Computer generated transcript

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

OK, let's get going. I introduce myself and people trickle in as we do go for the introduction, but welcome all to our third lecture of the year. And this one is on cardiology. This is one of the big, big medicine topics, often quite scary, often hard as well. But hopefully we might to kind of cover the big topics and hopefully make everyone understand a little bit better. By the end of this talk, I, you know, I'm always encouraging like interaction and you guys ask as many questions as possible and that's really part of the benefit of you guys coming and attending this live. So it's gonna be a mixture of SBA S, it's gonna be a mixture of kind of explanations as well. But also please, if you have any questions, just pop it in the chat, be very happy to answer. And we, you know, I want to make this really as interactive as possible as well just to kind of make everyone's learning a bit better too. Um This will be recorded. Yes. OK. And we'll publish it, we'll publish it hopefully on youtube and definitely on med too. OK. So to registry who asked that question? It will be recorded. Cool. So let's get going. My name is Eamon. I'm one, I'm a currently cardiology F one at New Hospital part of Barts Trust. My BSE was in cardiology and um at back at med school and it's kind of the subject I'm most interested in. I'm also the mind the final year lead as well. So we're kind of running this long month long a series for you guys really? And we're hoping to cover pretty much every single subject mapped to the UK. So this is only the third of really what should be about 30 different webinars. So, you know, just keep an eye out on our Facebook on our medal, but also we've got some med school reps as well you might hear from and they'll be kind of messaging along, keeping you guys updated as well. But right, let's get into the cardiology side of things. So today we're gonna cover really, I tried to pick the main topics and the things that are most likely to come up. Acute coronary syndrome by far, the, you know, the most depressing the most emergency and actually very common as well. So we're going to go for that heart failure, hypertension, atrial fibrillation and a little bit of heart block, but actually not too much and then valvular heart disease as well. Yeah, unfortunately, you know, we have an hour, we might go over, we very well could go over, but it's impossible to cover all of cardiology. So there's a lot of other things that we won't and I've just listed them there. Just so you guys are aware of, you know, if people want, then we can always do another lecture as well to kind of give a complete overview of cardiology. And that's something I'd be very happy to do in the future too. And this is your MLA curriculum content map. Now again, this is new, not everybody is going to be using this. But even if your med school isn't using this, it's still a good guide to kind of understand what you need to know. The annoying thing is they've kind of mixed cardio with vascular and it's not specific in the slightest. So you can look at things like pericardial disease like what does that mean? You know? So it's, it's not super, super useful, but at the same time, it's definitely a good guide to point you in the right direction and make sure you are taking everything off. So I would really, really recommend mapping your revision to this, especially especially if your med school is using it as part of your exams, which I think many are this year and more and more so definitely next year, right? So I said there will be S pa si am just gonna make a poll, the uh sorry, just give me a minute. OK. So this is the pulp and I just read through the question. So a 62 year old man presents to Ed with a 1.5 hour history of central crushing chest pain, radiating to his jaw. He's diuretic and nauseous but does not complain of any dizziness. His observations are stable. He has no known past medical history. An ECG is performed and is shown below. Let me show you next. This is, this is his E CG. I'll give you guys a few minutes to look at it. Ok? And these are the answers. I'll give you a minute from here. Mm So about half of you have answered the remaining people quickly get an answer in. No. Ok. Quickly, quickly, quickly, quickly, fine. So right there is a mix. I don't know if you guys can see, let me know if you can or can't, but I've stopped the polling. Can you, can someone measure the chart if they can see? Great, fine. So a bit of a spread here. Thank you very much, Miriam. Half of you really have gone for number two and the other half have gone for number four with a few other dotted about the rest of them. And this is a really mean question. I reckon most people who went for two or four were probably confused between the two. Would, would someone be able to kind of explain a little bit why they went for two or four? And while we're going through that, let's come. Ah, brilliant. That's exactly, it just has gone for the, the trick and that I was trying to get you guys to look at. Ok. So, yeah, Monna is definitely the, the way forward what's going on here? This is a man who's presented with central crushing, central crushing chest pain, radiating to the jaw. So that is very cardiac sounding, chest, chest pain. And the moment you hear that you really need to think, OK, we've got, could this be an A CS in our hands? Is this an emergency diaphoretic? So, very sweaty, very nauseous, often symptoms associated with acute coronary syndrome but no dizziness, which is another symptom and the crucial thing here, observations are stable. Everyone learns moac and everyone loves, you know, this mean to give morphine oxygen, nitrates, aspirin, clopidol do that. E CG give that antiemetic et cetera. But a lot of those things you actually only give if the patient needs. So what's the essentials out to the acronym Aspirin? If you've got aces in your hands, everybody needs to be loaded on 300 mg of aspirin. Almost everybody will be given a second antiplatelet as well. OK. And that can vary depending on trust from clopidogrel tool, Prasugrel. And we'll talk a little bit more about that later, oxygen only actually gets given if a patient has stats less than 94% and his observations are stable. So, you know, from that, that he doesn't actually need oxygen the other thing, I mean, for those people who went for one that is, you know, often the long term management, well, maybe not SGL T twos if they don't have heart failure, but definitely the rest of them are. And those who went for again, three and five, we wouldn't give statins or beta blockers in the acute phase. Here. We're really trying to manage the acute problem, which is, we have a blocked artery and we need to unblock it somehow. So we have a CS and I guess we can kind of guess that from the history, we look at the E CG and the E CG shows ST depression. All right. And it's really, it's quite in the lateral leads. Well, yeah, even these anterior leads as well. But V four, V five, V 61, Avil there's very clear ST depression, sort of a little bit of, I guess some TV conversion going on too. All right. A VF, you have a VF two as well. So there's very clear ST depression. And from that, the diagnosis with this is most likely going to be enemy. Ok. We would need a drop as well, but most likely we're going to be having an enemy on the hands and we need to treat this as a CS. And the answer therefore is number four. Ok. Aspirin tool and Fondaparinux when you have an, when you have a enemy, that's the treatment that we're going to give in the short term. And in terms of the fondaparinux, how much we give varies depending on the trust. Fondaparinux is kind of a similar to your heparins. It's an anticoagulant. So we've given dual antiplatelets in terms of aspirin and ticagrelor and that knocks out the platelets and then we're knocking out all the clotting factors as well of the fondaparinux too. And that is shown to be preferential compared to low molecular heparins, et cetera, which is why we give it typically, it can vary. But I think the trust I work out, for example, we give three days of fondaparinux. Yeah. And this brings us on to our first topic, acute coronary syndrome. Now, there's two main types that everyone knows about. There's your ST elevation, your sties and your non ST elevations, your ante. And we'll start off with the sties because these are probably the most the biggest emergencies that you are facing cardiology, really what they are. Patho pathophysiology, pathophysiologically is literally an occlusion. A total occlusion of a coronary vessel. Once you get that total coronary occlusion, there is a lack of blood supply downstream of the artery and actually the severity that you're going to be causing in terms of ischemia downstream of the artery, depends on the how sudden or how short term this occlusion has been. Ok. If it's a gradual chronic, slowly worsening occlusion, then actually the damage might not be so bad because you're more likely to get some collateral. But if it's a sudden occlusion, it's a thrombus that's blown up and completely blocked the artery, you're going to get very severe symptoms, very severe ST elevation, the way to look at it as well. In terms of the path of is that, that coronaries work and they run on the outside of the heart and they kind of engulf the heart from the outside, wrapping it around. So if you get to an occlusion, you are going to really cause ischemia to the whole wall, which is what we call a transmural ischemia. However, in ST elevation, what's going on is you've actually got a partial occlusion. So it's blocked, but there's still some supply going. Unfortunately, that blood supply is not enough to prevent ischemia, ok? And there is still myocardial damage occurring. But because the arteries wrap around the heart from the outside, the damage will be actually furthest away from those arteries, which is what we call subendocardial ischemia. So