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It, it will start to record. OK. Yeah. So can you change the slide? Have you, can you try? Mm How do I do that? If you say, can you see the number I II if you cannot see the slide number, then definitely you can't. Now, I can't see the slide number. Can you see the slide number? No. OK. It's fine. Then he me it means he can't. OK. So what do you have to do? I would say you can open your laptop as well. OK. And then um so you can open your s um laptop and you can take the slide and then um you can uh you can read from that as well during the presentation. That's OK. Yeah. Yeah. Uh My video is supposed to remain on uh Should I put my sorry? Should my video be on? Yeah. Yeah, it's on um I it it's up to you definitely doesn't matter. OK. Yeah. Thank you. So we start um at nine o'clock. Yeah, we'll see whether the other people they already joined or not. Mhm People you can shake. OK. So I think we have almost 15 people already joined. So um Yeah, we'll start nine o'clock. Ok. Right. Uh, hello, Kennedy here. Hello. Hi. Yeah. Can you hear me? Yeah, I can hear you. Ok. So I will say you can unmute yourself. Ok. And then, uh, and then if you just kindly have a look at the chat box in the meantime. Ok. Ok. Ok. And then, yeah, um, in a minute I will start the presentation then. Ok, thank you. Mhm. Yeah. Um, I think um we should start now. Otherwise we're not gonna able to finish on time. Um go good morning and good afternoon everyone. I hope all you are doing well. So I'm so happy that um we managed to organize another teaching session. Um And also I'm really grateful that my colleague, Doctor Kennedy kindly agreed to do this um to participate in this session as well. Um So, um today, our um topic is um that we will discuss about the interpretation especially to diagnose both cardiac arrhythmia and ischemia along with uh relevant uh management. So our learning objective is that um I hope um you will um able to understand and interpret common um E CG readings related to cardiac arrhythmia and ischemia. And also you will able to diagnose with different types of cardiac arrhythmia and ischemia accurately using E CG readings. And also to learn about the latest management strategies for cardiac arrhythmia and ischemia. Um And I hope um to uh it will help to engage in clinical case discussion for enhancing practical understanding and decision making skills in managing cardiac arrhythmia and ischemia. And also um you will gain a good knowledge that how can you apply the E CG interpretation in different clinical settings for effective patient management. So, our presentation um the isn't uh today is that um first of all, uh we'll discuss how to do the basic E CG interpretation and also common practical challenges while interpret E CG. And also that's important um problem is that um acute Coronary syndrome. So we'll discuss about more details about the evaluation and management of the um acute Coronary syndrome. And also we'll discuss heart block and conduction abnormalities, common brachy arrhythmia and common tachyarrhythmia. They take, you can have a li um you can encounter when your daily practice. And also we'll discuss more about the, you know, how to, how do you evaluate and manage this kind of problem and um in between our presentation. So I, I'm aiming to do one hour. And then after that, we'll give 10 minutes break that was basically suggested uh um from the feedback that we got uh from the last time. So we'll keep short break at around 10 minutes. And after that, uh my colleague will do another one hour uh presentation. So if we start from uh what is E CG and definitely we all know. So the E CG is um uh is the test that you can check your ele your heart's electrical activity. And um this is um in a, an, a noninvasive easily available test to diagnose um and monitor heart conditions, specifically. Um any heart arrhythmia or ischemia, the importance of doing the ecg interpretation correctly. Um That is uh is, it is very important because any misinterpretation can delay your care, um delay care or provide inappropriate treatment and can have life threating consequences for the patient. S um So, um if we say that ecg we all know uh in our, from our medical school that we learned that there were some OS in the ECG strip that you, you all, we know that is um you know, P wave um and then you have pr interval, you have QR S complex, you have ST segment and you also have T UF and it usually the labeled as um you know, P QR S and then T and then UF so the but important thing is that um I will say in order to understand my rest of my presentation, I will say please keep in mind the is line in the ECG which is a flat horizontal line when there is no electrical activity. So you have to remember and you have to know who, which segment should be on the is electric line. So I would say you should remember that point and also you should remember J point as well because when usually we see um we said uh we mark the ECG with the different um you know, marker like P or, or whatever, we usually don't know, don't mention about the J point. So J point is very, very important. Um So what is J point? So J point is the age of the QR S um and the beginning of the elevation and is at this point is, is you can say it's like a dot So it, at this point basically located on is electric line. So in order to understand the any cardiac ischemic changes in the ECG, we should be um very careful to understand about the J point because it will be, it will give you um a good idea to understand and interpret the ECG uh very quickly, especially if it's any, whether there is any ischemic changes or not. So, um so if I go sorry, I just uh wanted to mention another thing in um So what are the measurement usually use? So, you know, we use the graph paper we usually use to um record the ECG. So in that case, we all know that there is, there is a small scar and there is a large scar. So one is small scar uh equal to one millimeter. And then whole ECG paper usually is three like 25 millimeter per second. So one second, whatever the reading we got, we have it, it usually cover 25 millimeters or it means 25 small boxes and one is small square if you um uh say um that uh if you, you want to calculate the timing, so it will be like 0.04 2nd. So what is normal ECG looks like? So I will say the normal ECG we know all the P wave. So you will see the P UF that is positive deflection. And then you can see the QR is complex. Um And also you can see the, where the uh QR is complex finish uh means end, then you can see the J point and also you can see the ST segment. So um so the beginning of the J point and then you can see um so from SS and um um and the beginning of the T year, we can see the ST segment. So the important thing is that in is this is, is that pr segment, you can see that is on the is electric line and also your J point and also your ST segment should be in the is line. So that is important. And then rest of that wave like P wave or QR S and um the complex and T wave it will be either it will be positive deflection or it could be negative deflection. Um But uh it will not be in, in I normally, it will be not in the acidic, acidic line that is important. So if you, if uh if you do the daily practice, um I would say 95% patient or maybe more than that patient will have the ECG in the hospital. I mean, so whoever they admitted in the hospital who comes to eat it, um there's so many reasons we usually do the ECG but be honest, um you will get so many CT S for almost um 95% of patients. And then what happens usually does. So for the junior doctors, um for example, does not, they will do the E CG and they will bring you and they will say, um can you just sign it this E CT? So the part was because um um the purpose of signing is that you have to find out whether there is any problem acutely. So that's why the nurse usually bring the ECG to the doctors to find out any medical problem or any emergency that we should be aware of as soon as possible. And so we can take the action. So that's why they bring the ECG to the doctors. So definitely you will see the ECG and then you have to interpret it. So I will say whenever you see the A CD, um the way usually we interpret and then um it advised by the A course as well. If you, if anyone does the A course already you can see in the A book, they suggested some tips like what are the way that you can um um you can read the A CD. So I will say you can see just um negro. The first step is that is there any electrical activity? So that is important. If there is no electrical activity, it means you'll get the flat line. So this is just only you will get the is electric line. And that is that's condition we know all that. Um that is, yeah, so it means that patient is already date or patient has a cardiac arrest and that is nonshockable rhythm. Ok. So that is uh that is the thing. So you should have a look first, whether there is any elliptical activity. Next step is if there is any electrical activity, then what is the rate? So, um it is important to know whether it's um fast or is whether it's tacky or bready. What, what is the rate exactly? And then the next step is if you know that is there is a rate definitely, you know that, right? The question is whether it's a um it's a rhythm, what is the rhythm? So whether it's irregular or it's irregular, that is important because if it's regular and then patient has the like tachycardia like past heart rate, then you shouldn't be too much worried. But if this patient has an irregular heart rhythm and then now you have um um uh we know, so a and then now you have to be worried like whether it could be like PSA or um and also there is um you know, sometimes say you can see like SVT as well. So just you have to make sure that this is uh what is the reason and based on that you can uh categorize or whether there is um uh what you have to, you have to take it. And the next step is that your QR is complex. So that is important. It's very, very, very important, especially if your Q QR is complex, is a narrow or is a broad, that is the thing you have to know. So usually the QRS complex duration is 2 to 3 millimeter. So it's a 2 to 2 to 3 boxes that is normal, it more than three boxes, small boxes, then it means more than three millimeter, then you can label it as a broad QR S complex. So that case, so your diagnosis will be different as well based on the QR QR S complex duration. And also if it's narrow, it's like it's a very narrow, like less than two, then you have to think about if, if you, for example, if anyone has a narrow complex and then you have the heart rate is a bit high and also your rhythm is for example, regular, then you can think of it could be um SVT or if you rhythm is irregular, but heart rate is high and your cure is complex is narrow. Then you can think of is um if so my colleague will explain more about them all the um you know the I sorry T and, but I'm just, just uh telling you that the way the importance of um interpreting all the complexes. Um So this is the QR is complex and after the QR is complex now you have to focus on P wave. So where is the, is there any actual activity? So whether you, you can see pu or not, if you can see pu. So the first thing I should say, just diagnose pu or not, if you cannot see POF, then that is different problem, you know, that's a common problem is f so if you see the pu, then problem can be different as well or it could be. Um so that can, so if you see the P that you have to make sure whether it has correlated with the ventricular activity. So ventricular activity definitely be presented by the PR is complex and act activity is present by the pu. So you have to see whether P PU is following the QR is complex. If it's not following, then definitely uh that is another problem, another arrhythmia that is abnormal. Um And so we'll explain more about later on. Um No. Um So the next slide, basically, I just wanted to see some measurements. So um we have so many things to explain today. So I will, I, we already put some of the slide, but we don't want to explain, I will say for your information in your free time. You can have a look so self is starting. Um So this is just normal E CG that um um so it explained the duration and with the segment and um you can see the P RPR segment and also ST segment both on should be on the is electric line that is important to know. And also you can see the J point as well in this slide. So mm just one thing from this slide, I should say that um how would we say usually um whether it's T segment division, whether it's ST Y um means how do you measure that is still elevated or is still depressed? So I'll say uh usually the way we usually measure based on the PR segment. So pr segment is our, the Isac line that is the scale. So if that um if your ST segment above this line, uh then that is the elevation and below this line, then ST depression. But based on the how um how high this um elevation based on that, you can say that whether it is significant or not, we will explain shortly. So this is the normal inter I mentioned, if anyone interested, you can have a look as well. Um So next thing I will explain about a little bit about is elevation. So um so I already mentioned that, how would I measure the elevation? How do we know that is elevated or not? So, based on the pr segment or is line. So pr segment we can say is um uh you can make uh you can think of this is a uh along the is line. So based on that, you can measure on that one. So how do you know whether this ST est segment elevation is um significant or not? So, use it if it the segment um if it's elevated more than one millimeter or we can say one is small box um in two or more contiguous li limb leads or greater than two millimeter or two small boxes in two or more leads in the chest lead. So usually in chest lead, especially in V one and V two, V one to V three, if you want to see that, uh they still uh if you see there's still um segment elevated more than two millimeter, then that is significant. Uh But in li lead or in, in uh you know, uh 13 and then every and that um sorry, 123 in that lead, um then it has to be one millimeter or mo more than that um elevation. So you can say that is significant. Um So um definitely elevation is um measurement is very important because it usually caused by complete full thickness marker infarction. So this is acute AMI and then you have to take the action as very urgently. So, um now it ST depression. So uh again, so the, the ST depression will be significant if it is depressed, like uh 0.4 0.5 millimeter or more. Um um And definitely it has to be um in two