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basic will be going through the basic physiology, some hCGs and then our tacky and bread year with me is. So if you're a card of student, then these of the leading objectives that you need today, 11 to the sessions. So let's start off with a bit of heart electrical physiology. So I'm sure a lot of you know, the conduction system of the heart. Really, really well, um, but what I'm going to get us to do is just label the conduction system. So when anyone tell me on this diagram What? This little yellow part is here today? Move! Put that in the trap for me. What does that represent as? And wow, you guys already falsified pretty and okay. Great. And does anyone know what this little strip here collecting the two Atria is back ones bundle. You have really well done. So backwards bundle, as I just said, is a bundle of fibers traveling from the right atrial to the left atrium to make sure that the to eight year depolarizing in a synchronized way Brilliant said same one. Know what this circle part is here? Anyone talked about in the trap? Avian? Yeah, really, Well done, guys. Really good. Um, so this is one of this is basically the main connection to the atrium, the medicals, So really real world. Um, they won't know what this section is here. Just coming down from the Aviane bundle of his brilliant on these two are the two divisions of the bundle of HIST. What they called kindy five is just yet. Bundle Branch is pretty. And so yeah, we have our left on. All right, Bundle Branch is. And then finally, as you got said, we got the EKG five. It's already well done. So I'm gonna just flash up some really quick questions that often will get asked and exams just to check your knowledge. So does they. Won't know which coronary artery supplies the s a n on the Aviane. I'll see a brilliant yet. Really? Well, don't see that. That's quite common examinations. The right coronary artery supplies both of those. Which area of the electrical conduction system has the fastest conduction speed? And do you know what the speed is? So the fastest conduction pickin Gee, yeah, really Well done does. They won't know how fast it isn't a candy. The more if not so the yeah is the 25. It's around about 4 m per second on back in. The fiber's really need to be the fastest section off the conduction system because they need to make sure they allow the ventricles too quickly. Contract really quickly to allow an appropriate and adequate blood ejection out of the aorta and out of the pulmonary arteries to make sure that we can maintain our cardiac output. So the opposite question. Which area of the electrical conduction system has the slowest conduction on? Does anyone know the speed Avian? Yeah, really Well done. So yeah, it's the Avians. The avian is the slowest, cause it obviously needs to give time for the atrial to empty the blood into the ventricles after atrial contraction. Andi, does anyone know how long the delay is a PhD in How long does it delay between receiving the impulse and releasing it to the bundle tests? They will know in seconds. Yeah, you're close your close guys, it's know is about no 0.1 seconds roughly on. That just allows time for that. As I say, the blood content in ventricles and finally which part of the electrical conducting system depressurize the depolarizing, the intervention killer septum say one that so which part of the system keep it arises? The septum bundle branch is yet because they won't know which one left. Well done. Well done, two k Who got the right? Yep. So it's the left bundle branch that depolarizing is the septum, so really well done, guys. Also, in terms of the conduction system, it's really important to know that the interconnectedness of the myocardial cells with it within the heart determines how quickly impulses pass from cell to cell. So in sales, where there's lots of gap junctions, there's loads of kind of channels for this electrical impulse to pass through. Then you're gonna get really far speed because that impulse in trouble through multiple gap functions at once, whereas if so, hasn't got money. Gap junctions isn't really connected to its other cells, and conduction is a lot harder and a lot slower. So I hate her. That makes sense Well done. This is just another brief recap for you. Also, Just remember that there's two main types of action potential shapes that we see in the cells of the heart. So you have the pacemaker action potential, which is seen in the pacemaker cells such as the S, A N and the Avian. And then we have the ventricular action potential, which is seen in the rest of the conduction system so that the passenger fibers the wonder of hits that we just went through as well as the H one ventricular my sights as well. So in the pacemaker action potential we have our funny current with sodium slowly trickles into the cells, slowly depolarizing it. Then we have a rapid influx of calcium in our phase zero. And then, um, from potassium rectified channel slowly pump the potassium back out to report a rise. Whereas in our ventricular action potential, we have, um, our, um sodium, potassium ATPase and face forward just keeping everything on its baseline on. Then, when there's an impulse phase zero sodium rushes in, making it more depolarizing on, then we have our phase one where a task and slowly flows out. The potassium slowly flows out. It continues to flow out on. We also have cows, um, injuring face to to balance out. And then finally, we have potassium continue to flow out, face three so another thing that's really important for the cells is remembering the refractory periods. So a refractory period is basically just a period immediately following the stimulation of a cell, during which it's not gonna be responsive to any further signals. So we just said the in phase zero, we have the the sodium channels open on that. Let's thesis Diem flood into the cell after those channels have been open. They then become inactive, which is where they can't be activated again. So do you know longer flows through them? And they can't be activated if another impulse comes along and after they've been inactive, then then go into a coma state? And in a closed eight, they could be activated if another impulse comes. So there's four refractory period that you really need to know. You have the absolute refractory period or the AARP, and that represents the time that all of the sodium channels air in the inactive state. And that basically means that because none of the sodium channels can be activated, we can't have another action potential be propagated, and that basically helps you to prevent a really fast heart rhythm. So really intense, tacky arrhythmias. I'm also miss time rhythms or impulses heading in the wrong direction. We then have the ER p or the effective refractory period, which is basically when the majority of sodium channels are inactive. But there are a couple that have gone into that close date and could be activated if there was another impulse. But there isn't enough sodium channels that can be activated in order to get a new full action potential. So if in impulse came along in the er P rather than AARP, then you could extend the Q T interval, which is the period in between ventricular depolarizations MRI pressurization. But you're not going to get another action potential. Then you have the relative refractory period, which is the R. A. P on this occurs when a small number of sodium channels are still inactive, but a large enough number are able to propagate and new action potential if it comes along and then you have the super normal period, which is where the sodium channels are really hyper excitable. They're ready for another impulse on even a small impulse control of for action potential. So now I just wanted to go through some of the physiological changes to the heart that can happen. So let's test your knowledge. Does anyone know what I know Tropia is? If you have to define it, how do you define on a tray? Be force of contraction. Yet that's right. Really well done. So, yeah, it's the force or energy of the muscular contractivity in the heart saying, We'll know what, Lucy Trapeze relaxation speed yet really well done. So it's the rate of which the my cardio cells relax, crying to try to be heart rate yet. So it's a change in heart rate, really well done and drama. Trippy. Does anyone know what that one is? It's probably the hardest one. Same one no more If you don't this probably harder one. So it's the basically, it's a is able to quantify the conduction speed or how much delay there is within the IV note. So if there's an increased dramaturg be, that means that there is less less delay at the AB in So obviously, the heart can control its own heart rate. We know that it's got the S A n is has automaticity, so it fires without having to have external stimulation from an outside source because it's got that funny current that slowly, depolarizing is before the impulses sent off. But you can also receive sympathetic fibers and parasympathetic input from the vagus nerve in order to alter characteristics on physiological changes. Our in our heart. So does anyone know if those sympathetic stimulation to the heart what happens to each of these four factors? Does anybody know increases? Yeah, really well done. So, yeah, all of them increase if there's sympathetic stimulation to the heart, and the reason for that is because if you want to stimulate the heart, we usually think of that as increasing the heart rate. But it also does increase the force of your muscle contractivity of the heart. And because you're trying to cycle through the cardiac cycle a lot quicker, know only do you need to speed up the heart rate, increase how much energy it has, you need to increase how quickly it relaxes, and you need to reduce the conductions read within the A VN already well done guys. So that was our basic physiology, and I wanted to just go through. The