Home

All you need to know - Cardiology part 2

Share
 
 
 

Summary

Join Misha, a 4th year medical student at UCL, as she delves into the intricacies of the cardiac cycle and ECGs in the second lecture of the series. Gain insights into understanding diagrams of heart pressure, volume and sounds and relating them back to the phases of the cardiac cycle. Learn about the role of the sinoatrial node, the start of the cardiac cycle, ventricular systole and diastole, and ECG readings at different stages. Misha will also help you understand the pressure volume changes during the cardiac cycle and the specific sounds at different stages of the cardiac cycle. This lecture is filled with interactive questions to ensure participants fully grasp the material, and if time permits, it will end with a brief quiz.
Generated by MedBot

Description

All you need to know for your preclinical cardiology exams!

Cardioresp Mechanisms - 10am

Cardiac Cycle and ECGs - 11am

Heart Disease and Heart Failure - 12pm

Pharmacology of Cardiology - 1pm

Learning objectives

1. Understand the phases of the cardiac cycle, including atrial contraction, isovolumetric contraction, ventricular ejection, isovolumetric relaxation, and ventricular filling. 2. Learn to interpret pressure-volume diagrams to depict the key stages of the cardiac cycle and to differentiate between the right and left ventricular pressures. 3. Comprehend the principles of blood flow, particularly how blood flows from a higher to lower pressure and the role of contractions and pressure gradients in the opening and closing of valves. 4. Recognize normal and abnormal ECG readings and associate specific segments of an ECG trace with different phases of the cardiac cycle. 5. Distinguish between different heart sounds heard during the cardiac cycle, including the first and second heart sounds, and understand their relation to the opening and closing of heart valves.
Generated by MedBot

Related content

Similar communities

View all

Similar events and on demand videos

 
 
 
                
                