in en in enemies or non ST elevation, mis, it's a partial occlusion and the damage to the myocardial wall is subendocardial, it's not transmural. OK. However, there is a third part of our A CS and that is the unstable Angina. In terms of differentiating an NSTEMI from an unstable angina, it can be quite hard. And what we really need is that troponin level, OK? Because an unstable Angina can have very similar presentation, you know, you've got your chest pain it's not resolving. You've got ecg changes even, but the troponin is normal and that means there is no myocardial damage as of yet. Ok. The my myocytes aren't bursting and releasing troponin. Yeah. So this is a little bit of unstable angina. It's effectively defined as what we have here. Ok. So it's angina which is prolonged, lasting more than 20 minutes of a new onset and severe or it can be increasing in frequency longer in duration or lower in threshold. And this is often something known as crescendo Angina or it can also be an a a chest pain or angina that occurs after a recent episode of AMI. This is a clinical assessment. All right, we don't really need any other tests because if you have chest pain, you've got a normal drop. That's it, this unstable angina ecg changes may be present, but they don't really change diagnosis. Ok. Also, if you guys have any questions, just pop it in the chat and we'll go through in terms of angina again, a term which is often, you know, we all throw around but actually defining it is really, really important and what it is is it's typical chest pain related to the heart. So a constricting discomfort in the front of the chest or in the neck, shoulders, jaw or arms. So that radiating central chest pain to the neck or down the arm, it's precipitated by physical exertion and it's relieved by rest or by GTA in about five minutes. Ok. We often get these sympathetic symptoms as well, which are associated with them. And these are your nausea and vomiting, sweating, palpitations and dyspnea. And often when somebody does present with an acute myocardial infarction, they will have this whole myriad of symptoms associated with anginal pain as well. So, it's important to look out for them and notice them in your patients in terms of investigations. We've kind of mentioned them already. Does anybody know any investigations that we want to do? A troponin? Yeah, definitely ecg troponin observations. Exactly that functional testing and testing for Angina. Ok. Nice. So in terms of anything, how the best way to always present investigations is always your bedside, your laboratory and then your radiology. So your bedside investigations that we're going to want to do is definitely going to be an ECG, we're going to want to do uh a full set of bloods. But really, we're really focusing on that troponin and troponin. We want to get serial troponins and serial ecgs as well. Ok. The reason being we can have a change in our EC GST elevation ST depression T wave inversion or Q waves. But is this new, that's so important because if this is an old change that was present one year ago, then it's unlikely going to be an A CS. Ok. So we need these new ECG changes that are changing whilst you see them. So for example, if you see somebody who has only T wave inversion, you do a repeat CG in half an hour's time or an hour's time. And they now have ST depression alongside the T wave inversion that's already in keeping with this cardiac and semi picture. So dynamic ECG changes is good to look out for. And a dynamic raised troponin is also really important as well. It's one thing having a raised troponin, many things can cause a raised troponin. For example, poor renal function can cause a raised troponin. But is your troponin going up and then down if it is there has been an acute event which has caused a troponin leak. And that again, it points towards an A CS event. OK. So serial troponins, serial ecgs. And another thing that is really important is an echo. One echo will give us is one, the ejection fraction but two, it's also important to look for regional wall motion abnormalities. What these are is if you imagine the kind of the ventricle of the heart as it contracts as you contract symmetrically, all in one nice motion together, if you have myocardial ischemia or a lack of blood supply to a heart to the part of the heart, you often get territo territorial reduced motion. And this is called a regional wall motion abnormality. So if you have a lateral ischemia, then the lateral part of the wall will contract less well. And again, if we find this on a echo and this all points towards an A CS or a heart attack having happened. Uh We have a question about is Angina pain referring to stable angina. So Angina pain can refer to stable Angina, but also even a CS pain is also known as Angina. It is literally that central crushing, crushing, chest pain that radiates to jaw brought on by exercise or worsened by exercise. But really, it's just that typical pain there. OK. Stable angina is um the, you know, the weaker spectrum, which is where you have that pain. That kind of goes when you walk gets better when you rest, et cetera. OK. OK. So in terms of management, we've spoken a little about this already. But the first thing we want to do for a study is load and aspirin, OK, everyone needs to be loaded in and aspirin 300 mg as soon as possible. Then we kind of get to the next stage, which is how quickly have they presented? And are they fit for any me, any interventions? And these are really important because if somebody is, you know, 100 and something years old, they've had a stemi, they have huge comorbidities and they're not going to cyber PCI, then we're not going to treat them with a PCI. OK. In fact, you might not even give them fibrolysis either. We'll just go down the medical management route instead. So it's all red depending on the patients on the patient's condition with regards to um so that, yeah, so with regards to how long they've, how quickly they've presented is also important because we want to ideally be treating them before the myocytes have had time to die, which really in this kind of condition, we're looking at, we want to treat them within 12 hours of, of symptom onset. And it's really important that we, that we do that. So the numbers are need to be presented within 100 and 2012 hours and if we can PCI them within 120 minutes, then we'll PCI them immediately. Ok. In most places, especially in places like London, for example, that's going to happen. But in some of the more rural places where you're quite far away from a PC center or from a Cath lab and you may want to fibrinolyse them first. All right. Um We will get to the questions in a minute. Ok. But they're all really good questions. Mhm. Fine. So, in terms of, so we've gone down the PCI carbon analysis route. The other really important thing is giving a second antiplatelet. Now, typically this will vary on the trust. Nice tends to prefer tag law and I guess for exams, tag law is the way forward, but it will depend on what agreements your trust has made in terms of drug availability. Really, it can be from clopidogrel, which is, which confers the lowest bleeding risk. And also has the weakest action on antiplatelets to tag, which is kind of in the middle for both Tso, which has the strongest antiplatelet action, but also confers the highest bleeding risk. So naturally, which one of those you give depends on how worried are you about this patient's bleeding risk? Have they had a previous bleed at a critical site? For example, a stroke, et cetera? Are you uh do they have a present hematoma? These are all things that can happen? And you would want to take into consideration in terms of PC, what this says it literally a catheter that gets inserted into the radial artery or the femoral artery, we go into the, into the coronaries and we just put the stent with a balloon as well. The stent is normally drug eluting. So it helps anticoagulate and that all helps the cool just with these questions. Um Can you please repeat what the E CG changes were that you want to check in your serial E CG? It's, you're looking for any dynamic changes. OK. So the first thing is has this, how's the E CG that you've just seen? And you're querying an A CS? Is it any different to the previous ECG from 34 months ago? Ie prior to the event happening? Because often people can have long term changes in their EC G which may look like an A CS if you haven't seen the previous C GS? OK. So it's important to make sure that these changes that you are querying a CS for are new. And if they're not, then it's less likely going to be a CS. And that can literally be a, that can be at wave inversion, an ST elevation or depression or AQ wave. All right. So kind of make sure that those changes in you. Would you do a CT MRI Coronary angiogram? Um So this is a bit of a more niche question, but it's a good one in an acute stemmy situation, you would go straight to angio. So an angiogram is where you put a catheter in, as I described earlier and you literally just shoot dye into the arteries and you can visualize the coronaries that way. CT or MRI are noninvasive and they are used more for when it's a less clear cut case. So you might have a, some, some, you know, ST depression, you're querying an antemi, but it's not so clear and the patient is very stable. They're quite old. Let's go do a act or an MRI angiogram to kind of visualize the arteries before we actually do anything invasive. OK. So that's more for the stable patients who need less pressing urgent intervention, an LV ef reduced LV ef well reduced ejection fraction. You know, it means that the heart is pumping less blood out of it. If it's new, then you might have had a, you might have a new heart failure or I mean, it'll be typical in terms of the heart not pumping as well, especially in the acute phase of M I that might improve with time even so if there is a new sharp production in ef that should point you towards an ischemic event having