CGs is that's really important for arrhythmias, So the golden rule of Easy. Geez, if you take anything away from the session, please That it be this on is that a deep polarization towards the electrode is positive or an upward deflection on the Z D trace. So I'll just repeat that again at the polarization towards an electrode is positive on upward deflection on the CD tracer here there is a deep polarization towards our detector or electrode, and that causes the trace on the EKG to go up oppositely. If a report or is a shin occurs away from the detector or away from the electrode, that also causes a positive deflection on the C G. Because both of those variables that changed the depolarizations switched to repent or is a shin on it's now moving away from the electrode and therefore two negatives make positive and you still get a positive defection. However, if you have a deep red or is a shin, away from the electrode or re powder is a shin towards the electrode that will produce a negative defection, the easy to trace. I'm just a quick reminder of some of the characteristics of STD paper because it's really important for you to know. So one of these small squares here is equivalent to no point north for seconds of 40 milliseconds on one large square, which is five small squares, is equivalent to no 50.2 seconds or 200 milliseconds. And when you are given an E. C G, the total length of time recorded is 10 seconds on. I've just written here is, well, the key variables that you'll need to know for your skis or your written exams as well. So the speed of the trace is 25 millimeters per second, and the voltage or the Y axis is 10 millimeters per mil a ball. So a little recap on the lead. So when we do a 12 lead D C g, it actually involves placing. Tell electrodes that specific points on the patient. So we have our six test chest leads, which you can see in this diagram. Here we have our four limbs, leads is well, which are the right home, left arm, left leg and unearthly, which is placed on the right leg. A say it's named 12 lead EKG because it produces 12 different directions from which electrical information can be ascertained from the heart. So we have our be 1 to 6, which correspond Roger, sleep our leads 12 and three on I lead a V e r a v e l a v f. So I think the 16 is quite explanatory. Leads 12 and three. They measured the electrical impulses between two to limb leads. Basically. So when it does this, it basically labels one of the leaves is positive on one of the leads as a negative electrode. And then when you're thinking about the e z, e g and I was just explained the golden rule. When you're thinking about that, imagine that you have your eye sitting and looking from the positive electrode towards the negative electric when you're deciding whether the depolarizations coming towards your away from you. So, for example, in lead one, it measures the electrical difference between the right arm and the left arm and the depolarizations going from negative to positives. If it's heading in this direction in your eyes here, the the depolarizations is heading towards you on. That will cause a positive up strike. Then we have leads a V e r a v e l A v f and this is quite similar to leads 12 and three in that it's using two leads to work. How the the depolarizations the heart in a certain direction. But with these leads instead of it being only two electrodes in play, it actually uses three of thumb labels, one of them as the positive electrodes, and two of them is the negative electrode. So if you look at a VR, for example, the right arm is labeled as the positive electrode on the left arm. The left leg are labeled is the negative electrode In this, you could get a different direction of the heart because you're positive. Electrode is up here, be a negative. Electric is actually halfway between. In this case, the left arm, the left leg. Um and so you can get this direction instead. And once again, remember that your eye is effectively sitting at the positive electrode, looking at the negative one, so positive depolarizations a VR would be in this direction towards the right arm. So the components of any C g. So hopefully this is a revision for you. But just remember, a P wave is atrial depressurization. The Q wave as a separate for the Q. The intervention of the septum sorry is supplied by the left bundle branch, so the Q wave is a negative defection. So if we look at our little diagram here, if we imagine are left bundle, Branch Block is supplying the septum is kind of going from left to right. So in this direction, from left to right in the heart, right to left is you look at my mouth on. As you can see, that's kind of away from the detector says is the polarization occurring away from the electrode? So therefore, it makes a little negative deflection on the C. J. Then we have our wave, which is our ventricular depolarizations. That generally happens from top to bottom on that, therefore occurs towards the detector, and it's a depressurization, so it makes a very big upstroke on the EKG tracing. Then we have our X wave, which is the ventricular depolarizations along the potential fibers. So as you can see, the kidney fibers travel kind of from the apex of the heart back up, and therefore they're heading away from the detectors. They depressurized. That's why you get being negative deflection. There And then finally we have our T wave, which is all been treated a report or is a shin. You also need to remember the intervals and the segments as well. So we have the PR interval, which represents the Aveeno delay that we spoke about for about lot 0.1 seconds. The reason why it's on the eyes or electric drying and it's effectively neutral is because if you imagine it's a delay, the impulses and moving a relative to the detector so the eyes are electric line is whether it is. It just stays constant. And then we have our ST segment, which is the time in between ventricular depressurization a report over repolorization. Sorry, and this is flat as well, because it's basically where the charges a counseling out with each other. Another thing I wanted to mention is the difference between intervals and segments, so generally on interval typically includes the waves that they're talking about. So, for example, in the PR interval it includes a Z concede here includes the P wave, um, and the Q T interval includes the beginning of the Q wave all the way to the end of the T waves so it includes both the Q A volunteer eight. It's including the ways that it talks about in the name of the interval, just like in the PR interval. The P wave is included within that time, whereas the second is generally the the time between the two ways that are in the name. So, for example, the ST segments from the end of the S wave to the beginning of the T waves of those two ways and not included in the measurement I heard that makes sense. If that doesn't like, re explain it, so then this is just a slide that you can review in your in time, but during exams that often ask you about certain intervals and things. So it's really important that you remember these numbers here as to what the normal measurements of any CGs. So a P wave is usually less than or equal to two small squares and height. The cure us generally is less than three small squares, or 120 milliseconds. The PR interval is usually between 120 to 200 milliseconds, 3 to 5 small squares and for an ST segment elevation, it needs to be greater than one millimeter or greater than one small square above the eyes. Um, electric grind in more than two um, adjacent leads, however, in some, really does what it requires a larger level of elevation if you want to diagnose the same. But that's beyond your levels. So don't worry too much. As a general rule, it needs to be greater than one small square and then just a little recap of your HCG territories as well. So when interpreting and a C J, it's really important for you to be able to identify where the area of risky Miri's in order for you to be able to direct treatment if you want to. Um, unblock a second coronary artery, for example, says three main territories that you need to remember. So you have, uh, your inferior, which is leads to three and a V F, which are the areas of the myocardium, is pied by the right coronary artery. And I remember that as this looks of it, like a boot shape on boot goes on your feet, and that's inferior. That's the most inferior part of your body on their four. This is these your inferior leads. Also, F clue in the name for foot is well, that also means it's Imperia. Then we have our anterior septal territory, which is leads V one to be before on the chest, unless pie by the L. A. D or the left anterior descending. And then we have our lateral leads, which is one A V L M V five and B six. And they're the areas of the myocardium supplied by the left self circumplex artery. If you ever get confused on exams, just try and think about where these vessels are, where they lay on the heart, and also where the electrodes on the person hooked up to the E C G on where they're viewing the heart from that should give you an idea is as to what territory you can't and then presenting the CD so this will be very relevant to your skis. A swell, but I thought it was really important to have here. So when you're presenting any CG, start off with the basic someone's name that age and they're presenting to plate where they've come in to see check the CD date check. It's calibrated. Using those measurements I gave you on the first slides on offer to compare to any previous easy. Geez, because you might pick something up, but it might have been picked up before been treated previously. Then you need to calculate the rate. So for a regular rhythm, you can do this by dividing 300 by the number of big squares between the top of the R waves. Um, however, if you've got any regular rhythm, you can't do that because they are. Our interval will be