contiguous leads. And um and depression, you all know that it was significant because it's uh it indicates marker ischemia. Now. Um uh No, so I will just talk to a little bit about the tr because T is also sometimes indicates that um you might have some, um you might, might have a test M I as well. So, uh so um how do you measure? So if in your limb lead on 123 and if you, if you see that your limb lead your um um tw is more than five millimeter, then that is significant that you should think of. This is definitely TB is um tall. So TF could be tall because of two problems. So, um if his is tall, we usually called hyperacute. So, in that case, um in that case, in um that situation, you could think of whether patient has any hyperkalemia or hypo or hyper A A I and but if in chest lead, uh you just need to make sure that it has to be more than 10 millimeter. Um it, it has to be more than 10 millimeters in the chest lid. Um So it just uh so now we'll say now the common problem that you can see. So for example, if anyone asks you to take the ECG, we know how to interpret. That means uh we don't, we, we can go through uh um the basic interpretation. But the problem you will face when you uh see that ecg that um um lead mis displacement that is very common problem. You take, you can see um it's not too common also as well, but you can see that often. And so you can have uh uh it, it can, it, it can maybe see that is um benign early depolarization or high takeoff or um J point elevation. So that is problem. Um um We'll, we'll explain more details about it. So I will just say, first of all, if you have, how do you know that your mis mis displacement? Um So in order to know that your lead miss displacement, you can see that um um the common, I should say just look for R. So if you see that a VR lead um I II, usually if it's any dis mis displacement, you will see that it become or everything is positive. So you, you can see that um QR is complex is positive. So in that case, you can easily identify that this is one of the tips that you can have a look and you can. So definitely this is um a mid displace. Um So this is um a mis displacement of the lead. And then also mm uh you can uh you can have a look, there are some bit complicated finding. I don't know, ii, to be honest, I will not remember any of them. So you can say it said a lead one is completely inverted. Um Or sometimes you can say there may be marked uh right. But I would say it's easy to remember that you can say that your um um just on a just look at the A VR whether there is all the uh if it's uh everything, uh if it's positive, then definitely you have to think about it. This is likely mis diss and then you can ask the nurse to just guide it and they can do it again. So, um if you see the plasticity, this one and then you can see there is II, if you see the lead too, it looks like a little bit, you know, uh elevation and then um because of the mis dis you can see some of the invasion in uh V one as well and in uh VF you know, V four leads. So it will give you like II you can think of maybe it's um it, it just um um so some non elevated Mr looks like or maybe it elevated Mr as well. So it's a bit confusing um um picture. So if you after the correcting the uh placement, you can check the ECG, it's, it's just normal and this patient basically has a normal, just af but there is no elevation or any to in not like that. So, the next problem is benign early repolarization. So that is um important to know because it just um mimic the pericardial is um it picture and also it mimics with the um it's elevated in my picture. So that way it is very, very important. OK. So um so usually this kind of picture, you can see this kind of uh ECG picture you can see um especially with the young people and then also you can see some male innoculate. So what are the findings mean? So why is um what is the main worry? So the main worry is that in this kind of ECG picture, you can see that ECG pattern uh is uh there is a widespread segment elevation. Um And then um a and the problem is um that you can see this kind of picture like with uh 10 to 15% of ed patient presenting with the chest pain. So definitely you'll be confused whether this patient has any EV MRI or not. Um But um definitely the few points that you can have a look. So you can um so they, how would I differentiate whether this is a really elevated A I or not? So that way you can differentiate that is important and you have to remember, I should say in future as well, whenever you just have any confusion about the elevated A I or not, and then you also in your mind, just think about patient. Patient is a young patient and then there is no cardiovascular risk factor patient is having chest pain, but it just E CG shows like this. So you have to think about um whether it is um uh relevant or not. So, in order to know how do you um differentiate, I will say just remember a few points. First of all, um you can say that's widespread elevation and no reciprocal ST depression in any other lead. OK. So there is no any um uh sorry. So uh no depression to suggest occlusion A I and it's just generalized. H the question is whether uh general is common in pericarditis as well. So how would I differentiate between pericarditis and um pericarditis? And um B means benign early report, how can I differentiate? So I will say you can keep in mind. And the thing is that uh that um usually if anyone has a pericarditis, they have pure depression usually as well. So that's the one of the thing you can differentiate. Another thing is that sometimes you might see there is some notching or sliding at the G point in the inferior lead. And sometimes um you can see that with more prominent in um uh he four as well. So I will show you the ing so usually you see um uh this is, so if you see this V three lead, it's um so you can see it's um the way it's presenting is definitely like concave you know, the shape is the elevation. So, um and then if you see the next one, basically someone mentioned that it could be like the, the way it is still elevated, the morphosis looks like that is smiley face. So you can see that it looks like it smiley face. So the concavity um upwards um and then also there is some notches as well. Um So, um especially it more prominent in um lead V four. So you can see there's some notches, where is the JJ point? So in that point, uh II, this is the way that you can differentiate, this is benign polarization. Um And then yeah, so this is the nose you can see. So the not um at J point and is in 34 with a fish hook morphs characteristic of the B er and this is, this is a common E CG that you can have a look that is um B er um So um I already discussed like how do you differentiate the pericarditis? Um the same changes usually happens to pericarditis. And also B er so how can you differentiate? I already mentioned you can see the pr whether it's depressed or not that is common in Pericard. And also there is another parameter you can use as well. So um um ii it's usually that is called ST or a slash TU ratio. So if less than 0.25 then it then that is consistent with B er and if he pericarditis, then um ST um slash T ratio will be um more than 0.25. And now, um so how would I calculate the um this ratio? I'll say it's, it's already explained here. If you have time, you can have a look quickly later on. And um this is the my uh this is basically real patient that I um so I attended one Met call. Uh Then um so there was a one patient, a 35 year old gentleman presented with a chest pain in Argenti GP Clinic. So uh our gen GP clinic just next to our hospital. And then they put the med call because patient, they think patient had them. Um It's M I so um so when they put the med and we went and see the ECG and then it shows like this. So patient is pretty young, is 35 is very young, doesn't have any risk factor. But with this ECG, so um we discussed with the cardiology consultant quickly as well, like uh but definitely we are worried because whether it's a hyperacute um elevated edema or not. And then definitely the consultants say they have experience. So they, they know very well. So they said um no, it doesn't look like but do the troponin. And then based on the troponin, if it's um normal, then it is not significant. And then we did the troponin, basically, it was normal and patient was patient doesn't have symptoms that any chest pain at that time as well. And then patient basically said discharged by himself because um he was maybe not convinced as well that he had a heart attack anyway. So um so this is the way that um you can manage this patient, this kind of patient as well. But I will explain the management later on as well. So I will say, mm the important thing is that um if it's a young patient, I will say keep in mind that um it could be not a elevated M I, it could be something else, especially it could be. Um um you know, so how do you manage? Definitely, if you see this kind of um CG definitely would would we we just need to make sure we're not missing any urgent things because this can be lifethreatening as well if you miss the any M I and patient might have cardiac arrest any time. So just make sure you shouldn't miss any patient E elevated M I. So um usually b er is not a problem. But recently, there's some studies shows that there is a link between the benign and the early pattern of the E CG. And also there is some risk of idiopathic ventricular fibrillation. So they found out some patient has a cardiac artist who had uh before this kind of um ECG picture and then now developed um uh cardiac arrest and and they have um ventricular fibrillation. So that's why um it's with um uh it's scary that um we should do something. So it says like usually you shouldn't do, we shouldn't be worried if patient s less than 50 but patient is less than more than 50. So I will say we should investigate further to make sure there is no any ischemic heart disease um or no, any other patient has any um you know, any other um especially we, we have to consider whether patient is having, having any risk factor for ischemic heart disease or some and then we can, we can treat accordingly. So if anyone has the card b er before and then you, you you had the cardiac arrest, definitely if you know that story, then in that case, definitely you have to put the ICD um for that patient. So um I will say what is the Andrick? So if you, if you, if you see this kind of picture, then in that case, I will say no, just do the troponin, OK, take the proper history, definitely do the troponin and also repeat the E CG to see any um evolutional changes. And also ask um the expert opinion. Uh definitely you can speak to the cardiologist as as well, especially if patient has a like typical cardiac sound chest pain and also patient, his troponin is high. So in that case, I will just ask them uh whether they really want to do an investigation or not. Um Yeah, so this is the way that you can manage the b er, so now I'm going to talk about um acute coronary symptom um that you all know, that's the basically three different types of um traditional types of co acute coronary syndrome. Uh that is medical emergency and that is important uh for everyone that you should diagnose early as soon as possible. Um in order to avoid um any delaying of the, any treatment. Ok. So the first um uh type is um um so what are the types? So um it's ST elevation M I. So that is um uh one type and then another one is non elevated ami and another one is um unstable angina. So um it is important to differentiate the three different types of A CS because it will tell you what is the exactly exact plan of management you should give this patient. So if it's, for example, if it's anyone has the ST elevated M I, then um II, we have to consider about the rehab sc therapy and PCI as soon as possible. A as we know that the C point value is two hours. So within two hours, you have to send this patient to cat or primary PC or primary PCI center for uh PC. Now, next, the next, the other two types is nonelevated Mr and unstable enzyme. In that case, you can have some time but it's a advisable that you should start the treatment as soon as possible, especially medical treatment and then you have a little bit time so you can um just reassess and then cardiologist can see and then can they can consider for mm you know, further um um management plan. So based on the patients um history, patient's comorbidities and everything. So they will decide whether this uh these other two types of A A CS, whether they need any further interven intervention urgently or not. So, um so I will say um II will explain a little bit later on how gonna we differentiate all three kinds of um A CS. But I will say it doesn't matter w which kind of a CS you are saying it means dealing with. So the presenting complaint and then the evolution will be the same. So the evaluation, how do we evaluate? So you do evaluate by, by taking the history. Definitely. So the patient will definitely come to us because patient has some um usually um patient has a chest pain, that's where they come. Sometimes the patient might come because there is some incidental ECG findings. So that's why they come. Uh Patient doesn't have any symptoms now but GP did some uh did uh E CG or someone did the ECG for some different reason and they found out something in the ECG that that's why they sent to you. B So it means uh any chest pain or any uh suspicious. This is your findings. It means you have to evaluate, you have to consider this patient has any ac or not. Ok. So how do you evaluate that history? So if patient has any symptoms, then you can ask and evaluate the symptoms. So especially the chest pain, um uh you know, this is common presentation. Also, you can consider some atypical um uh symptoms as well. For example, someone said, ok, especially, you know, atypical chest pain, like burning like epigastric s um epigastric burning pain. So, in that case, um uh that is common uh that is very common in elderly people, you know, diabetes, patient and also women. So, um so you can, you can consider that symptoms, you should ask the symptoms as well and also you can uh ask for any breathing problem or not. So you have to take the details history. So I will say in order to differentiate whether this is cardiac chest pain or not. Um um you, you just ask few of the component of the history. One of the component I would say very, very important that is exertion, whether patients uh symptoms is worsened with exertion or patient's symptom, the way patient uh all set of the symptoms was after exertion. So that is very, very typical cardiac chest pain. And then also you