Computer generated transcript

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

Hi, everyone. Uh Welcome back. So we're gonna be doing the second lecture of the series now um on cardiac cycle and ECGS. So I will let you take over. Hi, everyone. Um So this hour we're gonna be doing. Yeah, cardiac cycle and EC GS. Um So just to preface my name is Misha. I'm 1/4 year medical student at UCL as well and I did my I BSC in Clinical Sciences last year. Um And if you're at UCL and I think of doing that, I would really recommend it as well. Um So what we're gonna be covering in this hour, we're gonna do the phase of the cardiac cycle. Um I'm gonna get the pressure volume and heart sound so we can understand this diagram here and then looking at the basics of EC GS um and some abnormal EC GS and then if we have time, do some SBA S. Um So we have a couple of questions throughout the presentation. So if you just drop the answers in the chat as well, if you can um or just think the answer to yourself, whichever's easier. Um So the first thing, so before we start. There's key things to remember when you come to the cardiac cycle. So blood will always flow from a higher to lower pressure. Um And if the pressure gradient is bigger, that means the rate of the flow will be quicker. Um contractions increase pressure. So obviously, if you contract the atria, the blood will go into ventricles and then valves open according to pressure gradients. So, um if the pressure is high in the atrium, then the ventricles, the aorta, the um atrioventricular valves will open. And then if the pressure in the ventricles are higher than the pressure in the aorta or in the pulmonary artery, then the semi unit valves will open. So to start off with, let's just name the phase of the cardiac cycle. So we've got um the two like phases, ventricular systole and ventricular diastole. Um there's also atrial systole. But in a context, if you were just, if they just say cyst or diastole, they are referring to ventricular syste and ventricular diastole. So we start off with, we have atrial contraction, then we have isovolumetric contraction, ventricular ejection, isovolumetric relaxation and ventricular filling. So, to start off with um if anyone wants to drop this in the chart, uh does anyone know what begins the cardiac cycle? So it begins the atrial contraction if we've had someone say a. Ok. Um So that's a good try. But it's not the ATRIO ventricular node, it's actually the sinoatrial node. So that's the starting one that's at the top of the atria which starts the contraction. Um And that's the first thing that depolarizes. Um sorry. There you go. Uh So let's go through atrial contraction. So that's our first phase in the cardiac cycle. So this first um bit in the diagram on the right. So we have the firing of the sinoatrial node um which depolarizes and causes contraction of the atrium. And we'll go on to more detail. But in an E CG, this is represented by the P wave. So the pressure in the atrium increases and we can see this on the little purple line um on the diagram. And so therefore, the blood moves from the atrium to the ventricles. Um However, this only accounts for a fraction of like the blood, uh the ventricular filling um because most of the blood that's filling the ventricles is from passive blood flow. Um because the AV valves are open. Um However, in when the um heart rate is a lot faster, um there's less time for passive filling. So it's more important and more blood is pushed into the ventricles from atrial contraction. Um And so we can see this on the diagram. So we've got the up to the beginning. So of that first phase, we've obviously got ap wave um and our atrial pressure increases. And so then our second phase, we've got isovolumetric ventricular contraction. So the ventricles er contract and um they depolarize And so at this point, both our atrioventricular valves and our semi Unna valves remain closed. Um And this causes a rapid increase in pressure. And isovolumetric means that no blood is in er ejected yet. And so the volume in the ventricle remains the same. Um So we have this point and then you can see that the pressure increases with that green line. So that represents the left ventricle um in that second er phase of the diagram. And you can also see that the QR S uh on the E CG is at that point as well. And this uh represents a depolarization and contraction of ventricles. We then move on to our next phase which is ventricular ejection. And this happens when um the pressure in the ventricles exceeds the pressure in the aorta or in the, depending on what side the aorta or the pulmonary artery. And you can see that the green line just overtakes the, in this case, the aortic line. So the blue line um and this is when blood is then ejected. And so in this phase, there's kind of two phases. Um so there's rapid ejection. So this is when the pressure in the ventricle is a lot higher. Um And so it forces the aortic and pulmonary valves open. And so blood is like rapidly ejected because the pressure gradient is the most it will be the biggest it will be at this point. Um And so most of the stroke volume has ejected here. Um And this is also where the aortic and pulmonary artery uh pressure reaches their peak. Um And this corresponds to the ST segment on uh ECG. So just keep that in mind. Um And then after that, we have the reduced ventricular ejection. So this is just when the uh there's still blood leaving the ventricles, but it's at a slower rate rate because the pressure gradient is reduced. So um the ventricular volume still drops and you can still see that and it's got like a that second phase in uh systole. Um And this is also marked by the beginning of t of the T wave in uh the E CG. And you can see this this where repolarization begins to happen. Um So then we move on and we have our next space which is isovolumetric ventricular reduction relaxation. Um So again, isovolumetric means means