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Hello, everybody. Um Phil just told me that some people are running late, so we'll give it a couple more minutes and then we'll start if that's OK. OK. I'm being commanded to start. So uh let's crack on, I've already tested this out with Phil. Hopefully you should be able to see these slides. Um So just a brief bit about myself. My name is Robin. I'm currently in internal medical trainee in year one at the raw Broten doing respiratory. Um You'll notice there's a theme that a lot of us are from the Ra Bronson and that's because Phil has just done a respiratory placement here and has recruited all of us. So, um welcome. I'm just going to run through how I'm going to break down this session for you. Um Oh, sorry. Firstly, I should say my interest is in cardiology. I studied up arts and did an integrated degree in uh at Imperial and Cardiovascular Sciences. And um my particular interest is in arrhythmia. I've done an F three and an F four in cardiology and intensive care respectively. Um And yeah, that's about it. I think let's move on session format. So how this is going to run is there's three main topics within cardiology. There's interventional cardiology which covers coronary artery pathology, electrophysiology, which is arrhythmia and devices and non invasive cardiology, which is heart failure and valvular pathology. I'm going to be covering those three broadly, but I don't have the time to be able to cover everything within your curriculum. So don't use this as a be all and end all to cover every single topic to revise for this is just to supplement your education and each topic is going to have lots of questions. None of them are going to be easy at all. Don't be disheartened. If by the end of this, you've not gotten many questions, right? The point of this is so that we can approach answering an exam question together where you may not even have heard of some of the answers, but you should have a systematic way of working through an SBO short based, um, sorry, a single best answer question or an OSI, there's going to be one OS station, we're going to work through everything together. So the most important principle in single best answers going forward, even past medical school is to read the question and also the options. Um, you'd be surprised how many times you'll go through a past paper and realize that you've actually misread the question completely or missed out one of the options that you just didn't read because you were too nervous. Um, with each topic, I'm going to be focusing on physiology primarily so that you actually understand what's going on behind the pathology. Even if you have no interest in pursuing cardiology as a career and will take breaks in between the, um, sbs to give, take home messages. So you can remember the key points. I don't expect you to remember everything. There's quite a lot of material to get through and you are going to be sent the slides. So, uh please don't try and take too many notes during this. There's going to be a recording as well. Just focus on listening and participating. Um Just a note on participation. There's going to be a lot of questions from me, whether it's within the physiology itself, whether it's in an SBA or whether it's in osk situation and I would be very grateful if you guys would interact. I know it's very daunting doing so in front of your peers. But you're never going to get a better opportunity outside of a mock exam or a real exam to put yourself under pressure and under spotlight to display your knowledge and display your thinking process at any given points. So either unmute your mic and say something or write in the chat, I don't really care. But please participate, you'll also see there's a mentee code in the bottom. So use that there's going to be I think 18 S bas in total. And um you can, we will go through it together. Um If you can just all take the time to log on to that now, it should just say cardiology quiz. And if, if people can just say when they're ready, I will give you a minute or so sorry as me. All right, let's crack on. So the first topic I'm going to be talking about is coronary ischemia and that is in the umbrella subspecialty of interventional cardiology. With each topic, we are going to be going through basic physiological principles that you should already know just so we can have the same base understanding going forwards when it comes to understanding the physiology of the pathology of itself. So what everything boils down to in cardiology is how pathology affects the function of the heart as a pump. And you have to understand that within the pump function, there are lots of different moving parts that contribute towards overall function within coronary heart disease. The main problem that they try to address is blood supply. So the blood supply to the heart is supplied during ventricular diastole. During ventricular systole, the ventricles empty a blood and oxygenated blood is delivered into the aorta and is distributed. Um ultimately arriving at the end organs when, when the heart is in the diastole and the atrioventricular valves, shut the backflow of blood against those closed valves, uh goes enters the coronary osa and fills the three main coronary vessels. So, uh myocardial oxygen supply is determined by blood or blood flow through those vessels. And any changes to the radius in those vessels at any point greatly affects blood supply and ultimately will cause ischemia. If there is a mismatch in supply and demand. Does anyone know the law, the physiological law that governs flow through a tube, lamina flow through a tube with respect to radius is this low of the class? No low. The plazo relates to surface tension um and uh a vessels diameter, but that's a good suggestion. It's Purcell's law. So essentially, if we just get the pen out, what it says is that it's quite a complicated equation. But ultimately, what you need to understand is that flow is proportional to radius to the power of four. So any changes in the radius are drastically going to affect flow. Um So if you were to have a coronary vessel or any kind of tubing like this, you reduce the flow by half. So this is half. Um And the ultimate effect on flow is you would get a 16 fold reduction in flow. So you can see how atherosclerosis can affect coronary artery flow just by reducing vessel diameter by a certain amount, not even 50%. And this is important for you to understand, I'm not going to go into the pathophysiology of atherosclerosis, foam cells, macrophages, whatever you can look that up in your own time. And you should all know that at this point. Um next is that inability to meet myocardial oxygen demand usually, but not always manifests as chest pain. And this is the way that a clinician can decide in combination with biochemistry and radiology. How likely they think it is that someone has genuine coronary artery disease. Because as an F one or as any kind of doctor, you are going to be seeing hundreds of people come into A&E with chest pain and your job, especially if you want to do cardiology is being able to form a picture in your, in your head about how likely it is that someone needs urgent intervention or that it probably isn't coronary artery disease present. So let's move on. Um We're going to be following the journey of Mr Jones throughout this series. Initially, he is a 68 year old male presenting with chest pain. He has a past medical history of diabetes, hypertension and smoking. Um So are there any features of a clinical history that you ask Mr Jones around his chest pain itself that make you concerned about Angina? So, so what features in a clinical history would, would make you worried? Does it worsen on exercise and gets relieved on rest? Exactly. Exactly. Well done. So there are two of the three principal features in the typical classification of Angina. There's one more so it's just surrounding the actual character of the pain. So it describes it as central crushing, chest pain, radiating, it doesn't even have to be crushing, just central chest pain that can radiate to the arms or jaw. Um So the traditional classification of Angina, so I don't know the names of the people saying, but I really appreciate it. That's, it's very brave to speak up in front of your peers. The, the, the three main features of Angina traditionally classified are constricting, discomfort in front of the chest or in the jaw, neck, shoulder or arm precipitated by physical exertion and relieved by rest or nitrates within five minutes. And um what they say is that if you have all three, you have typical Angina. If you have two of the three, you have atypical angina. And if you have one of the three, it's non anal chest pain. And this is not a rule. And actually, when they studied this, only 15% of people with coronary artery disease had all three of these features. So you cannot use this as a way to exclude coronary artery disease just by taking a history. And you can have someone presenting with a full anterolateral stemi that doesn't have any of these. So, and it's just important to note and as far as medical school goes, it's a very good way of classifying angina. Um If you have pain at rest, then obviously, you progress into the unstable Angina and acute Coronary syndrome treatment algorithm. Um I'm not going to go into detail about that. Now, you just had a lecture on that and it's going to feature later on. But um A CS has been covered a lot for you and I'm sure you'll know very well. And there's, to be honest, there's not that much, there's complexity to it. It's just following a uh an algorithm. Um So Mr Jones in this situation describes typical anginal chest pain. He has all three of these features, but he has none of them at rest. And so we're happy that he clinically has stable angina. So the European Society of Cardiology class one recommendations, which basically just means that everyone seems to agree on these um to risk stratify stable coronary artery disease are as follows. So um it recommends using biochemistry initially, you would look at their glucose profile, their lipid profile and their thyroid function. You would take resting and ambulatory ecg and do a resting echocardiogram. Now note this is with regards to investigating stable coronary artery disease and how you would risk stratify to form a natural diagnosis. This isn't how you would go about saying to someone they have for certain obstructive coronary artery disease, you can just use this to build a clinical picture and that's all it is. And what this goes to tell us is that if you have high risk ie if all of these things are worse and if you have worse symptoms, then it favors either invasive angiography or functional testing. So there's lots of different ways of testing coronary artery disease. And I'm sure you guys know a lot of them and we're going to ask you to list them, but understanding when and where to use them is, is very important. So, um let's look at the diagram that they give us. What they say is that if you have a from the previous eye, if you've formed a good picture that someone is very likely to have obstructive coronary artery disease. If they have lots of risk factors, if they have imaging, that shows that. And by imaging, I mean echocardiography that shows that they may have areas of ischemia. If they have an ambulatory ecg that shows ischemia on exertion, then you would favor doing these tests. So a stress echo is a functional test. This is a test that you perform under stress and you inject dobutamine to see whether or not there are areas of