different. And therefore, as I said before, the length of any CD traces 10 seconds and you want to work out the rate in 60 seconds. Therefore, you can count the number of cure complexes in the whole rhythm. Strip in that 10 seconds and turns it by six to work out how many there are in 60 seconds. Then you want to look at the rhythm, so I'll be going through Sonus rather Minnesota. But are there people ways present? Do they have a curious compacts associated with, um, is it regular? Is it regularly irregular, or is it irregularly irregular? And then you can check the access eso The way I do this, I just put this on the slide on the side here, so a normal access is between minus 32 90 degrees in this green zone here, and when you look, it leads one and two on any CG. If you look at the are ways of the kind of big defection off in the QRS complex, if they're both pointing upwards that generally suggest that somebody has a normal access if they have looking at least one and two. If lead one is negative and lead to, it's positive. So if you think lead one kind of sits above Lee to on easy G on D two is just below it. So if you leave, one is negative on need to. It's positive, that kind of reaching for each other on because they're reaching. It's a right axis deviation rays if you have lied. One positive, so facing upwards and lead to negative kind of leaving each other, and therefore it's a left axis deviation. And if both leave one onto a negative, that suggests it's an extreme axis deviation in this back zone here, then you want to look at the morphology of each of the waves, how long they are a swell. So the p wave curious, complex t wave on, then look at those segments and into walls and check. But they're the right length as well. I'll let you guys review this in your in time. So before I go on to arrhythmias, I think is really important to cover what Sinus rhythm is, because that's what we're ultimately going to be comparing Teo. So Sinus rhythm is basically any cardiac rhythm. In rich depolarizations, cardiac muscle begins at the S a note, and there are a few features on an a C G, which suggests that somebody is in Sinus rhythm. So as I loaded to before that is that each pee wave is followed by curious complex. And that's because, as I said before, a P wave is actual depolarizations and curious complex is ventricular depolarizations. So it suggests that the electrical activity of the heart is following the correct order the Atria Depolarizing and contracting and then the ventricles, a depolarizing contracting. So that's good, Then the PR interval should be between 120 to 200 milliseconds. If it's any different to that, that suggests there's probably a There's a difficulty there's a longer delay or a shorter delay, which could suggest a pathology that isn't encompass by Sinus rhythm. And then we also want to make sure that there's a regular rhythm as well, because if someone's not in a regular rhythm, then they're not in Sinus rhythm. So that's what Sinus rhythm is, what's in arrhythmia. But it's basically any disturbance to that normal cardiac rhythm does what it says on the 10. Um, it's really important for categorizing arrhythmias that you know the normal rate of the heart on that 60 to 100 BPM. So your heart rate should be between those two numbers. So when we described tacky arrhythmias and bradyarrhythmias attack, your arrhythmia is basically any abnormal rhythm, uh, with a right greater than 100 BPM and a bradyarrhythmia is any abnormal rhythm with a right less than 60 BPM. So let's start off with the attack, you arrhythmias. Now I'll let you guys made me review this in your own time, but I've drawn you a little tea tree diagrams to basically categorized the main tacky arrhythmias that you need to know in your pre clinical years. So let's quickly talk through this together so quickly. Can you guys really quickly type in the chart? What does the QRS represent on the C G been treated? I depolarizing well, I'm really good guys. Um, so if a arrhythmia has a narrow QRS complex in which there is 120 milliseconds, which he said is kind of the upper end of normal for a curious complex that's normal. So if a curious complexes narrow, that's good. That's where we want it to be. If it's brought. That suggests that there is potentially a problem in the ventricles, because if the ventricular depolarizations taking longer than normal, that suggests that some sort of activity and that depolarizations is impaired, which is why it's lengthening. Whereas if it's narrow, it suggests that ventricular depolarizations is fine because it's not. It's not being extended. It's not been delayed. So, as you can see, here are broad, complex tachycardia is tacky arrhythmias. Sorry on mainly pathologies with the vegetable. So specifically ventricular tachycardia. Ventricular fibrillation, whereas are narrow QRs complex is, but there's no problem with the ventricles. Depolarizing are mainly pathologies of either of the atria or parts of the electrical system above on the 80 note. So these convene further categorized into regular an irregular. So our our regular rhythms. We have Sinus tachycardia, super ventricular tachycardia, and we have irregular rhythms. Doesn't say which could be a tree or flatter, although that can also be regular in some cases and atrial fibrilation. So let's go into atrial fibrillation's start off with, because I think that's probably the most important one that you need to know for your pre clinical years. So what is atrial fibrilation? Well, it's a super ventricular tachycardia arrhythmia resulting from irregular, disorganized electrical activity and ineffective contraction off the Atria. So basically, the the Atria are contracting all together as one. They're basically just kind of fibrillating. They're just kind of waving about to that and not generating a really good atrial systole. So why does this occur? Well, basically, there will be an irritation to an area of the atria that can cause it to fire electrical impulses and stimulate action potentials when it shouldn't do when really, that should be left down to the S. A N. And there's those of reasons as to why that irritation can occur. It can be due to inflammation. Decreased oxygen's the scheme your stress to that piece of the myocardium increased sympathetic activity. Lots of different reasons. And the mechanism really isn't understood that Well, um, this area is usually the root of the poem. Revenge, Um, on what it does is it ever develops a ectopic atrial pacemaker is basically almost like a little new s a n that sends off impulses or a reentrant circuit, and I'll be going through reentrant circuit shortly. And basically, what happens is if you've got this part of the age of firing off impulses and the S am doing it, your atrial really don't know what to do. And the impulses basically just counteract each other. And as I say, there's no synchronized atrial systole because of that. And there's no uniform depressurization of the Atria, and it just causes them to fibrillate. Um, generally in a person this can present in many ways, it can be a symptomatic. And I had a patient today. He had absolutely no symptoms, but I felt his posted. It was irregularly irregular. Um, s so it can be completely asymptomatic. People won't know they have it. Um however, it can present as palpitations, shortness of breath, chest pain falls all things like stroke. A swell because where these atria fibrillating they can basically form clots because the blood flow in the atrial, where it's not moving and not being pushed into vegetables comes really turbulent on. We know that turbulent blood come together, and it forms clots, which can then be transported after other parts of the body. And these are some causes is, well, virtual fibrilation that I'll let you read later. So there are four main types of Rachel Fibrilation. So we have the first detected episode, which is basically, as it says on the 10, the first episode of effort. You detect that irrespective how long it is, how many, what symptoms it causes. It is just the first detected episode. Then we have paroxysmal. So this is when someone has two more upset, but they need to terminate spontaneously, so without electrical cardioversion or pharmacological cardioversion so cardioversion being when you put in someone back in Sinus rhythm, it needs to self terminated with in less than seven days. Persistent F is basically when you have tumor, so it's but it needs to last longer than seven days or needs to require either pharmacological or electrical cardioversion. And then we have permanent F, which is basically a if it fails to terminate when you called you about it or if it does terminate, it will come back again within 24 hours. Or you might have someone that's got a long standing. AFC is something that's all stayed longer Year on cardioversion just hasn't been indicated or attempted. So probably the main point that you guys need to know for a f Can you pop in the chapped for me? What? The two main SED changes that you see in someone with atrial fibrillations loss of peewee waves. Awesome. And the other one? Yep. Irregularly irregular. Amazing weather guys. So yep. So you haven't irregularly irregular rhythm. So that's where the distance between the our pizzas you can see here is not constant and it doesn't follow. A pattern is well, so you could have a regularly irregular rhythm where someone White House, two together, then too far apart and two together too far apart or something like that. Here, that doesn't happen. There's no pattern. They just the difference just keeps changing each time and then, as you said, well done, absent pee way. So you just get this kind of wavy baseline fibrillating baseline may correct, um and that's characteristic of of a f A swell, so well done. So the management of a, uh this is quite a busy side, so we're going to talk for it relatively slowly. So if someone is found to have a F and they're hemodynamically