the um volume remains the same. And so this happens cos the semilunar and atrioventricular valves are both closed and you can see that the pressure, so the green line drops rapidly um but the valves are closed. So the volume remains the same. And once uh the pressure has dropped below the pressure of the atrium, this causes the atrioventricular valves to then open. And then we get our next phase, which is our ventricular filling and this is where there's passive filling of the ventricles. So, before the atria have contracted blood is moving into the atrium and into the ventricles as the B valves are open. Um And so in this phase, again, you also have rapid and reduced ventricular filling. And this is just rapid is when the pressure gradient is the biggest. So when the pressure in the ventricles is much lower than the pressure in the atrium. And then as it gradually fills, the ventricular filling becomes slower, because the pressure gradient um gradually in like gradually decreases, the difference decreases. So now that we've had we kind of know the phases of the cardiac cycle. Let's just make sure we understand the pressure volume changes. Um So this is a good diagram to kind of explain it. So if we start off with the green, the atrial contraction, so like our first phase um on the, the graph, you can see that there's the volume is on our X axis and the pressure is on our y axis. So as our atria contract and this is also for a ventricle, by the way, not an atrium. So as our atriums contract the volume you can see increases. So a small amount about a third um increases in our the volume of blood increases into our um ventricles. And then at this point, our um essay, sorry uh semilunar valves and our atrioventricular valves both close and this is where we have our isovolumetric contraction. Um So this is a, you can see a picture, a nice diagram here And this is why the pressure rapidly increases, but the volume changes stays the same um once our pressure has increased above the point. So this is the square on the diagram is where the pressure in the ventricles is higher than the pressure in the aorta or the pulmonary artery. And this is where the semilunar valves then open. And you can see that this pressure is increasing cos of the contraction, but our volume is rapidly decreasing and this is getting rid of the blood through the contraction. So the blood is leaving the heart and this is also the stroke volume. So the volume lost here is the stroke volume. So the volume ejected from the heart. Um then once our pressure falls again, sorry before our pressure falls. So once our ventricular ejection, ventricular ejection is er complete, we see the isovolumetric relaxation stage. So um again isovolumetric. So the volume stays the same, but our pressure rapidly decreases. And that's shown by the straight pale line down. And then as we have passive filling, we've got the atrium is also relaxed at this point. And the majority you can see of the volume that's being uh volume of blood that's entering the ventricles is from the passive filling. And so that kind of shows you um what's happening pressure volume wise during the cardiac cycle. And so the image on the right, the other graft, it kind of shows you the difference between the right ventricle and the left ventricle, obviously, the left ventricle is gonna be a much um higher pressure because it's pushing it around the whole body, not just around the pulmonary system. Um That's the pressure volume changes. So now let's discuss about heart sounds during the cardiac cycle. So generally, everyone will have uh a 1st and 2nd heart sound. Um some people will have a third heart sound and it will be normal. Um And then occasionally people have 1/4 heart sound and that can be normal. But most of the time is indicative of something uh underlying going on. But let's talk about the first two first. So we've got obviously our lab dub. I think everyone should know that at the point when you listen to heart, you hear the Lb dub Love Dub. So our first heart sound, which is the LB. Um this occurs at the very beginning of systole uh as you can see on the diagram and specifically when the ventricle first contracts. Um and this is, this sound is primarily by the er A B valves, er, the tricuspid and mitral valves. Um this is the closure of them, that's what makes the sound. Um And obviously you hit there there to stop the back flow of blood into the atrium. Um Interestingly as well. This is also you can time this with the carotid pole. So you might see cardiologists listening to the heart with their hands on the patient's carotid to check um if there's any delays. Um and our second sound, our dub is, it marks the closure of the semilunar valves. And so this is er, at the beginning of diastole and at the end of the ventricular contraction basically. So that's why it's at the beginning of diastole. Um Yeah. And as I said, it's the closure of the semilunar valves. So the aortic and pulmonary um and same thing, it's to prevent the backflow. Uh And yeah. So where can you listen to these heart sounds? So, on a patient, you'd there's four places generally that you listen to the heart. So we've got on the right side of the sternum between the 2nd and 3rd intercostal space uh and same on the left side. Um And then we've got in the fifth intercostal space, um more medially like by the sternal border and then uh more under the CVI the clavicle. So when we're listening to our tricuspid and mitral valves, you wanna listen to the two at the base of the heart basically. So our tricuspid is where that green dot is um in the fifth intercostal space and by the sternal border. Um and you hear this valve when you're listening for your first sounds or your love. Um And then if you move it along slightly and you hit like the midclavicular space, um sorry, the fifth intercostal space, but midclavicular line, you hear the mitral valve there and that's where this blue dot is. Um