can ask um whether it was a relieving factor. So the the relieving factor might, they might say, ok, after having the GTN spray, they felt better or, or maybe pain completely gone or sometimes they relieve it factor could be like for example, patients like after the exertion patient started to have the pain. But when the patient um was taking the rest patients, uh pain feels better. It means this is this is still cardiac pain, but that is as stable angina. So, so and the importance of uh we're doing the differentiation is that so it will tell you and also it is important to know the details about the frequency of the symptoms as well. And also you should ask patient whether patient has any symptoms. Now, whenever a patient presenting to you, you should ask the symptom uh presenting symptom, uh whether it's any ongoing symptoms or not, that is important and also definitely any other symptoms associated symptoms, especially you should ask whether patient feel like bit sweaty with um you know, cold clammy. And also sometimes they feel like they're about to die, sometimes they feel like as well. So um y you can ask all those history as well, especially sweating, you know, a little bit of um bit dizzy or maybe presyncope um that is also important as well. Also sometimes they feel uh sick, feel sick as well. So those they are vomiting, you should ask those symptoms as well. So these are the associated is important to um you know, to establish your diagnosis. And then, so once you get the history. And then definitely the important part of the history is that patient past medical history. So that is very, very important, especially if the patient has any cardiovascular uh disease before patient, whether the patient has any um um like any um M I before or any um PC or anything done before any coronary artery bypass grafting done before or not. So this is very, very important and then you should ask about the details when it do oh, when it was done. And then um the other thing is important that is the other comorbidities. So you uh comorbidities is important and also the performance status as well. So the comorbidities is important. For example, if anyone has the cancer and this is metastasis, cancer patient, uh uh you know, the prognosis is very poor and the patient will die maybe in one in one. So usually if it's like uh the patient prognosis is less than one, usually this patient is not suitable for PCR. So that's why it's important to know. And also if you um you speak to the cardiologist, they will always ask you about the definitely past medical history and also the um you know, the Park status as well. If his annual Park status, you know that I like it very bad, like it's not independent. Uh they, they are requiring too much help for doing their daily activities. So if his status like three or four So they will just say, you know, they will, they will evaluate anyway, but maybe this patient will be not suitable for the PCI. Ok. So this, that's why it's important um to take all the history. And also definitely um last but not least that you have to take all the risk factor of cardiovascular risk factor history as well, the diabetes, high BP, high cholesterol or you know, family history as well. So, and then after the checking the history, definitely you will do the examination. But in order to examinations as your um it's just normal examination you will do. But in order to I'll say make sure that um patient is not any shock. So es especially patient is not on any cardiogenic shock. Our patient doesn't have uh for example, features of heart failure. Our patient doesn't have uh like any murmur or anything, any new. Because if the patient, if anyone has a chest pain and patient is now having this new old like patient is in cardiogenic shock or patient is having um like new heart failure features or uh any other problems. So in that case, you have to think about this, the way that patient had already ami N is now developing complications. So in order to just diagnose the complication, you have to, you know, do the thorough examination um in, in, in view of just find out the the complication of the AMI. So um then after the examination. Definitely, you can just um think of whether the patient is on uh on a high risk or not. So in order to uh do the risk assessment, like whether it uh why it's important to know the patient is, has the high risk of A I or patient is high risk or risk of patient already, for example, maybe had the A I. But whether is there any future high risk of death? because of the A I see. In that case, it is important to know because it will tell you that uh how soon we need to do the intervention. So uh the hormone um risk uh model we usually use to assess the risk is that is um grace risk score. So I will not go through everything because uh you can have a look and you can do the Google as well. So you can have a look. Um uh and then usually they usually see some of the parameter based on the parameter. They usually um do the scoring system. So the importance of doing the risk um crazy score is that it will tell you whether this patient um um like has a risk of six month, you know, the uh the patient. Um So it says like uh six month risk of death. So it will uh tell you um the severity of the problem. And then also we have another scoring system that is TB scoring system. So it will tell you like um uh for two week risk of death or A I in two weeks time. So usually use uh we usually use grace score and then um that I already mentioned that the role of these scores in, in the A V. How soon do you want to do it? Sorry, I didn't realize that II haven't changed the light. Um So what are the, so you have already, we have already taken the history and everything. So I would just say definitely you have to evaluate the risk factor for A CS. We all know that is factor for A CS is the older, is high BP, high blood, um high cholesterol. Uh There is smoking, lack of physical activities, uh diabetes, family history. Uh If you, if you anyone has a family history of heart attack, less than 50 years obese or uh around 50 years obese, then you have to think about that. They are um they are high risk of developing ami as well. So for example, after taking the history and everything, so you do realize that this patient might have cardiac sound, chest pain. So it's suspected a CS. So what other investigation you will do? So the investigation, we usually we do that. Um That is, I will say two investigation is usually enough. So one is to in order to uh in order to confirm your diagnosis. So if you take very good history, that is 50% your job is done. Another 50% is that if you do your ecg and uh troponin, then another 50% will be done to confirm the diagnosis. So the um so you will do the E CG and troponin definitely. And then we usually do the other test as well, especially if you're just not sure whether this patient is having any other lung problem or any other cause condition is causing this chest pain. Usually we do the chest X as well and also usually do the blood test. That is routine blood test, including CRP and then you can do the coagulation and venis as well. So why it is important? So, um if it's anyone has the infection, it's like high inflammatory marker, especially if it's more than 50 CRP. This patient is not for PC until unless your infection is getting better. And then if you have like uh and then also you have to see the kidney function as well, you have to see the uh patient platelet count and everything to assess whether this patient is suitable for angiography, whether you can give the anticoagulation, whether it's safe to give the anticoagulation as well. Uh And also uh that it is safe to give antiplatelet therapy. So that's why it's important to do the blood test as well. And also sometimes we do echo as well, especially if patient. Uh for example, it's like oral is M I but I'm not sure because this could be maybe patient doesn't have new E CG changes or maybe patients. Um it's a bit like confusing situation. In that case, usually we do the inpatient echo to see any disor wall motion motion abnormalities. Uh uh So, so if you, if you do the, then it will tell you if it's any ischemia or not. Um In that if it's anyone has ischemia in the particular part of the heart, then it will, that that part will not be moving. So it will be like hypokinetic, so it will not move. Um You know, the heart is always pump, isn't it? So it's moving all the time. So the particular area will be uh they, they will see if there is a hypokinesia. So in that case, um sometimes we do the echo but it's definitely not always. So, so now I will discuss more about this elevated A I. So, so how do now we'll just learn, how do we know this patient has the elevated MRI as per your E CG findings. How do you know because II just mentioned that E CG and troponin that is enough for your investigation. I will say uh means to diagnosis your condition, but I will say in, in, in order to diagnose TEV A I, your ECG is enough and then based on the ECG, you have to take the action, you don't have to wait for the troponin to come back. It doesn't matter whether your troponin positive or not. But if you see as a junior doctor or, or anyone, to be honest, if you see the ECG show just only limited in my picture, then you have to take the action and the rest of the thing you can do later on the other investigation. So, so that's why it's important to know how do we interpret, how do we know this is elevation in mind? So, um I would say um so the first thing is that I will say you can focus a few of the things. So I will say if you see the ECG and you are planning to find out the uh still and I will say focus three things. One is whether there is any gross elevation in any lead as already, I explained that. How would you know this is elevated if your in your limb lead, if your ST is elevated more than one millimeter? OK. And if you're in a chest lead, especially if you want to V three, if you see that um your ST elevated is more than two millimeter. OK. So in that case, and it, it has to be two an contagious leads. It means it has to be like two leads, not like only one lead randomly, not like that. So and it has to be the same, same surface lead. For example, if it's um V one, it changes. So it has to be B2 B3, not like um uh one is in uh uh there's some still you can see in lead two and you can see some elevation in V four. It will not be significant. So it has to be, it, it has to be like the same anatomical area and then same um so same anatomical area uh which is correspond with the, that lead. And then that is the one point you should have a look. The next point is that just have a look quickly whether there is any ST depression in V one to V three. Because if there's any ST depression in V one to V three, it will tell you that it's posterior mind. And the third point is I will say look for any new lip bundle brows block. So, so that's it, that's the, if you sort it out three things, I mean 33 features then uh it's done. So it means you, you will able to diagnose this patient has a still edema. So I would say you should do the practice like this. So you just um make a habit that whenever you see the ECG just look for three things first, it's still limited. I used to be honest, I as II usually don't bother about taking the rate and rhythm and everything. To be honest, I just usually try to focus whether the patient has any elevation or patient has any ST depression and we want to B2. Um if you want to be three or patient has any bundle block. If it's not, these three features are excluded, then OK. I have been II can consult in the rest of the things. OK. You can have no time. But if you have three things like in the ECG, then you don't have time. So you have to take the action um quickly and then um uh the other things you can have a look as well. Um You know, to diagnosis elevated A I that is a reciprocal ST depression and T inversion. Also, you can have a look pathological as well. So based on that definitely your time up on set of your patients symptoms and the time you are doing the um ECG based on that um you can see some other changes like as as I mentioned, like pathological Q wave or T wave inversion. So that is um um normal coronary artery anatomy. And then, you know, the relationship of this anatomy with the ACG leads we all know. So I just um put it as a reference so you can have a look later on. Um So now I will just um is another that I put this slide for a reference as well. So I will say in order to diagnose the elevation, just think about um your is line. So you know that your aspic line and also think about your J point, where is the location of your J point and your uh shape of your ST OK. So ST se shape of your ST segment. So for example, if you see uh this, there's so many more of ST elevation, the same, same um so whatever is present in your ECG, it will be counted as at elevated A I. So if you see that all ECGS, so the first one it mentioned, that's the, the first ECG is mentioned that is um conventional is still limited. It means in that case, your J point will be um will be um elevated. So it, it's not definitely it's not in the isolated line. So usually your J point will be in the isolated line. But if you see they still A I, in that case, you will see your J point is elevated. And then after the J point, you can have a look. What is the morphology, what is the pattern of your um ST segment? So if it's uh sometimes um you can see uh uh show the more other point as well. So if you see this slide, um you can see there's a different morphs. So it, it says that in acute elevated M I basically may produce a EV with either concave, convex or obliquely straight morphosis. So it could be um so it could be obliquely straight or concave as well. So that's why, but usually it could be usually maybe common is convex, but it is the concave as well. That, that why it is a bit confusing with the ve polarization G. So that could, so it, but it could be con anyway, so it can be any shape. But usually this is the common um E CG um you know, the more as you can see in the elevated MRI patient. So now next one is I showed that is if you have posterior M I, as I mentioned that in from P one to P three, just look for ST depression. So this is a common picture in ST depression. Um um if you have posterior M I, but definitely it's important to see where is the ST depression. Um uh whether it's definitely it has to be one to P three leads. And then this is the evolution of AMI, as I mentioned that based on your timing, you can see that um time of onset of the symptoms and based on the time that you definitely done the E CG and based on