unstable, meaning that their BP is low, they might have had a loss of consciousness. Basically, they're very very, Um well, then the first thing you need to do is DC Cardiovert them because you need to correct it straight away because it's causing the loss of BP. And if they have less BP, that could affect their profusion of their organs, and that's really dangerous. You need to call you about them, and you also need to give them heparin, which basically, um potentiates or stimulates anti from been three to inactivate factor 10 in are clotting cascade and if you inactivate a factor in the clotting cascade, not going to clot as well, so the blood becomes thinner. And, as I said before, a F conform clots Where the atria fibrillating. So we don't want to do that. We want the blood to be finished. Those crops don't form on. That's why we give heparin. Um, Then I'm gonna jump down here to this the tree map. So there's three main components to F medical management on that is rate control, rhythm control and anticoagulate until coagulation. So because a F is an irregular tachycardia, no only do you need to control the rate because it's a tachycardia, you also need to control the rhythm because it's irregular. And as I said, because of the risk of clots, you need to potentially undergo regulate them. So most patients have a rate control. If they're F has been going on for less than 48 hours, and it has a reversible cause, so you can use be two blockers, calcium channel blockers And if someone is elderly with heart failure, you should give them to Jackson. Then, if someone maybe allegedly from rhythm control. Um, and this is where we put them back pharmacologically into Sinus rhythm. So this is a pharmacological cardioversion. We can use either flecainide, which is a sodium channel blocker. Well, I'm the order and which is a calcium channel blocker? Or is it say we can electrically call you about them if that's indicated? And as I said before, because of the fibrillating atrium that causes turbulent blood flow. So we may need to look into anti coagulating the patient to prevent the risk of forming blood clots That could be two a stroke or a p a. A pulmonary embolism where a clock it's logged. It lodged in the vessels of the lungs. And for that we would use something called a dose pack, which is a direct for acting anti coagulant on what we use. That is something called a picks of on and apixaban is a factor. 10. A direct inhibitor on. I like to remember this as a picks about has got X ray in it on, but factor 10 A is written as ex A. So that's how I remember that the mechanism of action of apixaban and someone might also have their F managed non pharmacologically and so they can oblate or basically they get a piece of heat on the irritative part of the Atria and basically just burn away those cells. They don't fire off impulses anymore. And there's also non pharmacologic, other non pharmacologic for the pharmacological management method that more rarely use. If someone's a F has been going on for more than 48 hours, you need Teo. Get them on anti coagulation for three weeks before you called you about them. That's because because it's been going on for longer than 48 hours, there's a bigger risk. There's been more time where there's been that turbulent blood flow, and so we it's more likely that they formed a clock, basically, So we want to make sure that there aren't regulated s they don't form those clots, um, for three weeks before you try and put them back in Sinus rhythm. And if you're trying to decide for a patient, whether they should, um, be on long term anticoagulation is part of their management. We use something called the Chads Fast School, which I popped a little table here for your future reference. So we you should consider anticoagulations in a score of 22 or more in a woman one or more in a man. Does anyone know why there's a difference? Why is there a difference in the school. Brilliant. Yes. So one of the one of the point is for sex? Yeah. Being female. Exactly. Well done. So if we said it was one plus for everybody, then 50% of the population that a female roughly would get one point straight away. So that's why there's the difference on I did just see a question in the trap. What to do? Someone is human. Dinotopia on stable. That's in the box here. If it's less than 48 hours, then we need to look at these medical management parts here. I hate that makes sense. And she also had a wants the questions if no So then we have atrial flutter. So this is a super ventricular tachycardia characterized by rapid actual depolarizations waves, which is quite this down here. So they're called saw to flatter waves on what causes Atrial flutter is basically a small reentrant circuit in the right atrium which repeatedly conducts atrial impulses to the Aviane. So it basically sends those impulses to the avian on a regular basis. On that causes the atria to deport, arise as the atria. Um, all right, kind of involved in this reentrant circuit on that causes these flatter waves to basically depolarization area more often than they should do. And the reason why these flatter waves don't go down into the ventricles is because of that a V and delay. So because of the refractory period, we were talking about the star on the slower avian conduction. That means that the Aviane needs enough time to reset itself before it can conduct in the impulse on. So from that, a V and delay means that we have a few flutter waves before we have any of them go down to the ventricles. So the signs and symptoms are pretty similar to atrophic relation. But what I do want you to remember is often these reentrant circuits here cause the atria to be about 300 beats a minute. And often it's not the case with this diagram, but often with atrial flutter. People have a 2 to 1 ratio in which they have to pee waves, and then you have a cure s two p waves and a cure us. And if that's the case, that means that two of those a tree or contractions will be passed down. Sorry, One of those atrial contractions will then be passed down to the ventricles for every two of thumb that occur. So if your atria going at a pace of 300 BPM, but only one of them is conducted down to the ventricles, you often get a ventricular rate off 150 BPM. So if you ever see someone with an 18 year of 150 BPM, let atrial flutters thing to mine because it could be pointing towards that, as I said before is, well, it has a narrow QRS complex, and that's because the problem isn't with the ventricles depolarizing. It's with the Atria. So that's why they're curious, is normal. It's now on. The management is very similar to a F rate control river in control. And if the hemodynamically unstable so low BP, loss of consciousness, anything like that DC cardiovert them because we don't want them to lose profusion to their organs. So reentrant circuits. I've talked about them a lot. What actually, are they so I'm gonna talk through how impulses get from a to B in the heart. So in the heart, if you're going from a say at the top of the screen to be there will be two pathways that it can go through. You can go through a fast pathway on a slow pathway. So in the fast pathway, the impulse is conducted really, really fast, as the name suggests. But the time it takes for this pathway to reset itself or to report a rise takes a very long time. It's very slow, however, in the slow pathway. As the name suggests, the conduction is low, so the rate of which the impulse goes through. It's very slow. But after the impulse has gone through, it quickly resets itself so quickly report or others. So this is our impulsive little yellow circle here. This is what happened so it comes down. The impulse splits. It quickly goes through the fast pass by, takes a bit longer to go from slow pathway and then comes out the other side as one. And at this point, this X basically just means that they're report arising now in a reentrant tachycardia or on any of our pathologies that we talked about. Whether it's a reentrant circuit, an extra impulse will fire between to normal impulses during this time the fast pathway because it's slow to repolarization on its refractory. It can't conduct that impulse is it gets down to here, and therefore all that impulse does is it doesn't go down the fast pathway. It just goes down the slow pathway. And by the time that this impulse reaches the bottom of the slow, partly the fast pathway has finished. Report arising. It took a bit longer, but it got bad. It's now report arised. So not only does the impulse come out the bottom here, it also goes, Hang on. There's another way I can go and it goes back up the fast pathway. And that's because the fastball, if I have to say, is reported by that time. And when it gets to the top again, the slow pathway, it's really quick to report or is it would have report arised. By now, it can go back down the slope off and send the impulse back up to the Atria. And what happens is this impulse. Just keep going round in this circle all of the time and sending off impulses both up and down on this diagram. So it happens of it like this it goes out. But then it also things another impulse this way. And then it keeps going and it keeps going and it keeps going, and that causes really far circuits to build up. So I'm gonna play those two again. So this is all normal. The impulse comes down, splits, goes through the two pathways and then comes out the other side together. Then it report arises. This one takes a bit longer, but it's fish report a rising now so it can go back up and around and around again. I heard that makes sense. If it doesn't, don't worry. You'll get to review the slides in your own time. So why is this important? Well, as I said before, there are arrhythmias called super ventricular. Super ventricular tachycardia is on. These could be broken down into a V E N L T and a a V O. T. So a super ventricular tachycardia is basically just number litter