and then the same thing for the aortic valves and the pulmonary valves, er, you've got got that yellow, that orange dot which is the second intercostal space and the right sternal border and the pulmonary valve, which is the second intercostal space, but the left er sternal border and this is where you'll hear your S two. So your er second heart sound, so your dubs um and that will be those closing. Um So those are the normal heart sounds. So these are some heart sounds that uh you'll have to know about um that are abnormal. So if we start off, we've got uh aortic stenosis. So this is um it's a result of like turbulent blood flow during the ejection phase. So in the systole uh part of the cardiac cycle um and it's often it's like called a harsh crescendo decrescendo sound. Um I'm not really sure how to explain it but it's good to go in like actually the sympathies on like a youtube video um after to kind of understand the sounds a bit better. Um But you hear this in, there's a nice photo underneath so you can see where you need to hear this. So it's an aortic stenosis. So you'll listen to it where it says a so on the right er second intercostal space by the sternal border. Um and you'll hear this here during systole um and it can also radiate up the carotid artery. So you can also listen to it up there occasionally if it's bad. Um And then we've got our mitral regurgitation. So this is what we call holosystolic. So it extends throughout the whole of systole. Um and it's more of a uh high pitch um blowing sound again. I would listen to these videos on youtube. Um Yeah. So we've got our ma regurgitation, then we've got our aortic regurgitation. So this is a diastolic murmur. So it's from blood flows back into the left ventricle. Um You can kind of hear this and it's good to hear this in the lower left sternal border. Um and it can also radiate along that lower left um side. Um and then with mitral stenosis, same thing. It's also a diastolic murmur and you hear this with ventricular filling and this is um the same reason, obviously blood flowing back er into the atrium, er cos obviously, it hasn't closed properly, the ventricles hasn't closed properly. So those are some abnormal heart sounds to look out for. Um And so before we move on to our EC GS, let's just discuss the cardiac conduction system that kind of conducts the whole cardiac um cycle. So to start off with, we have our uh sa node. So what starts our cardiac cycle? Um So this is initiate, initiates our electrical impulse. Um and it's in the top of the right atrium. So uh good to know where that is um especially when it comes to dissect in the heart, um to know, to preserve it. So you've got your SA node. Um and it's often referred to as the pacemaker of the heart because it sets the rhythm for the cardiac cycle. Um obviously, in a normal patient who's not got any issues with it, um and no severed nerves. Uh so the electrical impulse generated by the SA node, it causes the atria to contract because the um electrical impulse goes down and you've got it through the back man's bundle and that goes around um the atria so that it's uh coordinated in its contraction. Um And so, yeah, so the contraction down there, um then we get to the A V node. So it, the electroimpulse travels down to the A V node. And um this is located between the atria and the ventricles. And what this node does is it temporally delays the impulse. So it allows the ventricles to time to fill with blood um before it then sends an electrical impulse down the bundle of his um and the other branches and which extends into the ventricles and well around the ventricles. Um So the bundle of hi divides into the left and right bundle um and it transmits the electric impulse down towards the apex of the heart and then the purkinje fibers er then spread throughout the myocardium. So, around the ventricles and er deliver the impulse to the ventricular muscles and make sure that it's coordinated and it's contraction. Um Obviously, if there's any non coordination, this is what causes arrhythmias, we'll discuss that in a bit. Um And so after this, and we've had our ventricular contraction or our systole, um and this is, after all, the electrical impulses have been uh um have gone and so on AE CG, we can see that our P wave was obviously our sa node depolarizing our QR S er complex is our um, a V node sending the electrical impulses and the contraction depolarization of those ventricles. And then our T wave is the repolarisation. So once you've had that massive deer depolarization, there's a smaller repolarisation so that this can happen again. Um And this happens during like ventricular filling, er and just after the contraction. Um And then this obviously starts again with the sino atrial node. And I think in the last lecture, um, we learnt the sino atrial node has a rougher depolarization about 60 BPM, obviously, depending on the person. Um and the, the vagus input and sympathetic input. Um, it will differ and whether obviously you're doing exercise. Um But yeah, so that's the cardiac conduction system. Uh And now we can move on to ECG waves. So let's uh label our E CG wave. So we've got RP wave which we know is our atria contracting our depolarization and then we've got what we call our pr interval. So this is the beginning of the P wave to the start of the QR S complex. Um And this is the PR interval, then we have Apr segment and this is the end of the P wave to the start of the QR S complex. Then we obviously have our Q wave, our R wave and our S wave which are RR QR S complex and that's our ventricles contracting. Um Then we have our ST segment and this is the end of our S wave or our QR S complex to the beginning of our T wave. So to the beginning of our repolarisation and then our QT interval is our beginning of our Q wave er to the end of our T wave. So the the beginning of the er depolarization of the ventricles to the end of the repot and so just bear in