occurred, especially if it's sudden. So for example, we have an echo six months ago or three months ago, an E LV EF was 60% and now it's 30. That is a big jump. Something has happened likely an ischemic event. Um Oh, loads of questions. Oh dear. OK. For the echo, would it be transthoracic or transferal? Generally, transthoracic trans requires sedation and is longer. So we wouldn't do that typically in Acs. Um So it choice of ap what do you mean by ap sorry for uh Katie's question. Can you please have access to the slides after this? Yeah, we'll get you access to the slides, don't worry. Antiplatelet. Uh huh. Yes. Typically it, it's trust dependent but for exams go tag law if you're gonna given the two just because tag law is your the one that I seem to prefer unless they're trying to push you down. This is a really high rate bleeding risk patient, go for Kloppy, et cetera. Um So you do an angiogram before the PCI. Yes, you do. So you always do the angiogram before the PCI. So you can visualize where the blockages are. What is the eligibility for reperfusion therapy? Is there a scoring system not really for sties for Nstemi, we have grace score which we're coming on to. Ok. And this is it. So end study management very similar. We give the dual antiplatelets, aspirin typically tool Fondaparinux as well. That's big difference. So everyone would get from the para. Now there is the grace score. How much this is used in clinical practice of the her I will say but for exams, I think it's probably the way to learn it. You do the grace score. If it gives you a low risk, then you kind of put on the conservative management. If it gives you a high risk or intermediate risk, then you want to go down the reperfusion route which is going to be a PCI. How urgent that PC is does vary depending on the patient's clinical condition. So if they're hemodynamically unstable, you know, for example, their BP is low, they're very tachycardic, then you would want to go down an urgent, you know, nearly immediate PC. But if they're completely stable, the symptoms have resolved, but an ischemic event did occur and you do have a little bit more time. And I think from how urgent that you need to give a A PCI for undergraduate exams, that is probably the amount that you need to know. I don't think you need to know, know anymore. Then that if another important point is on the bottom of both these nice flow charts and these are all available on. Nice, by the way. So I do have a look at them is cardiac rehabilitation and secondary prevention. Ok. So remember cardiac rehab, especially in your Aussies, it's a really good thing to say because it kind of is looking at the more holistic picture and it does really help patients too. OK. Next question. Have a look at this one. I'll get the pole ready. I OK, they should be there. You guys can answer OK. Five more seconds. It's good to get, go for it. And then cos I think we're running a bit behind. OK. Closing the pole, closing the pole, closing the pole closed fine. So a bit of a mix but largely number four with a few going for number one and number two. And I can understand that the diagnosis here is a stemi, particularly an i inferior stemi. If you look at the ST elevation from 23 and aVF and an inferior stemi means there's going most likely going to be a right coronary artery disease. OK. Those who went for one and two, I assume you're looking at the reciprocal ST depression in V one and V two. And again, that can happen. But remember when you get SST elevation in one region, often you will get a reciprocal ST depression in another. OK. So it's important to just take that into account that act the disease isn't in V one and V two. It's where the ST elevation is, which is 23 and A VF and therefore the answer is right to Coronary number four. And I'm hoping you guys have all seen something like this before. It's just one of those things you've got to remember unless you want to kind of visualize and work it out yourself, which again, you can do, but we're not going to, to go over that today. One A V LV, five V six lateral leads, lateral leads, typically going to be left circumflex or the diagonal branch of the left anterior descending. So these are all the br the coronaries which supply the lateral side of the heart. Inferior is RCA or, and, or left circumflex often because sometimes you can have a right dominant, which is where the right coronary artery supplies the inferior part of the heart or you can have in fewer rarer cases. The left cir complex left circumflex supplies the posterior heart instead. Ok. So yeah, can be annoying. But anyway, and then your anterior septal leads l ad left anterior descending, all right. And in terms of secondary prevention, these are the long term medicines after a myocardial infarction that someone is going to be on. The most important thing really is going to be modify risk factors. Ok. So if they're hypertensive treat, that type two diabetes treat that if they're smoking, get them to stop, improve diet exercise more. These are really, really important because they will prevent another heart attack happening or they will at least reduce the risk of one happening. Ok. The other things are generally everyone's going to be on dual antiplatelets at least for a year. More than one antiplatelet continued long term. It's again going to be aspirin and one of the three that we mentioned earlier, everyone will be given a statin unless contraindicated 80 mg compared to a normal dose of 20. So it's a high dose statin. We like to give an ace inhibitor as well that provides prognostic benefits to things like Ramipril. Atenolol is not really given. Generally, it's bisoprolol for the beta blocker. And then if they have heart failure and they're not really well controlled on the Ramipril and the Bisoprolol, then you can give it Plein or other other antagonists like spironolactone as well. OK? And we'll get to heart for you in a bit. But these are the long term secondary prevention medicines that we give to prevent another mr happening and they are really important. They really do make a difference. OK. Third SBA have a look. Oh questions. Um Hold on a minute. Let me just create the pole. So what do patients usually get in cardio rehab? There's a cardio often like a nurse or a PT or OT that come and they just help in terms of one what they can do in life um options they have. And also um yeah, I'm actually not really too sure to be honest what happens in cardio rehab, but one to a cup. So even if patient is very unstable and needs PCI immediately, we always do a coronary angiogram. CGRA before PCI. So if they're very unstable, then we do a normal angiogram not act just because when you've done the normal angiogram, you then do the PC afterwards. But it is important to do that initial angiogram because you won't know where the blockages are without visualizing the arteries. If they're more stable, that's when we get our CT angios or MRI S stress perfusion. MRI S done instead. Feng ho how V four V six, V six, I don't know what you mean about that story. Um Rare, sorry, what was right dominant again. So there's different types um of c cardiac coronary anatomy. A right, dominant coronary anatomy typically means the right coronary goes round, wraps around the heart and supplies the inferior side. Whilst a left dominant means the circumflex does that instead? Do you only give one dose of 300 mg? Yes. So it's one dose 300 mg, then a daily 75 mg different to stroke. And when do you start secondary prevention medications? Really once you've treated the initial problem, so you've had the reperfusion and then you give the secondary prevention medicines definitely before discharge. Um for a CS in the community, uh can you get 300 mg critical or patient has an aspirin allergy? Yeah, provided they also don't have a critical allergy and yeah, for HK. All right, get your last few answers in. I'm gonna close this pole. All right. Stop pulling. Cool. So again, a, a mix. People gone for two and gone for four. Fine with a few for 51 ft one. All right. So let's go through all these medicines are. Ok. Losartan. It's a angiotensin receptor blocker and A RB works similarly to an ace inhibitor and you don't give both. So this patient is on Ramipril already. So he wouldn't want to give Sara Perindopril. No one's gone for. But that is another ace inhibitor and they're already on Ramipril. So we didn't do that. Bendroflumethiazide is a thiazide diuretic. They're on indapamide. We wouldn't want to give that. And aide is a thiazide like diuretic. OK? And is the the third line medicine for hypertension Eplerenone is another good one and would be an option here. But there's one thing that makes it less likely. And that's the potassium, OK? The two drugs that we need to know that raise potassium are your ace inhibitors and your Mra S your mine mineralocorticoid receptor antagonists which are apar and spironolactone. OK? If it's potassium is above 4.5 we tend to lay off those drugs and not give them just because that can push someone into becoming hyperkalemic. And therefore by a process of elimination, the answer is Doxazosin, it's an alpha blocker. It's pretty good. But it does have some side effects as well. OK. And about 43% of you got it. So we're all done to those. So hypertension, I think, let's rush through this quickly just because there's a lot to get through. And I think it's one of the, the, the topics that people know better. Generally, we define that as said there above 100 and 40/19 clinic, reading A BPM is above 100 and 35/85. And there's two main types, the large majority of people are essential. This means that there's no really known cause it just kind of happens and often as we get older, then there are secondary causes as well that can be split into endocrine renal, other drugs such as steroids, nsaids and the C OCP. Other things like pregnancy and cooperation of the AORTA also can cause hypertension. You would generally only go and look for secondary causes if someone