Computer generated transcript

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

Hi guys, we just give it a couple of minutes for any last minute people to join and then we'll make a start. Ok. We'll make a start and hopefully a couple more people will, will, will come in in the next few minutes. Um So evening everyone, thanks for joining us again. Um So as I'm sure some of, you know, this our road final series, um, we're a good four or five sessions in now and, um, today I've got Ross and Jed who are gonna go through cardiology um, as you guys may or may not know, this is um, a long running series that we are med teaching, um, are running um, every Thursday around an hour and an hour and a half. Um, some SBA style questions with explanations which of looking at covering the new UK, Mra um syllabus. So our next session would be the same time, seven pm next Thursday. Um And we'd be doing uh M SK and orthopedics, um, just a couple of things. If you have any questions, please feel free to pop them in the chat. Um I, I'll keep an eye on, um, of course feedback and everything will be at the end. So we'll have certificates for you guys. Um And all we ask is that you, the Ross and Jedda favor, who've very kindly given up their time to teach you guys today. Um Just give them some feedback, it helps them out a lot. Um And I'm sure you and, and you guys will be in the same position in a, in a years' time. Hopefully. So, um I'll hand over to us and Jed. Thanks guys. Thanks for the intro. So, hi. Uh My name's Ross. And yeah, this is my colleague, Ed. So we um we both started our first rotation in cardiology together in Brighton. So we thought we'd er we'd be good to maybe help lead a session on this. Uh So the format of the session. So it's all M CQ based. Um We're not gonna delve, we, we'll go into detail as to why we've chosen for each option. Um But we won't cover the entire topic realistically, this is just exam content focus, what's gonna be high yield some of the questions. They might be a little bit harsh, but it's just to get you to think a wee bit and stop you falling into the common pitfalls. Um And yeah, so here's some of the topics we're gonna cover today. Uh Let you have a quick reread. Um But otherwise I don't wanna spoil some of the answers, so we'll get stuck into it. So this is the first question. So a 73 year old woman arrives in A&E having experienced three hours of sudden onset, severe crushing, central chest pain, radiating to her left shoulder and jaw. She has a history of type two diabetes, hypertension and moderate aortic stenosis. She takes Metformin and amLODIPine with no known drug allergies. Her observations in ECG are as followed. She's saturating 96% on room air. Her BP is 100 and 42/76 and her heart rate is 65 BPM. What is your initial management prior to senior review? Um I'll rely on y to put the pole up so just give it a sec. So I'll give you guys a minute to answer. OK? So we've got two responses. OK? We're getting a bit more now, I'll just give you guys another few seconds and then we'll go into it so I can see the, so I can see some of the responses so I can see a couple of you have gone for a there, there's a good, there's a good spread. Some of you have gone for CD and then it looks like three or four of you for have gone for e So the answer, the answer is actually c um So we'll go into a bit of why. Um There are a couple of trip ups there. So I hope you're able to gauge this lady is suffering from an end stemmy Um So, so fr from the question, you can see she's having a typical presentation, uh and she's got some risk factors. She's got the sudden onset, severe central chest pain, it's radiating to her left side. She's got the risk factors of age, increased age, diabetes, hypertension, and valve disease. Um And then hopefully the key and eye keen eye you would have seen on the ECG, she's got some ischemic changes. So she's got some ST depression in leeds. 1 to 3. It's in a VF there's a bit in V four, V three, V five and V six, but this is most likely an inferior lateral ends sty. So let's go into each option as to why it wasn't that. So for those of you who put a um so a is the only option with oxygen. So this this lady's saturating 96% on room air. So she doesn't have an oxygen requirement studies show if you, if you unnecessarily ventilate people, there's actually a worse outcome um in an A CS point of view. Um So then why wasn't it b um So can anyone write in the chart? Why did we cos the only difference there is the GTN. Why have we not given this lady a GTN? Is anyone able to say in the chat? Any takers GTN is for Angina? Yeah. Uh But why haven't we given GTN to this lady? There's one reason OK, I'm gonna, I'm gonna put you out your misery. Um So this lady's got, this lady's got um aortic stenosis. So, nitrates are contraindicated in aortic stenosis. Um So for her, um yeah, so she's got moderate aortic stenosis. These patients are dependent on their preload. So, preload is the volume of blood that fills up during diastole nitrates cause vasodilation and hence hypertension and therefore reduce the preload. But because these patients have got a stenotic uh valve, the er the aortic stenosis, they can increase their stroke volume in order to cope with the drop in BP. So hence it tanks, it tanks the their BP. So yeah, avoid GTN S in those with aortic stenosis in terms of antiplatelets. So why haven't we gone for D or E? Um So as an F one and this is the initial management prior to senior review as an F one, I wouldn't make any decisions regarding a secondary out platelet. In any acute coronary syndrome. You would need a really good reason to not start aspirin such as they have a very, very high bleeding risk. But this day, this lady doesn't look like she has one. So yeah, in terms of the, the second antiplatelet, we don't yet know what the definitive management plan is. She hasn't been seen by a senior. So we don't know if she's gonna be medically managed. We don't know if she's going for PCI I, we don't know if she's gonna have fibrinolysis adding a second antiplatelet will increase her bleeding risk and potentially influence the definitive management plan. So as a as a port of call, I would hold off starting a second antiplatelet, I hope that makes sense. So let's go a bit more detail to ATS ATS. So uh acute coronary syndrome refers to a spectrum of conditions. So really useful to think of it as a spectrum where the coronary arteries are becoming narrowed. So this image on the left, I think helps to, to display this the the differing pathophysiology between stable angina um unstable and the mis. So with a stable angina, you've got a stable atherosclerotic plaque that builds up on the the inside of the, of the arteries gradually over time. Um and then in unstable angina, there's some disruption or break in that plaque causing platelet aggregation. But um the pa the artery is still patent. There's no cell death, there's no infarction, there's still ischemia, ischemia being reduced oxygenation to the myocardium. So that's causing pain, but there's no infarction. Then we get to an end sty where there's a significant plaque rupture or a thrombus. Um and that's now causing non sustainable occlusion. So there's still some flow in an end Demi but um there's not enough collateral supply to supply the myocardium uh and the the patients resulting in myocardial infarctions. So they, there is cell death, that's why they're gonna get a troponin rise. And then finally, with stemi stemi, there's a total blockage of that vessel which is gonna result in critical ischemia and it's gonna warrant urgent investigation. Um So the three diagnostic tools that you're gonna use to, to narrow down on a CS. So history, I know that sounds obvious we've sent patients for an angiogram before to PCI just based off of the history alone, even when their troponin and E CG was negative. So history is really important. Troponin troponin is one of those tests. We're encouraged to think of not as diagnostic. Nowadays, it's really, really, really sensitive. So as in it'll pick up most um nearly everyone in A CS, but it has a poor specificity. So it'll have a lot of um negative positives. If I said that the right way round, it'll pick up a lot of individuals not having uh a sty or an end sty. So it can be raising chronic kidney disease, it could be raising sepsis and pneumonias, it could be raising myocarditis even a pe. Um And then finally, an ECG ECG s again, be careful because you won't always get ischemic changes initially, especially if they present really early. And then finally, the image on the right is from the European Society of Cardiology. Again, this is just helping to differentiate between the difference um on the A CS spectrum. The different investigation results most important here. Most important takeaway here being um the difference between an ente and unstable Angina. If you have a drop raise. That could be an Nstemi or a STEMI. If you don't have a trop raise, it's not that. So in an unstable Angina, you're not gonna have a trop rise, right? So next, this is a sort of summarized version of the nice A CS guidelines. Um So initially, so the top part, this is the initial management for all A CS and I want you to keep it really simple and especially as an I as, as an F one. This is all you're gonna have to do. Just think mona, not moat, not mon A, just think mona. So it's not any in any particular order, but it's just to encourage you to think about this sort of stuff. So morphine um obviously, to manage their pain, you can think about oxyCODONE as well. And metoclopramide again, they're gonna be feeling sick potentially because of the A CS. Be careful with metoclopramide if they're at risk of arrhythmia. Um So you might want to consider uh cyclizine instead, oxygen only if they have an oxygen requirement. So don't let that trip you up nitrites, as we said, avoiding those with a s nitrates can be really good though, if the sublingual GTN is not working, what you can do as well is you can set up an infusion of GTN and that's actually really effective. And then a aspirin load them on a loading dose of 300 mg. You would need a good reason as to why not to start it. Once you've done that, then you can think about your more definitive management plan, depending where on that spectrum, you think the patient is. So for an unstable Angina on the left here, so we would still risk stratify them and consider the benefit of sending them for coronary intervention and PCI. So patients with unstable Angina, if they've got a lot of risk factors, if you think they have a high clock button, you can still send them for PCI. Um But generally, if they're low risk, we'll opt for conservative medical management. Um So this will involve starting antianginals. There's a stepwise sort of approach. I've cld in the, the