any arrhythmia that manifests above the ventricles. So basically, any of with me that's no to do with the ventricles is called in SPT. So you will have heard me refer to atrial flutter and a f A supraventricular tachycardia, which they are. However, if you hear the temp, SPT it typically just refers to these two arrhythmias here, and what that does is it produces sudden onset, narrow, complex tachycardia. But you can see on this diagram once again because it's narrow complex because it's a tachycardia above the ventricles. The problem isn't with the ventricles. Therefore, the complexes narrow. It's normal, it's not been bored and ditto, and this can present as acute palpitations, chest pain or lost consciousness, loss of consciousness or syncope. So, as I said, you got a V a naughty and a V e r t so atrioventricular node or tachycardia reentrant tachycardia is a VLT on. That's basically when the reentrant circuit is within the ab ab Noda's you can see here there's an atrioventricular reentrant tachycardia is when the reentrant circuit is spread across the atria and the ventricles. So this is really important for a condition called Wolff Parkinson White Syndrome. So there is a bundle of fibers connecting the lateral side of the atrium in the ventricles. Does anyone know and come popping? The chap What is that bundle called? Yeah, brilliant. Really Well done, guys. It's the bundle of Ken. So this bundle can, as I said, is an extra conduction path way between the atrium. The ventricles, which basically allows impulses to bypass the avian and they can travel across the bundle, can't both directions. Normally, what happens is once the HR depressurize. As I said before, they have to wait. The A VN before the Aviane allows the impulse to go through before it can go into depolarizing ventricles. However, if the one of the Kennedys present, then the impulse contractile through the bundles can in this direction, from the 80 to the vegetables Onda begin depolarizing the ventricles ahead of time before the Aviane. That's the impulse through here, and what that does is that create something called a slurred QR up straight for adult weight, as you can see here on the C G. And this kind of makes sense because if the impulses coming to depolarizing vegetables, then your depolarizations basically starting a bit earlier and you're not having that period where there's no electrical movement when it's being delayed on the Aviane. Because that impulse is traveling toward the electrodes along the bundle of can't on their four that once again the PR interval was reduced at the time spent on the eyes or electric climb decreases. Because of that create citation, however, impulses can also travel the other way for the bundle of Kent. So if an impulse has come through the electrical conduction system, normally it could then hot back from the vegetables back up to the atria. And that can cause one of these reentrant circuits to appear. So you can imagine this circle that I showed on the previous light is occurring between the atria and the vegetables, and that can cause really fast atrial rates to be transferred to the ventricles, which can then be transferred back up to the atria and make a really, really fast and fast rate in a fast heart rate on that can lead to something called ventricular fibrillation. And also sometimes an MRI or cardiac arrest on that can be really dangerous. So how do we treat it? Well, there is a curative treatment, which is where we use radio frequency ablation off the bundle of cancers that said, before basically just firing lows of heat at these things, bundles to make sure that they can't conduct impulses anymore on bear four. The impulses have to travel for the normal conduction system. They can't buy cost in the bundle of can't on. This is a definitive curative treatment. This really helps people that suffer with this condition. Okay, so I lost track here with me. That I'm gonna go through is ventricular tachycardia. This's a broad, complex tachycardia. So this is when the cure is is greater than 120 milliseconds. And that's because once again, the problem is with the ventricles and they are taking longer to depolarizing, and therefore the cure s complex extends in its length. And the reason why this happens is because there's an ectopic focus in the ventricles, which is firing off impulses a bit like the one we had in a for there was one in nature and there was one in the ventricles. It's really important that the you assume or brought complex tachycardia is VT until proven otherwise because of their wrists of cardiac arrest. And here is, um, causes Here is well as to why be taken it now on an e. C. G. And there's probably two that you'll be presented with during your pre clinical years. You might get a monomorphic VT. Or just normal ventricular tachycardia, which is basically monomorphic just means all the cure is complex is a roughly the same right, and they will basically look the same. Well, you can get a polymorphic ventricular tachycardia, which looks like this one on the bottom and an example of this is something called course on the par, which is basically where the cure us complexes are varying in height, and they look really different. And this apparently looks like a twisting of the baseline some people could see it on. This is really dangerous, and why we should assume or brought complex tachycardia is, uh, HVT because this can lead to sudden cardiac death. And to manage this condition, we use rate control, rhythm control on. We can also use implantable cardiac defibrillators or CD's, which basically monitor the rhythm of the heart and deliver a shock if it's abnormal to prevent someone getting into sort, Uh, toes are the poor on heading into a cardiac arrest. So that was taken arrhythmias. That was probably the hardest bet. Now we're gonna go into our Broady arrhythmias. So once again, here's a little tree diagrams for you. So once again, we can category categorizes based on the length of the curious. So once again, if the curious is a normal duration that suggests that something isn't wrong with the ventricles. It's a problem with the Aviane odor up, so that, in this case would be something like a navy node block for which there's different types that will be going through in a second and abroad cure. I suggested there's something wrong with ventricular depolarizations, which is causing it to be longer on. That could be something to do with the bundle. Branch is so either left or right bundle branch block. Let's quickly go through heart blocks. A heart block is basically when you get impaired conduction of impulses from the atrial to vegetables, usually at the AB. Note where those two whether to set the train was connect, so there are different degrees of it. 12 and three, first, 2nd and 3rd degree in first degree. You have slowed a V node conduction, so basically there's nothing necessarily wrong with the ab nose. There's no block. As you know, it's called a heart block. There's nothing no physical like cutting of the fibers or anything like that. It's just a bit slow, so it just takes a bit longer for the impulses to come through. This can be normal. So, for example, if somebody has a high vagal turns to the vagus nerve is very active, such as enough weight on this can't be normal, or it can be due to a V know blocking drugs such as beat of pockets or C, CBC or digoxin. And this is often asymptomatic on on only See a GI. Because the PR interval is the time at which the A V node is kind of delaying the impulse, it will just be prolonged in someone with first degree heart block because the Aviane conduction is slower and therefore the delay is longer and therefore the PR and four is longer. Then we have second degree, and that's the next, more severe one up. So this is when we have intermittent conduction between the atrium, the ventricles, so this can cause symptoms so it can cause obviously a slow heartbeat, shortness of breath because you're not getting enough blood to the body presyncope pee or syncope. So when you feel that you're going to faint or you fall, and it also causes in the right regularly irregular post. And there's two types is move. It's type one a moment side, too, so move. It's type one can be normal and has similar causes to first degree relative move. It's Type two is more likely to be due to a skinnier or a V know blocking drugs, and the difference between these is in a Mobics type one. You have progressive lengthening of the PR interval until eventually a curious contractor beaters dropped. Where's in mobitz? Type two. You have a constant PR interval, and then, after a certain amount of curious complex is one of them is dropped. Then we have third degree, and this is the most severe. And that's when you have a complete conduction block between the atrium, the vegetables. So the heart rate is very slow because it's being solely controlled by the ventricles themselves, and this could be caused by a multiple different things. But it can be caused by right coronary artery and a collusion or an inferior M I. Can anyone type in the chapped for me? Why would those two first ones are right? Coronary artery occlusion or inferior and my cause, the third degree heart block because it supplies the A. Be a really good job allies. Yes, because it's applying the Aviane on also the essay node. The impulse basically can't get into the ventricles Onda. This concludes recent symptoms quite similar to a second degree, but even more severe on can lead to heart failure as well. Only see GI. This is showing is no association between the P waves and the curious complexes. So you can imagine, because there's a complete conduction block between the two, the atrium, the ventricles can talk to each other. The atria, just DiPoto rising and contracting at the rate they want to the ventricles are just doing the same bag depolarizing and contracting at the right. They want to as well. So you get the P waves