the heart which um start to not be contractile with the Dobutamine infusion. Um Does anyone know the mechanism of action of of dobutamine? Just gonna check the chat. Oh, someone actually guess sorry, I didn't see that well done. Ok. So Dobutamine is essentially the opposite of a beta blocker. It's it's a beta one agonist that um enhances cardiac contractility and um inotropy chronotropic et cetera. So what you get is normally when the heart can compensate for reductions in coronary vessel diameter at rest. As you begin to increase myocardial demand, the supply cannot keep up with that. So a stress echo is a good way of seeing. Is there actually any problem with coronary vessels that is dormant at when the patient is at rest? CMR is cardiac MRI and pet and SPECT are different forms of CT or radiological imaging. I'm not going to go into those. I don't really think you need to know the ins and outs of this. I think what you need to know is that if you have a low probability of obstructive coronary artery disease, from the test we mentioned before, you would do a coronary CT angiogram, which is just a normal ct of focusing on the heart and its vessels. And you would see how much calcium deposition there is in the coronary vessels. And that would give you a marker on how much atherosclerosis you think there is, it's not a very specific test, but it's useful for the population that has a low likelihood of obstructive coronary artery disease. As you, as you get more and more worried about a patient having obstructive coronary artery disease, then you would favor functional imaging, cardiac MRI and if you have a very high suspicion, then you would go straight ahead with invasive angiography. Um Mr Jones reports pain whenever he walks about more than 10 m. He has biochemical insulin resistance and a very high total cholesterol. His ambulatory ecg is normal sinus rhythm with frequent ST depression in anterolateral leads associated with higher heart rates. So what investigations do you think that we should proceed with? Where does he fall on the spectrum? Oh, sorry, I missed, managed as well. Yeah. Sympathy mimetic. Yeah, that's correct. For diamine. I'm just going to stick on the chart after I answer a question. Um, so the investigations you proceed with are in this gentleman, you, you'd probably consider a stress echo or a cardiac MRI, as we mentioned. Um, and, uh, that's that. So we'll go on to our first single best answer question. Uh It should update on your mentee that we've proceeded with the first SB A. OK. So there's 24 people. I'll probably wait until there's, I don't know, like a decent number of responses so far. There's 11, take your time. OK? Um So the correct answer is actually only one person got this right. The correct answer is dilTIAZem. A lot of people have put isosorbide dinitrate and I can see why. But the European Society of Cardiology guidelines and concurrently nice guidelines suggest that for treating stable angina, the first line is dilTIAZem or a cardioselective beta blocker. So um it doesn't have to be dilTIAZem, it can be verapamil. So essentially first line is a beta blocker or a nondihydropyridine calcium channel blocker. Um Ranolazine is a late sodium channel inhibitor and that's second line aspirin is as you know, an anti platelet and you would offer that for primary or secondary prevention. This is a, a good choice, but this is not answering the question. And um you'll see as we go on with this session. If you don't answer the question, you're not going to get any of the questions, right? Um dilTIAZem is the correct answer. If Aberdeen is a following channel inhibitor, that's also second line. Um and isosorbide dinitrate is a long acting nitrate, but that's also second line. So I'm just going to check the chart because I seem to be missing a lot. Ok. So there's no questions. Um If you have any questions, please interrupt me, by the way, stable angina. All patients with stable angina in terms of primary and secondary prevention should be on aspirin with a PPI and a statin. So this is every single patient who you've risk stratified as having a reasonable amount of certainty that they have obstructive coronary artery disease, whether that's through imaging or through high clinical suspicion, they should be on aspirin with a PPI and a statin. They should have GTN just as a PRN sublingual spray for short term relief. Um And you can use that to quantify how often their or how badly their angina is progressing. The first line antianginal that I mentioned um is a beta blocker or a nondihydropyridine channel blocker, not the two together. Um And the reasoning is because so this is the physiological breakdown of adrenergic stimulation in a cardiac myocyte and this is Americanized. I'm sorry, but epi and any refer to adrenaline and noradrenaline. And essentially what I want you to get from this diagram is that the effect of the beta adrenergic system on cardiac myocyte is to increase heart rate. So chronotropic contractility. So inotropy and conduction velocity. And while that system is useful, if you are exercising, if you're in shock, whatever in someone with a stable angina where their supply is barely meeting their demand. If you can't, if you are not happy to increase the supply by doing an doing an angioplasty, which isn't indicated in everyone, then you would think about reducing the demand and you would do that by medications. So that's why using a beta blocker or a nondihydropyridine calcium channel blocker is first line. I haven't done the physiology of the calcium channel blocker, but um essentially it works in the same way. Uh Just not through this mechanism. OK. Um So for second line antianginals, um II, I would say that long acting nitrates are actually second line and the rest are third and for the purposes of um your exam, I think it would be good to know that if you were to get a difficult question like this and they didn't have a first line, then long acting nitrate would probably be the right answer. Um If Aberdeen runs in and NICA, I'm not going to touch into the how they work something with respect to long acting nitrates, you can have immediate release or you can have modified release and oh my God, my drawing is terrible. If you were to have an immediate release preparation, then does anything know, does anyone know anything about the dosing regime? How you would, is there anything particular about the pharmacology of nitrates that, that anyone is aware of? Ok. So with nitrates, you can develop tolerance very quickly. So you should asymmetrically dose it just like if you were to give someone furosemide, you would asymmetrically dose a nitrate. There, there's a mechanism within physiology called tachyphylaxis. And certain medications experience that as you give someone more steady doses of something you reduce their efficacy. So just be aware of that for nitrates, just to summarize what we've done in the last few slides, proper history taking is key in risk stratifying likelihood of coronary artery disease. Uh If you have a high likelihood of obstructive coronary artery disease, then you would um undertake functional or stress imaging. If you have a low likelihood, then you would organize a CT coronary angiogram. Um These tests dictate whether invasive angiography is indicated. Um And usually you're not going to perform invasive angiography off the bat. All patients with stable coronary artery disease should receive aspirin with A PPI and atorvastatin. First line antianginals are beta blockers or nondihydropyridine calcium channel blockers. Ok. Next SB A um I'm just gonna move this along on this thing. Uh Mr Jones returns after established medical anginal therapy, he describes worsening chest pain on exertion and Now at rest, these are his troponins measured um at zero and six hours and this is his ECG. Um So if you can just pop onto many, you can see the question and the question stem if you hover over it, uh what's the most appropriate next step? This is a difficult question. Um And it is essentially a spot diagnosis. So, um the usual ways of ruling things out with exam technique isn't as appropriate here. And if anyone knows the answer to the spot diagnosis, just shout it out because um you get gold star, I'm gonna check the chance. OK. There's a decent amount of answers um split between urgent invasive angiography and angiography within 72 hours. Um So this is Wellen syndrome. So, um this T wave inversion here is a pathognomonic of a critical lad stenosis. And what that means is that there's a very high risk of this uh at ECG evolving into an acute anterior stemi. And it, it may indicate that a sty has already happened and the patient is flipping between um reperfus and not perfusing his left anterior descending artery. Um This actually came up in my finals, which is why I think it's relevant. But um again, it's just AAA useful clinical um useful ECG to know. And if you're interested in why this happens, then I'll go through it later, but I am running short on time. So the answer is urgent invasive angiography, well done. To those who got that right. So Mr Jones undergoes successful lad revascularization and a week later he presents again with worsening central chest pain. His troponin is 24 and his ECG is shown below. I'll give you some time to have a look at this as I change my ment. Ok, while you're looking at ECG, I'm just going to play what you're going to hear on auscultation. Yeah. Um And the question is uh on the, I'll go back to the slide. The question is which of the following is the most appropriate step? You should be able to see this on your ment. Now, um the options are urgent angiography, CT P DC cardioversion, Ibuprofen and Valvular assessment. Can I get it to play this again? Mhm Does anyone want to explain what you can hear on auscultation? Just play it again? OK. Again. Yeah. OK. Um So a lot of people on men have answered exactly uh Asher. It's a pericardial rub. So you get the gold star here. I think the reason why people are suggesting Barbu assessment is because they think that this is an ejection systolic murmur pertaining to aortic stenosis and a pericardial rub is actually what's being heard. It's the grating sound that you can hear on either side of the lob and the key points is again, reading this question, we are still talking about Mr Jones who we know has ischemic heart disease and has had and lad revascularization. A week, a single week later, he presents again with worsening central chest pain. So, in my mind, there are two things that could be happening. Number one is mechanical stent failure. Has his stent gone wrong. And if so he needs PCI, his troponin is not that high and it's nothing to really get excited about. You would probably be worried. But in this case, this is all the information that's given to you in the context of auscultating. A pericardial rub. The correct answer is ibuprofen. So I think two people got that right. Well done to you too. And so we'll touch on pericarditis. It's relevant in this case because it's occurring one week later than his initial procedure. And there's a specific name of this syndrome. If anyone wants to say it or put it in the chat while I just go on to explain pericarditis. Is it a dress syndrome? Yeah, well done. Well done. It's really annoying. It's not, it's not telling me who it is. Who is, is it Manish? Um But yeah, yeah, well done. So. Um pericarditis is inflammation of the pericardial sac and it can manifest as acute or chronic. The typical causes are actually infection and especially in third world countries, things like TB and viral