mind these er terms when it comes to talking about EC GS. Um and when exam questions might ask you um to measure, for example, the QR S complex or the length of the ST segment. Um but this is just a nice image uh on the right so that you can er picture what's happening in the phase of the cardiac cycle with each part of the E CG. So let's learn how to read CG. So this might be catch up for a lot of you. But um so we start off so on E CG paper, this is the same throughout the country. E CG paper is standardized. So we have our small squares which are worth naught point naught four seconds, a larger square which is naught 0.2 seconds. And then that means five larger squares are equal to one second. Um And then it's important to remember this 300 large squares equals one minute because the way generally a fast way to measure the heart rate in AE CG reading in a trace is to do 300. So that large square divided by the amount of big squares in an R interval. And so this is only obviously if there's a regular heart rate. Um So if there's a regular gaps in between, but the RR interval just represents the tip of the R wave. So between two of the R waves, you can see that by the arrows. Um And so, for example, you can see in this one, there's 2.5, big squares. So you can divide 300 by 2.5 and that should give you the heart rate. So, um sorry. So let's give it a go um If you guys want to try this, so focus on the bottom line um and try calculating what the heart rate of this E CG is and then write it in the chart if you guys can. So I give you a couple of minutes to try that and focus on the bottom line. That's our main trace that we're gonna focus on, we've had someone say 100. Amazing. Yeah, exactly. So 100. So uh you've got three big squares in between our RR interval and we do 300 divide by three and that gives us 100. So, yeah, perfect. Um So now, oh, let's try this as well. So this is moving on to our next topic. So, learning about the 12 D DCG um which obviously you saw in that, but how many electrodes are attached to a patient in a 12 lead E CG? Does anyone know C 10? Yeah, perfect. OK, great. So you guys already know all of this. So um this might have caught some people out because obviously it says 12 be CG, you expect 12, but you know, we have 10 electrodes um and leads are formed by the connection between the electrodes um and that becomes one lead. So uh it's important to know where you need to put your leads. Uh Sorry to put your electrodes on a patient. So here's just a little diagram and you can actually see uh it's labeled where you need to put the different um the different electrodes on an individual. Um And then with the limb leads, we've got a ra R la R RL and LL and uh you need to put these on the wrists, you need to put them on the ulnar silo process. Um And on the ankles, it can be either media medially or laterally. Um on one of the styloid processes. Um And that's how we would stick our electrodes onto a patient. And so the point of these electrodes is that they give us, they create leads. So connections between the two electrodes create leads and then we can have different views of the heart. So um our, we've got our three, our 12 and three leads and our A VRA VL and A VF, they give us horizontal views of our heart and our V one to V six, it gives us that views. Um, and so that's why you get an E CD trace with 12 different er, bits on it because those are the 12 leads. Um, and that helps us identify whether you have like where you might be having a, a cardiac like which uh coronary artery might be affected. Um, um, cardiac deviation. Basically, it gives you a really good view of the heart. Um, so on that topic, let's discuss cardiac axis. So this is something important to know. So we've got a cardiac axis generally, we know that it lies between about minus 30 degrees and plus 60 degrees. So what this means is that the, um, in, sorry, so what it means is that like the net directional electrical activity spreads toward where that yellow arrow is, it spreads that way. Um And so that's like the net direction of the electrical activity. And obviously that makes sense if that's the left ventricle. Um, and the heart's pointed that way, the uh electroactivity goes towards the apex of the heart. So that makes sense. Um So in a normal cardiac access, so in a nor in a patient with no pathologies, um you'll see a positive deflection in so if we look at leads 12 and three, um all of these leads, you should see a positive deflection. So you can see in these and where I lead to is obviously got the highest positive deflection because that's closest to the mo the net direction of the electrical impulse. Um And same thing in a normal person, you would see the A VR would have the most negative deflection. Um And this is because it's obviously going, it's looking at the opposite way to what the um, electrical er spread is the direction of the electrical spread. Um If that makes sense also, if you have any questions, please do drop them in the chart. Um This is a more complex topic to understand, but once you get it, it should be good. But so we've got um, those are our normal cardiac access. So in some pathologies, the cardiac axis can change. That's why we get our deviation. So we start with our left axis deviation. So generally this is when um the direction of depolarization uh distorts to the left. So between minus 30 minus 90 degrees. So you can see the yellow arrow signifies the kind of general direction of the electrical impulse on what where the whites left axis deviation. Um So usually this results in the deflection of lead three becoming like super negative. And then in significant issues, uh significant pathologies lead two can also become have a negative deflection. So you can kind of see that in this diagram. Um and left axis ST deviation is usually seen in things like conduction abnormalities, um hyperkalemia and sometimes congenital defects can cause left axis