top box up there. Um You would start with like for anti angina, you would start with a calcium channel blocker or a beta blocker. Uh The next step is you'd up titrate that dose. The third step, if they're still symptomatic, you would add in the other drug. You didn't start just be careful when you do. It needs to be a non rate limiting calcium channel blocker. You can't have a rate limiting and a beta blocker because then you get heart block. So a non rate limiting would be something like amLODIPine or Nifedipine. Um And then finally, if you're getting to the stage where you're having to think about adding a third drug, add the third drug. So that could be isosorbide mono nitrate, a longer acting nitrate or something like ivabradine. But consider rereview whether they would benefit from uh PC. And then also uh these patients, we'd start them on secondary prevention. So I always use the Pneumonic the, the four A's to remember that. So that's a for Atenolol. Uh We don't really use Atenolol. It's more beta blockers just to get you to think of a beta blocker ace inhibitor. So Ramipril atorvastatin, we, we would do 80 mg for a secondary preventative dose. And then aspirin, once they've had their loading dose, aspirin, then goes down to 75 mg. So then we come on to end stem eight. So again, we do a grace score gray score is one of these things that we never do in um uh in reality, it just looks good on paper and for exams. So always think about it in exams, but I don't think I ever saw anyone do it in like four months. Anyway. We do a gray score if it's a high risk. So over 3% and they're clinically unstable. So they're hypertensive, they've got signs of heart failure, et cetera. We think about immediate PCI and we give them unfractionated heparin there and then if they're just high risk. So again, over 3% but they're stable PC within 72 hours and we give them Fonda paranox, don't give Fo Fonda paranox if they're going uh for PC within the next couple of hours. And then finally, if they're low risk. We do conservative medical management um for those patients the same again, in unstable Angina, I forgot to mention, make sure with these patients whenever you do conservative management always safety net them. Um So say if, if they're having symptoms, ask them to sit down, try the um try not exerting themselves. If the pain's still there, then using the GTN and then moving on uh to call A&E if the, the symptoms are still present, then finally, with STEMI, we're nearly there, stemi is just symptom onset and PCI availability dependent. So you'll probably already know this. So if it's within 12 hours onset and PC is possible within two hours, primary PCI, primary PCI just simply means they go straight to the Cath labs, they don't go anywhere else. But if PCI is not available within two hours, then you would fibrial doing EC G again within 60 minutes to 90 minutes and then reconsider PC. But in reality, they're all gonna be going for PCI right? Next topic. So a tall and slender, 53 year old man presents to his GP with three weeks of worsening shortness of breath, which is affecting his sleep. He has a history of chronic kidney disease, hypertension and osteoarthritis of the left hip. He takes ramipril and acal with nail drug allergies. During your examination, you pay, you notice the patient has a slight rhythmic head nod. Observations are as follows. So his respiratory rate is 21 he's saturating 97% on room air. His BP is 100 and 56/61. His heart rate's 72. He's not got a temperature. What murmur would you expect on auscultation? So if y could put the pole up again, so I'll give you guys a minute. Ok. So I can see already. Yeah, there's a good spread. OK? Looks like a few of you are getting it right. OK. Let's go through the answer. So the answer was d it early diastolic for so for those of you who put d give yourself a pat on the back. Um So why was it d so this man er is suffering from aortic regurge, which is an early diastolic murmur. So why is it aortic regurge? So I hope you got a few hints there. So, first of all tall and slender. So whenever you hear tall and slender think Marfan syndrome, so it's a connective tissue disorder with connective tissue disorders. Always think aortic regurge in the back of your mind. Um He's got worsening shortness of breath, which is one of the clinical features of A R. Um the rhythmic head nod. I was trying to hint that's demus it's sign. So aortic regurge is one of those ones that's got all those weird clinical examination findings. So cos he's bobbing his head. That's demus. It's A R and then with the, with the BP, he's got a wide pulse pressure So that's, that's almost a difference in 90 millimeters mercury there. So wide pulse pressure, that's also a sign of aortic regurge. Um extra brownie points. Again, if you could say in the comments, do you think this, this murmur would be heard loudest during inspiration or expiration? When did we think it would be loudest? Ok. So I can see someone's gone for inspiration. OK. So we've got some divided Penina. OK. Right. Ok. So we've got a few going for inspiration and a few going for expiration. Um It would be during expiration. So it's left sided. So I'll go a bit into, I'll give you something useful to, to help you remember in the future. Um So murmurs are t the sound of turbulent blood flow either due to a stenotic valve or a leaky valve. So I think to understand murmurs properly is useful to un just go back to the basics and understand heart sounds in general. So I've included a link down there to a really useful video by zero to finals. Strongly recommend watching it. But essentially, so the first heart sound is when our atrioventricular valves close. So that's the tricuspid and the mitral valve and they, they close at the start of systole to stop the blood flowing back into the atria. The second heart sound is when um systole finishes and it's when the semi semilunar. So the aortic and the pulmonary valves are stopping the blood from flowing back into the ventricles. So if we think about it, systolic murmurs are gonna happen in between the first and the second heart sound. Anything else is diastolic? So, if it's between those systolic outside, diastolic, I hope that makes sense. Um, 3rd and 4th heart, heart sounds, I'll just briefly mention it. It comes up time to time in exams, but I think it's pretty low yield. Um S3 is heard directly after S two like nt 0.1 2nd. It's almost impossible to auscultate. Even regs would struggle. Um It's the sound of the Chordae Tendinae twanging like a guitar string when the um when the ventricle fills up with blood, um the chordae Tendinae being the, the bits of tendon stringy wee bits that are, that are attached to the valve. So it's normal generally in, in fit and healthy people under 30. But once you get above 4050 it's thought to be pathological and it's generally a sign of heart failure as the guitar string, if you think of it is reaching its limit, sort of sooner if that makes sense. And then s four S four is always abnormal. Uh It's heard just before S one and it, it's, it's due to be thought to turbulent blood flow. So as the atria is pushing against a non compliant, stiffened and hypertrophied ventricle. So it's again, it indicates uh heart failure. So how do you remember systolic versus diastolic? So this is, I still use this to this day. Um So this is a really useful mark. So I always remember systolic A S Mra S Mr being that um weird sleep stuff that people listen to. Um no judgment. Um So a S aortic stenosis and Mr mitral regurge. So just remember a systolic A S Mr and then diastolic arms. I remember, I even for exams, I wrote the word diastolic on my arm just to get me to remember that cos that's aortic regurg and mitral stenosis, which are both diastolic. So just remember that. Um And as I said, uh beforehand, so we've got the first and the second heart sounds, we can see all the systolic murmurs are happening within those two heart sounds. So, yeah, aortic stenosis there and mitral regurge and you can see uh aortic regurge and micro stenosis are happening outside of those in terms of whether it's left sided or right sided. So remember left for expiration, right? For inspiration, right sided murmurs being your your tricuspid, um your tricuspid regurge or your pulmonary stenosis generate the the right side, the right sided murmurs will mirror the opposite counterparts if that makes sense. So, aortic and pulmonary stenosis are both gonna be early systolic murmurs. So just think of it in the same way. OK. And then again, just some high yield facts for each type of murmur. So, a se ejection systolic murmur just commit that to memory radiates to the carotids and in terms of clinical features, just think sad. So I think all aortic stenotic patients are sad cos they're gonna experience syncope, angina and dyspnea, breathlessness for Mr. Um So Mr is a pan systolic murmur. It's thought of as a high pitched whistling murmur. Um really, it's the left axilla. It's uh because it's a leaky valve. Patients can develop symptoms of congestive heart failure because of that backlog of, of, of blood. Um and the causes are rheumatic heart disease, collagen disorders. So your, your um Marfans uh an SL E and poster M I complication as well, aortic regurg. So that's what um was in the stem of the question. So it's an early diastolic murmur. It's got some of the same causes rheumatic fever, uh collagen disorders, bicuspid aorta though. That's, that's independent. Um But then as I said, it's got all these weird clinical findings. So it's got a wide pulse pressure, it's got a collapsing or what's known as a Corrigan's pulse. So when you lift a patient's arm up, you'll feel their pulse, their radial pulse will become bounding, collapsing doesn't mean it disappears. It, it becomes bounding when you lift their arm up. Quint, which is the, the pulsation of the nail bed and then damoose it. The, the stupid way I remember it is like if you think of a head banger and they're bobbing their head to the music. I know it's stupid but it, it helps me remember it and then finally, mitral stenosis, there's not too much to remember for this except uh malar flush. So they'll get that, that perfect sort of butterfly distribution r er rash and then they can have P mitrale. So uh a bifid P wave on their EC G. So just remember those. Ok. Third question. So a 47 year old man presents the A&E with sudden onset tearing chest pain that radiates to his back. He has a heart rate of 100 and five BPM. ABP of 100 and 52/76 no signs of end organ ischemia. Um He has a past medical history including hypertension and ischemic heart disease. A ct thorax, abdomen, pelvis is ordered and confirms the suspected diagnosis as a false lumen is seen in the descending aorta. What is the definitive management? So again, if you can go up a