and curious complexes that there's no real pattern between them because the two systems are talking to each other. So this is a bit more about what they look like on the C. J. So you can see there's a problem. PR interval in first degree. You can see this is a mobitz type one, so you can see the PR interval is gradually lengthening on, then a curious has dropped, whereas in a mobitz type two, the PR interval was the same each time. And then the cure. A sister on this is unexamined of the third degree, and you can see they're peewee waves on their curious complexes. But that register best. They're not coordinating with each other toe in terms of management, first degree or secondary mobitz one can be normal, as I said, and you should treat your underlying course if they're on a navy know blocking drug like beat it back or a calcium channel blocker, you could stop that drug. If it's appropriate on, do you should monitor them as well, just to make sure there's no complications, whereas with a second degree that you say mobitz to Sorry about that, I will change that. So a secondary moments to or a third degree. This is always pathological that's never normal, and often that's treated with a permanent pacemaker to make sure that they the bradycardia, isn't causing a lack of blood flow out of the heart and preventing them getting enough and blood, too. And they're bite walk ins. So our final a reading of the day is a bundle branch block, so bundle Branch book is basically when it's impaired electrical conduction through over the left or the right bundle branch of the electrical conducting conduction system. So in a left bundle branch block, the right bundle branch has to depolarizing the left side of the intervention the septum which, as we said before the left bundle branch, would normally depo to rise. So that causes a wave of depolarizations towards the V six electrode, which you can see here. So imagine this is the heart in the trust in the chest wall is kind of around here. The V one is kind of on the front of the chest. Um and B six is in the midaxillary line. So it's in the Examiner on the lateral side of the patient. So is the right one of broached depolarizing is the left side in this direction. It's heading towards the V six electrode, and we said before, if you're getting a depolarizations towards the detector, that's gonna cause a positive defection. The CJ. So if we look at a left bundle branch broken any CJ you can see on the V six electrode that the DEPOLARIZATIONS is producing a positive defection. The C G um envy six. So if you look at this hour from the perspective of the one, it's heading away so you can see that this creates a negative defection. The C G right bundle branch block. It's basically the opposite. So if the bundle right bundle branch is about the left, one takes over on it. Deep arises the intervention conceptive in this direction, as you can see by the arrow, that's a positive defection towards the one a negative one from the viewing of the six So we can see here. There's a big positive defection and B one, um, on a negative one in 36. And the way you need to remember, this is the term William Marrow. So William is because in a left bundle branch block the one So office, um, electrode on the CT looks a bit. I can kind of commit you. It looks a bit like a W shape on D. V six. It kind of looks like a M shape, and the girls in the middle show you that it's a left bundle branch block almost for a right bundle branch block on the V one looks a bit like an M, and the V six looks a bit like a W on the hours in the middle tell you that it's a right bundle branch block, and that's how you should remember what they look like on any CJ and another really important point to know. That is, if you have any CD with someone that's got a new left bundle branch block, so it's the first time that's being detected. That could be the sign of the same. So that was the end of my presentation. We're just gonna do some questions now, so thank you for launching the pole. So a 61 year old male presents to any with a temporary loss of consciousness. His vital signs are shown. His partner told you that he had a heart attack last week. You look at his SED for months, which, which shows ST Depression leads. We want to be full. Unless the elevation needs to three in a V F. You perform another E c G. But you're still waiting for the results. Which part of the electrical conduction system of the heart is most likely to be damaged leading to his presentation. I'm just gonna read on the pole. Hopefully that should be going bring you guys get yours is in nice and fast. Keeping coming. Okay, I'm going to get 10 more seconds. Last few ounces in. Okay, I'm gonna end the pole. That brilliant. So the majority of you got this question right? Really Well done. So the correct answer here is he? So let's talk through this question. So it talks about he have hay had a heart attack last week on these were the findings on the E C. G. So can anyone tell me with his presentation last week what's happens? They have Nestea depression. Leads be 1234 get a ST elevation Needs to three and a VSL name on top of the chat. More happened. Brilliant. Yeah, he had an inferior stemi. Really good job. So the ST Depression is just showing receptible change in the anterior leads. But the ST elevations is what's important. And that's in the inferior temp territory. No, he said if someone has an inferior stemi What cardiology tree is involved? The right, Brilliant. On what do we say? The right coronary artery supplies Brilliant. The avian. So he's coming today with a temporary loss of consciousness. And he's pretty human. Genome McPhee on stable So he's got a low heart rate. Sorry. That should say 33 36 breast per minute on low BP on days. Temperature is normal. So can anyone tell me what's happened today? Well, that kind of tells you on the screen. Same one? Yeah. Yeah, he's a navy block. So he's now presented with a third degree complete heart broke. Brilliant, because he's not getting a blood supply to his avian. But, um So next question, a 70 year old man is attending the cardiology crank for a review of his medication for his atrial fibrilation. His BP reading in clinic today was 150 over 95. You notice he has bilateral pity and Dema and he has no history of stroke or a TIA. His current medications include atorvastatin, digoxin, ramipril on metformin. What is the most appropriate next stage of managing his A f keep balance is coming in. Okay, Brilliant. I'm gonna end the hole there, so we got a bit of a split between a and see which is what I expected. Um, well done. Total of those of you that perch see? Well done. That's the correct answer. So the reason why it's know I and I can see why you put that because he's got the bilateral pitting edema is because the questions specifically asked what is the most appropriate next stage of his management of his A f so no, necessarily managing this patient, but specifically the atrial fibrilation that he's got. And we said that for atrial fibrilation, it's got three main components are rate control our regimen control on our, um, and struggle a shin. Um So for him, he, um we need to look into basically whether he needs any anti coagulation on because he's not on any already. So then we use the chads score to calculate it. So in this case, has he got congestive heart failure? Well, yes, he's got the bilateral pretty edema on. Also, he's under Doc saying which I said is a form of rate control for a F in order patients with heart failure. So that gets him one point. Has he got hypertension? Well, yes, he's got the reading in clinic to get today, which is high. And he's also on ramipril, which gives us a bit of a crude that kids this one point then we have our age greater than or equal to 75. He's not. He seventies. We don't get any points there. Has he got diabetes? Well, yes, he's on metformin, which you would have learned in our case. 11 session is a commonly used drug to treat diabetes. It says he has no history of stroke or TIA a on. We can assume that because he's got a lot of cardiovascular pathologies on. He's on a statin. It's likely that he has vascular disease on been terms of his age. It does get a point in the 65 to 74 category on. He's obviously mail, not female. So whether or not you include the vascular disease, he's got four or five points, which basically just means he definitely school and regulation because our cut off in men is one on their four because he needs a regulation, we give him a picks around and come. Anyone remember what the mechanism of action is? Back to 10 in a inhibitor. Really? Well, don't guys. So next question a 54 year old man presents to the cardiology clinic to discuss his actual population. He tells you that he is experiencing palpitations. And this year, despite rate control medications, you offer him a radiofrequency ablation procedure. How well, in an ablation procedure helped to manage his old batch of, say, atrial fibrilation or atrial flutter, but can even tell me what that she does. We didn't keep those owns is coming in this clear majority, which is really good guys. Pretty. And I'm going to end the pole that I've really well done. So we have a clear majority for the correct answer, which is really good. So the correct answers be so just remember that radiofrequency ablation procedures is the most common use high energy to destroy tissue that is causing the arrhythmia which, er for atrial fibrillations is commonly, as I said around the pulmonary very roots of the pulmonary vein Trim on this can be used in a four h will flatter. So our last S p a, a 23 year old rugby player, presents to his GP experiencing palpitations and occasionally feeling faint. He has an irregular pulse of 55 beats a minute and the CD is performed. Which shows the following What is the most likely diagnosis? Keep your eyes is coming in looking really good so far. If you don't know, give give it a