deviation. That's just something to keep in mind when you're learning to read an E CG. Um So then we have our right axis deviation. Um And this is obviously when the depolarization direction distorts and goes towards the right. So between plus 90 degrees and plus 180 degrees um in this uh the most common cause of right axis deviation is right ventricular hypertrophy. So, in things like uh pulmonary hypertension, so when your right side of your heart, so the right ventricle is having to work a lot harder. So the muscle tone increases and there's an increase in electrical, um there has to be an increase in electro stimulation that way. And that's what can kind of turn the depolarization direction towards the right side. Um And you can see that in this case, the deflection in needs three become a lot stronger, like a lot more positive and can sometimes um look more positive than D2. Uh A VR can also become either less negative or in serious condition become more positive, become positive, um not just less negative uh because of that direction of the electrical impulse. Um And so obviously, we said that you can see this quite commonly in right ventricular hypertrophy. But you can also if you've got a very tall, skinny patient, um it's quite common for them just to have right aci deviation, but with no cause of pathology, um just because of their anatomy. So the heart tends to kind of turn slightly uh in taller patients. Um And so now let's discuss some abnormal EC GS. Um So let's start off with our sinus arrhythmias. So, sinus arrhythmias are what we've got normal are no, oh sorry, our normal um QR S are normal ec like a normal E CG trace but sorry, not normal E CG trace just like a normal um wave. So normal heart rate, normal pumping. But um it's not a regular rhythm and most of the time sinus arrhythmias are going with your um ventilation. So when you breathe in the heart rate increases and when you breathe out, the heart rate decreases and you can kind of see this on this E CG wave where it's not regular intervals between each um contraction. So each uh sorry, each cardiac cycle. Um And so that's what a sinus arrhythmia is. Uh but the contraction is still um normal, it's just different uh time between each contraction. Um then we have signs tachycardia. So that's a normal heart rate just a lot faster. Um So the time between um uh depolarization, sorry, the time between our repolarization um RT wave and our P wave um increase uh sorry, decreases. So we've got sinus tachycardia. So faster heart rate, then sinus bradycardia. So the opposite of that. So as much slower heart rate, so we have a much more increased distance between our T wave and our P wave. Um And so those are our sinus rhythms, then we'll have our atrial fibrillation. Um And this is when our atria aren't contracting properly. Um And so you can kind of see that there's like a quivering uh QR S complex. Um cos the ventricles are still contracting but the before like our P wave is not a normal P wave. So there's no um segment in between our P wave and our QR S complex. Um So our, our atriums are just like uh not contracting once it's just, it's not contracting, right? But it's um it's like not a coordinated contraction and then we have our atrial flutter. So, um when our atria are rapidly depolarizing, um the waves are sorry, the waves are too rapid for the um Aveno to keep up um like to keep up with and pass the excitation onto the ventricles. So, um only now like only occasionally does the depolarization of the ventricles actually occur. And so this causes a misshape of the P QR S er signal. So, you can kind of see that here. So you've only got occasional QR S er complexes within a bunch of P waves and that's what is caused by atrial flutter. And then we have our ventricular fib fibrillation. Um And since when our atria just not contracting at all properly, and you can see that it's just quivering, um sorry, a ventricular fibrillation, it's just uncontrollably contracting. Um The patient can survive from this but it's just not regulated contraction. Um And then we have ventricular tachycardia. Um and this is sorry, I got on the opposite way around. So, ventricular tachycardia um is when there's not regulated ventricular contraction. So that's why it's just up constant P QR er constant QR S um eleva er elevations and then, and that's what's in our ventricular tachycardia. Um and then in our ventricular fibrillation. So that's the one above the ventricular tachycardia, there's like an uncoordinated electrical conduction. Um So the contractions are not coordinated, so the heart can't pump uh any. So the heart isn't pumping any blood um out. So there's no ejection. Um and this is when, if it's not treated. So, obviously, you have to treat this with a defibrillator um to shock the patient out of this rhythm and get the contraction coordinated again. So the heart can start pumping um blood out, but that's what leads to this E CG trace. So you can just see um no coordination, just constant electrical conduction. Um and nothing. So it's just almost like the heart is like flailing around and so those are, are abnormal EC GS. Um So let's before we finish, just talk about a um syndrome that might come up, especially as a pre clean. This is one of the most common uh syndromes to come up when you're talking about EC GS. Um and this is Wolf Parkinson White syndrome. Um, so in Wolf Parkinson white, er, you've got an accessory pathway. So obviously you've got the P Kinji fibers and the bundle of hiss. Um but in Wolff Parkinson's white, these patients have this like extra pathway called er the bundle of Kent and it kind of goes around the other side. Um like it skips where you can see this blue arrow, it comes around and this is the accessory pathway and er this causes the electrical conduction to be able to bypass the ATRIO ventricular nodes. Um So in a healthy patient, the AV node, uh the impulses travel through the bundle of hi and its