pool and we'll give it a, a minute or so. Ok, I think good result. Ok. Yeah. In the interest of time, let's reveal the answer. So most of you actually got that. So, yeah, the answer is d so I hope you're able to sus from this, that this patient. Yeah, is having an aortic dissection. Um So we can see from the question. Yeah. So typical presentation as soon as you hear tearing chest pain, think aortic dissection, it's more common in descending uh to have tearing. But um anyway, it radiates to his back as well. Um Important to, to know he's got no signs of end organ ischemia. So it's uncomplicated. Uh He's got a risk factor of hypertension, which is a big risk factor and it's in the descending aorta. So the descending aspect is key cos that will impact on our, the, it's, it's termed as a Stanford type B dissection. Um So we'll get into why specifically, it was d so aorta dissection is when there's a tear or a break that forms in the inner layers of the aorta wall. So you've got three layers, you've got the, the intima, the media and the adventitia layer. The where the tear happens where the false lumen presents is in between the intima and the media. Um key main points for exams to remember. So if there's a greater than 20 point difference in BP between the arms, that's, that's a sign of aortic dissection. Hypertension is a big risk factor. Um You might hear a diastolic murmur on examination cos it can cause aortic regurge, which is a sort of late presenter present er presentation find um it can present with focal neurology. So sometimes you get patients who uh are experiencing uh paraplegia in the legs or change in sensation, even sometimes critical ischemia in the legs. So that's, that's if um there's involvement of the spinal arteries. So yeah, that's generally a late sign, but it's something to keep an eye out for hypotension is a sign of progression. So, again, it's a late uh presenting find in these patients. So it's generally a poor prognostic factor in terms of investigations, chest x rays, it's non diagnostic, but it's gonna help you to build a picture. Uh It will show a widened mediastinum, a CT angiogram, chest, abdomen, pelvis, that's the gold standard. Um However, if the patient's too clinically unstable and you think they're not gonna be able to, to stay still in act, then you can go for at oea transesophageal echo. Um So yeah, getting to the classification. So there's, there's two types of classifying systems, there's Stanford and there's DeBakey, I for exam purposes only listen to, to Stanford. DeBakey is the one where in the image, there it goes type one, type two, type three. Uh It's just to make you aware of it. It's I think type one and two in um in a grade, the ascending aorta and type three or four about the de just pay attention to the Stanford for exam purposes. So, Stanford A being um if there's any involvement of the ascending, so even if you've got it in your ascending and your descending, it would still be a type A type B is when it's just confined to the, to the descending. Um So then, yeah, in, in terms of management, so for type A, we would opt for surgical management uh most likely via open repair. So that's gonna involve midline steno and you're replacing the ace ending aorta with a synthetic graft. And in the meantime, up until you get that patient there, you're going to control their BP and their heart rate with IV. Labetalol, IV, labetalol is just the one everyone uses and it's just to control the exerting pressure on the aorta. In the meantime, cos obviously, they're quite high risk. These patients are managed surgically. Um cos I think the there's a 50% mortality in 48 hours if these patients don't receive any surgical intervention. So these guys are high risk type B were less concerned about. We're just gonna manage them with labetalol. We're gonna control their BP, control their symptoms. Um They can go for surgery. Uh If, if we think there are signs that they're clinically unstable, they develop focal neurology, et cetera, but most of the times it's gonna be conservative. So question four, a 67 year old. Do you just have one question? Sorry. Oh, yeah. So one question, no child, by the way, uh when would you do A to e over a CT Chest Abdel? So as a to e, so as I said, it's when you think the patient's clinically unstable, there's, there's A to e and then there's an uh an abdominal ultrasound, abdominal ultrasound is gonna be non diagnostic. It's gonna let you know that it's there T OE is gonna be diagnostic. And again, it's, if the patient is clinically unstable. So they've got signs of hypotension uh they're tachycardic, they're developing signs of heart failure, et cetera. They've got critical limb ischemia. Um So yeah, if you think a patient cos just, just appreciate when you send someone to act, they're gonna have to be still for what about 15 minutes or so? And you're not gonna be able to do any urgent intervention. So just look at them from the end of the bed and say is this patient gonna be alright for the next 10 to 15 minutes if not do at oe cos that's much quicker. Does that make sense? Ok. You've got one more um the difference in BP. Sorry. Would the difference in BP also show cooptation of the ooh Now you're testing me, I think. Yeah. Uh w when they say difference, do they mean uh difference between the arms or a wide pulse pressure? What what, what are they saying? Just waiting for more details, I guess uh the the difference between the arms I think cos we we said in the stem of the question if I go back. Um Yeah, so, oh I don't think I'd said it there but the answer is yes, yes. Um If you find a difference between the arms as well. Uh then yeah, that that's a sign of um aortic dissection. Yeah, it's there. And the key points the first point. Yeah. A a difference of greater than 20 millimeters. Mercury between the arms is a sign. Yeah, that answers any more questions. I can't see this. That's all. So, I'm just lying. That's all. Yeah. Oh. Did someone have one there? Did someone come on to the mic? No, no. I think that's all all right. Ok. Right. I'm gonna go into question four. so 67 year old woman presents to A&E with a four day history of fevers and rigo. She's also noticed she's got some new onset thoracic back pain. Today she has a past medical history of childhood rheumatic fever, hypertension and aortic valve replacement three weeks ago for severe aortic stenosis on examination. You note some painless erythematous macules on the femur eminences and hear a diastolic murmur over the aortic valve. What is the most likely causative organism? This is a typical exam question. So I'll give you guys a second. Ok. She can interesting spread. So, yeah. Ok. Right. Yeah, I think some of you are starting to get it. Right. Let's let's look at the answer. So answer was B staphylococcus epidermis. So um this is just like a typical exam question. It's come up in finals pap er final papers like a lot. I think I even had something like this. Um So the most common organisms have switched around. Um So yeah, this, this was infective endocarditis. Why? So she's presented with fevers and rigger, these patients can present really variably and generically. Um So always have in the back of your mind if someone's presenting with pyrexia or symptoms with no clear cause. These patients will just generally feel rubbish. Um, but I hope there's, there's some more clues in there. So she's got some thoracic back pain. Um, these patients are prone to developing discitis, which that could be hinting at she's had some previous rheumatic fever and recent valve surgeries. Those greatly increase your risk. Uh The painless erythematous macules on her hands. I hope you saw her Janeway lesions. Uh And finally, she's got a diastolic murmur, which is probably because the infection is now in her new prosthetic valve, which is causing some retrograde leaking. Uh So some regurg. So why, why is staph epidermis? So this is the, so staph aureus is the most common bug. Uh Now it used to be, it used to be strep viridans, but it's now staph aureus, but because she had valve surgery within the last two months, so it's recent. So it's within two months, it's most likely um staph epidermis. So let's go into why? So, infective endocarditis. So this is a life threatening infection of the endocardium ie the inner lining of the heart. Uh and it's usually not always but usually situr around the valves. It's most commonly bacterial, but again, not always, it can be fungal or it can even be seen in sl E um it's usually as a result of a bacteremia. So, bacteria being present elsewhere in the blood uh that have found their, their way to the valves. Uh, however, there's um other risk factors that can increase someone's susceptibility. So, er, for instance, valve surgery, so if you're directly um introducing pathogens of bacteria, um less than two month old prosthetic valve. So why, why two months? Um, so valves, whenever you put a device inside a heart, it undergoes what's called endothelialization. So it forms its own endothelial layer after two months. But before that time, it's susceptible to staphylococcus epidermis. So that's why within that two months, it's most likely Staph staph epidermis. Um if patients are IVD use or if they've had recent dental procedures, however, the, the endocardium is usually protective against the bug and it forms its own protective layer. So then if we have damage or insult to this layer, that could also facilitate infection. So that's how I've split the two risk factors. So for that, we're thinking uh previous valve disease. So, in stenosis or if there's any sort of turbulent blood flow that'll damage the valve, congenital heart disease, hypertrophic, um cardiomyopathies and previous uh or chronic inflammation. So, an sl e or, or rheumatic fever. Um So these are the causative bugs. Just try to commit these to memory cos these will come up. Er So the most common, as I said is staph aureus, as I said, um less than two months, staphylococcus epidermis, poor oral hygiene or dental surgery. Think streptococcus viridans that u it used to be the most popular, but no longer, it's, it's more present in developing countries. Um, viridans refers to a group of bacteria. Um, so it's not a specific bacterium. So, uh mitis and sanguineus is, yeah, part of that group. And then lastly if somebody has streptococcus bovis, you have to screen for bowel cancer. It's, it's just, yeah, one of those weird past med things. Yeah, that's associated with bowel cancer. And then how are they gonna present, what's the signs and symptoms? So again, as I say, it can present really generically. Um they'll, they'll describe themselves as having a, a persistent fever and persistent fatigue. They'll feel really run down, they'll have chest pain for obvious reasons. They might have hematuria if there's renal