the, based on that, you can see there'll be different, more fluid and different changes of the elevation. So um initially, if within minutes, two hours, you can see there initially just started to have ha have hyperacute ta and then uh you can have a look that um uh within 0 to 12 hours, you can see that it's just segment, it started to elevate. And then after one to within 1 to 12 hours, you can see there is AQ sa pathological Q wave and then after that, you can see that's pro elevation M I with T infarction that is common, uh you know, findings in elevated M I. So I also mentioned some of the other causes of elevation. Um But to be honest, in practical point of view, you if you see any M I just make sure this is not a CS, this is the main, main purpose, the rest of the thing. Um the cardiologist student, to be honest, diagnosed, that's all the condition, but I'm not too, too much worried about other problem. Um So that I just mentioned, so you can keep in mind. So, um and also we, as we, as we mentioned, there are so many other causes of ST segment um elevation. So, but uh in that case, the morph a little bit different. So you can have a look the morph if, if Penny carat is usually this called give shape. So if you see the j uh we can see that J point is elevated, but there is some uh if you see the ST segment, it looks like more concave, concave are poor. So it is very typical for um you know, the pericarditis patients and also pericarditis, we know that there will be widespread still. So this this um the still will be will affect all the leaves, not only just um you know, the particular uh surface, not like that. So it it will also help you to differentiate and also we already discussed about the B er and um uh also my colleague will speak to you about the left bundle browns block and everything. OK. Uh So definitely if you see that is still elevated M I, which is very straightforward, you know, this is you can manage quickly, you can send this patient to cat lab. But if it's any other changes, especially if it just only segment depression or um uh so in that case, or maybe just nope in. So, in that definitely that is the common CG findings for non elevated A and I was stable. So I will say in E CG um uh So if you do the ECG for uh uh the patient has a, for example, chest pain and you did the ECG and it shows um maybe normal or maybe it shows some like nope to, to, to inversion or some nonspecific a depression. So in that case, we'll say that is um likely diagnosed is elevated and stable angina. But the way you just only differentiate that whether this is non, is still limited A I or uh unstable angina that is troponin. So if your troponin is high, then that is known is still limited A I. But if your troponin is normal, then that is unstable angina. But ECG changes usually will not able to help you to differentiate whether it is non, is elevated or unstable angina, just only blood test. So there's a couple of the ECG test. I um you know, just um put, just to, for reference, so you can have a look. So that is inferior M I. So you can have a look the um L2 3 and um aVF. So there is a, you can see there is some ST um and elevation, you can see the morphs is uh just to start a little bit uh con cave shape. And then the important thing is that you can have a look where there is some reciprocal changes. So if you see the A VO so um so if you see that in the uh lead A VL um and also um lead to one as well, there's some reciprocal changes, there's some ST depression. Um and then this is high lateral A I. So you can see it's a elevation in lead to one and also lead A VL. Um there's some changes in V four to be successful. So that is um that is uh highlight I, so that is post I. So I just mentioned that we want to be three. You can see there is ast depression and that is very, very typical of her. Um It's elevated um uh means this is a elevated M I definitely there, but that is posterior M I and this is um this is the E CG from my practical life experience. So uh another M call we got from urgent GP clinic. The patient was 48 year old gentleman came with a history of um chest pain and then uh they did the ECG and then it shows there is a uh still a patient in V two V three. And you can see um uh so this is AP one mil and then V one to V uh V two and V three as well as there is a mild reciprocal changes in lead two of especially lead three. we can see there are some little bit ST depression and also lead um two as well. Ok. So that is um another um an T or M I um E CG. So um as I mentioned, there's another investigation we should do um to confirm the diagnosis that is troponin. So we already discussed about the ECG that is first primary investigation. The next investigation is troponin is important. So, um but just keep in mind that troponin can be limited for so many reasons. That is very, very important to remember because in every day practice, believe me, you will see so many patients with troponin elevated but there is no any um basically coronary artery disease. But patients is because of so many reasons. The important uh usually uh scenario we usually see that is patient has a kidney problem. So patient has a renal failure. So they usually have the troponin high as well. But so many other reasons can cause that to put in high. So the important thing is that, for example, patient has um um hypoxia a patient has in a patient is, has an infection patient uh is in shock. Um And that can cause cause the troponin high as well. Even if you have anyone has the like sub he and then um they can have have the high troponin as well. So, so, so just keep in mind um that it can be elevated. So, so in that case, definitely it would not be significant. So, um so how do you evaluate? So for example, you were su from your history from your ecg findings. So you just said, OK, I'm suspecting patient has the A CS. So I will say if you have a CS and it is elevated M I, then you don't have time just send this patient to Cath Lab. So you do don't have to worry about that patient anymore. But uh if, if, if you have other two types of A CS, then how good are you manage? The thing is that the question is whether we can send this patient home, whether we can keep this patient in the hospital, if we keep this patient in the hospital and then how long we'll keep this patient in the hospital? So that is another question. So in order to in order to know like, what would I do, what would be the next step? So I will say is based on your patient, you know, the current presentation for example, patient had the pain and everything was suspected CS. But now patient currently doesn't have any symptoms at all. And you did the ECG it's normal or it could be some changes, but your troponin is normal. So it means your diagnosis unstable enzy. Then in that case, patient doesn't have any symptoms at this moment. Now, so what gonna we do? We say we should admit this patient um and then we just observe 1212 hours and then we can send the patient home based on that assessment on that time. Definitely. And then now the next question is, for example, patient has known limited a and patient has the um um you know, the troponin high as well. So what would we do in that case? Definitely, um you have to admit the patient and I this patient needs um urgent treatment and everything as well. So this is the way that you can think of. So it means I'm just trying to say you that um based on your diagnosis either you can um you can prioritize. So if it is, this is your first priority, then one is still limited and your second priority and you're on stable and is your third priority. So, um but usually all the patient will be reviewed by the cardiology. But what you can do um at the beginning, so I will say um you uh especially if you say you have IDE so you can start a treatment straight away. So that is uh in order to start a treatment, you have to give loading dose aspirin, 300 mg, andre 1 60 mg uh straight away. And then you can just, or this patient uh you have uh you know, the transplant to the Cath lab. So it's a so whenever the, wherever the hospital you work, you should know where is your PCI center. So um in our hospital, we have the different protocols. So we usually have like until five o'clock. So 9 to 5, we have the PCI. Um uh uh we have the cat lab, they usually um do the PCI. And then after five o'clock, we have to speak to the another hospital. Um then um so if it's anything, any, any, I usually just uh call them and then um we just trans organize the transfer to the patient to them. So while you are waiting for the transport to patient to the PC center, I will say in the meantime, make sure you give this loading dose of, of dual anti plain, also keep patient um in cardiac monitor bed because if patient, anyone has a elevated aide, they are more prone to develop of any arrhythmia at any time. So just need to make sure you, you keep this patient in a cardiac monitor bed and also um you can give some symptomatic treatment. So for example, if it usually it is very common that patient has um the chest pain. So you can, then I, in, in that case, you can give some IV morphine that is usually a 10 mg you can give and then um it also helps uh to reduce the oxygen uh needs in the heart as well by reducing the sympathetic nervous system activation. So that's why uh it's preferable that you should give morphine rather, rather than giving any other painkiller and also give us some antiemetic as well. Because if he give morphine, it can cause um nausea, vomiting as well. So just make sure you keep that one, they are vomiting. So you have to keep that antiemetic as well. So if patient has a low is elevated M I, so what would we do? So if it known is M I or unable angina treatment nearly the same, but just approach a little bit different or prioritize, it is a little bit different. So I will say in both cases, if it's a non limited Mr and stable Angina, just start the medical management. So the medical management for everyone is nearly the same. Like you have to give aspirin 300 tag, you can give 160 miligram loading dose. But usually uh if the patient is for PCI, as I mentioned, we shouldn't give um uh coo we shouldn't give anticoagulant straight away because this patient will go for PCI. But in case of your is still limited Ami and on his table and we usually give the paradox as well uh because they will not go for the PCI um urgently. So, yy, you can just keep that one straight away. So, and now as I mentioned that usually, no, you have to admit the patient in the hospital. And also you have to evaluate all the symp you know, the uh patient has any uh persistent, any um pain or anything. Uh in that case, um if patient has ongoing symptoms and patient is unwell, then you have to uh you have to prioritize that. Whether it's this patient might need um PC within 24 hours. Ok. And sometimes usually if patient doesn't have that much pain and patient responded with the medical treatment, patient was a little bit stable. Then in that case, uh PC should be done usually within 48 hours of presentation, but patient will be in the hospital for inpatient uh you know PCI. Now he's unstable are the same as you mentioned. So medical treatment you can start. And then the question is the, if anyone has un and the question is whether uh with this patient needs to be in the hospital um and then whether need inpatient, any investigation or patient, any PCI or not. So usually it says that usually we monitor for 12 hours and definitely based on the monitoring me means it will evaluate the patient. If patient has ongoing signs, symptoms of ischemia or infarction, then you can consider for in inpatient invasive um eny that is PCI if patient doesn't have any symptoms, for example, patient is um is stable, is ok. And then in that case, you can send patient home with outpatient investigation, like it's just A and CT coronary angiogram and then you can just uh do the cardiology, heart clinic, um you know, outpatient uh referral as well. So they will have a look but if patient on a stable angina and but patient has some ecg changes as well, um then also patient has some significant risk factor. But for example, patient has the um already had a little diabetes, BP and everything. So in that case, if it has a significant risk factor, then um you can um you can consider of doing uh we'll say um all the investigation especially uh preferable investigation is a stress sequence order or prior to discharge. Ok. Um but uh definitely you have to assess are usually ii usually, usually guided by the cardiologist as well. If he's anyone who has recent PCI or cardiac bypass, I'll say just make sure he should seek for help as soon as possible because this kind of patient, they are very, you know, um more prone to um develop another um you know, the cardiac events again. So we just need to make sure that you seek for cardiologist advice as soon as possible. So I will say tricks about diagnostic cardiac ischemia by signs and symptoms and it is interpretation. So what is, what is, what is your focus will be? So I will say your focus will be just take the proper history to establish your cardiac chest pain. And just keep in mind that that will be like um usually cardiac chest pain, usually exertional and also really by GTN. And also then just um don't forget about that typical chest pain patient might have just only shortness of breath and you could have patient could have some A CS. So just make sure you um just keep in mind that one as well. And also I will say when you see the A CG, as I mentioned that uh just remember three things and if it's three things sorted, if there is patient doesn't have that um three features, then just constant, you can just think of, OK, you can, you can be relaxed and it can consider the other findings. And also I will say if you see ECG and then you can see that it's not, for example, but it just ECG some shows some ST depression or t inversion of some, some know specific changes. So I will say it's very, it's preferable that you always compare this ECG with the previous ECG. So the E CG will be uh the previous E CG will be available in the system. So you can double check whether the same changes or not. If it's same, then you shouldn't be worried this is the chronic changes, uh nothing will happen now. So this is not um uh any problem at this moment. So, and then uh and I also mentioned that um troponin basically only can differentiate, known is elevated amount stable angina. So because in ECG could be normal in both cases. And um you also keep in mind troponin can be elevated for so many reasons. And then I will say um ask for help if you, if any confusion. But it's still