is hypertensive and they're less than 40 years old. All right, or they're really, really hypertensive and they're a little bit older than them and they're very resistant to medications, lifestyle management that we can give are there. So, you know, these are kind of your classic of what's good for the heart lifestyle medications, reducing salt, reducing caffeine, you know, reducing alcohol, don't smoke that Mediterranean kind of diet that everyone goes on about exercising more losing weight, et cetera. Stuff that I don't forget to say in your Aussies because these are marks and they're so easy to miss cos everyone always goes down the medical route. But again, when you're talking about medicat about treatment, always think, first of all, what are the lifestyle changes that can be made? What's the pharmacological changes that can be given or medications that can be given and then what interventions can then be given. So things like for example, a P CIA surgery, et cetera. Ok. And I'm sure most of you have seen this. It's definitely a figure that I looked at loads. It's one of our best friend past med and it kind of walks you through pretty well to be fair how to approach hypertension from a GP perspective. So you have a clinic reading of 100 and 40/90 white, her hypertension does exist, it can make someone's BP seem higher than it actually is. So we always want to do a home, BP monitoring, ambulatory BP monitoring where we send them home and they record their own readings, ok? Depending on what comes back from that. As said here is how it depends on whether we treat. So if they're less than 100 and 35 we don't treat, but we monitor very closely, especially if it's just under, if it's more than 100 and 35/85 with the following problems. So target organ damage, which can be literally things like uh retinopathy or you know, hypertensive retinopathy, er kidney disease, et cetera, then we treat established cardiovascular disease, renal disease, diabetes or a 10 year cardiovascular risk equivalent to 10% or greater. Probably the reason why I included this image is because I learnt this figure as like my gospel for hypertension. But I kind of come to realize there are a few things it misses and this is one of them. If someone is less than 60 they have a cure risk of less than 10%. Nice says to consider still giving treatment because that cure risk can under play their actual risk rating a CS or a cardiac event. Ok. So we would still consider treating somebody less than 60 if they have a key risk of less than 10% the other um the other changes will come to you in a minute. Do both systolic and diastolic need to be raised or no, it's just as long as you have one of them you can treat. And then if someone has a BP of more than 100 and 50/95 you treat immediately. Ok. Another question, why don't you treat stage one hypertension in patients over 80? The reason being as people get older, the whole point of treating hypertension is reducing the secondary, the risk of a secondary cardiac event occurring. Ok. Or a or a cardiac event occurring even as a primary event. So if someone is reaching 1890 they're a little bit older. The long term benefit we're going to give them by very tightly controlling their BP is actually less. And we know that people as they get older naturally get a higher BP anyway. So we're a bit more relaxed in terms of trying to maintain their BP into a narrow range or low range. And we only really treat them if they reached above 150 stage, et cetera. I hope that answers that. Now, this is probably the most important part that this, that pass med figure does not include. And it's this bit at the bottom where it says BP of 180/100 and 20. Ok. This could be a medical emergency and you need to refer for a specialist same day review. So send them to A&E ambulatory care, et cetera. If they have a retinal hemorrhage or papilledema, they have life threatening symptoms or have a suspected pheochromocytoma. Ok. So they've got malignant hypertension, very, very high hypertension and it's, and you're worried about them. This, there could be, you know, some problem going on here. We need to do a same day referral. Often these will be the hypertensive patients who suddenly become hypertensive and it's not a more gradual, chronic thing because if it's gradual and chronic, your body adapts and responds accordingly. If it's a sudden change, your body is like, whoa what's going on, it can't respond and that's when you get problems. Otherwise, if it's above 100 and 80 you still assess for target. Um, but there's no like w immediately life threatening or worrying symptoms and you go down the similar route as before. Um, but you would still treat anyway. Ok. And I've gone for the nice flow chart here just because I like this one. I think it kind of covers it really well. I'm sure you guys kind of know this fairly well. By now, first lines, if you're diabetic, if you're less than 55 and not Caribbean, Afro Caribbean, then it's an ace inhibitor. And ARB typically, if people are um not responsive or they, you know, they can't tolerate an ace inhibitor. And then we give the A RB, a question that often gets asked is what if the Afro Caribbean and, and diabetic, then you go for the A RB. OK. If they're older than 55 then we go for the CCB, then we kind of like to add the two together. So you can literally either do an ace inhibitor of plus A CCB or a Thiazide like diuretic or you kind of mix and match with those two. Thiazide like diuretic generally tends to be indapamide. OK? Step three is you add all three together. Step four is the question that I asked earlier, which was quite mean. I'm sorry, but I was trying to emphasize a point where if potassium is less than 4.5 we give Spiro or a Perenne. If it's more than 4.5 we give an alpha blocker or a beta blocker. Doxazosin generally tends to be given, but it has lots of side effects like postural hypotension. Ok. Another thing that you don't really appreciate but can be useful in OSS is you're perfectly within your rights to say, just up titrate a dose. So someone's on 1.25 ami they've got a long way to go. You know, maximum dose is 10. You can up, rate up. You should really up titrate that before you start another agent. So always keep that in mind as well. OK. That's hypertension. Done. Next question. Sorry, I have to make a new poll every time. Yeah. OK. All right. The last few responses in good, good closing the poll soon. OK. Closed. Fine. So nice. 90% of people are gone for ir good job. And so what we do have here, we have a man of heart failure. He's known heart failure, ejection fraction of 28%. So it's reduced ejection fraction. He's on a whole load of medicines and we want to change one and add Sacro Valsartan. Does anybody know what Sacco Beryl Valsartan is? It's a new medicine. It's came out whilst I think probably all of us a few, all final years have been at UNI It's an RNI Yep. Entresto. Entresto is the brand name re stands for angiotensin receptor, neprolyzin inhibitor. So it does include an A RB, that's the Valsartan part, but also includes uh Neprolyzin inhibitor, which is the sacrovir. And together they're meant to really, they're meant to provide a good, a good benefit. I think the last time I checked the study showed it was equivalent to an ace inhibitor, but there might have been more since I'm not gonna, I'm not gonna bet my career on that one. But anyway, what we, what do we know? We know if you're giving a, you cannot give an A RB and an Ace inhibitor together. Therefore, we must stop the Ramipril before starting the entresto. And that's the correct answer well done by us and this brings on to heart failure. Now, heart failure can be tricky. I think the reason it's tricky is because there's so many different ways of defining it. The best way of looking at it is heart failure is an inability of the heart to regenerate a cardiac output that meets the demand of the body. OK. And that can then be subclassify into certain different types. The most common one is preserved ejection fraction versus reduced ejection fraction. And if that wasn't un confusing enough, the European guidelines then came up with a midrange ejection fraction as well. The numbers are about more than 50% is preserved, less than 40% is reduced. 40 to 50 is midrange reduced ejection fraction. We can treat fairly well. We have loads of medicines, preserved ejection fraction. We have very few. I think we have one and that's just, that's the SGL T two inhibitors. Ok. Very hard to treat preserved ejection fraction. It's a real problem in cardiology. Midrange is a little bit of both. It kind of has signs of both, but it's still easier to treat them. Preserved. A lot of the reduced ejection fraction. Medicines still work. Another way of looking at it is left versus right versus biventricular. The reason why that's helpful is because often it tells you what symptoms you're likely to expect and just think of it in terms of backlog, right. So if you have a left ventricular heart failure, you're going to be pumping less blood to the body, you've got more backlog backwards into the atria, left atria and then into the pulmonary circulation. And that's when you get all your symptoms such as dyspnea, paroxysmal nocturnal dyspnea, your nocturnal cough, orthopnea, et cetera. All right, if you've got right heart failure and the backlog is the other way you get into the right atria into the vena cava. And then that's where you get your peripheral edema and fluid overload. Since that, all right, biventricular is the worst. You get symptoms and symptoms of both. Typically, it starts off as a left causes backlog into the pulmonary arteries and palmary circulation into the right and then the right can't pump enough and then you get right heart failure as well. And then you get there's biventricular heart failure, which is very hard to treat. Indeed, another way is systolic versus diastolic reduced ejection fraction that we call systolic. The reason being your ejection fraction is