involvement uh in terms of signs, rough spots, you'll see on fundoscopy as they appear as small. You can see there on, on uh on the fundoscope, they appear small white centered retinal hemorrhages. Um don't confuse Janeway lesions in Osler's nodes. So Janeway lesions are micro emboli on the hands. So they shouldn't be painful. So they're painless. There's no reason they should be painful. Osler's nodes are generally located on the fingers and they're thought to be localized immune responses. So the loop and hence they're tender, so tender, non tender. OK. Hope that helps you remember it. And then in terms of actually diagnosing because it presents. So generally we follow modified duke criteria in order to make a diagnosis. So you can see that you've got a different combination of when you can rule it in. So if they meet any of the pathological criteria, it instant diagnosis if they have two major criteria, um one major, three minor or five minor, um in terms of the specific imaging findings at the end of major, that's gonna be on an echo. Um A vegetation, by the way is a, is a clump of infective bacteria held together by fibrin and platelets. If you're just wondering where that is. And then for the minor criteria, vascular phenomenon that's gonna involve major emboli splenomegaly, clubbing, splinter hemorrhages, janeway lesions in any Petitti I uh immunologic phenomena. So that's glom and nephritis. As I said, if you've got renal involvement, osler's nodes and raw spots, then finally, microbiological evidence that just means a blood culture that didn't meet the standards of the major criteria. OK. Um If there's any questions, yeah, put them in the chart. Otherwise we'll move on to question five. So a 39 year old man presents to the ward complaining of new onset palpitations moments later he becomes unresponsive. There is no palpable pulse CPR is started and DFI PS are attached. The following is shown during the first rhythm check what I is the next step in your management. So if you think you had started the pull, have we got the pool going there yet? Oh, sorry, just give me two seconds. Sorry, apologies. All right. Should be, should be going out. Yeah. Ok. Yeah, I think most of you have got it. So let's, yeah, let's show the answer. So it is answer. D so I hope you're able to guess. Yes. So this guy is obviously in cardiac arrest but he's got what looks to be on his rhythm strip, er, normal electrical activity, but he's not got a palpable pulse. So I think those of you who got d were able to, able to pick out. So yeah, he's got P EA pulseless electrical activity. Um I know this wasn't nice not giving you a full E CG, but in reality, you're not gonna have a full E CG. This is what you're gonna see on the D FB machine. But yeah, we'll go into, why was it option D? So this is from the, the 2021 guidelines from the Research Council UK. Um It's pretty good in terms of differentiating how we manage a shockable versus a non shockable rhythm. My problem with this, with this um algorithm is it, it doesn't really tell you when to use what medications and when. Um so thankfully, they've also, they've also provided a chapter in the Advanced Life support booklet, which is there on the right. Um So I've summarized this on the next slide as well. So this is a summarized version of how to manage shockable versus non shockable rhythms. So imagine. So we've started CPR um the and then we get to the first rhythm check and we've identified VT, er, pulseless VT or VF. So we've identified a shockable rhythm. Um, so in that instance, we would then do a first single shock of unsynchronized DC Cardia version. Um, in the reality. So, or in, in the scenario where they've already got DFIB pads and they're in a PCI center and you watch them, you physically see them have or go into VF or pulseless VT. That is when you would do three successes, initial shocks. In reality, that will almost never happen. It only really happens when patients are, are undergoing PCI. And they've got the pads on because the, the, um, they're sort of assuming they're gonna go into VF or, or, or VT, they're at high risk anyway. So we've done the first shock. We do two minutes of CPR and then we get to the next pulse check. They're still in, in VT or, or VF, we do another two minutes and then we get to the third rhythm check they're still in. So after the third shock, that is when we give the 1 mg adrenaline and we give amiodarone 300 mg. So after the third shot, after that third shot, we continue CPR and then we do a rhythm check every two minutes regardless of what stage of rhythm check. And CPR, we're at, we keep giving the adrenaline every 3 to 5 minutes and with the amiodarone. So we're only giving it twice the amiodarone we give the 1st 300 mg, the 2nd 100 and 50 mg we give after the fifth shock. So we only give amiodarone twice. OK. And essentially, we keep doing this until the patient develops a pulse or signs of life. And um and we achieve ROSC, which is the return of spontaneous circulation for asystole. It's a little bit different Asystole. We're gonna keep doing until the patient goes into a shockable rhythm. It's unlikely you're gonna be able to resuscitate a patient in a non shockable rhythm. So we, and then once we get them into a shockable, we switch into the other algorithm on the left anyway, so we've got a non shockable on the first rhythm check. Um We immediately give them adrenaline. We do two minutes of CPR, we check the rhythm in another two minutes. Um There's still an ass er er P EA. So we just keep giving adrenaline every 3 to 5 minutes. I hope that sort of made things a bit clearer. Um So if we go back to the E exam question, so yeah, it was option D. So this patient's in P EA immediate adrenaline. I hope that clears things up a bit. And then finally, so this is more gauge towards um an AK station if you ever had to manage a cardiac arrest. I have heard of it before, but I think this is just really good to know as well. Um So this is for the individual who's gonna be standing at the end of the bed, leading a cardiac arrest, who is usually the most senior doctor and they're gonna run through the four Hs in the forties of reversible uh cardiac arrest. So we think hypoxia. So we're gonna look at recent trends. Have they been hypoxic recently? I sure somebody is ventilating them adequately. We do, we look at hypovolemia. So again, look, are there any recent uh signs of trauma, any signs of bleeding? Think um on the floor and for more uh hypothermia take the temperature if they're cold, think about a bear hugger, which is this inflatable blanket. Some hospitals have it. Some don't. Uh we can give them warmed IV fluids or we can retrofill their catheter with warm saline and then er hypokalemia, you are not gonna get a radial pulse in a patient um who is pulseless. So you're gonna have to go for their femoral. So a femoral stab and then in terms of the ts so tension, if you think you tension, pneumothorax is the cause, get someone to auscultate and percuss the chest um during the two breaths or during the rhythm check. If it's a tamponade you're worried about. Again, think of recent history of trauma or surgery and get a bedside echo. That's the only thing that's gonna confirm it. Uh a thrombus. Again, look for a history of any recent clots or if they've got a pe if they had any chest pain recently, any A CS, if you've got any signs of A DVT, any swollen calves. Um, once, one thing with a thrombus, once you thromb, you then have to, you have to keep doing CPR for 60 to 90 minutes. And that's a lot of time to be doing CPR for. So, just be careful. Um, and then finally toxins. So is the patient in IVD U, um, check their pupils if they're constricted, check their recent drug history and their drug chart and yeah. OK. So I'll hand over to Y now. So I think I went over a wee bit, I can, sorry, it's just a couple of questions that come through about that. Oh yeah. The first one is any idea of when to give a synchronized versus an unsynchronized shock? Yeah. So synchronized and unsynchronized. So just think unsynchronized is um defibrillation, synchronized is where? So that's your D CCV. Um So that is when you're trying to get a patient, for instance, out of atrial fibrillation. Um So they're not having a cardiac arrest or it's, it's when someone in, in S VT. Um So, and it has to be synchronized to the R wave. So yeah, just remember unsynchronised is defibrillation. And then, yeah, there's all, there's a whole host of indications for synchronized cardioversion. I hope that answers your question. Was there any others? Um There's one more, but I think it's been answered in the chat. So all right. Ok, cool. Anyway, I'll hand over to Ed. All right. Can you hear me now? Ross? Can you tell me? Yeah. All good. Ok, perfect. Uh My internet's been coming out of the last few minutes, so just let me know if something, um, goes wrong when you, if you can't hear me. Um, all right, I think. Can you take the pool? Oh, no, I just closed the pool. Perfect. Um, so I've got a couple of questions as well. Uh I'll try to get through them reasonably quickly. So you guys don't need to, um, sit here until very late hours, uh, but hopefully they'll be useful. So the 1st 1, 15 year old student presents to your office and advice of his football coach. He started playing football this year, suffered a syncopal episodes of practice. Um, he was sprinting, um, with the rest of the team and became lightheaded. He lost consciousness, fell to the ground, regained his consciousness within one or two minutes. Um, no. And on the exam you hear a systolic murmur, uh, at the left lower sternal border and apex and you've got some changes on the ECG. Um, so what would you expect to hear, uh, on examination? All right, let's give it a minute. Try to get a few more answers. Ok, I think I'm moving in the right direction. Ok. So the general topic of this question is cardiomyopathies. So generally if you've got a 20 or a teenager year old person doing some sports and passing out. Um you think of a cardiomyopathy? So luckily a genetic cause. Um so, can I have the next slide, Ross? Sorry. Um So the correct answer for this will be a as uh many of you have, have chosen. Um So what we're thinking of here, um Why aren't we thinking this is the correct answer, the most common question that will obviously point towards hypertrophic cardiomyopathy. Um So, and I'll explain um the findings of hypertrophic cardiopathy in a second, which will obviously explain the question as well. Um So, can I have the next slide? Right. So, when we're thinking of cardiomyopathies, we've got several different types. Um the most important one is obviously the hypertrophic cardiomyopathy. So that's your average teenager, 20 year old who just out of the blue kind of passes out generally on, on exertion, then we'll