pericarditis and myocarditis are common in this case. Um We can see that he's, the patient has just had an mi and we know that or at least now, you know that infarction and revascularization can cause pericarditis. Um And the name of that is Dressler syndrome. Um, other causes that I hadn't mentioned are malignancy, um, connective tissue disorders and uremia. Um The treatment is nsaids and colchicine. Together, those are the updated guidelines for recommended first line treatment. Uh The second line is to add corticosteroids. It's important to know you don't go straight ahead with corticosteroids, you would add them second line. Um Most of the time in any pathology you would like to avoid using steroids. Um Third line is azaTHIOprine. I don't think you'll be asked what the third line is for pericarditis, but it's important that you know that the first line treatment is nsaids and colchicine and these are the um particular conditions where pericarditis can manifest. Ok. So let's move on to our OSI Mr Jones has aged a bit. He is now 75 and he reports increasing chest pain on exertion, but none at rest. Thankfully. Um He has the same medical history and you are asked to perform a cardiovascular examination and report your findings. So, um on examination, um I don't know if you want to take some time now to think about how you would approach this station, but we don't have very much time. So let's crack on these are the findings and there are no other notable ones. Um I don't know if anyone wants to have a go at presenting this uh and giving a reasonable idea about diagnosis, investigations and management plan. But please speak. Now if you do want to do that. I mean, from the pictures, it seems like they've had a midline steno toy and potential vein graft harvests from the forearm and the lower leg. So they could have had potentially a cabbage. And then in the hand, I mean, it seems like there's like pigmentation either like tar staining or, um, I don't know if this could be some kind of like splinter hemorrhage or something. It's tar staining. Um But yeah, well done, Manna. Thank you for that. Um And you're entirely right, the patient has had a coronary artery bypass graft with vein harvesting. Um The vein harvesting was actually done from the radial artery. You can see here from the left arm. This is just a red herring and actually featured in my end of year OSI someone had a random leg scar and the examiners were seeing if they, if people thought this was sain vein harvesting. So just something to note that the saphenous vein runs medially. It wraps around from the dorsum of the toe and wraps around media uh up the leg and this is, this is the area of the vein that's harvested. This is a keloid scar. Um So uh it's pretty harsh if they do that, but the examiners do whatever they want. So, so this patient has had a coronary artery bypass graft and that entails um arteries that are artificially inserted to bypass lesions in multiple coronary vessels. So, you would only be referred for a bypass graft if you had multivessel coronary artery disease. And typically, this is the coronary artery. This is the artery that goes to the left anterior descending and this would be your um left internal mammary. Uh And this is just uh usually a venous graft, but in this case, has been an radial artery graft. Um So just to note that you can have venous uh graft harvesting in the leg or you can have arterial graft harvesting in the arm and arterial graft harvesting is actually the long term studies show that it's better for you. Um But it's a more risky procedure. So, clearly, bad things have happened since we last saw Mr Jones. Um What aspects of their history would you go about trying to ascertain? What, what things would you be interested in? Um Perhaps when he had the procedure? Yeah, exactly. So you want to know the events surrounding his, his cabbage? Do you want to know whether it was an acute semi with and out of hospital VF arrest or was it just an elective cabbage done? Because he had bad coronary arteries in this case? And in any case of someone who's had an mi, you want to know three things, the events leading up to and including the mi what were the consequences of the mi and what therapy is he on now? Um And is he on the appropriate therapy? So, if I wanted to present this case, then I would go about it as follows. Today, I examined a 75 year old male called Mr Jones who complains of worsening, exertional chest pain. There was evidence of tar staining in the hands. No clinical evidence of valvular disease or endocarditis. He had a left radial artery harvesting scar and a midline stot toy scar which suggests that he has multi vessel coronary artery disease and has undergone bypass grafting. My working diagnosis is angina secondary to coronary artery disease. I would proceed by taking a full history of his pain and the circumstances surrounding his history of myocardial infarction. I would also request clinical observations and the 12 B DCG routine blood tests as well as a chest x-ray. Further specialist imaging, which includes echocardiography and potentially invasive angiography. I would ensure he receives smoking cessation advice and is established on anti platelet therapy with gastric protection. A statin, an ace inhibitor and a beta blocker. So if you gave this presentation after doing this kind of OSI, then you would inevitably have to be given full marks. Because outside of providing a differential diagnosis, you've covered all of the bases and you've covered the salient positive and negative findings, no one, if you've ever marked an Osco, then you'll know that no one wants to sit through and listen to you presenting every single negative finding. Um But if you just mentioned the important ones in a succinct way, then the examiner will be very grateful and it will make you look a lot more slick and that's the case with all specialties, not just cardiology. So just things to remember here. Um Pericarditis can occur following myocardial infarction. Typically after 1 to 2 weeks, the main stay of treating pericarditis is nsaids and colchicine deep or biphasic anterior T wave inversion may indicate critical proximal lad stenosis A K A Welling syndrome. That's the ECG that we saw before and must be acted upon urgently. Clinical evidence of cabbage should be highlighted in a pa station. Ok. Cool. Um Next topic, arrhythmia. So the basic principles behind arrhythmia are that the conduction system, uh the cardiac conduction system initiates and propagates electrical impulses through the atria and then the ventricles. So, originating from the sinoatrial node av node down the perk and fibers and up down the bundle of this and up the perkin jay fibers to coordinate ventricular contraction from the apex. And that results in a narrow QRS on the surface. Ecg um defects in the sinoatrial node affect impulse initiation and defects in the atrioventricular node, affect impulse propagation and being able to differentiate between sinoatrial node and atrioventricular node pathology is something that you are definitely expected to do. Um or at least just looking at an ecg uh the most common cause of sinoatrial node dysfunction is age and the most common cause of ventricular arrhythmia is ischemic heart disease. Everyone happy. Any questions so far? Cool. So as I was saying, this is just the normal cardiac conduction anatomy and just something I want to say here is that the purposes of this and the purposes of there being an atrioventricular septum that prevents conduction from the atria. And the ventricles is as I was saying to coordinate ventricular contraction. It's very important that the ventricles empty together and from the apex. And in conditions like left bundle branch block in situations where you have a pacemaker. Any other situation where you have asynchronous cardiac contraction, most notably in heart failure, then you would get a broad QRS on an ECG and the ventricles would by definition not be working as well as if they were contracting together. And so the whole function of the conduction system is to deliver coordinated ventricular contraction. OK. That's something that you have to understand. Um So next SB going forward, augment a 75 year old presents with lightheadedness. He has a to the DCG. Where is the defect again? If anyone wants to present this ECG, then be very impressed. I'll give you a couple of minutes to answer this. OK. I'm just going to go ahead and explain this ECG if the last people want to answer. Um So it's a totally DCG. Uh we can see that it's in a regular rhythm and um that there are P waves which um are always, um oh sorry, there is a P wave that always precedes every QRS complex. OK. So P wave Q and every time there's a QRS complex, there's a P wave before it, the most obvious abnormality is that there is a gap here and a gap here. So this is a period of asystole and it's not just asystole of the ventricles, it's asystole of the atria as well. Um So essentially the, both the atria and the ventricles aren't contracting. So um the correct answer here is the defect is in the sinoatrial node. And um the reasoning is because um this is, this is what's called sick sinus syndrome. So the the sinoatrial node, which is the source of impulse initiation is not working very well. If it was working fine, then there would be a P wave here. OK. If it was a defect in the atrioventricular node, then there would be a P wave here and there would be no QRS or there would be some evidence of P QR S dys. OK. But as we can see each QR S is preceded by a P wave. So we know that the AV node is working fine or at least OK, right. The fact that there are periods where there is completely no P waves and they've actually done a nice little diagram here for time. Um This is 1 90 there's a P wave here. This is 1 91. There should be A P wave here. So the fact that there are no P waves at all indicates that this is a sinoatrial node defect. There is a problem within impulse initiation. OK. Not impulse propagation. Does that make sense to everybody or does anyone want to explain that in another way? OK. Move on. You're going to have to get used to this. There's quite a lot of ECG. So a 75 year old male has a routine 12 lead ECG and the options. So I'll just skip ahead on mental again. Where is the defect? It's the same choices, but it's a different question and a different ECG and again, just scrutinize the ECG do it methodically PQSS ST segment T wave and again, bonus points. If anyone can tell me what this rhythm is, what is the name of this rhythm? OK. Um I'm not sure if I'm sort of like creating this wrong. Um Just because the E CT is a little bit small on my screen. Um uh But I'm just wondering because I can't seem to see any P waves and the rate is quite slow. So, is it like a junction or Brady card here? Yeah, well done. Really good. So this is a junctional rhythm and a junctional rhythm essentially just means that the rhythm is coming from the A V node or below. OK. Um The reason why is because the sinoatrial node normally governs impulse initiation, but it's not the be all and end all if this isn't working and the heart is falling below a certain rate, usually it kicks in around 40 beats a minute, then the rest of the conduction system take over, but they take over at a slower rate. So that if this kicks in again, this will be the main driving force. But all of these parts here and even further down here can initiate their own rhythm, but it just takes longer. So here, this ecg that defect is again in the sinoatrial node. And that's evidenced by the lack of P