despite him uh doing all this, uh there are sometimes uh most of the time, I'll say it will be might be difficult. For example, if it's uh is it like um usually the new left bundle bronze block is important to because it's mimic that elevated M I. But how do you know this is new or old? So that is very difficult question. So I will say in that case, if there is no previous G available and you don't know whether this is a new left bundle bronch block or not, I will say in that case, do the troponin quickly if it's troponin high and then new left bundle and then this is um left bundle bo block and then this is this will be significant. So you can take the action accordingly. And always, if there's any confusing, you know it M I, then I will say you can speak to your senior. And then if to be honest, if you are senior. Then in that case, I will say we should speak to the cardiologist. Um and also you should do the troponin as soon as possible. Um And I would say if you have any confusion about the elevated M I, please start the treatment and no one will blame you. Espe especially just give the loading dose. No one will say you to be honest that you did wrong. OK. So um this is the way we can deal with all the cardiac chest pain and the E CGI relevant E CG findings. So I think I have already taken 10 minutes more. So we should go for break now and after 10 minutes we'll start um the next part. Um And my colleague will explain about all the heart block and conduction abnormalities and arrhythmias. OK. Thank you. Can you can you hear me? Yeah, I can hear you. OK. Uh So is there any questions I sh I shouldn't. Um I didn't ask. Uh No, I think uh in the chat box. None at the moment. Sorry, no questions on the chat post. OK. Um Out here pa was talking about uh a slide which was talking about evolution of stemming. Uh I should say evolution. That is mistake. Sorry. Yeah. What is the question? Yeah, I think uh let me check with the same person. He said, if you go to that side, he said, so would you be able to go through identifying the QR S complexes place. Um um We slide, yeah, this, this uh evolution. Yeah. Yeah. So what is the question she said, uh would you be able to go through, identify the QR s complex place? I think we will have to do that after we come back from the break. So that would be around um OK. 10 2, 1022. It, it means of uh whether we can identify the QR is complex in this um oh my God. He said, please go through what is the P wave QR S and S ti think he's talking about basic explanation of uh the waves of um of the um G I think you can just go when we come back from break, just show them the, the upward deflection of the P wave QR S complex. And then, oh OK. So um because it's just the basic explanation of all the waves and the, no, I think it's on that slide once, identify the QR S like different waves for the QR S on that slide. Mm I think I will go, that will be the first, maybe one of the first ECG S. That's just the basic waves of No, no, no, no, no. I don't think that is the question. The question is this one. No, no, not that, not that I think the question is on that evolution of uh CRS of uh stemi. He wants to know how to identify the different ways the the one that is Q, the one that is the one that is not on this basic one? Oh OK. Yeah. As I said uh in the, what is the QR s here? OK. OK. So the, the, the problem is I can uh I cannot um use the mouse, isn't it? So you cannot figure out um you know what is the exactly location you wanted to show them? Do you understand what I mean? So I would say we can see that QR is complex but how can I trace that? I mean, how, how can I show them? I think uh maybe next time. Uh So how to use the mouse? A pointer. Yeah, exactly. A pointer. Exactly. Very, very important next time for the next presentation. Uh uh um I think, yeah, we, we should have a look at that one to be honest. Yeah, I would just say you uh tend to eat after the break. Um um I think the patient is listen to us so they can because they are sending for no of um comments. So if you can just move back to that um to that slide. Yeah, we talking about evolution. Um Yeah, I'll go back. OK. So we can see. Um OK. OK. This one. OK. Yeah. Yeah, I think the, the, the, the thing there is that the Q wave uh I think the thing I want you to know is that, that it's not everywhere they have Q, in fact, most of the QR S companies don't start with Q wave. So, yeah, exactly. Yeah. So uh like there is a PT with now, I think it's only as the, is that, is that a key wave? Now, can you point out that one? I can point, I'm talking about the, the first one. OK. So first one, it looks like pathological Q wave, isn't it? Maybe, maybe Q wave or a deep S wave. Yeah, exactly. So, yeah, so that is at the confusion. So it could be Q wave or, you know, a deep S wave. Yes, maybe that. Yeah, exactly. But you can see if after that wave you can see some J point and also your point basically. Yeah, it's March with the TF Yes. Exactly. Yeah. Like an indentation. Yeah. So, exactly. And then the other one, the second one, the second box talking about the ST elevation, I think um the Q wave is the, you know, the, the, the first part um elevation followed by a uh convex um uh elevation. I think the one that, the way that comes down that comes down between the he in the, in, in the limbs of the hem that will be the S wave. Yeah, that would be the S wave. And then the ST elevation is the one that uh goes up uh uh in a convex manner. Um Yeah, and that's the box. And uh the third one, I think. Um the first uh downward deflection, the other Q wave or deepest wave, as we said earlier in the first box. Yeah. So, but it says it's key wave. This one, it said it's Q, this is the key. Yeah. Clear cut Q. Yeah. You Yeah, exactly. Yeah. Clear co Q wave. Yeah. And then you can see the J point as well in that, in that. Yeah, in that complex you can see the jet um J point and then it's elevated and this is a little bit convexity rather than concavity. Can you see that it's elevated? It is more like more convex rather than concave. Yes. Yes, it's more convex. Yeah. Yeah, that it's indentation. Yeah. So um and the next one is, is definitely there is a QR S complex and then rescue. Uh the person said she got it now. Oh, sorry. We tried to explain. I'm so sorry, just uh you know, we cannot point out. So that's the problem. But thank you so much for your patience. Anyway, everyone is uh um it just listening so patiently. Yeah, it's difficult because you cannot participate, isn't it? So that's another problem. I think eventually they will maybe update in some point um in future, maybe they will update that the, all the people that can participate. So let me just go through the comments again. Someone said two in late in a patient with chest without any abnormal e abnormality. Uh I'm just trying to see what? Ok, can you use a, uh, let me just tell them we are sorry, we can't use this this time around. No, we can't use it. That's the problem. I'm using it. Um, from my mobile. It means I'm, uh, I logged in, in my mobile and I'm doing the presentation. Yeah. So that's the problem. I think next time you want to try with your computer it makes life easier. Yeah, I think so. No, no, that's true. Yeah. So, um is it 10 minute already? Yes, we just explained verbally. Ok. The person say it's, it's the AQ wave that was convincing. Yeah, I think we've cleared that whatever it is, it's uh that would be two negative deflection either or the best wave. But it, it, it's immaterial anyway to the diagnosis. So I think um uh uh you can start now. It's 10 minutes already. We are starting now. Ok. Sure. Can you ask, can you to join, sit down here? Uh So would you mind to start then? I think we should start on who do not? We are still online so we can start first? Ok. So I'm going to change the slide. Yeah, I will help you to change the slide. Um Yeah, you're gonna stop. Ok. Uh Good morning, good afternoon. Depend on where you're listening from. As I continue to what my colleague discussed this time around, we want to talk about some arrhythmias and some conduction abnormalities. And we'll be starting with heart block. So as we all know already, the heart blocks are divided into three. Basically, we have the first degree A V blocks, the second degree A V blocks and then the third degree A V blocks uh just more like a summary of them or the first degree A V block is just when there is a prolonged pr interval, she already explained the different parts of an E CG. And uh the different, she, she started out the P waves, the KRS complex and the T waves. So when the P, the uh the interval between the P wave and the PR complex does the pr between the P and the R is great than 0.2 seconds. We say the patient has uh physically have block. Well, in second degree heart block, there are two different types. You have the one we call the Mobi type one and I Mobi type two. I Mobi type one, we notice a progressive lengthening of the PR interval. And after a while, we will see a nonconducted B wave whereby you see the PR interval, keep increasing with each beat. And then subsequently, we see a dropped beat. It is different from the Mobi type two whereby there is uh and in and dense dropping of the ventricular conduction, we see that the PR wave is very constant but the PT is very constant. And then after a while you have some drop beats one in 10 degree A V block. There is no relationship between the PWA and the RS complex. OK. So just a little bit on an in depth description. The first we have block. First of all, we should know, like I said earlier is when the parental greater than 0.2 seconds, that is about five small boxes. So whenever you have the parental admitted than five small boxes, then you, you can say the patient has a physically a block in basically a block. There is a delay without interruption in the conduction from the atria to the ventricles. And it said to be marked if the period is greater than 300 milliseconds that uh 0.3 seconds. So uh there are a lot of causes of physically a block, but we need to know that it can also be normal of a, a normal variant in certain people. But then you can also find physically heart block in patients with some electrolyte disturbances like hyperkalemia and those who take some a blocking drugs like beta blockers and digoxin. Then like I said, it's normal, you can get it to some outlets and it can also be an indication that someone has an inferior M I or post retro surgery. Then the first a block is an isolated finding and most times usually benign and does not really cause any symptoms or any stability. And then most times we don't treat them. Ok. Uh I want to show the presentation of the, the next slide list. Yeah. So uh looking at these slides, uh like I said, the pr interval is prolonged, usually more than five small boxes. And if you look at the place where the P wave was isolated between the P wave and then the arrow wave, you can see that it's over five small boxes. And then in uh index A CG, the one on top, you can see that the P RT is more than 300 millisecond, 0.3 seconds. And because of the distance between the P wave and the uh arrow wave, you can see that it's almost embedded in the pre P wave. So the one below is a, an of a patient that has sinus bradycardia which basically the avid blocker by the parent is more than 300. Why? This is uh patients with normal sinus shading with uh Yeah. Next one. Yeah, this uh a patient with a normal sinus rhythm with first degree heart block invariably when the uh PR interval is greater than 200 milliseconds. So going to the second review a block, we said it has two types, you have the MOS type one and then the MOS type two. So I Mobi type one. Like I said earlier, there is a progressive prolongation of the PR interval followed by a, a nonconducted P wave. So you get to see uh AP wave without a EKK complex. Following it and they need to know that the pr O interval is usually longest immediately before the drugs beats. And then the shortest is that after the drug beats means that with each beat, the pr interval keeps prolonging until it's, there is a disappearance of a carious complex and then the cycle continues again. So, but then, uh we also need to know that the easiest to whenever I look at an, the way to notice that a patient has uh some uh secondary a block of type one, you see that the uh carious complexes are usually lodged into clusters and they're followed by short spaces. Like you can see that they are, you look and see if they are clustered in one place. And then after you see a small space and then you see on that cluster. So that's the first thing first play, you get whenever you get an E CG of a patient that has a second degree A V block. And then there's another thing we also need to know is that the P to P intervals are despite uh as uh P to P intervals are constant. That's why glides in the curious complex. So in as much as that, there is a drop beat, a drop in curious complex. If you begin to make sure the P to P interval, they are usually very constant. OK. So this is another uh of a patient that has second degree A V block of the movies type one. Like I said earlier, the first thing that will catch your eye when you look at this kind of ECG is how the complex are lodged into clusters. And then you see like a gap, then see on clusters, I see like a gap. So that's how it appears. Yeah. And then if you look at the uh uh yeah. OK. If you look at the uh P waves, the pr you can see that they keep increasing. I wish I had a s they keep increasing with each beat until final. You see car doesn't Yeah, this is different from uh Mobi type two whereby there is a constant uh pr interval and then unexpectedly you have a drug beat, you have ap that wasn't conducted. So, but then uh looking at the mechanism whereby these things happen, you see that in type one, it's usually occurs you to a reversible conduction block at the level of the A V node. So a multi type one, you see that there is malfunctioning of the A cells. And since they are malfunctioning, they progressively get fatigued or they fail to conduct an impulse. But this is different from the uh Hispo system that tends to fail suddenly and unexpectedly. Like you don't, it's not like mo like why is that the cells get getting fatigued, fatigued and then they don't come up. But this one just happened abruptly. Uh which is, which is which makes it more serious. OK. So like I said, difference between the Mobi type one, Mobi type is a Mobi type one is that there is progressive prolongation of the period before you have the drop speeds. But in MOS type two, the period remains constant and then you suddenly have dropped speed. OK? So uh these