talk quickly about dilated cardiomyopathies. And then we'll say a few words about the other two types, the erythrogenic cardiopathy and the restrictive cardiomyopathy. Um So, the first thing that we talk about is the hypertrophic cardiomyopathy. Um So, here, we're talking about hypertrophy, the thickening of the myocardium in absence of another cause. Uh We're talking about aortic stenosis or hypertension. That's why it usually affects younger people. Uh It's the most common cause of sudden cardiac death. Um And it's usually autosomal dominant in terms of inheritance or can be inherited in syndromes. I don't know if you've heard of Fabris disease. So, um disease of the um lipo glycosides or Pompe disease. So, um glycogen transport disease, um your clinical features would be if, if you were to cut out and put it under a microscope, just a small biopsy, uh it would be hypertrophy and disorganization of your myocytes. So you'd have chunky big cells, but the organization will be off if you looked at it and compared it to normal um heart muscle and it will be particularly affecting the septum, the septum, as you can see um on, on the, on the image that septum also at the same time, anatomically is quite close to your um uh to the valve to the aortic valve, which is sometimes you've got the subtypes of hypertrophic uh cardiomyopathy, which is called um hypertrophic obstructive cardiomyopathy, which is when the thickening of the muscle is such that also cause this um ii impairs the outflow. Um We've also got issues with um systolic uh motion of the mitral valve. So, so, so sometimes the mitral valve might not close properly and in fact, might um additionally add up to the, to the er obstruction through the optic valve um symptoms. So, generally, the symptoms um are not really very evident. Most people are completely asymptomatic. Um if someone is lucky to be symptomatic. So that is, it gets picked up early and you can do something about it. Um they present with symptoms generally sim similar to aortic stenosis. Um so that your chest pains, as Ross mentioned, a dyspnea uh can be the syncope. Um you can get arrhythmias and in many cases, people have gone through life with it as, as asymptomatic. And unfortunately, in some cases, it release uh it results in a just sudden cardiac death um signs. So that would be the double uh double apical pulsation. So you can hear us ros mentioned before the S four sound. So that sounds just before S one. that is because the, the atria trying to forcefully additionally contract uh which produces the, the S four. As you can imagine, the, the left ventricle is quite beefy, quite strong. So you've got a very jerky kind of strong carotid pulse. Um You'll have an ejection systolic murmur. Um And that, that's the important thing. So the ejection systolic murmur is increased with maneuvers that decrease afterload, um such as standing or valsalva. So, uh any maneuvers that pull the blood kind of far away and uh decrease your, your a road, decrease your BP will increase. Um the murmur um and the murmur will be decreased by maneuvers that increase um preload, um such as um squatting, for example. Um So they'll have, they will lead, they will result in more blood being, being transferred to the ventricle. Um The ventricle will feel much better and the outflow obstruction will be much smaller because of that, that dilation. Um when you look at it in the investigations, um you're gonna see left ventricular hypertrophy on the ECG um echo, which is usually diagnostic will show you this is asymmetrical thickening. Uh You can do an MRI as well and the important thing is to do genetic analysis, especially if you've got some family history um regarding management. Um there's two key things if you've got someone first. So, so the main aim in terms of management of your hypertrophic cardiomyopathy is to keep the preload high. So you wanna keep that ventricle nice and distended, um filled up nicely so that there's no outflow um obstruction through the optic buff. You can do that by two main um strategies. The first one, the simple one is making sure that the patient's always really well hydrated. So the reason why the synoptic episodes happen usually in sports is that you get really dehydrated, uh which increases the actual obstruction, you get shortness of breath, you get your chest pain and then you just pass out. Um and then you can also treat it medically by decreasing by kind of increasing preload um via beta blockers or calcium channel blockers, which obviously slow down your heart, uh enable your um uh your ventricle to fill in uh much faster, sorry, much faster, much fuller. Um And then therefore increasing the preload and decreasing the obstruction. Uh can you go back slightly to the questions and the answers? So, as you see that basically correlates uh with answer A, I'll just quickly go through BC and D. So I would normally ask you about just in order to save time, I'll just quickly explain. So, answer B is a typical murmur for mitral valve prolapse. Um So it's a mid or late systolic click um to see uh it's mitral regurgitation. Um The tricuspid regurgitation and is aortic stenosis, but I think ross covered a fair bit. Uh So I'll not go further into it. Uh Can you go two slides forward? Sorry. Right. So this is just a good table. I'll just quickly talk about the other types um of uh myopathies. So the next one will be um it appears in questions quite rarely, quite rarely. That's why I'd only say a few words about it is the uh it's not here on the table. It's the erythrogenic cardiomyopathy. So it usually affects the right ventricle. It's also uh basically your muscle is replaced with um fatty tissue. Um And then since that's a fatty tissue and not muscle, your right ventricle gets dilated. Um with dilation, you usually get arrhythmias because your conduction is not synchronized anymore and you can eventually get your right ventricular failure. Um Clinical features with um myopathies are generally very similar for all of them. So, most of them are asymptomatic and then if you get symptoms, depending on which ventricle is affected, uh you end up with syncope, you can have sudden deaths and um arrhythmias. And in this um case, obviously, you can have heart heart failure. Um In this cardiomyopathy, your ecg will be normal echo is the really good diagnostic tool uh which can show you your uh right ventricular dilation. Um But you'll see a lot more if you do a cardiac MRI because you'll be able to tell that the muscle is not quite a muscle that there's some um fibro fatty tissue And your gold standard for diagnosis is just genetic testing. And since at least arrhythmia, you're gonna use your um drugs to prevent arrhythmias. So you're gonna start with beta blockers if you are non symptomatic. Uh and then you can move to stronger drugs, you can move to amiodarone or sotalol, which is a beta blocker with some potassium um channel blocking activities. And then if you're worried uh of life-threatening arrhythmias, uh you can implant um on CD. So the second, the sorry, the third type that um comes up in questions quite often is the dilated cardiomyopathy. Um that is usually not genetic. So you would look for additional causes. Uh but it also can be genetic, but it's a much rarer genetic cause than for hypertrophic cardiomyopathy. So, with dilated cardiomyopathy, you've obviously got dilation of the chambers. Uh And because you've got dilation, you've got um worsened systolic uh function. Um The usual cause is your kind of alcohol consumption for 40 years. Uh Chemotherapy. So, DOXOrubicin is a medication that commonly is associated with dilated cardiomyopathy. Uh You've got your tropical diseases. So, parasite Chagas disease um causes dilation and then you've got many, many more um the clinical features, it basically presents with like heart failure. Um So you've got your impaired heart pump pumping because it's dilated all the circuits that work in a normal heart uh somehow off in terms of synchrony. So you can um just have some uh arrhythmias and conduction defects because the heart isn't squeezing very well. Uh You can get some thrombus um in the uh in the ventricles and result in emboli and obviously, sudden death is associated with all cardiomyopathies. Um And the gut test here is an echo uh which will show the dilation of the ventricles and all general function. Um and then management for it is the same management as for heart failure. So, medical management, which we'll talk about a bit later and you can implant your ICD the fourth type. And the last one that I wanted to talk about is the restrictive cardiomyopathy. So, it's kind of like you look at the heart and it looks fairly normal. Um It's, but for some reason, it really expand very well. Um it's usually caused by um just fibrosis um of the heart wall most commonly. Uh it's associated with amyloidosis or sarcoidosis. Uh but can also be genetic. Um Features are very similar. Um So dyspnea, fatigue, uh edema uh and on the examination you're gonna have some nice signs um ascites, uh edema. Um Once again, um you're gonna do your ecg, your heart's not gonna be pumping very well. So your QR s will be low in terms of voltage. Um your cardiac MRI will be a good test, but we'll show you that fibrosis. Uh But biopsy is probably the best um the best test to confirm the, the diagnosis uh in terms of management, you try and treat your amyloid and sarcoid uh as appropriate. But in other causes, often transplantation is the only kind of effective treatment. Um Can I have the next one, please? Um And here, what I just wanted to touch on is the kind of the acquired and usually reversible with two cardiomyopathies. The first one is your Takotsubo, which basically presents like a um heart attack. Uh But when you do an angiogram, um you don't see obstruction in your coronaries, but you see this weird shape of the heart. So hopefully on the image you can appreciate on the left side you've got in diastole. So it looks fairly normal, uh slightly abnormal, but you know, heart has generally look different in everyone, but then insistently on the right hand side, you can see that the, the basal part of the heart um is pumping quite well. But then you've got this ballooning or dilatation. Those are the the key words in terms of your apical uh part of the heart. So it doesn't really squeeze, squeeze too well. Um So that's tach of sub cardiomyopathy. It's generally reversible within 4 to 6 weeks. Um You can hate the symptoms with beta block blockers generally affects middle aged women. We don't quite know what causes it. We think it's RS due to stress. Um So elevated level of catecholamines, but we're not quite sure. But the most important thing is that it's in most cases reversible and not really associated with um recurrences, frequent recurrences. And then the