waves in every single preceding, every single QRS. This rhythm is entirely coming from the avian node and below. And this is called a junctional rhythm. Um So as you can see here, again, this is the only point of this diagram is just to illustrate the intrinsic um activity of myocardial cells. So the sinoatrial node has the quickest, then atrial muscle, then AV node, then ventricular muscle. So it just goes down the conduction pathway um like that. So as you go further down the conduction pathway, the intrinsic rhythm gets slower and slower. Um So again, that's evidence of sinoatrial node disease. Ok. Next 75 year old male with a history of stents to the right coronary artery presents with lightheadedness. And this is ecg these are the options whereas the defect, it's the same options. And again, just take the approach that we've been talking about for every UCG just take it methodically. Is it a regular rhythm? Is it fast or slow? What are the P waves like? What is the PQ relationship ST segments? T wave just do that with every single ECG and you won't be able to misread one at least for the purposes of the exam. And if a, again, if anyone wants to tell me what they can see in this ECG, that would be great. Uh Yeah, it's interesting. It feels like I can see um there are P waves which aren't necessarily related, like they're not always followed by QR S. Um Yeah, I agree. But then there are also is I can't tell if sometimes there's a drop in the P wave but that might just be in certain leads. So it could be some kind of, I mean, it's narrow complex QRS so it could be like complete heart block maybe. So what I would say about the PQ relationship is that you're right, there are certain instances like here where you can't see a P wave. But remember that the ECG is a recording in time and time is across the X axis and you can see here that there are P waves. So this is just, this is just a lead, not reading the P wave. And what you can say about this PQ relationship is that it's intermittent. So there's a P. So if we start from the beginning, there's PE Q and then this is a P nonconducted P wave. This is a PQ PQ PQ nonconducted P wave. So, so therefore, you, you can say that with some degree of certainty that this is type two second degree heart block type two because the pr interval is staying the same. So it's not type one, there's intermittent uh P QR S non conduction. So this is type two, second degree heart block. And the reason why it's not third degree is because um there is still preserved PQ relationship we can see in actually a good amount of the qas complexes. So the reason why it's not sinoatrial node is we can see that the P wave activity pe pe pe oh my God, my drawing pee pee pee the P wave activity is relatively regular. OK. So we are happy with the P waves. The QS are intermittent and they aren't always after a P wave. So, so the problem is an impulse propagation, right? The problem is, is, is this is working fine, this is working fine, but this AV node isn't conducting every single impulse. And that's evidenced by the fact that there are P waves and no Qs. OK. Um But most people got that right. I think so well done. What would you do if you saw this ECG? OK. Is it dangerous? Is it not dangerous? Um So it's not good, right? It's not good. It's second degree type two heart block, which means that and the patient has come in with lightheadedness. So he's got symptomatic second degree type two heart block. So you have first degree, which, you know, is just increased. Pr you have second degree type one and type two and then you have third degree, anything below this line is bad. So a first degree and second degree type one are ok, sometimes normal, sometimes physiological, second degree type two or third degree with symptoms. Um If either of these have symptoms, then that's bad. And another clue in the history is that the patient has a history of right coronary artery stents, right coronary artery ischemia um often involves the AV node because of the way the coronary artery wraps around the heart and um perfuse it posteriorly. So you often see in patients with inferior mi is that they are complicated by some degree of heart block and that's what this patient has. So second degree type two and third degree AV block are dangerous rhythms. And if you get asked to see a patient that has um a new presentation of either of these, then you should follow the bra adult Bradycardia algorithm. Um And I'm not going to touch too much about that, but you just need to know that here. Um It's actually got what I said that mob is type two. So second degree type two A V block and third degree block are bad. And that is when you would think about doing these measures. Um So when would you put in a pacemaker? We've talked about that. So that's if you have end organ dysfunction, ie you're symptomatic. Most patients who present with bradycardia are symptomatic in way of syncope. So most of them present with either pre syncope. So lightheaded, lightheadedness, dizziness or actual syncope itself. And if that coincides with um documented Mobics type two or complete heart block, then you would think about putting in a permanent pacemaker. Um So usually permanent pacemakers are dual chamber. You can see either on the diagram or on the chest x-ray. This is in the right atrium and this is in the right ventricle. This is a dual chamber pacemaker. And um this is what um can be captured on ecg of a dual chamber pacemaker. I'm just going to briefly touch into how it works. Nothing about the specifics. So this patient, what's happening is nothing is happening, nothing is happening in the heart and then the pacemaker decides nothing's happened for long enough. It has a backup rhythm and it goes OK. I'm going to pace the atria. So the atria been paced and then it waits is anything happening is anything happening? No, nothing happens. So then it paces the ventricles. So it's actually initiated a shock here and a shock here. And in this patient, they clearly have both sinoatrial node dysfunction, evidenced by the lack of P wave here. There's no P wave here and they clearly also have atrioventricular node dysfunction because this P wave or this atrial impulse hasn't been propagated to the ventricle ventricles. So the ventricles have had to be paced by the device, right. So you just need to understand that there's sinoatrial nodal disease, which you can see on an ECG in terms of P waves. And there's also atrioventricular nodal disease, which you can see on the ECG by PQ relationship and both of which can be treated by a dual chamber pacemaker and sometimes more often than not, they coexist, sinoatrial node disease and avian node disease. Does that make sense? Yeah. Any questions? Ok. So just a um summarize bradyarrhythmias are usually due to defects in either impulse initiation which implicates the S or atrial node and can be evidenced by lack of P wave activity for impulse propagation. So, impulses going between the atria and the ventricles um which implicates the AV node. And that's evidenced by um a dysfunctional PQ relationship. Second degree type two or third degree AV block carries a high risk of asystole if this occurs with evidence of end organ perfusion. Sorry, this should say dysfunctional end organ perfusion. Ie syncope. A pacemaker is likely indicated. A dual chamber pacemaker can sense and pace both atria and ventricles depending on the pathology. Tom. Next SB A OK. All right. Sp seven. Yeah. So a 47 year old male presents with palpitations. This is the ECG um where is the defect? Does anyone want to summarize ECG. Yeah. Um, it seems like there's, it's, it's regular tachycardia with, um, absent P waves and narrow complex QR S so it, it could be something like SVT. Yeah. Agreed. Well done. So this is by definition an SVT. So it's a tachycardia because you can see that the, um, for every two big squares there's a Q. So it's around 1 50. Um, so you guys know that if there's, and if there's one big square, then it's going at 300 which is unlikely there's two big squares, it's going at 150 there's three big squares, it's going at 104 big squares going at 75 5 big squares going at 60. So this is going at one, around 150 beats a minute. It's a narrow complex, regular tachycardia as managed, correctly said. And there's no discernible P waves preceding the QRS if I was to zoom in, I don't know if you guys can see it when I zoom in. But um in B one, there's um a small little dent here and that's actually a P wave being conducted in a retrograde manner. So after the Q, so that means that this rhythm is AVNRT. So the defect is in the atrioventricular node. I know that before I was just talking about how P waves, if there's no P waves, then it's a sinoatrial node pathology. That's the case in bradyarrhythmia here. This is a tachyarrhythmia. There is no discernible P waves because there's been another impulse generator that's taken over the sinoatrial node. The sinoatrial node has been overridden by something else. And AVNRT stands for atrioventricular node reentry into tachycardia. So it's the re entrance circuit that has formed that has now taken over impulse generation. So again, what would you do if you saw the CCG stable versus unstable blah, blah blah blah blah? So I'm not going to go too much into these algorithms because these are something that you can learn in your own time. And also that in terms of asking you on exams, the only real important bit is this bit, is it unstable or is it stable? And then you just go synchronized shock, narrow, broad etcetera? And I think in your exam they'll probably just try and make you discern is the patient stable or unstable by giving you clinical signs or symptoms that correlates with the adverse features here? Um But why is it a synchronized shock? Does anyone know by, can you not just shock whenever someone has a tachy arrhythmia and they're unstable? Is it like if you shock them during the ventricular repolarization, can it precipitate a ventricular like tachyarrhythmia or fibrillation? Yeah. Why I'm not sure. So if you have a, you're right. If you have a AP A oh my God, if you have a PQ and a T wave, right? The point of synchronization is to shock it exactly on the r, if you were to shock it in the T wave, then what you need to understand is that the ventricular repolarization isn't homogenous. It doesn't happen all at the same time, if you were to have a set of ventricles, only some of them will be rep polarized at the time of the T wave and some of them will be refractory. So some of them will be ready to get shocked again. Some of them will be ready to get conducted again and some of them will not be, they'll be still being like, please give me some more time. So in that situation, you're shocking a myocardium where half of it is ready, half of it is not ready. And then what you get is the ready part just goes OK, fine. I'm going to start contracting and then the, but the part that was not ready then goes actually, I'm ready. So then what happens is you just get a re entrance cir circuit where it just goes from the part that was ready to the part that was non ready and it just goes round and round and round and round. And that's why you get ventricular tachycardia. And in that same line, that's how you get AVNRT. So or any kind of reentrant tachycardia is you have some kind of heterogeneity in um the cell repolarization where they are in the action potential. So just to very quickly cover AVNRT what happens is in your atrioventricular node, you have a fast pathway and a slow pathway. So in the fast pathway, the conduction speed is high