? And if you go back and so basically, what, so if you, so if you have ST elevation in leads 23 and aVF, so there's green leads. So if you look at this diagram on the top, right, um you can see those three leads are closest to the underside of the heart. Yeah. And if we go back, um you can see that the underside of the heart is supplied by the right coronary artery. Yeah. So if you see ST elevation in leads 23 and aVF, then you know there is infarction, myocardial ischemia and myocardial infarction in the right coronary artery. So that's also known as an inferior Mr because it's on the, it's on the inferior side of the heart. Ok. Similarly, if you have a look at BL leads one and V five and V six, you know, that's on the lateral side of the heart and you know, that's supplied by the uh left circumflex artery. Yeah. So that's where, you know where the infarction is. And then once again, lastly, you've got the VV two to V four, the middle section that is supplied by the left anterior descending artery and that's also known as an anterior MRI. Ok. So that's how you have a look at the E CG and that's how you determine where the um infarction is, if that makes sense. Yeah. Um I'm not gonna go into the slide um investigations, you guys already spoke about it before. Um ECG you do routine blood tests, serial troponins. Um You wanna do um a chest X ray and, and you obviously want to do an angiography and you wanna eventually do a cardiac MRI because a cardiac MRI in a non urgent scenario will allow you to see if there are any regional wall motion abnormalities and see if there's any ischemia uh affecting the myocardium. Ok. So the immediate management of a patient with heart. So if you go back to that patient, I think his name was John. I can't remember. Um you go, you're by the bedside, you've done an E CG, you've seen an inferior MRI for this patient. Er, and as every junior doctor does, when you start working, you start panicking and you're like, oh my gosh, what do I do. So straight away, what you do is you need to manage um the patient immediately. So you give him some analgesia. So you start with morphine, give morphine, a metoclopramide. Give GTN spray under the tongue, causes vasodilation of the coronary arteries. And it basically improves the blood flow to the myocardium. And basically, it helps soothe the pain, breathing wise. You only give oxygen to patients if they are, it should actually be less than 94%. But if they are desaturated, less than 94% if you over oxygenate them there, I think there was a study showing that there's an increased risk of free oxygen free radicals being formed and that's very toxic to the patients. So you only oxygenate them if they're desaturated. Um And then you start the patient on dual antiplatelet therapy. So, aspirin and clopidogrel 303 100 a stat dose. Ok. Um And the reason why I need to give you antiplatelets is because the reason for the ischemia or the infarction is because the platelets are, if you think back to your pathology lectures, the platelets accumulating, they're clogging up the arteries causing, causing the infarction, you need to prevent further platelets from accumulating there and causing a worsening of the, of the infarction. Um So you give aspirin and clopidogrel or you can give aglo instead of clopidogrel. Um And then you give Fondaparinux um uh in the context of an Nstemi. OK. So that's what you do in terms of managing the patient. Um And then obviously you wanna send them for an angiography, uh plus or minus PC. Um And then this once again, varies, same thing. So in terms of PC, you only do it if it's within, um if it's within 12 hours of their symptoms, if it's greater than 12 hours of the symptoms, you would basically assume that the damage is already done and you would treat them medically and you can do a non urgent um angiography plus or minus PCI. OK. Um And um when you're there with the patient, obviously you escalate to a senior once you start and then want antiplatelets and then obviously you refer to cardiology and they should go on to a cardiology ward to be treated. Ok. So, er endosy management is very similar to study management. Uh The only difference is you give from the paradox. Um um but you give it for 72 hours until the angio is done and essentially what Fonda Parex is basically an anticoagulation medication. Um uh if you can do some reading on it later, but uh it affects and it, it acts on the factor 10 A. Um and it inhibits that and it sort of prevents um clots and stuff from forming. So it prevents certain complications and stuff. Um So that's very important for you to know if that's what you're doing at semi and an angiography plus or minus PCI. Um what is a PC? Essentially, you, it's a, it's a way for you to image the coronary arteries and also intervene as well. So you insert a wire um through the radial artery in your wrist and the guide wire is inserted and it goes all the way um to your coronary arteries. And you, you have a look at the coronary arteries with this image that you can see on the bottom, right. Uh So you can see exactly which coronary artery is narrowed and then you feed through a stent through the wire and you keep the stent inside one of the coronary arteries and it keeps the coronary arteries open. And that is good treatment because the issue in heart, heart attack or not heart attack. Sorry. Yeah, in heart attack, sorry, in my heart is infarction is the narrowing or the clogging up of the vessels. So what you want to do is you want to keep a stent to keep it open to allow good blood flow going to the myocardium. Yeah. So that is what PCI I is basically during this once again, just a quick sign that you give unfractionated heparin because um you're inducing metal into the patient, increase the risk of um clots and things forming. So that is what you do in terms of definitive management of um myocardial infarction. But for you, for you guys, the most important thing to know is this um A to re assessment, um, treat the patient immediately escalate to senior get cardiology involved. Move them on to a cardiology ward. Yeah. Um and then long term management on discharge, they need to be on aspirin and clopidogrel together um for one year and then aspirin 75 once a day lifelong, give them statins to reduce or control their cholesterol, give bisoprolol 1.25 mgs once a day and Ramipril 2.5. Uh because that's a prognostic medication, it helps their um life expectancy and then GTN great if ever they develop any angina in the future. Ok. Um And then in terms of treatment for stable angina, it's different to um uh to myocardial infarction because you're not trying to treat a blood clot or platelets that are just accumulated, causing a clogging of the arteries. You're just managing the um supply and demand of the um of the myocardium. So essentially you treat the symptoms obviously by giving GTN spray which causes vasodilation. Um and then you prevent future angina by giving uh rate, control to control the heart rate at a certain level so that you keep the oxygen mismatch or the oxygen demand supply at a good level so that they're not experiencing any pain. Uh So you can give bisoprolol or dilTIAZem, which we spoke about earlier in the context of atrial fibrillation. Uh You can also give long acting nitrates, which obviously will help as well once again prevent angina. Um And then obviously secondary prevention, like before you would give statins, antihypertensives and antidiabetic medications because obviously hypertension, high cholesterol diabetes are all risk factors for heart attacks and angina and things and the heart disease, which obviously this patient that we're talking about now had all three of them. Um, so, yeah, that is everything. I'm so sorry. It was very long. Um, I do hope it was helpful. Um, yeah. Yeah, I hope, I hope it was helpful. I think the areas that I spoke about I think are high, your topics which you need to know when you are working properly in the NHS. Um And I think it's just important for you guys to prioritize areas of your learning where you know, you, it's gonna benefit you uh when you're on your own faced with a situation or scenario, um where a patient is deteriorating, you need to know how to manage the patient or at least at least initiate a management on before your senior arri arrives. Um But yeah, hopefully that was helpful. Uh Once again, apologies for running over. Firstly, thank you, Doctor Jacobs. Your lecture was very informative and useful and I'm sure it's gonna be useful for everyone else on middle. Er, thank you again once and just a quick one before we all before we do exit today. Er, if you could or er so sorry, your feedback forms will be sent out to you via email. Please fill them in and your certificates will come after that if you get any problems, contact Medipap International at and email or social media Medipap International. And uh next week Thursday guys at 7 p.m. there's a talk on acute kidney injuries by doctor. Uh so hopefully do register and we shall see you there. Thank you very much. Thank you, Doctor Jacobs. Once again. Thank you so much.