last one is um peri partum cardiomyopathy. So, in women who are in the last trimester or within five months after delivery, the risk of um dilated cardiomyopathy by you should recover within six months. But that's also something that's quite important if, if you've got a question about a pregnant lady who's got some heart issues. Ok. Can I have the next um question. All right. Question seven. So you've got a 55 year old man this time. Uh who's getting um progressively worsening, shortness of breath and some leg swelling that occurred when he was on a business trip. He has a diagnostic, a diagnosis of a congestive heart failure. Um and he's uh he's symptomatic with it. His BP is 1 40/90. So, no JLO venous distension or gallop. So, there's no S3 or S four and he's got only minimal swelling. Uh His echo shows ejection fraction of 45%. He's currently on aspirin and a statin. Uh, he doesn't like taking too many medications, which is quite common. Um, so what additional treatments are indicated at this time? Ok. Ok. Perfect. Um, so the correct answer, can I get the next slide? Sorry. So the correct answer is b so we hopefully we're gonna appreciate that the patient as the, the question says he's got heart failure. Um, the very important thing is that he's currently, uh, becoming symptomatic. So we do need to do something about his treatments. Uh and we'll talk about all the medication but generally the first medications that we start in order to improve someone's treatment, uh will be an ace inhibitor and a beta blocker. Um We can start all of the, all of the management. All of those management options are uh available and are used in patients with heart failure. Unfortunately, those questions, try and trick you and um try and ask you for which ones you would introduce in what order? The first thing with general E Ace inhibitor and a beta blocker, um spirolactone. So, an aldosterone antagonist is something that we use frequently as well. But that's for people with um a lot more significant heart failure, uh generally class three or four. So your ejection fraction is expected to be under 35%. Um And uh you introduced them in patients who are already on an ace inhibitor and a beta blocker. Um Digoxin can be used to control arrhythmias but this would be something kind of that we, we don't really have in this question. Um, furosemide can be used if we've got evidence of edema. Uh, all the other medications we start them. Uh, and we're still struggling. Uh, interestingly enough, whilst Furosemide helps you with your symptoms, it doesn't really increase in morbidity so it can help you with the pedal edema, it help you with the breathing. Uh, but at the moment, um there are better options for it. Um Can I have the next night? Right? So we'll just quickly talk about heart failure. Um The most important thing about heart failure is that it's not a diagnosis, it's not a condition itself. So it's a sy syndrome um that results from either structural or functional cardiac um disorder. So, if you've got heart, someone with heart failure, it's incredibly important that you still look for the cause. Um because you might be able to treat the cause and then improve someone's um heart function without necessarily having to start someone on the heart failure medications. Um Heart failure is kind of a vicious cycle. So at the beginning, when your heart function starts dropping, you activate all these mechanisms to try and uh improve the way your heart works. Um And those me, those uh mechanisms work really, really well at the very beginning. But unfortunately, as you keep adding um increasing your age or keep adding your risk factors or, you know, keep your BP, high, keep um smoking or have a heart attack. Those um risk factors eventually overwhelm uh those mechanisms, those corrective mechanisms. So, some of the main mechanisms, for example, is the release of the atrial natriuretic peptide uh which causes uh natriuresis diuresis and vasodilation at the same time. Um As you've got decreased renal perfusion in someone who's got um who's got heart failure. Uh you increase the production of the renin Um And then you activate the renin angiotensin aldosterone uh pathway. Um which as it says here leads to vasoconstriction and then leads to salts and water retention and then that creates that vicious cycle. Um You also, as you um pump less out of your uh out of your heart, uh your carotid bodies feel like you're being in kind of more of a hypotensive state. So your sympathetic system is stimulated. Um tries to make your heart pump harder and and quicker, but that gets um overstimulated uh leading to myocyte exhaustion, exhaustion and apoptosis, which further obviously can uh contributes to um to, to your heart failure. And uh lastly as you're pumping um less um you have peripheral vasoconstriction because you obviously try and um try and preserve the blood flow to, to your important organs to your brain um to your gut uh to your liver and throughout uh so you've got an increase in afterload which further decreases ejection fraction, which causes further ventricular dilatation. So, as you can uh appreciate. Um It's OK. Um What? So in terms of uh different types of heart failure. Um So we generally have two. Sometimes you can um uh encounter the third type uh which is just the in between of the two. So you've got your heart failure with reduced ejection fraction, um which is the same as uh heart failure with systolic dysfunction, uh which generally occurs when your ejection fraction is below 40. The most common cause is uh heart attacks, issues with your valves, hypertension. Um And then you've got your heart failure with preserved ejection fraction. So, ejection fraction, about 50 that is usually due to hypertension. Uh because hypertension causes stiffness of the ventricular wall and uh decreases the ventricular compliance. So it decreases the ability of your heart to relax, which then impairs your diastolic function. And then the third thing is this heart failure with moderate ejection fraction, which is literally um when your ejection fraction is between the 4050 but something a bit recent, more recent uh symptoms uh generally depend on which ventricle is affected. So if your left ventricle is affected, uh then you're gonna get symptoms primarily of pulmonary nature. Uh So you're gonna have your exertional dyspnea. Uh You can have your paroxysmal nocturnal dyspnea, uh you can have your cough as well. Uh If it's your right ventricle that's affected, uh you can have your ascites, peripheral edema. Um and such uh when it comes to signs you have tachycardia elevated JVP S. Um Oh, actually sorry. Can I have the next slide for that? Thank you. So you've got your cardiomegaly. Um So increased cardiothoracic uh ratio. So your heart becomes more than um 50% of that uh thoracic um diameter. Uh You've got your 3rd and 4th heart sounds, third heart sounds particularly if it's heart failure with reduced ejection fraction. So if it's a reduced ejection fraction, your heart, it leads to cardiomegaly, your heart dilates and it, you end up with a kind of like a dilated cardiomyopathy. Hence the S3 um injection, you've got that stiffness. So you end up with the, with the S four, you've got your bibasal crackles, uh pleural effusions. Uh You've got the curly B lines, um which you can see if you really go over chest X rays. I always struggle. Uh You've got your peripheral ankle edema ascitis and hepatomegaly regarding investigations, if you wanna just diagnose heart failure, uh the syndrome, uh the test that we usually do is BNP uh which is elevated um and is released from your ventricles. And then what you do, obviously, you can do a chest X ray and an ECG which can show you that someone's in heart failure, but you, what you really wanna do is try and look for an underlying cause. So you do an ECG and look for signs of ischemia. You look for an arrhythmias. Um You can do an echo just to look at your what uh valve function. Uh you will also look for signs of uh previous mis by looking at wall motion abnormalities. And then if you can't find anything, you can do um cardiac catheterization um or you can do um cardiac MRI or a nuclear scan to just look at that muscle. Um even closer. Can I have the next slide? And then the very important thing is your four pillars um when it comes to treatment of your heart uh of your um heart failure. So, don't forget about the first thing, which is just um what you do in terms of conservative management. So the first thing is trying to limit um sodium intake to try and um stimulate the diuresis. Um so that people are not in um retention, but then you quickly move on to uh to treatments. Um So, like I said, the first thing you do is start them on a beta blocker. Um And then you can start them on the an ace inhibitor uh or an uh aldosterone receptor blocker if they uh have a reaction to the ace, um you then move on to an aldosterone antagonist. So you've got your two options. Uh generally in use, you've got your spironolactone and the plein um spironol lactone, you have to be always cautious of the side effect, which is gynecomastia in men. Uh And then you call your SGL T two inhibitors. So your Empoli Flosin and Depo Gliflozin. You might be familiar with them and if not, you might be familiar with them since they're diabetes medication. Uh, but they were shown to promote, uh, diuresis and generally help, um, with heart function. Um, you also have been to this new class of medications, uh, which is called Neprilysin inhibitors. Uh, usually, um, in a combination with an A B. So it's your s, uh, Secure Valsartan or SAC B as you might uh encounter it on the wards. Uh which is something that we introduce after we have all the four pilots. Uh but we still can't really uh control the heart failure. Well, um so we can, uh we can introduce that instead of the ace inhibitor or the ARB. And then like I've mentioned furosemide, bumetanide, I do loop diuretics just for the symptomatic relief. So just to offload some fluid. Uh but don't really use them in the long term if you don't have to. And after you obviously got your intervention, so no surgical method, uh you can um use cardiac resynchronization therapy. So basically as your heart dilates, um as I said before, you're at the risk of um getting into arrhythmias. Um So you wanna put in a device that would resynchronise your heart uh in case your ventricles start pumping somewhat independently. Um So you can implant a CRT device, uh which simultaneously will pace both ventricles. Uh if they go out of rhythm and then you can add an ICD and that becomes a C RTD, uh, in case they also go into an arrhythmia, so that shock can be done at bringing them back to normal rhythm. Could I get the next question? Right. So, question eight, you've got an otherwise asymptomatic 65 year old