and usually the impulse goes down this pathway most of the time. OK. The problem with this pathway is that it rep polarizes slowly. So it recovers slowly. There's a slow pathway as well where the impulse jumps around instead of just going in a straight line and this rep polarizes quickly. OK. So what happens is normally in contraction, they both get depolarized. But the the slow one takes a lot longer. So it doesn't really matter what happens to the slow one because the fast one has already depolarized everything. And the impulse has been sent to the ventricles if a oh shit, if a premature atrial complex happens. So an ectopic within the atria and the fast pathway is still rep polarizing. So this part is not OK, there is no way through this part. This part is actually fully rep polarized the slow pathway because we've said it has a short refractory period, then the impulse goes down the slow pathway. And by the time it gets to the end of the slow pathway, the fast pathway is actually ready now. So not only does the impulse still go to the ventricles, but it actually goes all the way back up the fast pathway and to the atria. So now you just have this AV node that's just going ham it's just doing whatever it wants to do, depolarizing, both the atria and the ventricles in a like just a big circuit, right? So that's how AVNRT manifests. And that's why the only real way to treat this is with Adena Zine. Adena zine can be used as a diagnostic measure in SVT. If you're not sure about what's happening. For example, in flutter, it will reveal an underlying flutter, but it won't treat it in AVNRT. It will treat it because what you're doing, Adena um slows down depolarization across the AV node completely. So as a result, both both pathways become refractory and then the sinoatrial node takes over. OK. So just so you're aware that re entrance circuits are essentially how most arrhythmias form, most tachyarrhythmias form. Um Next question SBA 80 and also well done to everyone. With the last question, most people got it right. A 30 year old woman presents with a four hour history of palpitations. She has no significant medical history. Where is the defect? So again, none of these are easy questions. Please don't be disheartened if you don't get them right. And does anyone want to tell me what this, what this rhythm is? Just checking the chart? No one's talking the chat. Feel free to present this rhythm. Don't let me hold you back. OK. Feel free if anyone wants to. So it's a narrow complex, irregularly irregular rhythm with um no real discernible P waves. You can argue that there are P waves. Um but this is most likely to be atrial fibrillation. OK. So that's the first step of this question. This is a two part question because not only do you have to recognize what the ECG is showing, you have to be able to identify where the defect is and none of these say atria, um which you would be inclined to put as an answer. Actually, the defect in atrial fibrillation is from the pulmonary veins. Um And I think only one person got that right, well done whoever that is the formation of impulses, all of the studies and evidence have shown that the bulk of the impulse formation is in the pulmonary veins and those act as little micro reentry points where the impulses take over sinoatrial node conduction. So what they do in advanced atrial fibrillation is they will ablate these circuits, they will essentially just cut off the pulmonary veins from the atria completely. So there is no communication between the two. So that is important to know it's important to be able to recognize this is atrial fibrillation and also to know that the origin of the impulses is in the pulmonary veins. Um And this is a diagram of both the ectopic circulation within the atria around the pulmonary veins and the actual ablation itself. Ok. Next question, which drug is most likely to restore sinus rhythm in this patient? Please read the question and the answer is well done, well done, everybody. OK. So um well done. Most people got that right. The answer is flecainide, uh bonus points and we know how flecainide works. What is the mechanism of action? So there's a specific, there's a specific classification of antiarrhythmic medications and that's called the Vaughan Williams classification. And that just categorizes antiarrhythmics into four broad categories depending on what receptor they block. So, um class one is sodium two is um the beta receptor three is potassium, four is calcium. The most relevant ones are one and three. So the and within one and three, the most relevant ones are flecainide which is a one C sodium channel blocker and amiodarone in class III which is mainly a potassium channel blocker. OK. So flecainide is a one C Vaughan Williams antiarrhythmic that blocks sodium channels. And that is the correct answer here because of the options that you are given. It is the only rhythm control that can be used in af so Adena slows av node conduction used in SVT irrelevant here. Bisoprolol is a form of rate control medication. It slows down heart rate but does not restore rhythm. ASM OL you may not have heard of but it has lol at the end. So you would think it's like Bisoprolol, it's a beta adrenergic antagonist as well. Flecainide is the correct answer. Verapamil is a nondihydropyridine calcium channel blocker. So this is another form of rate control. So flecainide is the only correct choice here. OK. Um If I was to present the question to you like this, a 60 year old man. So compared to a 30 year old woman presenting with a four hour history of palpitations, this is a 60 year old man presenting with a three day history of palpitations. The ECG is the exact same. How does your management change? Would you prescribe rhythm control in this patient? And if not, why? If so why does anyone know? Do you do anticoagulate first? Yeah, exactly. Well done. Barbara, that, that's spot on. So if the patient has presented less, more than 48 hours after symptom onset, this man has presented three days after, then you would never initiate rhythm control unless you've established anticoagulation. So rhythm control only if presentation within 48 hours of symptom onset or you've established anticoagulation for three weeks or if you, or if you've had a te which not many people are going to have had. Um The reason why you've had a toe allows you to give rhythm control is because there is a particular anatomical um part of the heart which you are interested in in af does anyone know the anatomical part of the heart which is implicated in thromboembolic formation in A F is it the uh left atrial appendix? Yeah, exactly. Well done. So it's the left atrial appendage. Um There is this embryonic structure within the left atrium called the left atrial appendage that predisposes thrombus formation and it is the culprit in why af patients get strokes. So there are two tools that nice guidelines recommend you using the A chances tool and the orbit tool to wrist stratify a patient in terms of how likely they are to get a clot and get a stroke versus how likely are they to bleed and die from the bleed. And if you are happy that the chance of a score outweighs the orbit score, then you would commence every patient that you see with atrial fibrillation on long acting anticoagulation. And that's because of possible thromboembolic formation within the left atrial appendage. OK. Does that make sense? Cool. So, as usual with management of any arrhythmia, you would see whether the patient is stable versus unstable and we are assuming that both patients we've looked at are stable. So you would use the trans vas and orbit scores to proceed with anticoagulation and that's all patients rate control. Um If you were to opt for it would be in the form of beta blockers and calcium channel blockers again. And um second line would be digoxin, third line would be a combination of all three of the above and this is most recent, nice guidelines. So um if you're going to be us on anything, then it will be this and how would you appropriately rate control? Af and the fourth option is quite an extreme option, but you would essentially ablate the AV node. So you would stop any kind of conduction going between the atrium and the ventricles and then you just put in a pacemaker so that you could pace the heart yourself. Um Cool rhythm control would only be instigated if there was a new presentation of AF or if they were young and outside of that, I don't think you need to know very much more. I think in an exam setting, if they ever ask you this, it will be in a new presentation in a young patient. And then you would opt opt for rhythm control. Um Other circumstances would be heart failure if you have af secondary to something like sepsis or pneumonia. And um if you were unsuccessful in rate control, but I would say these two are the um things that you, you could get asked about in an exam. Um So rhythm control control strategies for af people usually use amiodarone and just some things to note about amiodarone. As we've mentioned, it's a Va Williams class three. It has a long half life. So that um you have to give loading doses in the initial period, you have to regularly monitor the liver, lungs, eyes, skin and thyroid. And it can cause many bad things. The most notable of which is hypotension. So that's relevant if you were to have an acutely unwell patient, their BP is 70 40 you would not be so keen on giving them amiodarone as a first line treatment. It can also cause arrhythmia and it can widen your QT interval. And this is just a um like a blue blob that was on the internet and um can be useful in remembering the side effects of amiodarone, which are often topics in medical school and MRC P questions. So you have issues with the thyroid with the lungs, particularly you get um pulmonary fibrosis, hepatotoxic and you get blue colored skin, which is why he's blue. Um And you get sensitive to light. OK. So just to summarize AVNRT is the most common SVT and it's caused by reentry, unstable SVT requires synchronized DCC V, stable SVT requires vagal maneuvers. And Adena Zine, we didn't really actually talk about this, but um this is from the guidelines and it's just something that you should remember. Um I'm sure you all know that by now the trans Vasant orbit scores are used to decide whether or not you would anticoagulate an AF and rhythm control. Usually in the form of amiodarone can be used in some AF patients. Um amiodarone has a long half life and causes toxicity. OK. We've got one topic to go. I know that this is timeline to go until 8 30. So, um do you want a break or do you want me to just carry on this one is shorter unless anyone take a break in the chat. OK, I'm just gonna carry on. Ok. So heart failure again, basic principles. The heart is a pump and the function of this pump is to match the oxygen demand of the organs. That's what it does. Ok. Ultimately, any kind of problem with the heart, the end outcome is gonna be damaging end organ perfusion. Ok. What is the formula for cardiac output? What are the determinants of cardiac output? It's heart rate and stroke volume. Yeah, that will will diminish heart rate and stroke volume. That's correct. Um So as you can see in this equation, that's what it's equal to any changes in either of these will directly affect cardiac output. So if you were to have an acute shock situation, then the physiological mechanisms for compensating for that increase in need for cardiac output would be to increase heart rate or to increase stroke volume or both. And the compensatory mechanisms in the heart are the adrenergic