reduced, which means that your heart is contracting less well, is unable to pump enough blood. We kind of go down, for example, dilated cardiomyopathies where your ventricles, very big narrow walls, very weak myocardium can't pump very well reduced ejection fraction, systolic dysfunction. Ok. Preserved ejection fraction typically typically is more diastolic dysfunction. You very hypertrophic heart, very thick, myocardium doesn't relax very well. And that impaired relaxation means you're not pumping enough blood to meet the demands of the body crucially. However, you are pumping a normal ejection fraction. It's just not enough. Um And those are some of the commons called in the UK registry. What's the mechanism of SGL T two inhibitors and preserved ejection function, heart failure? I don't know. It's, yeah, it's more, it's literally in the new guidelines and the European guidelines this year only included it and the American ones from last year. Um in terms of how it helps. Um I don't know, sorry, but fine. Another important thing to note, I really kind of memorize is the N yh A heart failure classification. It's a, it's a pain to memorize. It's really long, but just I need to get familiar with it. One is the best, no symptoms, no limitation of physical activity four is the worst symptoms at rest. Two and three are somewhere in the middle. All right. Typically a question will give you one where the answers two or three. So they're not gonna be as nice as that. But it's definitely one to look at in terms of investigations, heart phone investigations. What do people have, what do you think we would want to do to investigate? An echo? Yeah. BNP. BNP Echo. Yeah, you're on the right page. So do an EKG the reason being often an arrhythmia can cause heart failure, especially if it's sudden if you've got sudden heart failure, that's worrying. Ok. And the causes of heart failure, we should really be splitting into ischemic versus non ischemic. All right, if you have an ischemic heart failure, that suggests there has been something like a myocardial infarction which has caused a sudden reduction, ejection fraction and weakness of the myocardium. And you're not pumping enough blood that can be treated non ischemic has many other causes. That's where you go down in the cardiomyopathy route, your hypertension arrhythmias, et cetera. So each is very important. For example, af is, provides 20% of cardiac output. Sorry, the atria provide 20% of cardiac output in af you lose that atrial contraction and therefore you're losing 20% of your s chronic outcome that can push somebody into heart failure if they have already some risk factors. All right. Likewise, bundle branch block is another cause of heart failure. And that is treatable with cardiac resynchronization therapy, which we're not gonna go into today. But it's interesting if you want to look into it, it's where the oso quickly in remember, branch block, your ventricles aren't pumping, synchronously, they're pumping at different times that can reduce ejection fraction. If you synchronize the ventricular um pumping and contraction with a cardiac resynchronization therapy device, you can improve ejection fraction and actually quite well treat somebody's heart failure. So that is a really interesting aspect to management as well in terms of exams, CG NT pro P MP before the echo. All right. So you do this B MP and if it comes in like raised but not super high echo, sorry, swap those two around. OK. Raise but not super high echo in six weeks. Very, very high echo in two weeks. OK. Um Sorry, written the wrong thing there. Other other investigations do a chest X ray and look for the cause as we said earlier about your ischemic versus non ischemic. All right, this is your chest X ray. And I kind of remember splitting it in terms of ABCD E. So look for your alveolar edema for A. So this is going to be, you know your per peripheral edema, just look at loads of pictures, get familiar with it on X rays. It's got quite a characteristic look B being the curdy bee lines. So if you look at the edges along the the chest wall, there are some thickened lines that come out to the chest wall. That's your curdy bee lines. It shows fluid uh C being an increased cardiothoracic ratio. M. Make sure you're looking at APA film on an AP film and on the PA film. If it's more than 50% then you have an increased ratio D is dilated up the lobe diversion. So that's your dilated vessels, this can be quite hard to spot. But if you can kind of look at this picture, there's some tubes, you can kind of see or th thickening alongside um kind of alongside the vessels and that's your dilated vessels that is literally backlog of blood going up into the lungs. Ok? And then e is effusions. So you can get a pleural effusion often as such as blunting in the costophrenic angles, but you can also get horizontal er fissure fluid as well, which is what we have in this picture here. Ok. But do get used to looking at chest x rays for heart failure because they can come up in exams and this is the heart failure management. I'm going to rush through this just because you know how much time. Um but juice and we have preserved er and they are, as I mentioned earlier, have different treatments. The mainstay of treatment are your ace inhibitors and beta blockers. If that's not doing enough, then you start a Spiro or Aleen often with the ace inhibitors and beta blockers, you don't start, tend to not start both at once. You start one titrate upwards and then start the other. Just because if you start both at once, you can drop somebody's BP. OK. Following the MRA the Peroneal Spiro, we then have a few other options. And this really depends on, I guess what the, the specific patient's phenotype and what's going on. So for example, of Aberdeen slows down the heart very similarly to, well, not similarly, but it slows down the heart like bisoprolol does, for example, OK, it reduces sinus rhythm. So if someone's in sinus rhythm and the blood, the heart rate is quite high, the N is definitely an option because it reduces that sinal node activity, that sinus node activity. If you can always, as we mentioned that question, uh start entresto or Scovil Valsartan. If they have a very low ejection fraction, hydrALAZINE is an A digoxin are also options. Digoxin can be useful with af as well because it helps slow that heart down in af the problem with digoxin is it's not very good with exercise. So if someone is doing lots of exercise, we don't like to give it and it's given much less now, especially in heart failure. OK? We don't really give it too much. Um This is just skip through that. OK. So it's hit eight. I know we said it would be one hour and I'm very sorry, I've got about another 20 slides left. We're going to talk through Bowels, going to talk through. Uh, I've got a few EC GS at the end as well and, um, af, so feel free to stay if you're going to leave, that's absolutely fine. But can you please please do this feedback form for me? Um, it's really helpful one because it helps guide us what we need to do next. And two helps us understand how we can improve our series as well, especially because we're at the start of the series, any suggestions you guys want to include, just put it in there and we can include it. OK. So that's the form and actually, I'll just get a link as well. Um That's a feedback link too. If you're staying until the end, that's absolutely fine. But whenever you're leaving, just do that, please. OK. Next question. OK. Get your on to them guys. All right. Last few minutes closing the pole, closing the pole pole is closed. OK. So majority of people have gone for three with a few others going for two for and a few more for one and five. Interesting. Yeah. So what's the diagnosis here? Someone tell me and on top of that, someone tell me why they've gone for three af fast ventricular rate. Yeah, exactly. That, yeah, we have someone who is in af and they're hemodynamically unstable. Perfect. Really good job guys. Yeah. So w what's the clues here? You have an irregular irregular heartbeat, you know, that screams af at you no real cardiac history previously. But they do have a lot of risk factors for, yeah, they've got anxiety, they've got big work deadline, upcoming, very stressed and they're fast running 100 and 47 BPM and that has caused them to drop their BP. Ok. Similarly to what we said earlier about how arrhythmias can reduce cardiac output when you're reducing cardiac output. That can then because the heart is beating so fast that can then drop someone's BP and that becomes an emergency that needs urgent treatment. Now, the urgent treatment in this case is going to be a DC cardio version. OK? And that's the right answer. So well done. Ignore the heparin I that is meant to be DD. Now, this is a busy slide and I'll just kind of break it down bit by bit. What is AFA F is chaotic, irregular atrial rhythm? So the atria are contracting at multiple different focus points all across the right and the left atria such that they're basically just quivering, they're just shaking. There's no regular contraction of the atria, which means you have impaired pushing of blood down into the ventricles. OK? Because you have this constant electrical excitation going from the atria to the A V node, the A V node then just gets confused and kind of just responds intermittently irregularly. And whenever it can and that's what causes the classical irregularly irregular pattern found in E CG life in the Fast Lane, described the causes of atrial fibrillation really well. And that's what I've included here. So it's a no lot of text, but I just wanted to highlight you guys this way of categorizing it. And that's one atrial distension, atrial distension works because you're stretching the atria and as you stretch the atria, they all, they have their own automaticity. So they have their own electrical excitation. And as you damage that they can then start exciting themselves and start creating an atrial fibrillation, arrhythmia. Ok? You