are other concepts when we talk about uh second degree heart block and it's what we call fixed ratio, a blocks. The second degree heart blocks with fixed ratio could be, it's usually a ratio between the DS and the complexes and it can be 2 to 13 to 1 and it can even be up to 4 to 1. And then it can either be due to Mobi type one or type two conduction. So this is a, an E CG of uh like a victoria presentation of a patient that has uh the A 2 to 1 block. If you calculate the atri rates, you can see it's about 75 bits per minute and the rate is about uh that's eight bits per minute, meaning that you can see about two D US before a KRS complex. So if you look at the ECG clearly, you can see the QR S complex well delineated, they can see the T uh T wave and they can see there are two T waves before each K Rs complex. So that's why it's a 2 to 1 block. So the next slide also shows uh an E CG of similar presentation. You can see the uh let's look at the two, which is the strip, you can see the KS complex was stated that uh well represented and they can see it as a at wave after the K RS complex. And you get to see two other P waves before you get under carriage complex. So because there are two P waves to one K RS complex, we call it a 2 to 1 block. So it's one of the fixed uh blocks. So the next one, you can also see in the next slide that there can also be a 3 to 1 block. And in this case, you can see that A I rates could be probably 90 with ventri being just one third of the uh atrial rate. And if you begin to look at for, for from, from the diagram given from the EC GS given, you can see that there are three different P waves. But then it seems that the third P wave is almost embedded in the, in the uh previous, the top period is almost embedded in the uh T wave. So, but then incidence, the A rate is three times that of the me because you get to see three P waves before each P RA is complex. So uh still part of the fixed ratio A blocks, you can have what we call high grade A block where you have up to 4 to 1 conduction ratio by 4 to 1. I mean get four P waves before a cars complex. So because of that, I can see that the rate is about 1/4 of the Atria rates. And from the Victoria differentation, you can see that there are four different B waves before you have a conduction that before you have a conducted that you have a complex. And then most times the first one is also embedded in the uh presidency wave. So under close to I'm sorry to interrupt you, there is one question that what is the reason that wave usually get invaded into T waves? Sorry, it says. So the question is the question is what is the reason that P wave usually gets embedded into T waves? Is it just due to hyperactive atria? Yeah, it's due to hepatic atria because you know what happens in uh uh for example, what happens in second degree A V blocks is that there is usually failure of conduction at that level. So the atria is more, most of the things actually in the Atria are not conducted to the ventricle. So the chance is due to like essentially due to a hepatic uh atrial. Yeah. And then most of them are not conduct. Yeah. And most of them are not conducted to the Yeah, that's good. Eventually the car is complex. Yeah. So there's another question, what is the, what is the clinical significance of knowing to each two or 3 to 1 block. Uh The thing about the clinical significance is that uh Mobi type two generally uh sorry, I need to know what they mean by clinical significance. It's just the concept of uh fixed blocks is that it's just a concept here. But remember that irrespective of the uh number of uh how is the number of uh the fixed block? Whether it is 221321421 is still mob type one and type two. OK. So it's still a second degree A V block. And then it's treated as such. I don't know if I answered the question. Yeah, you can carry on now. It's fine, I think. Uh yeah, they got the sir. Thank you. OK. It doesn't have, let me know. OK. So the next slide is talking about axis, I want to another concepts that you talk about when you talk about bradyarrhythmias is to check the axis of an E CG when it is given to you. And then there are two key ways of checking axis in an E CG. The first method is what we call the method. And as I calculating the axis like the proper way to look at an in and know what the axis looks like is by looking at the lead one and then the A VF So when you look at the lead one and it is positive, the next uh lead you need to look at is the A FF lead. If by, by, by mean, like uh before you say a, a lead is positive, we look at the Kr complex and when the R wave is more than the S wave that in terms of number of small boxes, you can say it's positive, it can be when it adhere to the A and then when the S is more, you can say it's negative. So when you look at the first and it's positive, the next thing to look at is the A VF, if you look at a VF and it's also positive, you can say the axis is normal without uh being wrong. And then if you look at the lead one and it's positive and you look at the VF and it's negative. The chances are that the patient has uh left a deviation, which could be physiologic or pathologic. And then when you get a negative uh a negative TRS complex in one and then it's positive in AF patient, you said to have right axis deviation. And then when it is completely negative both in one and a VF, then it says extreme axis. But then the second method which is a three analysis whereby introduce the lead to the lead two. Basically, it's not, doesn't make so much difference from using the first method, but it, that helps us to delineate the possibility of a pathologic of S left a deviation. Remember that when it is positive, um when the car complex is positive in li one, it can either be a normal axis or a left axis deviation. If the uh you check in VF and it's still positive, the chances are that it's a normal ace G or if it is negative, then you can be pathological physiologic. And that's why you look at the lead through. If lead two is epiphys or even positive, then you think it's not a ap left a deviation. But when you look at the true and it's also negative, just like the aVF, then the chances are that it's a pathological that so it's an easy way to actually know the axis of an ECG by just looking at it without having to the axis. So the next E CG just shows us uh I just need to talk just to give us an idea of how to arrive at it. If you look at the little one here, you can see that the S wave, the arrow wave is more than the S wave and it's positively skewed. Like you see that the uh KS on the one is positively skewed. The next one you look at is uh the F and you can see that it's also positive. So in this patient has right, a de so it has a normal axis. But then if you look at the next one, you can see that the uh QR S complex on one is negative. The next place you look at is the AF UF and you can see it is positive. So since uh L1 is negative and it uh the A VF is positive, then you can say the patient has a right, a deviation. Then the next slide, you see that uh the patient has a positive if the person has a positive uh QR S complex on lead one and a negative QR S complex on lead af like the next slide, you would say the patient has a left at deviation. Then the next place you need to look at is the lead two. Why you take the lead two? And you see that like in this case, the next likely. So like this one, I'm trying to talk about like you can see that the lead one is positive leads aVF is negative. So in patient has left a deviation. So the next thing is to look at this lead too, looking at it. So you can see is basically epiphys and that's why you say the patient has a surgical left axis infection. But then if we had dumped the uh lead two and it's negative you that say it's more of a pathological left disease devi it's an easy way of just getting a without even having to go to calculate, especially where in the ED is given to you. So we talked about in this case. Now, I can see that the lead one is negative, the VF is negative and then the two is negative. So that's what we call a stream a deviation. Yeah. So another concept I want to talk about, we are talking about bradyarrhythmias is the uh concept of fascicular blocks. And we have the some blocks, we have the left an club block, we have left club block and uh then we have uh bifascicular and trifascicular block. So as a matter of definition, these are things you find out in an E CG that makes you see a patient has a left anterior fcul block. The truth is that in most ECG S, if you check the block individually, looking at an E CgA, the has left and block, most it manifests as a left axis, uh left axis deviation like we first described whereby you have a positive uh K complex in the one and then a negative K complex in the A VF. So they really have this uh left a deviation in people that come down with a left atrophy block. Then they, they have, they usually have a small Q and AD R complex in the one and A VL. So when they have a small Q and a deep uh that means in the one and A, that means one will definitely be positive, then they have a small R and DS complex in these 23 and A VF meaning that it's gonna be negative. And then in most patients or some patients, they can have prolonged arrow arrow peak time in a field of more than 45 minutes. So when you see a patient that has a small Q and big a complex in one and Avil, so this one is positive and then small R and DS wave complexes in the 23 and A VF, meaning that they are both uh it's negative only 23 and a VF. So most times they manifest as left a deviation as you earlier described. So let's look at some CS like that, that will show more of what I'm talking about. So now you can see in this patient now they have a small AR wave and a deep wave in the two three and F. So making it negative because your R wave is small and S wave is deep. Well, if you look at one and Avio you can see that uh the patient has a small Q and deep Arwa which makes it positive. So in the patient will manifest with uh left axis deviation. So when you see a picture like this, the patient has what we call a left eye as club block, but then like on face, face value, looking at it this way to suggest is that most times it manifests as uh left eye de like earlier described. OK. So if you go to the next slide, it's similar to what we discussed. The patients who have a one, a small Q and deep wave can see how small the Q wave is and then how the wave is that's seen in the one and the A V, then when you go to the two, you see a small R and a deep S waves in the uh three and SA VF. So looking at this uh E CG on face value, the patient has a positive uh KRS complex on the one and a negative KRS complex on the. So the patient uh presents function that look like a left axis deviation. But then in this patient, this patient has a left anterior vascular block, considering the uh definitions we've given already for it. So uh the next slide is just to tell us that the uh the ROF P can be as high as five milliseconds or 0.45 seconds in a. So they have a prolonged AOF time. So the next slide is just to still what further portrays what an left and Asri look looks like you look at the uh small arrow uh small QR wave when you go on an A VL and then the sa small R and DS complex is in the 23 and A VF and they can have the prolonged arrow wave in A VL which is at 45. So why you have this in an E CG which manifests as left axis, as you described as a definition of left axis when you have this kind of thing. And E CG, they can say the patient has a left anterior for block. So that's for the left and blood block. But they will have the second uh one which we call the left postal block of the can also be blocked. And then in left postural blood block, they usually manifest as right axis deviation. It's almost opposite to what we get in the left anterior vascular block in this case. Now, the uh lead one and the A VL will not have a small R and a deep s while the uh inferior leads will not have a small Q and deep arrow wave. So it's like opposite. This is more like a sharp contrast, the opposite, same thing we have in the left vascular block. So when you have a small arrow and deep s complex in lead one and A VL, and they have a small here and deep arrow wave in lead in the inferior leads, then you will now see that manufacture has the right axis because lead one will now become negative and then uh the VF will not become positive. So that's what was going to give us a picture of a right, a deviation in patients who come down with left antivascular block, who the first E CG after this is a Yeah. So we can see in this patient that this patient in lead one and lead A L, we can see that the QRS complex is negative because the arrow wave is small and we have a very deep s complex, a very deep wave. Why the uh inferior leads? We can see that you have a small Q wave and a very deep arrow wave in lead. 23. Sorry, sorry, Doctor Kennedy. Do you mean tall wave? Yeah, cause yeah, that's what I mean. Sorry, not deep Arwa sorrys in and the inferior it's just OK. So when you see pictures like this, it's manifests as a right axis deviation because uh the RS complex is negative on one. And then when you look at uh F is positive and then it is positive. So it manifests as a but with these features is uh right at your A block. So under concept is that of bundle branch block. So you can see an E CG shows a right bundle branch block when you have a duration of more than uh 120 milliseconds. And they have what they call a ASR prime pattern in V one to V three which gives it an appearance of an M shaped cars complex in V one to V three. And they notice some slurring of the S wave in natural leads that did one did AF and G six. So let me show you what the end looks like on the next slide. D Yeah. So if you look at this slide, you see what the RSR prime pattern is. If you want to see if you want to view in patients with right bundle branch block. And then there is something we call discordance. When people have a right bundle brand block, there's a concept of appropriate discordance whereby uh we refer to the fact that there is an abnormal depolarization that should follow an abnormal depolarization. So it usually appears to go down to the president carriers complex. So in patients who have right bundle branch block, this appropriate scores can manifest as depression or two in one to lead one to lead V three. So that's why it appears the patient has a negative, it has uh a two in, in the few on this one I'm showing now. So like I said earlier, this RSR prime is seen in V one to V in most patients with uh right bundle branch block while there is some slurring of the S