system and the ras system and that extends to the kidneys as well. So these systems are initially compensatory and can make up for either reduced supply or increased demand in the acute setting. Ok. While they can initially compensate over time, they become deleterious. So they become pathological and bad. And are the reason why heart failure is a self perpetuating syndrome that just gets worse over time unless it's treated. So just again, the sympathetic nervous system, just the thing to note that compensatory wise, the beta adrenergic system increases the rate of heart contractility increases the strength of contractivity. Luso is just the rate of relaxation and other things are not really relevant, but there are downsides to constant exposure to beta adrenergic stimulation. And that's all of this crap here. The renin angiotensin system, what the point of that is as you have decreasing blood volume, the kidneys detect that and they release the renin and start the rennin angiotensin cascade initially. What that does is increasing circulatory blood volume by increasing sodium retention. Ok. And that will compensate for shock and increased end organ oxygen demand initially. But over time that becomes pathological. And as you take on more and more water, you retain more and more sodium, um your heart becomes, starts to decompensate. And that's why you get the evidence of that clinically peripheral edema, pulmonary edema, raised AVP, et cetera and both of these mechanisms feed into each other. So the renin angiotensin aldosterone system stimulates the adrenergic system and vice versa. So how the European society of cardiology defines heart failure is if you have an LV ejection fraction, under 40% you have reduced ejection fraction. And if you have over 50% you have preserved ejection fraction. Ok. That, that is just what I want you to remember and don't worry about mildly reduced. And but sometimes people say this is severe, less than 40% is severe. And then they would say 41 to 49 is moderate. So just just remember, less than 40% is severe. Um So next SB A mono SB 10. So we're back to Mr Jones. He's now 78 and we know that he has ischemic heart disease. He's attending routine clinic. His echo shows an lb ejection fraction of 38% and he's a euvolemic. He's on Enalapril Bisoprolol bumetanide and Eplerenone. What'd you do? Ok. For the purposes of time, you're only gonna have 30 seconds now to answer these questions. So, um be quick with the men. Uh most people have put the correct answer well done. And the correct answer is add Dapagliflozin. So let's just go through these very quickly. No action. Incorrect. The patient has an LV ejection fraction of 38%. That's not good. Um You need to do something and you need to improve their heart failure management. How do you do that? Arrange coronary angiography? Incorrect? There's no evidence of chest pain. There's nothing mentioned in the stem that the patient needs further investigation for optimizing coronary artery disease. OK? You just know that he has ischemic heart disease. The point of this question is answering, how do you manage worsening heart failure? So, Dapagliflozin is correct, we'll move on to why. Bendroflumethiazide is a thiazide like diuretic and that's used for hypotension and diuretic resistant heart failure. He's euvolemic. You wouldn't add bendroflumethiazide here, increase bumetanide. Same rationale you wouldn't, you wouldn't increase bumetanide. OK? There's no complaints of shortness of breath, oxygen requirements, whatever Dapagliflozin is. Um a medication that's oh I thought it was on the next slide. Um OK. Dapagliflozin is a medication that inhibits proximal tubular sodium and glucose reabsorption. So it acts here and it acts on the co transporter that allows for reabsorption of sodium and glucose into the blood. So essentially, it is a glyco uric agent and a natriuretic agent. It promotes sodium and glucose excretion. As we've spoken about the renin angiotensin system is implicated in the pathogenesis of heart failure. So, anything that will help to excrete sodium is good. And that's why ace inhibitors, ace inhibitors, et cetera, mineralocorticoid receptor inhibitors work and dapagliflozin works in a similar way and that's why it benefits the side effect. It also increases weight loss, which is good, recurrent genital thrush, which is less good and euglycemic diabetic ketoacidosis. And this is probably the one that will get asked about in exam is recurrent genital thrush. And it's a common side effect of starting this medication. If you think about it, you're peeing out more glucose, which is, which is a substrate for um bacterial metabolism. So you're going to get more infections around that area when you pee. So um just touching on chronic heart failure management, all patients, I'm sure that you guys know this because most of you got a question, right. All patients should be on an ace inhibitor and a beta blocker. Um and then you would add a mineralocorticoid receptor antagonist like spironolactone or eplerenone and then you would add dapagliflozin. This is the nice guidance. Um And this is what you should learn. So if the patient is congested, so if they had pitting edema, whatever, if they had evidence of pulmonary edema, you would add diuretics or increased diuretics. If they had um a reduced ejection fraction and bad symptoms. Nyha is a way of classifying heart failure symptoms, then you would replace your ace inhibitor with Entresto. I don't know if you guys have heard about Entresto before. If you haven't, I'm not going to open that kind of worms now. And fluid restriction is not routinely recommended by nice. So you wouldn't put someone on long term fluid restriction with chronic heart failure. That would not be very kind unless they were drinking like three liters of four liters a day. OK. So again, this is why ace inhibitors beta blockers and spironolactone and Eplerenone are the mainstay of heart failure management because you're stopping all of this detrimental effect and you're stopping this increased blood volume, increased sodium retention by blocking these two mechanisms, right? OK. So we've gone through this next SB A so same guy. Oh OK. OK. I've given away the answer but it's fine. You guys would have gotten that. All right. Anyway, I'm sure um it's essentially the same case and the only difference is in the question stem. He's now short of breath. He's got pitting edema to the proximal tibia and happily he's on dapagliflozin. That's the only thing that's changed. So, working through the question together, this, as we've already said is not right. You would not do this to a patient. Um Add dilTIAZem, you would never add dilTIAZem with bisoprolol together because you're increasing your risk of heart block. That's wrong because there's no mention of BP, that's wrong. There's no mention of BP. Um and the patient isn't actually on any loop diuretics. So you would add furosemide. Does everyone understand why you have a patient with heart failure? Presenting with shortness of breath and pitting edema, they're already on most of the prognostic medication to treat heart failure. You're going to add a loop diuretic. Ok? I totally did that on purpose. Definitely. So this is just a study that was done to show that loop diuretics actually improve mortality in patients who are congested with heart failure. So I know that often you get asked questions which of furosemide is the odd one out because it doesn't improve mortality. It does improve mortality if the patient is congested. If the patient has um pitting edema, pulmonary edema, if they have any evidence of fluid retention, it improves all cause mortality. Ok. So get that idea out of your head. Um I'll probably finish off with this one because uh we're rapidly running out of time. So, and I won't. So the answer this time. So same man presenting to Ed with shortness of breath we know his history. His JVP has raised course creps. This is his chest radiograph. Can you see he's got steno wires. He's saturating on 30 mL oxygen saturating. 90% BP is 94/44. His heart rate is 1 20. So you should be able to see on many. What are the options? I'm not going to flick over to them so you can still see this slide. But the question is essentially what is the next step in management? And it's a choice between hemofiltration, cpap, increase bisoprolol, invasive coronary, angiography and stop antiplatelet therapy and put in a drain. Ok? OK. Quick, quick, 30 seconds. OK. Yeah, everyone is answering the question, right. You guys are amazing, well done, well done. I'll ignore the last person who answered. So the correct answer is CPAP again, going through these options. Hemofiltration is only indicated in diuretic resistant acute pulmonary edema. OK? And it's usually when the patient is a ric, not producing urine, there's no mention there's no mention of diuretics and urine here. Hemofiltration is incorrect. Increasing bisoprolol to 10 mg, you would actually stop the bisoprolol because bisoprolol is negatively inotropic and negatively chronotropic. And you actually want that to be happening in someone with acute heart failure. OK? II, I know we spoke about it in um a chronic heart failure. But in acute heart failure, you don't want the bisoprolol to be there. Ok? You want the heart to be pumping as hard and as, as quick and as hard as possible. So you would not do this. You would do the opposite of this invasive coronary an angiography. Um It's a good idea, but there's no mention of chest pain troponin. This is the most appropriate initial management. You would not do an invasive coronary angiogram without treating the initial pulmonary edema. Even if there was lots of evidence for acute coronary syndrome. And um you would not do this, don't ever do this. Um Pleural drains are are rarely used in the treatment of heart failure, especially acute heart failure and it's not going to help physiologically. Um So this is just why CPAP works in heart failure. The most important things here is that it decreases extravascular lung water. So what happens in heart failure is your alveolus looks like this and it's actually collapsing on itself because of how much water there is in the interstitial. Ok. There is so much water that the alveolus is collapsing. And the person who mentioned La Plazo before La Plata law states that that increased surface tension from all of this water increases the pressure needed to blow up this thing and you need this thing to be blown up so that you can transfer gas. So that's why CPAP is very effective because it forces air in, expands this and pushes all this water away. It also increases intrathoracic pressure which puts pressure on the IVC and the pulmonary arteries, so you're decreasing venous return. So by putting lots of pressure on the venous system, the right atrium and the right ventricle, which are more compliant, you are reducing venous return and ultimately reducing the amount of blood that the heart has to pump around. And those are the most important things I'm going to mention here. So in the treatment of acute heart failure, just remember that the mainstay of treatment, even though it wasn't mentioned in the previous slide because it wasn't an option is that loop diuresis is the most important thing with someone suffering from acute heart failure. Please, if you've learned the mnemonic, MMP, please just delete that from your brain. That's just incorrect. Loop diuresis is the most important thing. Alongside, you can keep the pee positioning is also good and positive airway pressure is also good. So loop loop