can also get conduction abnormalities. And for example, ischemic heart disease, if you have damage to some parts of the myocytes, these can also become a focus point for electrical excitation, increased atrial automaticity, meaning the atria, uh the electrical signals a amounting or emanating from the atria increase in frequency. And these can follow things like caffeine binge, drinking or electrolyte abnormalities as well. And there's many other causes, too important thing to know. Often we don't find a cause. Loan af is really what we've described. We don't find a cause. OK. The other way, the other important thing is classification of AF and we kind of classify it as I've written here. So first episode it's happened once, hasn't happened again and you kind of just look and you think is there a clear cause, have they just had a cardiac surgery? If so we don't really need to treat it. It shouldn't really happen again. All right. Or if they have recurrent episodes, then this is where it starts getting a little bit more important to classify. It's had two more episodes, but it's sponte, but it's terminated spontaneously in less than seven days. Typically less than 24 hours. We call that paroxysmal. If it's not self terminating, then we call that persistent af and the episode usually lasts for more than seven days. But you can still normally cardiovert these ones. Hopefully with, you know, pharmacological cardioversion, like flecainide or DC cardioversion as well. Ok. Permanent AF is someone who is in constant af they cannot be cardioverted or we just think, you know what, we're not going to get involved, we're going to leave them in af that's probably what's safest for them. And I think there's been a huge amount of research again while we've been at med school or while, you know, I was at med school and while you guys are now, which has really kind of said, actually rate control is often better than rhythm control because rate control, we know someone has af we're treating it accordingly and actually, if we treat it very well, it shouldn't really reduce someone's life expectancy. Rhythm control can be difficult because you're trying and trying and they kind of go back into af and then it gets a little bit more challenging to kind of manage them. This is your classical E CG. The thing to note, probably I've just seen this a lot. And again, I don't know if this is science or not, but what I've noticed is often you'll look at V one you think, oh, that looks quite atrial fluttery because you can see these flutter waves. But a lot of af tends to have those flutter waves in that V one lead and if you don't really see them anywhere else, then you can think. Ok, actually, it's more likely going to be af atrial flutter often is a bit typically regular but doesn't have to be. And it tends to be kind of comes as multiples, not multiples, I forgot the mathematical word, but they can, uh there's a heart rate that can divide into 300. So 1 5175 et cetera. Ok. Cool. So atrial fibri atrial fibrillation symptoms are these often they're asymptomatic and you know, there are loads of patients running, you know, going out there who are in AF don't realize. And that's why it's so so important, especially for GPS to always check a patient's pulse because you can often pick up incidental asymptomatic af remember as you said earlier, it really becomes asymptomatic when that lack of 20% causes the cardiac output ejection fraction to drop and push them into heart failure. But if they're able to compensate for that lost cardiac output and they're not running too fast, then actually they won't have any symptoms. Ok. The symptoms that you often experience with your palpitations, that's the main one. But you can also get dyspnea, chest pain and rarely you can also get syncope or dizziness. But dizziness is a bit more common than syncope because I guess think about it, syncope is where cardiac output is not enough to supply the brain and it's cardiac syncope can be described as that. Ok? And to get to that stage is quite tackled in terms of management. The first thing you need to ask yourself as we did in that previous question is, is this patient hemodynamically stable if no s that meet DC cardio event? OK. And often it becomes a risk benefit ratio. I know II wrote Heparin eyes earlier. But in reality, if someone is anticoagulated, then you kind of take into the risk that you may cause a stroke by cardioverting. But because they're hemodynamically unstable, it's worth doing that anyway, if they are hemodynamically stable, then look, is there a reversible cause? Ok. Do they have an infection? Are they dehydrated or do they have some thyroid abnormalities? So always check for thyroid function tests. Uh Do they have electrolyte derangements if so treat them and see if that fixes the af if it fixes the AF and it's the first detected episode and you done the chads vas score and you think, well, actually this person doesn't need any further anticoagulation, et cetera. Then you know what you are, then you're right to say, OK, but if it persists, they need to start thinking. Do this, does this patient need the right to rhythm control? Do they need anticoagulation? And will an ablation be beneficial for undergraduate exams? Ablation is I think a bit above don't need to get into involved in that. But anticoagulation is something that we should probably try and work on to kind of work out who needs anticoagulation. No, for an undergraduate level, I don't think you would really ever get given a patient. I don't know, you might have a mean med school, but I don't think you get given a patient and they say are you gonna rate to rhythm control? But it's important to kind of know the information that's required to feed into that decision. At least. So nice advocate a rate control strategy generally unless they have coexisting heart failure first onset af or when there is an obvious reversible cause. OK, I guess that's important to know. So heart failure, first onset af or obvious reversible cause if they have those three, then you can try go down the rhythm route and try and cardiovert them back into simus rhythm, sinus rhythm, meaning ap wave precedes every QR s complex rate control. The medicines we typically give are beta blockers or calcium channel blockers such as dilTIAZem over amen. You can consider digoxin if that's not working or helping sometimes or gets given again. It's not very good. We don't like to give it so much and it doesn't really help. The patient does exercise in terms of rhythm control. There's a few options. You have cardio uh electrical cardioversion and chemical cardioversion. The two main types of chemical cardioversion are amiodarone and flecainide. Sotalol are sometimes also given contraindications to flecainide are structural heart disease or ischemic heart disease. So if they're very young, you go on the flecainide route. If they're a bit older, then we go on the amiodarone route or if they have, you know, for example, structural or ischemic heart disease. That moment when you cardiovert someone, it is the highest risk for causing a stroke because in your left atrial, you have the left atrial appendage, which is kind of like a sock that just sits there. And if it's not contracting very well, it's very easy for blood to get pooled in there. All right, what can then happen is once you've got blood stasis, you kind of a triad and you get the increased risk of clots and that clot can just sit there. It's on the left side of the heart. Remember? So when you cardiovert someone and you push them back into sinus rhythm, your atria suddenly contract again. And any clots that are sitting on that left atrial appendage can get pushed into the right into the left ventricle and pumped across the body. Worst case scenario that gets pumped to the brain and you get a stroke. So we only cardiovert if they are unstable, short duration of symptoms, less than 48 hours. So, there's a clear history. Either you've seen it or the patient is very clear in their history or if it's only started a few hours ago. Doctor, I've never had any palpitations before or you anticoagulate them for at least three weeks before cardioverting or you do a transesophageal echo to exclude your left atrial thrombus. Again, that doesn't happen too often. Would you still do cardioversion for a hemodynamically unstable patient of permanent? If Yeah. So if it's a hard one, I think if you've tried your medical management. So you've got somebody in af they're hemato unstable and you've, you can initially give things like metoprolol or high dose loading dose digoxin if they are not on it. Metoprolol is a fast acting but uh beta blocker, but it has a short half life. So it kind of goes quickly. And if they're not really helping you try your medical management, then yeah, I mean cardioversion is the next way forward when you chemically cardiovert and hemodynamically unstable but symptoms over 48 hours, we tend to do electrical cardioversion for hemo dynamically unstable to answer Stephanie's question. Ok. No anticoagulation. Anyone who presents with af even if it's paroxysmal, you need to do chads vas orbit school. Alright. You'll often see has blood floating around when I was doing my cardiology, rotation orbit didn't exist, but in the last couple of years, it's kind of become more, more, it's been adopted already by nice. And now we have to use that over. Has blood child f score is your risk of plotting and the risk of a stroke orbits scores your risk of bleeding. You do both and you kind of make a risk assessment or a cost benefit assessment of which way to go for anticoagulation. First line is Doac second line is warfarin. Often you give Warfarin when somebody has things like a uh um mitral valve replacement, et cetera. Ok. Well, I think it's mitral, it's one of the valves replacements, then you get warfarin um or any other contraindications, one might have to a dog. But I think the key thing here is even if you have paroxysmal E and you've