guess. You have 20% chance. Okay, five more seconds. Okay. I'm gonna end the pole. That so you had a bit of a split mainly between, I think see on D. So one of those is the correct answer. So well done. Total of those of you that put d so secondary heart block, Mobic type mobitz type of one. So looking at this question here we have a young rugby player. So that, to me, suggests that he's quite young. And then these fittings well, and he's come in with palpitation on syncope, which, as we said it a signs of an arrhythmia and reduce cardiac output. No, he has an irregular pulse, which I didn't necessarily say. It was irregularly irregular, which could suggest a f, but it could also be regular irregular, which isn't a sign of a second degree heart block. So that points us towards one of these too. Doesn't it day and say so? Well done on because it's a 55 BPM, right, that is bradycardic. So it definitely is pointing us more towards heart block than a F. So if we look at the ACG in the rhythm strip at the bottom, we have nine curious complexes. So if we turned it by six to work out how many, there are 60 seconds. We have 54 BPM, which is roughly what it said in the question, and it shows an irregular rhythm. Now, if we look at the P R interval, we can see that, um, you can just about see day. It's extending each time and therefore, after it started three times, it's been dropping a beat. It's a bit hard to see on this one, I will admit, but you can just about see that the interval was extending before we drop to be so. Therefore, it's a second degree heart block mobitz type one on go. What you need to remember is a mobitz type one is a lengthening PR interval which time resident took two. That should say sorry is a constant PR interval. So well done, everyone. You did really, really well and it was quite a long part of the sessions, and we'll give you a bit of a break before Sahara starts on. If you have any questions, do problem in the trap. And I think someone is just gonna We're just getting quickly talk about the 1 to 2 series for college students as well. Yeah. Oh, my God. That was, I think, one of the best sessions we've had in all skis of our, uh I think Megan Slide, I think we can all agree with amazing, really comprehensive. I was like a crash course on arrhythmias have seen one that was so good when I had this last year. Um, so like we mentioned earlier, if you want the only first introduced yet, if you are a second your student at Cardiff, you have probably have your risk is coming up on if anything like us to probably very anxious about it and don't really know how to prepare for it. And don't know if what you're doing is kind of along the right lines. Um and I don't know about you, but I definitely felt like I could do with a bit of personalized feedback on technique history exams on whether you didn't think of skills right and things so well. We have our annual event called the Osteo Easy wanted to escape training events on Basically, what happens if you sign up you on one more person, you're you're get paired up to a third year student a 30 or do toe on. We'll organize weekly, and they'll organize weekly sessions with you either zoom or in person based regulations to go over specific station that would come up in your issues like a cardiology station or a respiration, or get so station or perfect vascular station. You get a scenario on that station and you work through it with your tutor and you'll get personalized feedback so it purposely really helps me on these. Want to want to do one Sessions will also be accompanied by weekly lectures provided by me Megan Knish off our ski see as well as external doctors and other medical student as well. Um, and these lectures will drawn through each of this to every single station we can think off on, and the best way we think you could approach the station, so this sounds like a skin that you're interested in or would like to get involved with on first lies feedback. I'm going to pop the link to the sign up sheet in the chat. Now, Onda, give me a second and you can sign up on it. Um, yeah, we'd really recommend this game. We're sorry. We can't open it up to everyone who's any from anywhere. Sadly, we have to keep it limited to college students only. We already sorry about that and hopefully in the future will be able to open it up further. I would really recommend this. I know both of her and I did it as second years and we found it really, really helpful. But I would not like to say as well to those of you that aren't studying Cardiff as the Honda said, we're gonna have the lectures surrounding Oscars. Which is you guys know is what is osteo is all about s Oh, please turn up to those because they should be really, really good and really helpful for your osteo. Your risk a revision wherever you are will be covering all the signs that you may say as well as how to approach those exams on hopefully set you up for success. If you are quite a student as well, we do have limited places. So it comes on a first come, first served basis. So make sure to, um, son of this quickly as you come. You could sign up shortly, So I was just putting in the chapter on in terms of the Oscars. He lectures. They are going to be held. Um, I think they're much starting much 18. Time of loose 100? That's right. Yes. We'll get all the events will be up on Facebook Well advertised everywhere. So keeping on our socials on them, we will update You're not on the feet. Battling for this presentation will be released shortly into Sinus presentation. Yeah, definitely. We'll definitely have. Once you signed up, we'll have a specific lecture to everyone who signed up going through how it works exactly in, like, how to organize the sessions and two best benefit from them and things like that as well. So have you look at for that story to have some trouble getting that formally and go, But I've got it now. Okay. Okay. There we go. Make sure to fill that in. No, we'll give you guys a couple of minutes if you want signed up for it, or just take a break. Um, And then, Sana, when you're ready for free to begin your presentation, give it a minute. Yeah, I'm probably over the feedback up from up now as well. Just cause I'm a little late. I understand. I'm gonna be going over heart failure. The pathophysiology in management, Andre. Well, as the pathophysiology off from Bumble is, um, issues be back. It's a Google phone. With the survey, you complete the global from at the very end of it. You have a link to the medal feedback form, which is what you have to fill in to give Megan and I feed back for our sessions and also to get the slides on the recording. If you have any questions about anything, if you stay till the very end of session, you can on meet yourself and then ask us questions personally, um, I will also be in the chart. So if anyone has any questions about anything I've talked about or anything for Sahan Oh, she goes, I'll try not to, um, back on the track. I'll be going through that now, So we've got 20. Responsible already are. Thanks, guys. Very exciting. Um, definitely check with your friends as well, because it's just fill up really quickly. Like last year. It filled up really quickly for my year. Um, so share with your friends. If they want a zoo. Well, on D Luke Perry up. You know, in Cardiff. Yeah, really Sorry. Because we've only done Cardiff skis because only provide advice and card of skis. That's why it's a difficult of medical students. Um, sorry about that. If anyone has any questions, then feel free to put him in the channel into them. Um, like, I get it going. And then All right, Cool. Before I started told, my friend told me, give him a shot out. So told me you're here. Hello? Um, and always, right. So how everybody money, Mr. Hana on Gary. Excited to be talking about heart failure today, Uh, cardiology happens to be my favorite subspecialty at the moment, Actually, always has been and really passionate about it on. I'm going to try and share this passion with you. Um, today. So let's talk about the heart. I don't make it already done a phenomenal job of your brain cells are still around. Please ask him to stay, so that's talk about the heart to see what it does, right? So we know that the hot, in essence, is a pump on the purpose of the heart. The reason your heart exists is because you have to pump blood on. The reason have to pump blood is because you have to maintain a specific amount of cardiac output. Anyone tell me why it's vital to maintain a certain cardiac output. Why do you have to maintain cardiac organ profusion? Exactly. Yeah, that's exactly it. Like pretty much every organ in your heart, including your skin and everything depends on the ability to receive blood to receive oxygen. And it's going to be done when the heart works perfectly and or seven perfectly and is able to pump an appropriate amount of blood around the body. So as you know, each cardiac cycle that is each pumping cycle of the heart consists of systole and I athlete. In Diastole, your heart is filling with blood. It's relaxed. It's filling up with enough blood so that in systole it can eject this amount of blood into the into the aorta and then to the rest of your body to do all the perfusion. And therefore it's important that you have both diastole and systole working in a good condition. That's that. Firstly, you can get enough blood in the first place, and then you can also have the ability to release this blood. Her profuse your organs appropriately so either if you have dysfunction and diastole or systole, you're having problems with the volume of blood that your heart can get on there for the volume of blood it can inject, and therefore you get end organ damage because you know, being refused, Um, that's that's essentially the most summarized way of telling you were heart failure, basically is. So how do you categorize heart failure? Well, Lynn Ically heart failure is either categorize a systolic or