wave in the uh L1 lead area and then five and the electric leads. OK. Then possible causes of right bundle brand block. It's in people with pe uh right ventricular hypertrophy, ischemic heart disease, myocarditis, uh some cardiomyopathies. So in this, that is currently showing now, we've seen a patient that has uh an isolated dry bundle branch block who can see the M shaped K Rx complex in V one in V two and in V three. And when we look at the lateral, it's it's not so evident about, you know, some patients that have slurring of I va V five V six and then one and a V. But in this is just to let us know that it's not always cast in stone. You can see some features that can highly suggest a right bundle brand block without having some slurring. Like in this one, the slurring is not so obvious and it a patient has a normal eye disease. And yeah. So in this one too, this patient has a model brand block. I can look at the V one V two V three where they have the M shaped that the RSR prime uh part time of car complex giving it the M shape in V one V two V three, suggestive of uh a right bundle branch block. And the way you look at the, I don't know how clear it is. The later its look at V five, look at the S UF and V five. It looks slow as it doesn't look as sharp as it's supposed to be. So you can see V four V five, the S UF and V four V five and then V six, you can see how slow it is. So um remember I talked about appropriate discordance in that case, that some form of two infections. So uh talking about bundle branch blocks, uh duration is also more than 100 and 20 milliseconds and then they usually have a dominant in in view one and then the patient can also in the later, this patient can have a broad monophasic arrow wave. It really has different patterns like arrows, but I'll talk about it in such point slides. And then they can have a sense of Q wave in the lateral leads. Why they pro they have a prolonged Arwa peak time of 60 milliseconds and five and six. OK. So uh some psoriasis can cause left bundle block. You can have things like aortic stenosis even in hypertensive. And patients with uh the cardiomyopathy, there are patients with hyperkalaemia and also the gentos can come down with left bundle branch block. But then like uh my colleagues said earlier, when you find a new left branch block in the context of chest pain, uh it's highly suspicious of an I but then you should also have in the back of your mind that so many causes can some of these uh conditions can cause it? And then it's for you to be able to investigate and then be sure that you are dealing with a more benign one. So this like on the screen shows what I mean by a dominant wave in V one and then you can have uh some slurring or some much in uh the later needs. Like this one is what I mean by uh a slow or a broad or not wave on G six or any of the lateral leads. The next slide shows uh next slide. Yeah. So these are different uh car morphologies you can see in the lateral leads. So, like I said, uh in the lateral leads, the Arwa can actually be notched like uh the diagram on the upper left screen. It can also be I have an M shaped like the last one I showed this one showing the A. Then you can also have the RS wave like RS complex looking like this one level in a five. And then you can also have the uh monophasic or the yeah, monophasic arrow wave. So these are different patterns of Arwa you can see in patients that have a left bundle brand block and you can see this pattern in the lateral which are the L1 with A VL and then with five and six. So still as I talked about in right bundle brand block, uh we also have this concept of appropriate discordance in patients with left bundle brand block. And by appropriate discordance, we refer to the fact that there is an abnormal depolarization that should follow abnormal depolarization and then usually appears this going on to the present complex. So we look at the natural in patients with uh uh with store broad airwaves, they have ST segment depression or G invasion. Yeah. So this is like a representation of patients who left bond brand block. Yeah, you can see the small R like the very deep wave in view one. And then when you look at the lateral leads like here showing us V five and V six, you can see the pattern, we have the ra s complex pattern and they can have the monophasic arrow wave. So these are kind of things you see in patients. So when you see a complex monophasic arrow wave in uh arrow wave and marching and all those things in any of the in theater needs, and they now have a deep wave in the U one that is highly suggestive of a left bundle branch block. OK. So this is similar to what we talked about here. You can see broad uh most arrow wave basically in uh some of the lateral, you can see it clearly in uh L1 and then lead Avio and then when you look at the lead V one, you can see a very dominant uh swa and then like I said, they don't know the future is absence of QV five and V six. So we can't even find any uh Q wave in V four, V six. That, that we see in V five can see the arrays pattern and they can also see a monophasic arrow wave in V six. So this is an infection street uh left bundle branch block. OK. Then this patient is, is an issue of a patient that has a left bundle branch block. When you look at the V one, you can see that there is a deep wave sensor V two and V three but then our targets on the V one, which is diagnostic of a left bundle branch block. And they can see the uh uh lateral, it's can see notch in in can see the notch in view one, sorry in lead one. Then can also look at the uh Motha uh arrow in V five and V six, that V five looks more much and then V six. So this is uh suggestive of a right bundle branch block. Yeah. So this is similar, hey look, there is a concept of what we call incomplete left bundle block. Remember we talked about carrier duration being less than uh 120 milliseconds. So when you have all those typical features of patients uh due to features that will find a left bundle branch block, but then the current duration is less than 100 and 20 mills. Then you can say the patient has an incomplete left bundle branch block. So the current duration here is less than 100 and 20 milliseconds. We look at the uh arrow wave, deep arrow wave, uh sorry, deep wave in V one. And then we can look at the arrow wave in lead one, lead A V and then five and six. So this patient has the typical morphology of a low bundle branch block. But then the current duration is less than 100 and 20 milliseconds. So in this case, I can say the patient has an incomplete bundle branch block. Yeah. So now talking, we've talked about uh the 1st, 2nd and 3rd degree A V blocks. We've talked about the uh axis, left axis, right axis and uh ex axis with normal axis. We have talked about the fascicular blocks as uh left avascular blocks and the uh left blocks, right bundle brand blocks and the left bundle brand blocks. So we want to look at what we call a bis block. So patients uh who have bis in that two fascicles are blocked are usually people with right bundle branch, a bundle branch block with left anterior fla block. Remember what I said, like you through the ECG morphology left an F block, it manifests as a left axis deviation because you see that the P wave, the complex is positive in the one and negative in the F. So most times when you have that left a block on the face value, it gives you this left acid presentation and they, they now have feature of right bundle brand block in the same EG that you said the patient has a bi FCI block. Also though less commonly when a future, when you find features of right bundle brand block in an E CG with uh less block manifesting as a right deviation. And when you cannot define another cause the patient has by firstar block. So uh the next E CG. Yeah. So if you look at this E CG, you can see that uh the patient has a left a ation because the QR S complex is positive on the one and negative on lead. VF So that is the patient uh look, look at other features of this and block manifesting as L ad. And then now look at, look for features of bundle brand block. Let's look at uh V one, the N shape, not so clear as you have in which you can see the N shape, the RSR prime in V one V two. And then V three, the way I look at the uh lead one does later, you can see that the S wave is slowed. So this patient has features suggestive of a right bundle brand block and it has a left trola block which manifests as led. So this patient is said to have a yeah by block. So this is a typical ECG here. So in this one, so we can see you the Mr complex in V one V two. Yeah, basically V one and V two here. And then you can see that the patient has uh left a vascular block because complex is positive in lead one and negative in the A FF. So another choice of left avascular block. So because the patient has, yeah, because the patient has features of both right bundle branch block as you've seen in view of it. Yeah. And then you've seen that the patient has left aci deviation. So this patient has bivascular block. So uh this one, you can see that the uh axis is uh negative. So you can see that the axis is uh right axis ation with features of uh uh left and posture fcul block. And then when you look at this, you can see features of uh what do you call it, the effi of right bundle brand block. So in this kind of patient, now, the patient has what we call bis blood block, affecting the right bundle brand block and left block. Next slide. Next slide. Yeah. OK. So talking about Triphala block now uh in block, remember we said that uh two fascicles are blocked or in Tris Club block, the block, the refers to uh the presence of conduction, delaying all the three fascicles of the A you know, you have the right bundle, the left antifa block and then left cul block. So we have this, it manifests as a either a blockage or that is when you have a bis block, which is the right bole blocker and left and block with a third degree heart block. That is one manifestation of a Triphala block. But when you also have a a blockage of the, that's right model brand block, right? For surface block and then with third degree A V block, it's also referred to as TRFA Club block. In this TRFA Club block is just having a patient with bifascicular block coming down with a third degree A V block. So an E showing third degree A V block or shows a heart block with right onto ground block and left anterior or left postural block makes it a trip block. So the first E CG uh it shows a patient who has a trip block. You can see that the patient has features of right branch block. You can see the M shaped pattern in V two. You can see the MS shape pattern in a pattern in V three. You can see the slurring in V five and VC does the S one of the SV five and V six and even in the one. So that suggests a uh right bundle branch block. Then like I said, the left atrophic club usually manifests as left that division. You can see that there's a positive q uh positive carious complex in the one and uh negative in uh AF so that makes it uh left axis and you can see the heart block multiple period. This patient has, I think uh if I look at the OK, the is not so long, but I can see the multiple periods before each pr is complex. So which is suggestive of a heart block. So when you have this like a third degree, a block have left axis deviation. And the right blood block patient has a, a true trar block. So you can see that there's no relationship between the PS and then the QR S complex. They operate on their own. So similar thing to the next slide, thereby you have the M shaped pattern in V two, V one and V three. And they can see some, especially this patient also has uh some left axis deviation. You can see the uh the one is positive and a VF is negative. And then you can also see the uh 2 to 1 block whereby the patient has, yeah, can see, can even say the P wave has relationships with the RS complex. So this person has a bis block and then with a heart block so that making it tr blood block, then the next CGI want to show you is just to let you know that patient can also have an incomplete trar block whereby just having a effect, a block which is a prolonged pr interval of 200 milliseconds with a bis block can also be a trip var block. But since it's now occurring in the context of first degree heart block, then we refer to it as uh an incomplete triphala block. Now, in this E CG, you can see the M shaped pattern in V one, you can see the M shaped pattern in V two V three. And then you can see the slurring in some of the lateral leads like lead one, you can see the slurring of the wave in the A VL so that this patient has right bundle branch block. The axis is uh of left axis. And then if you treat the pr interval, it is greater than a hun uh 200 milliseconds. So this patient has a trip block but it has incomplete because it will occur in the context of degree block. So, but again, the good thing about yeah, the management of patients who have heart blocks and all these uh ranic uh that uh how have these heart block is that many of many times? We don't really do so much about them. Many of them are quite normal and they don't manifest with symptoms. But there are some people who manifest with symptoms, then it actually need to treat. So most patients with AAB block, like I said earlier can occur in alerts, can be a normal of variants and then can also uh signify something more se but in most times, it's usually of no uh real significance. So when patients have fail to heavy block, we don't usually go ahead to treat them. And then especially when you rule out other causes and there is nothing suspicious or anything on to, then you can let the patient be and just monitor the same thing with second degree every block B type one. When the patient does have symptoms like synopia and all that, there is no and we rule out other causes other symptoms and no other thing like that you don't have any other concerning symptoms or any other uh like patients uh essentially don't treat because especially when the person has symptoms. And that's why he now that considering maybe a pacemaker and all that. But then once the patient has a degree, a V block from Mobi type to down to third degree a V block, the patient will need a pacemaker. Then uh like I said, we have to, we have uh a third degree block. You need a pacemaker. They regarding the uh branch blocks to most times when patient is more symptomatic, we don't bother treating the patient. But then when the patient, the, when it progresses and or the patient becomes symptomatic, then we can consider giving a pacemaker and patients with trip Acular block. So it's a pacemaker, but