put someone back into sinus rhythm. If that child's F score and orbit school, say so, then you should still anticoagulate the reason being you don't know when this person is gonna go back into af and when they go back into af that risk of stroke happens again, just a little bit on uh atrial fibrillation as well. Uh Compared to atrial flutter and multifocal atrial tachycardia, we would anticoagulate all three of these. That's important because the risk of you have impaired atrial contraction. And when you have impaired atrial contraction, the risk of a clot always exists. And um where in atrial flutter, you kind of got that very sore tooth, you know, characteristic sore tooth appearance. You all know how that looks multifocal atrial tachycardia is where you have very different looking P waves. And if you look at this picture, the P waves all look slightly different, you no one's negative, one's very high, one's low. And what that means is that the focus point of the start of atrial contraction is not actually in the sinus node. It's coming from various points along the atria. And that's causing this multifocal what we call multi focus points, initiation atrial tachycardia that also needs to get anticoagulated. What are other contraindications to a doac? So, Doac are fairly new medications. I think the evidence base isn't there for a few things. So for example, if you have a large body habitus, I think, I think maybe above 100 kg, we don't like to give Donax because evidence space isn't there. We don't know how much to give. Uh you need to sometimes consider renal function as well. And also if you have valve replacements, there's certain valves which are replaced in which you can't give Dox and you'd rather give warfarin instead. Ok? And the I nr range for some of these is generally higher because with valve replacements, you have an increased risk of clotting. I hope that answers your question regarding contraindications to do. Ok. Next question. Sorry guys, we're running very late. Um And I mean, I'm doing this and then I will upload it anyway, but feel free to stay. I really appreciate it. And if you want to leave, just please leave the feedback form. Ok. Get your answers in nasty, want close the pole going to close it, going to close it, it is closed. Ok. So for uh most people, 61% have gone for number four, a few gone for number two. Yours? 135. Ok. So maus valve disease, in terms of what's this question saying? So this question is saying someone who's come with symptoms of heart failure, they've got worsening dyspnea. Ok. And we have multiple courses of heart failure, as you mentioned earlier. One of those is valve disease. The GP has a mid to late diastolic murmur and therefore, which of the following is the most likely cause a me to late diastolic murmur. So, out of these, the diastolic murmurs are going to be aortic regurge and mi stenosis. So we know it's going to be one of two or four aortic regurg is an early decrescendo murmur. So what does that mean? It's loudest at the start of the study and gets quieter. The reason being at the start of dias when is what is aortic regurge? Aortic regurge is the flow of blood from the aorta back into the left ventricle. Ok. At the start of the, the systolic pressure is highest. Its greatest. The reason being you've just pumped a whole load of blood into the arteries, very high pressure, equally ventricular um pressure is at its lowest because you haven't got much blood flowing into it. It's a kind of an open cavity that increased pressure gradient means you have a lot of black backflow of blood um going through the aorta through the aortic valve back into the ventricle. Ok. That's why you therefore get a decrescendo murmur ie it's loudest at the start and gets quieter along to think of mis stenosis. The atria contract. Wh wh where is mitrano mitral stenosis is a small opening of the mi or, or is a reduction in the size of the opening of the mitral valve which connects the left atria to left ventricle. Now, there will typically be blood flowing through it and in more mild to moderate mis stenosis. What happens is when normal flow of blood that doesn't make any noise. But once you get atrial contraction, you suddenly push a whole load of more blood through that narrow gap. And that creates a murmur and that can create a mid to late diastolic murmur. Ok. So as mitral stenosis gets more and more severe, that murmur becomes earlier and earlier. But if you hear a mid to late diastolic murmur, think mitral stenosis and that's the answer. All right. Next question, what, what is the cause? Mhm Let me see. I right. This is like a, a classic pass me question. They love this. Ok. Last few votes and I'm going to stop pulling. All right. So they have a mix between one and two and then a couple of people go four. So this is one of those things that you've either seen it or you haven't. The most common cause of my stenosis is rheumatic fever. Rheumatic fever is much more common amongst, um, people from developing countries. But even in the UK, the most common cause is the rheumatic fever. Ok. Many other valves classification would be the right answer. But for mitral stenosis, it's rheumatically, it's just one of those things that can come an SBA and it's good to know. This is a nice image. I got it from some website, I think maybe GKI medics. Um and it kind of explains a little bit whilst talking about the decrescendo aortic regurge murmur. As you can see, it's kind of the wavelength is greatest at the start and then gets quieter and quieter throughout the study. Whilst mitral stenosis, you can kind of see the rumble only really starts midway through, gets worse later on with an ejection systolic murmur. Um What is a really good way of, of kind of doing it is if you have a stethoscope, put it on, hold your um the diaphragm of your stethoscope and then kind of trace a circle as you trace a circle. What you'll hear kind of sounds like an ejection systolic murmur. And then when you go like that on the diaphragm, what you'll hear more is a pansystolic moment. OK. And it actually does kind of sound like that in real life as well. Some doctor taught me that when I was at med school but it, it is useful. OK. Think about sic murmur. It's crescendo, decrescendo, quieter to louder and then quieter again. Whilst the pan systolic is more just the same. It's just a consistent flow and a consistent sound effectively. All right. Cool. Now, aortic stenosis is the most common disease. Many causes degenerative calcification. It's a big one, especially amongst the, the elderly, if you're a bit younger and you've got aortic stenosis and think, ok, there's something going on here. So for example, bicuspid aortic valve disease. Yeah, I mean, Williams syndrome is always one of those ones that is great to say not oy, but like in real life, how often you're going to see it? It's where you get a supravalvular stenosis still causes that ejection. Sic murmur. Um, posttraumatic heart disease hum as well. Hoca causes left outflow tract obstruction. So you get that obstruction just below the aortic valve and that's from the, the the main signs is hypertrophic obstructive, obstructive means you get that left outro tract obstruction, cardiomyopathy. And the symptoms are, as we said earlier, often about the heart failure. So you're going to get your, you know, dyspnea, P ND or th apnea, et cetera, especially if it's quite bad. If it's very bad, you can even get mitral regurg and often as part of the work up to aortic stenosis replacement, we need to assess the mitral valve as well because sometimes what you need to do is actually say, well, they're both now not working well just because we've missed the boat. And actually it makes sense to do to treat both at the same time, the mitral valve and the aortic valve, other signs and symptoms you can get are syncope, sync, you know, aortic stenosis is always a important thing to consider and syncope, a narrow pulse pressure, a slow rising pulse, soft or absent. S two. The reason being S two is caused by closure of the aortic valve leaflets. If they're very calcified, if they're not opening very much as it is, then as they close, it's gonna create less noise and a thrill is literally a palpable murmur, fine investigations E CG but E CG to look for an arrhythmia that can sometimes be caused by aortic stenosis. The reason being the heart has to kind of pump way harder to get that blood out into the systemic circulation as it does that it can become hypertrophied, you can get some ECG changes. The other thing is uh echo because echo will let you characterize very well. How severe that's aortic stenosis is OK. And I've kind of made this aortic stenosis management flow chart. How useful this is for exams, I'm not sure, but it's good to kind of have an appreciation of it. The first thing is always, you know, again, think is this person medically fit for surgery. If no, then you're going with the medical management, you're gonna kind of treat the heart failure symptoms. If yes, they are medically fit for surgery, then think, ok. Are they symptomatic? And if they're symptomatic and you go down uh surgical aortic valve replacement or tabbing the difference being surgical aortic valve replacement is cardiothoracic. They get involved and they open the heart and they change the valve at is transcatheter. So it's kind of like a, you know, you go through the arteries and you put a catheter in up into the aortic valve and you replace the valve. That way, typically, tabbies are for patients who can't, who don't, aren't medically fit enough for a surgical aortic valve replacement. Ok. And then there's this whole criteria found on echo. So for example, a narrow aortic valve area, if you have a very peak velocity, low ejection fraction, et cetera, or you can do exercise testing. And if exercise, testing causes symptoms such as angina dyspnea, et cetera, then that can also be an indication for valve replacement. Mitral regurge is the second most commonest