branches and reaches the ventricles and that's what causes contraction. But in Wolf Parkinson White syndrome, um you've got this abnormal accessory pathway which is the bundle of Kent. Um and this is in addition to the normal pathway, but this bundle of Kent allows the electrical impulses to basically bypass the atrioventricular node and directly connect to the atria, directly connect the atria to the ventricles. Um and this causes pre excitation of the ventricles. So um the pulse travel, there's no pause and pulse um between. So the where the atrioventricular node usually pauses, um the electrical conduction so that the ventricles can fill, um the accessory pathway can stop that from happening. And the uh electrical impulses go quicker through um from the essay. No down to the ventricles and this is what we call preexcitation. Um So the ventricles are activated earlier than it should have been. Um And so, in patients with Wolf Parkton white, this can cause things like uh tachyarrhythmias, atrial fibrillation, um and supraventricular tachycardia. And so often patients will present with like uh syncope or dizziness um or like rapid heart rates. Um and they'll, they can present straight to A&E and often this might be the first time that they've um experience this. And then um obviously, when you come in like that, they'll do an E CG and in an E CG. So what you'll see is um if the patient has Wolff Parkinson white, you'll see a short pr interval um which you can kind of see on this image. Um So it's the shortened pr interval. So there's shortened time for the atria to activate ventri from atrial activation to ventricular activation. So that's why there's a shortened pr interval. Um you might see a delta wave. So instead of doing QR S complex, it's like a direct up and then down. But a delta wave is where it's like more slanted up. Um, and you can kind of see on this image, sorry, it's a bit small, you can kind of see where it's slanted up rather than just a direct straight line upwards. Um, and then you also see a widening QRS complex. So the ventricles are contracting for longer. Um, and this is obviously the investigations here and what you'll see. Um, and then in patients with Wolf Parkinson's why the management. Um, so most of the time patients will only experience occasional symptoms. And, um, if it doesn't really bother them, there's no treatment needed, they just need to be regularly followed up by a cardiologist. Um, but if they're getting more like triggered, um, they're having more episodes often it's a lifestyle can trigger episodes of things like stress, alcohol, caffeine. Um, and it's about modifying your lifestyle to prevent, um, these occurring, these events occurring, um, during an event, you either can you first try the Valsalva maneuver. So that's where you, like, close your nose and you try and breathe, like you push all the air out without letting any out. So, like when you're popping your ears, that's what we call the Valsalva maneuver. Um, if that doesn't work, then IV adenosine can be admitted, uh, like, can be given and if that doesn't work, then cardio, um, then you need to cardio. Uh, I forgot the word. Um, I basically use a defibrillator to restart the right, um, contractions. Um, and in severe cases. You, uh, uh, you can get the, you can have, you can undergo surgery, um abolition surgery, ab ablation surgery. Um, and they can remove this connection, the accessory pathway. So this won't happen anymore. Um, but obviously surgery comes with risks. So, unless it's seriously affecting your quality of life, um, you probably wouldn't do that. Um And so the prognosis and complications of all Parkinson's whites. So, again, palpitations, dizziness and syncope. Um most common symptoms of this. Um And then in a very, very small percentage of patients, uh sudden cardiac death can occur. Um but it's very rare. Um and mainly this is seen in men aged about 30 to 40 it's usually hereditary. Um It's inherited uh but it can also be associated with some congenital heart defects. But uh yeah, so that's basically Wolff Parkinson's white. So we've kind of covered everything we need to uh we have some SBA S as well if we have time. Yeah, we have time. Um So uh should we do the SBA S before the? Um Yeah, let's try some. Um OK, so if you guys wanna try and put your uh answers into the chat, if you wanna try, give these a go, some of these are quite easy, but just to kind of get your basic knowledge underway, we've got about four of these. Yeah, so you've got CNC perfect. So it's on the left anterior Axillary line. Um So between B6 and B four. So basically like just under the nipple um in the fifth intercostal space. Perfect. Uh So what about this one? Uh if you wanna give this a go. Yep. So we've got our, I think it's b um so our RR intervals. So, um yes, that's between our two tops of our uh QR S complex. Um And that's the time between the ventricles depolarizing. Um cos that downward after that top, you've got your downward um R part, part of the R wave down into S um and that's our depolarization there. So obviously to the next depolarization. So that's our RR interval. Um And then this, how much time has elapsed across seven small squares with an E CG trace? Yeah. Perfect. B naught 0.28 seconds. So obviously, our little squares are naught point naught four. So naught point naught four times seven. Perfect. And our last question, which E CD trace uh shows atrial fibrillation. Yeah, perfect. So we've got a, so you can see the quivers uh in the trace. Amazing. So, uh that's all that I've got to do. Um And I'll give you guys a bit of a break, but uh sh great. Yes. Um I'm gonna put a feedback form again into the chat so that again, just get it done so that you can access the recording and the notes. Um And we'll come back in about 10 minutes again. I think that's fair. Um So we'll start at about 1155 in the next one. But thank you for presenting today. Um And yeah, thanks guys.