then sometimes when they come in and uh it's not possible to get a permanent pacemaker in place at that time. It's really when they are very symptomatic, you can just put a temporary pacing wire or external pacing and then sometimes the rate is too slow and not responsive to drugs. It can also give a pacemaker. So the uh temporary pacing wire and external pacing are more like uh stop gaps to you're able to get a permanent pacemaker. But the only patient comes in the Ed. It's uh bradycardia most time when they come to the ED is that they have the uh the, the blood syncopy or even palpitations. First thing we need to do is to check the BP and there are some medications we can give, especially when the patient is symptomatic, you can give atropine, which can be given 500 mcg and can repeat it for, uh, after every 3 to 5 minutes to either you achieve a, a good rate or to a maximum of 3 mg. The other options are isoprenaline adrenaline and then of course, temporary pacing. Uh, the MLA shows the, uh, and A G UK guideline on managing patients who come in in emergency with uh adult bradycardia. So when once they come in, we assess them using the primary survey. That's the ABCD approach. Then if, if you feel the patient needs oxygen, maybe the saturating or acu well, we can give and then obtain IV access, then patient should be connected to a cardiac monitor, have the BP checked oxygen saturation to know if it's fine. If it's low, we give oxygen and then record the two of the ECG with that. You can know the particular and the patient has come down with. Then you also try to identify some causes like electrolyte abnormalities like magnesium and potassium, then also check if the patient is already on any previous medications like that can tamper with a conduction. Like all these beta blockers, digoxin assess the patient and the way you look at the patient. And there are evidence of life threating signs like patient is in shock, low BP patient came with syncope and then other features of an M I or even a heart failure, then it's always best you start giving your medications and that's why you start with your atropine, which we can give uh 500 mcg bonus and repeat it every 3 to 5 minutes until you achieve a maximum of 3 mg or you achieve improvement in symptoms. So if you give and a s response, then you now assess the patient for risk of a like, uh it does a recent to Mobi type so that something more serious, uh, complete heart block or even me over more than three seconds. If they are there, then you can also give more medications and then see a cardiologist with you to arrange for, uh, pacing. If your medications have not helped, then you carry it for temporary pacing and keep the patient and then, uh, to arrange for uh, more of permanent, uh, permanent pacemaker insertion. But then if you assess the patient and there are no life threatening signs, just the symptom, just no life threatening signs, just the fact that the patient had an E CG finding of bradycardia, you can just give the person and there are no risk of a, like I listed earlier, just admit the person for observation. So essentially, if the patient has, uh, life threatening features, there is always need to be medication for patient. But then if patient doesn't have life threatening features, just ecg findings, it is just to observe the patient. And then essentially well, patients that have type two tri fcul block or complete heart block, then they will definitely require a patient. So just uh uh thought uh over overview of uh the narrow complex tachycardias. So, uh by N complex is uh my colleague told us when she was uh discussing es generally, that's the normal duration of a complex. So if it's more than 120 milliseconds, then it's now said to be broad complex. So, invariably cardia are less than 120 milliseconds. So look at sinus tardia, atrial fibrillation, and atrial flutter are the key, most commonest ones we come across in a clinical practice. So the first one sinus cardia, cardia can come due to many causes. It could be normal, it could be fever. A lot of things can cause uh sinus ping in patients. Then even patients with uh pe can also have a uh the only finding I find in them is just sinus like cardia. But I'm talking about the common ones like atrial fibrillation, common pathologic ones, atrial fib in patients with af you can see that their rhythms are not regular. And the way you look out for P waves, you might not be able to find any P waves and then you might be able to find not be able to find absence of X baseline. And then you can have variable ventricular, sometimes they have it fast ventricular response. Sometimes it has no response really when someone is already on uh a blocking medications. And like I said, this is a narrow complex tachycardia and the KS complex is usually less than 100 and 20 milliseconds, except when there has preexisting condition that will make it uh broader. Like someone with preexisting bundle branch block. Then the thing about H I fibrillation is that you can also find fibrillatory waves which can be fine when the amplitude is less than 0.5 millimeters. Or it can be cause with of greater than 0.5 millimeters. And then it's always easy to uh mistake defibrillatory waves in A two B waves which are nonexistent in atrial fibrillation. So the E CG after this slide, choose a patient with uh Yeah. So you can see these patients how I OK. Yeah. So you look at these patients, you can see uh the IRI is irregular, it's regularly irregular. And the way you look at the V one, you can see some cause uh fibrillatory waves. So when you see an irregular uh you can look at it down here, you can see an irregular and they can't even find all, you can find a fibrillatory waves, you can't find any B wave. So it's highly so of uh atrial fibrillation. So the next slide is also similar patient has a rate of about 135 BPM. I can also see defibrillatory waves that occurs on the V one, you can see the fine ones and then yeah, no waves, the rate, the uh rhythm is irregular. So that's a significant of af and you can see that the ventricular rate is also high in this patient, he has a first ventricular response. But in the next slide, the patient has af but you can see that uh KS complex is uh sparse. So the patient has a slow ventricular response. So in this kind of patient, it's possible that he has been on medications like beta blocker or has other causes of that can slow the heart rate like uh hypoten and they can see no clearing waves and they can see define fibrillatory waves on the strip. Then another colon uh under common arrhythmia that has a narrow uh complex is atrial flutter. It's a narrow complex tachycardia, usually the atrial rate hits about 300 BPM and there's also lots of iso baseline like in e but the difference is that in this patient, they usually have what we call a so pattern or an inva float and it is true three and eight that in it. And then the floater waves in V one that means PS but there are no PS then differently, it depends on the conduction ratio just like in af So the next slide, you see a patient with uh atrial flutter with 2 to 1 block, you can see the fluttery waves looking at the er, is the two, the three and a VF, you can see the inverted floaty waves. And then while in V one, you can see that it's upright. Yeah. So this patient has got to one block. So the vent rate is about 150. Why? The ATRA rate is about 300. Yeah. OK. So the next slide is a patient with variable block with atrial floater. You can see the inferior leads having uh you can see the in, in, you can see the flu where the T VF as in the future needs, then the, if you look at the red strip down there, that is lead too, you can see that it has, it has variable a blocks, you can see some uh 2 to 1 and 4 to 1 blocks. Ok. Thank you. Hello. Sorry. So if you can just briefly explain the uh the uh the remaining slides, uh because um uh uh we are running out of time. Uh E CG is a very broad topic. So you can just rush through the rest of the slides. Now, just I like the important points and then, so that we can finish. Ok. So, yes. So, so invariably we've talked about the floater and the fluctuates you can find and we just need to know that the car variable blocks and then with different rates. So another uh I want to talk about are the wide complex ones. The ones that have uh a white Claris complex. And then the commonest ones are a ventricular tachycardia and ventricular fibrillation. So, amongst the uh uh the common is a monomorphic one. And as you can see this monomorphic one, they have a uniform KRS complexes within each lead and they, you cannot identify AP wave and just see a uniform mhm oh uniform KRS complex that would identify it UWA and then look at the axis it in the terminate because it's uh negative in V one negative in uh 12, negative in a VF. And then it has a broad complex. The QR S is more than 100 and 20. OK. Then other important uh another important uh tachy arrhythmia is ventricular fibrillation. This one has a chaotic and irregular deflection of ovarian amplitudes. You can't find any people with PR S complex. So you, you can't even identify anything. I usually rates are between like the rate usually between 100 and 50 to 500 per minute and then the amplitude decreases with duration. So it can be caused and it can define ventricular fibrillation. So the next slide shows us a patient with uh ventricular fibrillation. You can see that it's so chaotic irregular, no player baseline and no identifiable PQ. Are you with the next slide? Yeah. So you can see that there is no identifiable PQ RST wave. Everything is OK. No baseline. Just, yeah. So that's uh a patient that has a ventricular fibrillation. So talking about the management of ventricular of uh adult tachycardias according to the air. When a patient comes in, you do your primary survey give oxygen if it's needed, obtain IV access ECG BP like the basic things you do for a patient when they come in, they look out for uh identifiable causes like uh electrolytes like magnesium, potassium and all that are incorrect. Most times a magnesium target is usually more than one in my center. So you, you place an electrolyte that is missing. They look out for lifethreatening fea features like syncope shock, mycotic ischemia. If if they are life threat features like stroke, then patients will need a synchronized cardioversion. That uh yeah, it is correct. But this uh patient has no life threating features, then we use medications. So in conclusion, uh we need to keep in mind that's derisive for doing an E CG and then don't miss a diagnosis of S ami or electric me arrhythmias like complete heart block or even tachy arrhythmias like ASV T and VC. Then you also look for any acute M I features like ST elevation in any lead new left bundle branch block, ST depression in V one to V three. Thank you. So if at any time you have any confusion, you always seek to ask for help so that uh someone who is more experienced in interpreting can help you with the management and the interpretation of these. Yeah, thank you. So I don't know if you have any questions from the presentation, please, if you have any question, please send it in the chat box. Uh, here, if you can hear me, please, you can come up to say one of two things before we conclude the something we can't hear you. Probably your, uh internet connection is, um, not so great at the moment. Uh So that's why we can't hear you. Um, anyway, I think, uh, this is the end of the um presentation. And I, right, if you can just say something in the chat box, um uh because we can't hear you. There's an exclamation mark on your, on your um on your network. So we can't hear you. Can you hear me now? Yeah, we can hear you. Oh, sorry, I just reconnected again. OK. So there's one thing I just want to let you know if you want, if it's any patient is conscious, OK? And if you see this chaotic irregular, I know the QR is complex is an ecg don't diagnose this VF OK? Because this kind of patients might have some, you know, the patient might have some tremor and things. So in that case, you can might see this irregular chaotic um Curis complexes. So any pa patient patient will uh patient will be, you know, the either will be like, you know, cardiac arrest, definitely patient will be unconscious. So that is another errors you might encounter. Um And thank you, everyone. For your patience. Um And thank you, my or um two colleagues as well. Um I hope it will be useful. I uh we definitely, we're trying our best so we'll organize more that we can't still hear you anymore. Oh, sorry. Can you hear me now? Now? We can. Yeah. Yeah. So if you are interested about any topic that is, um, I would say uh medicine related. So that will be uh grateful if you let us know. So we'll try to organize those topics. And also I'm trying to sort it out whether we can ask the, you know, the surgical um doctor or, and gynecological and uh doctors as well to join with us to do their presentation. Um But definitely our aim is to spread the masses that how does the NHS work and also the practical point of view that how we manage all the common scenarios um in your daily practice. So this is our aim. So, um and thank you everyone again and I'll be uh very grateful if you kindly spend your little bit time to give us a feedback. And also, um definitely it's very inspiring that we got a very good feedback last time. So, um um it definitely you an encouraging feature that um we can organize uh that this kind of teaching session again. Um um Thank you again. Um I think that's all. Sorry, sorry, you repeat yourself. Maybe the other part of your uh concluding part. So maybe you couldn't hear you. There was a time we have a, we had to break in your, uh, audio, um, communication. Uh, and I think for, for another, another thing that we need to, uh, do that, I think I'm not sure whether your email is, um, showing in, in the, uh, bio. I think if you can just pop in your email in the chat box so that if they have any question or any suggestion about topics they want us to do, I'll put my email now and you can put your own to, in the chat box so that they can, uh, communicate with us via the emails. Yeah. Ok. No problem. Yeah. So what you said earlier? I don't know. Yeah. Um, I don't know. I think what you mentioned at that point was that we organized more, um, more sessions, uh, with different specialties, maybe surgical team, team and your team. But if you want to, if you have topics you want to suggest for us to, uh, to talk about, you can send them to us via the, any of the email that we put, um, put up there in the chat box. Yeah. Yeah. I think we can end a decision now. Yep, we can end it now. Yeah. Yeah. Yeah.