with diabetes presenting to your A&E with a sports related right shoulder injury. Um, his heart rate is noted to be irregular and you do an E CG and you see this, uh, what is the best immediate therapy? Okie dokes. So, uh, can we move on to the next slide just for the answer? Right. So if you look at the question, there is a few very important key bits of information. Um, we've got someone who comes in asymptomatic comes into A&E with a completely unrelated, uh, issue. Um, and we kind of incidentally as we do our basic OBS just we, as we do our basic EC G, we notice that his heart rate is slightly irregular. Uh, we do an ECG and this is what we, what we see. Um, that's just the basic kind of bit of information and I hope that we can appreciate that we're on a certain kind of heart block. Um, just because we can see that we've got some dropped heartbeats, then it means that it's not, um, first degree heart block, which I'll talk about in a second. Um, but then we look at it. Uh And we see that we've got some drop beats. So then the next thing we look at is whether there's correlation between P waves and QR s, which I hope um you can see that there is. So there's the P wave before every QR s. Um So we look at say heart block and now the second thing we look at is whether the pr interval um gets longer um as uh and eventually there's a skipped heartbeat and I hope we can appreciate that. At the beginning, we've got a very short pr interval, it gets a little bit longer. And then, um there is a, there was a skipped cure. So we're on the MOS type one. So the thank you back, um, a second degree heart block. Um So usually with your 1st and 2nd degree heart blocks, uh unless they're symptomatic, um, you don't need to do an intervention. You have to remember that even though it doesn't look nice that the heart rhythm doesn't look nice. Uh And you really wanna fix it and the fix for it is quite easy. Every single intervention is a, is associated with side effects. So if someone is asymptomatic, um you generally, the first thought that you should have is do I need to do anything about it? Uh And in the case of asymptomatic, 1st and 2nd degree heart blocks, um that generally produce a normal kind of heart rate. Um You are not required to do anything about it. Um When we talk about third degree heart blocks, that's a completely um other issue. Can I have the next slide, please? So when we talk about hard blocks, I'll just quickly get through it. Uh You've got your first degree heart block, which just means that your pr interval is prolonged. So it's more than 0.2 2nd. means that every atrial depolarization is followed by conduction of the ventricles, but there is some delay. Um You've got your second degree heart blocks. Uh means when some PA S are conducted, but some pa s are not conducted, you've got your Mobi type one. So the you back, which means that your pr interval gets progressively longer uh until ap wave fails to conduct. Um That means you've got a, some issue at the V node. Um And generally, you can just go with um with observation as in this case. Uh unless obviously, we're talking about someone who's uh fairly symptomatic. You've got a mobs type two with a drop complex. It's not preceded by a progressive pr interval, prolongation and usually uh your QR S complex is wide. Uh So it's above 100 and 20 milliseconds. That means that your block is below the AV node, usually at the hi S bundle. Uh And as just at the same time, it requires pacing if it's symptomatic. Um The second degree heart block is often caused by um inferior mis because as you, as you might know, the uh right coronary artery, which uh corresponds to the inferior territory um supplies the A V node. Uh And then we call your third degree heart blocks. Uh which basically means that there's no sync in A and V, of course. Um And with those, you definitely need to um and the main thing to do is establish basically what's the cause, what's the etiology? It's usually an M I and usually you can, you can treat it with a pacemaker. Um And then you've got your um can I have the next slide? Sorry. So that's something that I've always been struggling with, struggling with. Um because you notice them quite often and quite often also, there's just nothing um that they kind of add to in terms of your diagnoses, but they're quite a common diagnosis. Um So as you might know that his bundle, once it goes um distally, uh it gets right right to first the right and then the left bundle branches and then the left bundle because it supplies that big, big left ventricle, it has to sub divide into the anterior and posterior divisions. Um If you've got a complete bundle branch block, so either your left or your right bundle branch uh blocked. That means that your propagation of that signal um throughout your uh your ventricles is slower. So you can expect a QR S complex to be um wider. So above 100 and you, you're probably looking at your Q RSS. Um So you've got that classic marrow shape. So you've got an M in a V one and what looks like a V uh what it looks like a W in your V six. So if you've got an A S wave in your V one, um and your V six in your V one and then S wave uh and in your V six B brand block, you've got the opposite. So you've got of the William um structure. They've got a deep S wave in B1 and a toll V six. They usually asymptomatic like I've said. So usually you'll do an ECG and you'll get this right bundle or left bundle branch block, but they're usually um asymptomatic uh in questions, if you new onset, a new left bundle branch block, you've got to be careful if it's an M I. Um So you also always look, once you get to clinical practice, you always look at previous EC GS whether that left bundle branch block was already present. Uh But for question's sake, you have to be, be careful if you've got someone with a new left bundle branch block. Um and regarding the causes, so your right bundle branch block um is usually conge congenital abnormality in a large percentage of people or it can be associated with some pulmonary conditions. So, anything that puts stress on the right heart uh can give you a right bundle branch block. So, pulmonary stenosis, pulmonary hypertension, pulmonary embolism, pulse, obviously mis and then fibrosis your left bundle branch block um is usually caused by um left ventricular disease. So, aortic stenosis hypertension, uh mis or other kind of severe coronary disease. And then can I have the next question? Ok. Dokes. Uh probably, I don't know if I'll get the to the last one. I'll probably finish off this one. Maybe we'll see. So, a 36 year old man presents with a sensation of a racing heart. Um His BP is 1 10/70 respirate, 1402 SATS are normal. Um ECG shows a narrow complex tachycardia with a rate of 180 you diagnose axis or atrial tachycardia. You do carotid massage and valsalva, which do not help. What do you do next? Ok. All right. Looks good. OK. The next slide was perfect. OK. So most of you are absolutely correct. Um So what you do here is give the patient adenosine. Um Usually, I don't know if you know that you try to give it to as proximal uh an artery as you can. So usually if you've got someone with a cannula in, let's say the, the handle or the wrist, um that wouldn't work. Uh You have to have a cannula at least in the ACF uh if possible higher up. Uh That's because the heart of life of Aine is like half a minute or a minute or something like this. Um So it's very, very short and you want it to get a second, so you need to get it to the heart as quickly as possible. Um Can I get the next note? So we're gonna talk about tachycardia real quickly and how to diagnose um tachycardia that you're dealing with. So just instead of learning of learning what the sign and the ECG changes and the symptoms for each one of them are. Um It's just quite nice to learn the ways to kind of narrowing down your options. Um So the first thing we're talking about tachycardia over the pulse because uh Ross has talked about um vs um sorry VA and a studies a little bit uh earlier. Uh But generally, what we look at first is your QR S duration. So you look at your Q RSS if you've got a narrow complex CRS, um we think it's generally coming up from uh your, your atria. Uh But obviously, there are some um there are some rare occurrences where it comes can come from the ventricles. And then if you got a wide complex, um you're more thinking of um your a ventricular cause, but obviously, there are some exceptions as well as always uh what you then look at is the regularity. So if you've got a narrow complex tachycardia that's irregular, um most often it's gonna be your atrial fibrillation. Uh and it can be also your your atrial flutter. Uh If you've got something that's regular, you think of a um S VT. So supraventricular tachycardia, that basically means tachycardia originating from the atria. That's a regular tachycardia. So that's your sinus tachycardia. Um Your atrial premature beats could be an atrial flatter as well and then several other different types. And then if you go into white complex, uh you start thinking of your VT uh VF it's also important that you have some um aberrancy versions which can um look, have, look at um can be quite complex, but you're a at the next slide, some of EC GS just so that we're clear as to um what we're talking about. The first one, I think we can all appreciate atrial fibrillation. Um So we've got the uncoordinated atrial electroactivation and so this irregular irregular heart rate. So you've got the, the RR intervals are not distances from each other. And we can't also see PA S do not originate generally from the um SA N. They originate throughout kind of the, the atria. It's something that you gotta encounter very often on the wards and appears very often in questions. And that's there's a lot, a lot, a lot of risk factors, generally, anything that distends your heart um can cause af because like I said before, distention impairs the the circuitry in the heart. So age causes obviously some distention hypertension, uh also contributes to AF valve disease, heart failure, all the lung diseases uh but also substance abuse. So, caffeine drugs and then hyperthyroidism is something that commonly comes up in question as well. Um Right. I don't think I'll get it through every single bit. Uh because that's quite a lot of information. So, can we have the next E CG? All right. So here is the E CG that looks uh looks a bit different. So, going back the diagram, it's not like tachycardia. Um If we were to plot the RR intervals, they look fairly regular. But what we can see is that sore tooth kind of a baseline. So we don't have that nice uh flat baseline between, between uh uh between the, the, the, the uh so that, that things are um sorry, everyone, we'll just give you a second cos he keeps phasing in and out, but