diuretics are advocated by nice morphine. Actually, the studies have shown that morphine increases in hospital mortality and rates of invasive ventilation. So you would not give morphine, you would actually cross off morphine beta blockers. No, there's no good studies because no one in their right mind is going to give beta blockers to someone with acute heart failure because as I said, you are reducing chronotropic and inotropy, which in the acute situation you want to be happening. Nitrates, there was a good study done which shows that there is no improvement in in mortality with uh nitrate administration. So um nitrates don't cause harm like morphine and beta blockers, but they are only advocated by NIS in this situation where there is severe hypertension requiring nitrates or evidence of myocardial ischemia. So just remember, loop diuretics are the most important thing with a catheter, please. A CPAP as mentioned in that scenario is useful if there is severe dyspnea and that patient was on 30 liters via um high flow nasal cannula, it is clear that they were in respiratory failure. And you could see on the x-ray that there was evidence of pulmonary edema hemofiltration. As I've mentioned is only if the patient is resistant to increased diuresis. So, just to summarize for heart failure, it's a result of pathological processes that occur from initially compensatory mechanisms involving the adrenergic and ras systems. And long term treatment of heart failure with reduced ejection fraction involves ace inhibitors, beta blockers, uh mineralocorticoid receptor antagonists that shouldn't be an either. And SGLT two inhibitors, loop diuretics improve prognosis. If congestion is present, acute heart failure is treated with loop diuretics. CPAPs used in severe respiratory dysfunction and nitrates are used used in severe hypertension or myocardial ischemia, avoid morphine and beta blockers. Um cool. Right. So that's the end. Um And uh yeah, that there are a bunch of bonus sbas that I threw in just in case I was going to go under time, but I'm overtime. So I won't go through those. Um unless anyone actually wants to stay and go through them. They, they're all quite hard and, um, but they do have good learning points from them. So it's up to you whether or not you want to stay. Uh, Phil, what do you think? Well, to be, to be fair. Um, I kind of want to, I kind of want to hear them but it's up to everybody else. I mean, you can flash your feedback maybe on the screen if people want to leave it. Yeah. Yeah. Yeah. If you want to go, then please fill in my feedback. Sorry. Just something to mention about this chest x-ray. So this is acute pulmonary edema. I didn't actually mention this before because running out of time, but just something that you have to be aware of this patient has tenotomy wires which we know he's had a cabbage. Good thing to spot on a chest X ray, especially in a OSI. You know that the patient has ischemic heart disease. There's a small right sided pleural effusion and there's fluid in between the upper and middle lobes here. OK. Um There's pulmonary uh uh upper load, pulmonary vessel diversion and there is um cardiomegaly assuming this is a pa film. So this is an x-ray of acute heart failure and you should always be able to recognize this. Ok? And, and present it. Cool, right? I'll show you my feedback uh discard. Ok. Cool. Please scan that. Um Robin, we can't see it mate. Oh, sorry. Sorry. Uh one sec. Ok. Ok. Scan that. Yeah, we can see it now. Thanks everyone for attending. I know that that was longer than your normal sessions. But um I wanted to cover the main topics. Uh Please ask me any questions if you do have any questions. Uh Hi. Yeah, sorry. Thank you. Thank you for the it was really useful. I've got a couple of questions. So um is there like is there a cut off age for like rhythm control in? Because I know it's like younger patients who do, usually you see that people write over 65 that you would rate control, but it depend on the individual. And in the European Society guidelines, there's no cut off. It's just there are factors which would make you favor rhythm control over rate control in an exam. I don't think you are ever going to get asked. Would you, would you give rate control or rhythm control in someone who's a borderline age in your exam? You're going to get asked if someone's like 25 and they have new onset af then it's a or rhythm control. All right. Thank you. Um And then my last question is just um so you mentioned how like um or a f like the bulk of impulse formation happens in like the pulmonary veins. And so like, you basically cut, cut it off from the atrium. Is this like, does that happen in people with like sort of a F or it just like does it happen in everyone? Like the impulse formation in a, in a? So it doesn't happen like sort of, if you're not having in a normal person, you shouldn't have impulses coming anywhere outside of the sinoatrial node, the sinoatrial node should be the source of all impulse initiation in the cardiac conduction system in pathology. Particularly if someone has a history of alcohol exposure, thyroid disease or anything that would cause the atria to be dilated, then you're more at risk of af um So the, yeah, as you begin to stretch the pulmonary veins or expose them to toxicity like an alcohol thyrotoxicosis, then you predispose someone to forming um pathological re entrance circuits that would cause a cool, all right, I had a question um again about a f actually. So if um if you have um a person who's, you know, been in a f over 48 hours and let's say they're 60 but their chance of ask is zero. Would they actually need any anticoagulation or would you be OK? Just rate controlling with their anticoagulation. If someone's under, if it's a male under 60 then you would not. And if you don't have any of the risk factors, you would not anticoagulate them because their chances would be zero. You, you would, you would only anticoagulate someone if their chance vasco was one or above. And usually, um as you increase your chance score you increase your annual rate of stroke. So as you get, as you get past a chance score of three, your annual rate of stroke goes to 5%. So, um yeah, usually usually in, in, in this gentleman um o obviously, yeah, he's a 60 year old man. So you, you, you wouldn't anticoagulate him unless he had any other predisposing conditions which we've said he doesn't. Ok. And just to clarify. So is that like in the acute setting as well? You just don't need it at all because the chance basket is zero. Yeah. So in the acute setting, I think if you look at the algorithm, there is a point where it says to decide whether or not it's, it's appropriate to shock them. Um No, it's not in here. But in the, you'll be able to see in the e guidance on acute management of af that's a clinical decision to shock someone just because their BP goes below 90. So their BP is 85. That doesn't mean that you automatically shock someone if they weighing in the fact that their symptom onset might have been over 48 hours because what you don't want to do is great. You've rhythm controlled them, but now you've given them a massive stroke and they are probably going to die. So it's always just finding a balance as a clinician on gauging risk. And um yeah, if the person is Perret with and you think it's secondary to af, then you have to shock them. But if it's someone who's not been anticoagulated, you know, that the symptoms have been going on for a while, you would probably err on the side of caution. Oh, God, I don't want to show you that and, and you wouldn't anticoagulate them. Does that make sense? And you wouldn't shock them? Sorry. Uh, thank you very much. No worries. Any other questions? Yeah, Robin. I was just wondering, oh, sorry. I was just wondering um how long you think this will take? Whether in the interest of time it might be better just to like upload the slides and explanation. I appreciate. Obviously, it's already been an hour and a half for you. Yeah, probably about like I'd say 15 to 20 minutes if we go through it, probably 15 minutes. Oh, fine. Ok. It's only, it's only five, it's only five questions so you can stay. It's literally just five questions. Ok. Um I'm just moving on the mentee, please log log back onto the mentee if you do want to stick around. Thank you for coming. If you don't want to stick around. I appreciate you guys coming. Um So the next question, a 72 year old man presents following an episode of collapse, there have been two episodes previously. Um each lasting about a minute and he's had a history of anterior myocardial infarction. This is his examination findings and that's what his ECG shows what is the most likely diagnosis? Ok. Let's just see what people are saying real quick. People still reading. Ok. Oh, ok. Ok. So we have one of every single answer which is good, as I said, these are all extremely hard questions. So don't be disheartened if you get it wrong. But, um, everyone is than one person who's got it wrong so far. So we'll keep going. But I'm gonna wait a bit longer for people to read and respond. OK. OK. Let's go. So two people got this right. Um I'm just going to go through the rationale as to why the answer is VT here. So it's a 72 year old man. He has a history of ischemic heart disease and he's presented with syncope. OK. So that immediately should make you think. Is there some kind of arrhythmia going on? Is it a brady arrhythmia? Is it a tachyarrhythmia? There's something going on that's causing him to collapse. Acute mi is not likely without a history of chest pain and there's no ischemic features at least acutely, ischemic features on the ECG Q waves represent old ischemia. Um So this is wrong, right. SVT does not usually cause syncope, not usually. And in this history, it's an older man presenting with a history of ischemic heart disease and we know that VT and ischemic heart disease are very closely tied together. So the correct answer is VT a lot of you have put Brugada syndrome, no one has put heart failure. Thank you. The answer is not heart failure. Brugada syndrome is an inherited genetic condition where you are predisposed to VT. So I can see why you are thinking that if that's why you put it. It's a channelopathy where you usually occurring in younger people who present with syncope. You are never going to get an exam question, exam question where that answer is Brugada in a 72 year old man because it's a genetic condition. It's usually picked up very early and patients don't usually go on to live until their seventies with an anterior mi before they get diagnosed with it. So Brugada is wrong. The correct answer is VT well done to the two people that got that right. Um These are just like things to make you think. Then I'm not going to go on ramble about physiology for too long about this. Um OK. Next SB a 37 year old woman presents with a history of intermittent lightheadedness and one episode of syncope. OK. Well done everyone. Even though the last question, I went on to talk about Brugada syndrome for a long time. So the most appropriate thing to do is always the most general and most sensitive test to do. You are not going to go about screening someone for Brugada syndrome just because I've just spent the last minute talking about Brugada syndrome. Ok. The most sensible thing to do here is to do a holter monitor because you are investigating someone with a very generic Insys with concern over cardiogenic syncope. So you have a young lady with concern over cardiogenic cardiogenic syncope with no other medical history. You're going