and we'll talk about that it can be acute or chronic and acute is an emergency. It can also be ischemic versus non ischemic. These are some of the causes, I'm going to kind of brush through it very quickly. The main thing to know, is the mitral regurg there and the tricuspid regurge, you get the pan systolic murmur. Um, again, you can get LV hypertrophy as well. Um, because the, the heart is trying to pump harder to get that blood out into the systemic circulation rather than the atria. And as a result you can get everything is too, there's this whole a degree go up pony of signs. I'm not gonna go into them, but they are important to know they come up my oy um and they can come up in others, I'm sure. Yeah, I'm not gonna go through them. This is more just rote learning. Um The thing to note of aortic regurge. Typically, typically you hear it loudest, not over the aortic region but over the tricuspid region. Why I guess it's because as you think about it, the what's causing that murmur is, is the turbulent flow of blood through the atria, sorry, through the aorta into the ventricles. And therefore that tub of flow into the ventricles is where that murmur emanates from. And typically you can hear that loudest over the tricuspid valve, uh check hospital region. All right. Aortic Grego is more common than tricuspid stenosis. So if you hear a diastolic murmur of the tri thus of the tricuspid region do have a aortic regurge as a differential. Just really sorry. What did you say you could do on the stethoscope to make a pansystolic murmur, have, hold the diaphragm out in front of you and just kind of place two fingers and go like that and you get like a rush of blood basically that you can hear. It's quite cool, very quickly. Heart adapts to valve problems. It can either hypertrophy or it can dilate. This is just a quick bit in terms of what causes hypertrophy, what causes dilation. Ok. But for interests of time, we will ignore that. Ok. All right. 58 people still on. So we're doing well. We've lost about half, but we're doing all right. Thank you guys for staying. Really appreciate it. So, introduce podcasts. Let's go through EC GS, let's go through them. Have a look. I'm just making the poll. OK? OK. Most responses, stopping pulling now. Nice. So 75% of you have gone for number five, second degree heart block. Well done. That's the right answer. Yeah. And I want to talk, use this talk a little about heart block but not too much heart block is what it is where you have a V node. There's something in the A V node that's preventing or reducing the electrical excitation from the atrium ventricles. OK? Pr that pr interval is effectively giving you telling you the function of that A V node. OK. So when you have an increased pr interval, there are some something going on the A B note that's meaning that signals are, are taking a little bit longer to posture it normal pr interval is 120 to 200 milliseconds, anything more than 200 milliseconds, fast degree heart block. Then we have secondary heart block. Secondary heart block has two types. Maybe it's one, maybe it's two. Maybe its one is where the pr interval gradually. As you can see in this E CG gets longer and longer and longer. Before suddenly dropping, you have a drop beat P wave no QR S and you can see that kind of in this E CG here. Remember it's type two is where there's really, it's just normal pr interval. QR S normal Pr interval, QR SB um sudden or like no, no, but like a consistent pr interval, consistent pr interval, consistent pr interval and then I dropped beat. OK. And that is much more serious and much more severe just because there's less er predictability about why that beat is dropping. And we would want to, we would be more likely to treat Amobi type two than Amobi type one. The other thing is an complete heart block which is where there is complete A V dissociation. P waves are firing. QR S are firing, they're not talking to each other. The A V no is not working and they're both just kind of going off and doing their own thing. All right, the thing to note is on an E CG, take your E CG, take a blanket piece of paper and just mark out the, the ventricular beats, mark out the P wave beats. And if you have a consistent space between the P wave beats and a consistent space between the ventricular beats, but they're not really in line with each other. There are different gaps. Then you can think. OK, there's, there's a V node dysfunction. It's a third degree heart. I hope that makes sense. Right. Next one. Just for the interests of time. Do you guys want? Just shout out the answers in the chat. Mhm Just put in the chart. Let me know. OK anymore. Seven sprain fried can't look at an ECG anymore. I know. Can imagine how you guys are feeling. OK. Cool. So one left bundle and majority going for right bundle. Uh Yeah, this is right P OK. No, why is it right bundle in right bundle branch block. The characteristic thing is in B1. Everyone knows William marrow. I find William Marrow impossible to interpret like I know WV one for her bundle, et cetera. But how often do you see a W you barely see it and you spend half the time like, oh I don't know. So how I've done it is always look at B1. OK. First of all approaching, how do you approach the QR S? If the QR S is great in 100 and 20 milliseconds, then there are some disease there. OK? You either have ventricular tachycardia where the heart rate is beating very fast. It's going on its own. It's creating its own um waves and, and beats. I had s 120 mis because what that means is if it's less than 100 and 20 milliseconds, the wave is going through the A B node down the purkinje fibers and down the bundle of hitting the purkinje fibers which really transmit electrical excitation very quickly all across the heart, all across the ventricles. If you have that signal coming from anywhere else, then you will have a longer time to excite both ventricles simply because they don't go down those bundle of hiss and bikin fibers which are very fast that portrays an ECG as acr us more than 100 and 20 milliseconds. So if you fast think ventricle tachycardia if you're normal or your fast, but have morphology typical of a bundle branch block than think a bundle branch block. All right. So in the back of your mind, always, always think when you have a increased QR S, it's a bundle branch block with fee with right branch block in V one and sometimes in V two and V three, you have a very characteristic RSR pattern. OK. So what does that mean in your QR Sq? Is that downward deflection initially, not every lead will have it R is the first awkward defection. S is that another downward reflection? And then you go to normal. OK. When you say RSR, you are literally saying one upward, one downward another up and that's your M for marrow, OK. And if you start really nicely in V one V two V three, you have that RSR pattern, which is the M with right bundle. The other way of looking at it is you look at V six, you often have a slurred up stroke in the S wave. So as the S wave comes back up to the isoelectric baseline, it can kind of take a little bit longer and it's quite slurred. And that is also generally what I've found to be quite characteristic of right bundle branch block two. OK. In left bundle branch block, it's a little bit different. You'll see there's no RSR pattern and actually you have a very, very deep S wave in B1 B2. OK. And this is quite characteristic of left bundle branch block. So you have a raised QR s think is this right or is this left? There's RSR and V one, it's right. If there is a deep thick S wave in V one, it's left. And that is a fairly good way of trying to distinguish and differentiate between right and left bundle branch block. Ok. Next one again, you guys just put in the chat, sorry, might be a bit small. All these EC GS are from life in the fast lane. By the way, life in the fast lane is amazing. I'm sure you know, it's great another OK. Sty sty sty sty anymore. OK. Fine. And keep like this interesting. OK. So two main things here that you're gonna really gonna consider semi acute pericarditis. Ok. What's going to differentiate them, differentiate really between the 21? Really? Whenever you see ST elevation, think those two things most likely going to be stemmy. That's your real worry. Ok. But if there is global ST elevation across all leaves, not really inconsistent with one co coronary territory and think, oh, that's not normal. That's not your typical ST elevation that you expect if it's very sadly, so kind of as you've seen B1 in V five V six lead one, you know, like a saddle shape that's quite consistent with acute pericarditis ST elevation. Ok. So ST elevation in acute pericarditis is typically global. It's subtle shaped and you'll get some pr depression between the P wave and the QR s. So you can see it a little bit and need one. For example, that pr interval was just slightly lower than the baseline and a few of the other leads as well. Ok. So those are, those are your pericarditis stuff? Cool. Ok. So we got there. Thank you guys very much for staying. I hope that was useful. Do let me know, uh keen answer the feedback. Let me know if you would want more lectures on cardiology. What I was thinking is doing one specifically on EC GS. Um I think EC GS are really difficult and that would be quite useful for people. I mean, I like cardio So I was even thinking of doing like an echo course for final years. I don't know if you find that interesting. Um What else? I guess it's a lot about things we didn't cover. So, you know, all other things like tampon um et cetera we can do on the lecture for that. Um But yeah, please do the feedback form. Really appreciate you all coming. Do you have any questions? Pop in the chat now? Happy to stay another five minutes and talk through things. I'm sorry, I was a bit rushed towards the end and you're welcome everybody. Thank you for coming. Uh Gastro session is this Thursday? So that should be the second. Ok. All right. All welcome. Thank you guys.