hopefully he comes back, Jenny Heros. Yeah. Yeah. Yeah, you're back now. Oh yeah, sorry. Sorry. Can I have the next one? I don't know why I disconnected. Sorry. All right. So that the CG um same as last time. So the first thing we look at is whether it's a narrow or wide, you can obviously see that's a narrow complex tachycardia. Then we look whether it's regular or irregular. Um And then we can see that it is generally very much regular. There's two large squares between uh each QR s can we see the P waves? Uh We can't really see the P waves and which trade away brings us to the conclusion that it's most likely um just um supraventricular tachycardia. Those P waves do exist, but the distance between the, the CRS is so small that they get basically better. So this is what's happening with our patient right now. Um And generally the treatment where you start with, um is your valsalva maneuvers or your um carotid massage, why you do it? Uh because both those maneuvers increase your BP briefly. Um, as your BP goes up, your, the amount of blood, um, your heart pumps will go up, down, less blood is coming back to your heart, uh, causing your heart rate to speed up. And, um, at that point, once it speeds up even higher, um, your, um, your heart kind of re synchronizes. Uh, hopefully, um, the medical option is to go for the adenosine, uh, which has kind of the opposite effect. Um, if you ever give someone adenosine, uh, it's quite a scary thing to do because when you look at them associated with in textbooks and questions that censor them impending doom and they're gonna be sitting over there with the eyes open, kind of talking to you feeling like something's gonna go wrong and then they're gonna go into a second or two of complete like asystole and then the heart's kind of just gonna reset. Uh, but it generally works very well. If it doesn't work, you can try your beta blockers and calcium channel blockers. If that doesn't work, you can call them usually. Uh, can I have the next E CG? Um, this one is a bit more tricky because it's a bit difficult to tell what it is. But that's basically a wolf Parkinson white. So that is similar kind of question as the cardiomyopathy question. Um, but in this time you've got, let's say you're a 3040 year old gentleman, um, who has done some things, um exercise a little bit. But then, um you do the A CG and you see this tachy arrhythmia and you notice the delta waves, uh which are the, the quicker kind of upstrokes uh at the beginning of your QR S. That is because you've got an accessory pathway, it's called a bundle of cat. So instead of the, the heart signal from your atria instead of going through A VN and then being slowed down at the VN because the AVN is really good at slowing uh the signal down so that your left atrium can be depolarized as well before the ventricles. Um That signal goes through the bundle of Kent skipping the, um the, the, the AVN goes directly to the ventricles. So your QR S kind of starts a little bit faster, um which is where you get that delta wave uh regarding the treatment if it's um symptomatic, um you can also put them on some antiarrhythmics. Um All of them are the ones that we talked uh kind of uh but the best treatment is ablation. So you can e easily map where you've got that bundle of can and uh using kind of cold or, or heat or radio frequencies. Uh You can ablate it to uh completely, basically eliminate it. Can I have the next one, please? So this hopefully we know. Um So first of all, it's a white complex tachycardia. Um generally it looks regular um which makes us think it's a, it's a VT. Sorry. Yeah. Broad complex. Yeah, it's a VT. Um And then there's a few kind of common signs uh when it comes to, to VT. Um So generally in a VT, you've got your P waves and Q RSS occurring at different rates, um You can have something that's called capture beats. Uh that occurs when your sinoatrial node transiently captures the ventricles. Uh Meaning you've got a normal QR S at some point. Um And then you can have your fusion beats as well. Uh Which is when your sinus and ventricular beats coincide to produce what's called a hybrid complex. Um The next thing that we talk about is concordance. So generally in a monomorphic V VT, uh you've got your uniform QR S complex uh complexes within each lead like in this one, but you also have kind of polymorphic um VT which is when QR S um changes PL and access uh which I have on the next slide can I have it, Ross. Uh This is your polymorphic VT also known in this example, it's tools um and the treatment uh would be uh if someone is hemodynamically unstable. Uh But there is a pulse um you can uh cardiovert them or you can start them infusion. Uh If someone has P you decide your CPR uh I do what, what Ross told you to do um earlier and then the last one, can I decide that is basically your, what looks kind of like chaos? That's your VF uh that's your bit of bit of panic. That's your chaotic um irregular deflection. So yours is a very varying amplitudes. Uh Your amplitudes will eventually decrease with duration. You have no identifiable P waves, not really identifiable kind of perfect complex QR S complexes or T waves. Uh You need to start your ACL S as soon as possible cause otherwise you don't really have patients reverting back to normal rhythm from um VF. Um And then the next one and just quickly through the answer, it shouldn't take us more than 23 minutes. Um So we got a 45 year old female patient on uh on the ward. Um A review of the patient's medical record shows that her systolic BP was greater than 140 at both her last clinic appointments. Her medical history is significant only for diabetes. Her BP is 1 64/90. What is the best step in her BP management. All right. Just so. So we don't go over by too much. Can I have the next one? OK. So the correct answer here is C so start an ace inhibitor. So this is someone who's got um hypertension, uh who's also a diabetic, which is important in the question of this context and who's under 55 years old. Um Generally what we do with patients who are um who come in and have high BP. All you need at the beginning is repeated measurements. So as you're gonna encounter on the wards, uh if you've got patients coming in the BP, they don't like hospitals that are a bit scared of why, why you need to see them so often, I've had patients in my preoperative clinics whose BP was in the 100 eighties, 100 and nineties. Uh But if you, they do it at home, they send you the readings and it's like 120 or 130 it's absolutely fine. Um So you need some repeated measurements. So you want them to do it at home. Um Or you just ask them for several measurements whilst they come to, to your clinic or GPS. Um And then if they're persistently eve elevated, then you start with management options, you can go to the next slide. So first with all the management, you've got your three options. There is your conservative, there's your medical. Um And then you've got two options. Um, I think, uh, if you've got your medical options, sorry, conservative options. Um, you've got several, um, possibilities. The most effective is asking them to, to lose weight if they're overweight. Um, you've got your, uh, dietary changes that are also very effective and then you can do some things that are less effective. So, try and eat less salt, increase the physical activity and decrease your alcohol consumption. But in most cases we go to medical treatment. So, can I have the last note? I think that's my last. No. Mm, you're still there. We give you. Yeah. Yeah, we can hear you. Sorry people, we'll, uh, we'll be finishing up. Um, he's disconnected. He might, he might be able to rejoin if not, this is the last slide anyway. So we can just briefly talk through it. So, yeah, this is just a treatment of hypertension. Um So again, just following the algorithm. So, yeah, if they're less than 55 we're starting them on a, on an Ace inhibitor or if they're diabetic. Uh, otherwise if they're over 55 and the oh Ace back there he is m anyway, I'll keep going through it. Er, otherwise we'll put him on a calcium channel blocker. Um, and yeah, we just need to follow, I think the most for exams, er, exam purposes where they'll catch you out the most is where they'll give you a potassium level and they'll be at stage four, uh, and they'll be asking you what to add in. So it all depends if their potassium is over and above 4.5. So if it's less than 4.5 then you consider starting something like spironolactone, um, or if it's over 4.5 then you would think about starting something like a calcium blocker or a beta blocker because, um, that's not going to impact your potassium level spironolactone is potassium wasting. Um So you don't wanna be lowering it if it's, even if it's low enough as it is, otherwise you could see on the right hand column, er when or what sort of BP targets you would aim for. I'm not gonna go into too much detail cos we've, we've run over quite a bit. Um So otherwise we will finish the session there. So thank you very much. II apologize. I realize we went quite a bit over time. Um Thank you very much for those of you who stuck around towards the very end. I appreciate it. Me and Ed would be immensely thankful if you could fill out the feedback link. So I remember when I was asked to do that and I never really seemed to give a toss back then, but now you, you actually realize for our portfolios and stuff that is immensely helpful. So I would really appreciate that. Um If you've got any questions, I'm happy to hang around for a few wee minutes, um, and happy to answer them in the chat or if you wanna come on the mic. Um, otherwise, yeah, we will end there. Oops. Sorry, I think we are disconnected again. Oh, yeah. Yeah. Sorry. We're just, we were just finishing up. Don't worry. I went through the last slide. Oh, amazing. You're the best. Thank you so much. Thanks everyone. I hope it was the least remotely useful and good luck with everything. Yeah, good luck with your exams guys. You smash it. I'm just saying. Um Yeah, if anyone wants to answer questions, we're happy to hang around for a couple of minutes. Uh, where will recordings be updated? Um, uploaded? I think Harry said that um, earlier on. I'm not too familiar, I imagine. Um, if you signed on with an email, you'll be sent a link uh, afterwards. I think it might actually be if you fill in the feedback as well. I can't remember if sometimes it's like that. Um, they'll be sent to you via an email most likely. Um Yeah, they'll, they'll share you. Yeah. So that's what Harry says. Um, they'll share it with you. So if you've signed into this session, yeah, don't worry the the will be with you in a bit, right? Otherwise I'm not seeing anything in the chat. I'm gonna end it there. See you later. Have a goodnight everyone. Thanks so much. See you. See you. Bye.