to do a holter monitor. Ok. Angiography, wrong Brugada syndrome, wrong right heart cath, no MRI brain possibility. But again that you're doing an MRI brain to rule out either a space occupying lesion, a ischemic stroke. MS none of these things are in your top differentials here. So Holter Ecg is the most appropriate thing as if someone has a history of palpitations that you are trying to investigate anything that you are trying to find out. Is there a pathological heart rhythm happening when I am not physically seeing the patient? Then a halter monitor is very useful because it gives you a snapshot of it gives you a visualization of their heart rhythm over a certain period of time. So that will be first line in any investigation of syncope. So let's go on to the next question. Her 24 hour ECG shows this which abnormality is clinically the most important. So just remember the history why she came in, why you did the investigation and which one is clinically the most important? It's not saying which one sounds the most dangerous. Like what sounds the most scary is which one is clinically the most relevant here? OK. Good number of responses. Um So three of you got that right. Well done. The answer is um SVT. So let's break it down again. The um atrial premature, no, no, no, no, no, no atrial premature beats. So this is a benign feature. Everyone gets atrial premature beats. These don't usually cause any problems. However, they are relevant because we spoke about AVNRT before. If you have lots of these, then they can predispose you to avnrt because of that AV node thing that we were talking about. I don't know why it came out like that lagging. So that's not clinically important here in the context of syncope, is it ventricular premature beats? A lot of people have put that ventricular premature beats are just ectopics and premature beats refers to a single ectopic. Once you have two ectopic beats, that's a cot. And as soon as you have three, you have non sustained VT in between three ventricular premature beats and 30 seconds of ventricular beats. That's nonsustained. VT anything over 30 seconds is VT. OK. So ventricular premature beats are just single ventricular ectopics that by themselves are not clinically relevant in this situation. It's a 37 year old woman with syncope. If she had runs of VT, then you could argue. Ok. Her circulation is probably being compromised. She probably has reduced end organ perfusion, but she is just having premature beats, nocturnal, bradycardia, everyone gets nocturnal bradycardia because of increased vagal tone at night. Mobic is type one AV block this is wrong because as we said, this is physiological and very rarely causes harm. Supraventricular tachycardia is the right answer. So this is why. Um Well, yeah, this is the clinically the most important thing from this 24 hour E CG because this is the cause of her syncope. OK. None of the other things by themselves cause syncope. Cool. Does that make sense? Right. Second to last one, a 48 year old man presents with a four hour history of severe chest pain. His ECG is shown and the question is which coronary artery is most likely to be affected? And the options are un many and on the next side, but I'll keep it on this side. So you can see the gene, right? Could you swim to the ECG a bit? Oh Yeah. Yeah, sorry. So thank you. Can, can you see it if I zoom in, by the way? Like does it show up? Uh Yeah, it does. OK. Cool. This is a very hard question. It is a very hard question. Yeah. Have a go. If anyone knows this, then I'm actually going to be so impressed. If anyone knows like what, what, what the answer is. Yeah. OK. All right. So um let's do out real quick. OK. So the answer is the circumflex artery and this is a real case. This is what happens when they put the ECG S instead of being on the front of the chest, they put them on the back, the chest leads. And you can see that there's clear ST elevation in V seven, V eight and V nine. So this is a posterior myocardial infarction for the purposes of your exam, just know that this exists like this is a thing that can happen. And it's because when you usually supply the posterior aspect of the heart, it's either through the right coronary artery or through the left to wrap around and whichever one dominates depends on how you were born. So, in this case, the answer is circumplex. A right coronary artery was not an option. So it's asking you the question is asking you which artery supplies the back of the heart. And the answer is circumplex. Ok. OK. All right. So we're nearly there guys. 26 year old male was referred to the outpatient assessment clinic um with breathlessness, he had asthma and a history of recurrent chest and sinus infections. No other history. What is the most likely diagnosis? Wow. Well done, well done. You guys hold on. Does anyone care to explain why? Uh Yeah, the history and the ECG seem like um like car cartagena with um A P CD and Dextrocardia. So well done, well done. Manish gold star. Um So yeah, Cartage syndrome, you guys know it's a, a recessive condition where the, the features are cys inverters. In this case, it's manifested in dextrocardia alongside bronchiectasis and recurrent sinus infections and that's due to a defect in cilia and their function and how cilia are responsible embryologically for the correct sighting of the heart. And that's evidenced here by the fact that AVR is positive and then negative. So it's isoelectric aVL is negative aVF is positive. So you know that something is something weird is happening that the chest leads are all very low q low amplitude QRS complexes. So you can tell that the electrical access is going away from aVL aVL measures here. So you can tell that the axis is going away from a VL um and towards a VR or isoelectric to a VR. So um the axis is completely wrong, there's low voltage Q complexes. So this is dextrocardia, the heart is on the wrong side. Um I won't go into why the rest of these are wrong. OK. Very last one, very, very last one. SB A 18. Oh yeah, I'll show you the rest. Uh OK. So this is just e either you know this or you don't know this. So I'm not going to give you very much time to work it out because you can't use the exam technique to rule, rule in or rule out any of these e either you know it or you don't know it. And if you know it then well done, you're a superstar. If I was given this in an exam, I, I would just rule off the things which I knew it wasn't. And then just guess. And if you didn't know what any of them were, then you would just guess. Um But they like testing on clinical things in exams. OK. I think that's enough time. Um So the correct answer well done is Pulsus paradoxus. So very quickly arotic pulses. So this is a feature in severe aortic stenosis. And it's visualized here if, if you imagine the Y axis is amplitude of the pulse. So here there is a reduced amplitude and that's because of low flow across a stenotic aortic valve. Um the LV is unable to generate sufficient pressure to match a normal pulse. Um So anac aortic stenosis, the second option is a collapsing pulse, also known as water hammer and Corrigan. So that looks like this compared to a normal pulse, we are looking at a marked high and a marked low. So the reason is because in aortic regurgitation, you have an increased end diastolic volume um because of all the regurgitant flow. And as a result, um the heart has to pump out a lot more. So on Starling's curve, you are further across the curve and you are pumping harder and you also have a much lower low, much lower trough because of all the blood going back into the ventricle. Ok? I hope that makes sense. It can be pathological and aortic regurgitation is the most notable thing or physiological in the case of pregnancy and exercise. Ok. So that's collapsing pulse. A K A Corrigan sign A K water hammer pulse. So pulses alternans, I can see why some of you would have put this, uh this relates to severe heart failure. And that's uh it's characterized by an alternating amplitude in pulse. And the reason why is again to mention Starling's curve or Starling's law. Um as you increase your end diastolic volume, you increase your contractility. So this is preload or end diastolic volume. OK. My computer is really laggy but um essentially yeah, on the, on the X axis it's preload on the Y axis, it's contractility. And as you increase your preload, you increase your contractility in severe LV, dysfunction, you have a weak beat and as a result, you have more blood left over. So then you get a strong beat and then you have a weak beat, more blood left over, you have a strong beat. Bis ends is a, a defect in flow seen in either mixed aortic valve or severe A R. No one really knows why this happens and no one cares because this doesn't really have any clinical significance and isn't going to change anything. So there's not been very much research done in this um Pulsus paradoxes. So this is I promise you my last slide. So what happens normally in inspiration is as you breathe in, you're decreasing your intrathoracic pressure because you're pulling everything down. So there's less pressure building up in your chest, you're pulling everything down and you increase preload because the veins have less resistance to fight against. So you're increasing, you're decreasing the intrathoracic pressure, you're increasing your preload. So how much blood is going into your heart as the pulmonary vasculature expands as you breathe in, all the vessels are allowed to expand, less blood enters the left circulation. So you get a drop in BP during inspiration and that's normal. So you breathe in all of your vasculature expands, you have less blood going into the left side and you have a drop in BP because we know that blood, that cardiac BP is proportional to your end diastolic volume. So um that's normal. Ok. So whoever called this pulsus paradoxus is a moron because in Taminol, what happens is you get exaggeration of this effect. So it's not a paradox, it's just a worsening of a normal physiological effect. And um what happens is as you breathe in during tamponade, instead of your preload being increased with your nice RV, getting more preload, the RV can't get bigger because there's a bigger fusion in the way. So instead of getting bigger on the outside, it gets bigger on the inside and it pushes into the LV by bulging the septum. So because inspiration and the beating of the heart are not related as you breathe in. It could be during systole halfway through systole and your LV suddenly has much less blood to pump out. So as a result you have reduced cardiac output and reduced BP. Ok. So does that make sense? So pulse is paradox isn't a paradox. It's an exaggeration of a normal physiological response where your BP drops during inspiration. OK. Um But in cardiac tamponade, that extra blood in the RV, from breathing in all that um extra blood going into the right heart presses against the left heart and then you get less cardiac output. OK. Benito, the end the end, I promise. Thank you everyone for um staying behind, this is the feedback form in case you haven't filled it out. Sorry, it uh went on for quite a long time. But um there we go. Thanks very much. I really appreciate that. I hope other people appreciate it as much as I did. No worries. Um Yeah, I think everyone's leaving now. So um yeah, thanks very much. No worries. If anything didn't make sense, then tell people they can message me. Yeah, I'll pass on any questions if, if people have raised them. But um yeah, it was really good. Thanks. Um Yeah, I guess that's it. I'll stop the recording.