diastolic dysfunction. Okay, and then, after you recognize whether it's systolic diastolic, you can see whether it's left sided or right sided. So let's talk about systolic and diastolic heart failure. When you go in a ward in see people saying whether somebody has have pef or half breath and these are basically acronyms were saying heart failure with reduced ejection faction have rough or heart failure with preserved ejection fraction, which is have pets. So this fancy word ejection fraction. What does it mean? Let's talk about what injection fraction is. So this is a heart that is being perfused with blood. Okay, you have a certain amount of blood. Let's say in this instance we have about 50 miles of blood entering the left atrium. This is a normal heart. Let's say this. If you move the blood, then enters ventricles in Diastole, where it fails, and then finally, you get some of this blood that is removed and therefore ejected out of the heart. As you can see, there's been a small reduction in the volume. So while your ventricles field of 50 mills of blood, it's only managed to eject 30 miles of blood. This is normal because the way your heart pumps doesn't realize in a lot of factors, and 100% 100% injection factors extremely rare and actually basically doesn't exist. A normal ejection fraction is basically where, um, you have the right amount of cardiac output that is divined by the amount of blood leading the heart on the amount of blood that entered the heart in the first place, so that sounds complicated. So the equation for this that won't make it easier is stroke volume, which is the amount of blood that has managed to leave the heart over the amount of blood that was in the heart to begin with, which is, and diastolic volume over 100. To get a percentage in this instance, you would apply it. The stroke volume here would be 30 mills, which is the amount of brother has left the heart by end diastolic value, which is our 50 mills, which is the amount of blood in the ventricles at the end of diastole in 200. It's in this case, the ejection fraction off this heart was 60%. This is normal. So the normal ejection fraction and normal in you and me is about 50 to 70%. That is normal, and that's what you kind of look for in a normal person. Stephanie. That's how you, um, Kathy injection fraction. How does this become relevant in heart failure? Let's talk about the systolic failure or half breath. So in half, ref, As you can imagine, you have a reduced ejection fraction because that's what the word says. But how does this work again? We have the same heart diagram, and you have a certain amount of blood entering, so you have the same 50 million entering left atrium. No problem. The problem here is later, so this 50 mills is able to get in the ventricles. It's fine. So far, so good. You got the same amount of blood entering the ventricles, and it's all right. The problem in systolic dysfunction is, as you know, in systole, the myocardium contracts to eject blood. Therefore, you're myocardium is dysfunctional for any reason. Or if there's a problem with Contractility, then you're not going to be able to pump the blood out, and therefore you're going to pump a smaller volume of blood so you'll be pumping out 20 minutes of blood instead of your usual 30 or 40 and therefore you have a reduced stroke volume. If you input these values into your ejection fraction equation, you find your ejection fraction is greatly reduced. About maybe 40% and 40% is actually a sign off heart failure, and that is, you know, pretty pretty early on heart failure. But at his heart failure. I've seen people in the world who have 15% ejection fraction on D. I can't even that is that is such a little amount of blood that it makes you wonder how any of the organs are working. It's it's incredible of the heart's still functions. But it's 15% and lot of people have it, especially if the elderly. So that's what systolic heart failure is defined by. On a reduced ejection fraction I I started dysfunction. The other hand is associated with preserved ejection fraction where you don't have a change in injection fraction. How does this work? This is the same heart again, okay? And you have the 50 miles entering the left atrium again. No problem. Except as the world says in Diastole, your heart is filling with blood. Therefore, if your heart has a problem with feeling off the blood, all the blood from the left atrium is not going to make it in your left ventricle, and therefore you only get about 20 mils, making it from the atrium to ventricle. So you contrast this to systolic dysfunction, a systolic heart where the blood was getting to the ventricles the problem was later here. You have a problem with early on where the vet nickels are not filling with blood in the first place. Onda as a result, obviously going to inject a smaller fraction of blood. So in this case, your myocardium is having problems with feeling. However, this does not necessarily mean that it has a problem with injecting. So your myocardium can still eject about it can still pump it just can't feel very well. So here you still get the 20 mils of blood leaving ventricles. So if you put this into the equation, you have the stroke. Volume here is 20 mils and the end diastolic volume is altered 20 mils. It's definitely you have 100% ejection fraction. So in theory, you're like Oh my God, that's amazing. What is the problem? The problem is that if you actually look at the volume of this blood, it's 20 mils, which is very little and is not enough to perfused all your organs. And that is what I started. Card failure is so we contrast systolic and diastolic heart failure. Broadly, systolic heart failure is the failure to pump, whereas diastolic is the failure to fill in systolic heart failure. You have a normal and diastolic volume, and your stroke volume is reduced in diastolic heart failure. You're reduced it and I still it volume on a reduced stroke volume. And obviously, as you can tell, the ejection fraction is reduced in systolic and preserved and diastolic. I hope that makes sense in terms of what systolic and diastolic dysfunction is and how it comes about. So what is that for the causes of heart failure? So you have different causes, sometimes the systolic and diastolic heart failure. And obviously there's the whole list off problems that can cause both kinds. But in terms of systolic heart failure, you can have things like diet do myopathy, where your whether my card for the myocardium itself is dysfunctional and therefore it's not able to contract well. And this can cause problems in systole, and they're figured I systolic heart failure or with your Micardis is inflamed like in my car itis common general causes off um, heart failure that cause the Starlix and I solid hard failure are things like coronary artery disease. For example, if you have your left and here descending artery that has got a storm business through sclerotic of the terrorist dealer cyst, and therefore you get a Am I. This is going to, in fact, a region of your myocardium, and it's going to disrupt either its ability to fill or its ability to contract. And this really depends on where Which part of it my card is. In fact, you can't really tell. Generally depends on you can see the semester G leads and things. Other common cardiovascular risk factors, like hypertension and diabetes and is specifically valvular heart disease can cause heart failure can cause both types in terms of diastolic heart failure. Specifically, things like restrictive cardiomyopathy can cause it where basically, my cardio is really restrictive, really stiff, and therefore it doesn't have the elasticity to to spread and to fill with enough blood. And because it's a restrictive, it's unable to fill, and therefore it's reduced volume of blood that's in pump it out so you get confused cardiac output in the context off a pericardial tampon on. What's happening is that your pericardium was full of fluid, right? So there's no there's nothing wrong with the myocardium itself. Your Micardis is completely normal Let's say your pericardium is full of fluid, which is the sac which hold your heart. And this is going to compress on the bio cardio from the outside. And it's not going to let it fill enough, and therefore you get a reduction in volume and a reduction in cardiac output. Right? So here I have a picture of three different hearts on D. This doesn't have much to do with systolic and diastolic dysfunction, but I want you guys to tell me, I'll tell you, Number two was a normal heart that Can someone tell me what the difference in the pathophysiology off heart one and heart three years? Why did they look so different from each other? Three days it and one hypertrophy? Yeah, Exactly. Perfect. Okay, can someone tell me why one is hypertrophied? But three is dilated. Anyone think off the path of physiological cause of this? Not like I'm not looking for a name like HX nose is something just like a physiological cause Consenting was in Santa. Yeah, Amazing. Yeah, really clever. That's exactly it's. Let's talk about concentric. Most is eccentric hypertrophy. Let's talk about why some hearts look different from others even though they're both in heart failure. So this has to do with changes in the myocardium itself. And I'm gonna ask you to recall from your memory from PCs that has to do with, like, fibers, my oh fibers and like psycho meals and things. Okay, it's going to be a bit of, ah bit of, ah, recapping session. So essentially what happens is is when you're in heart failure. Obviously, your heart is under pressure to pump harder, right? Something is stopping it from doing its usual work and therefore has to work harder to produce the same amount of cardiac output. Now this workloads, this increased workload can result in different structural changes. In the first instance, let's talk about pressure overload, and this is an instance where the pressure to pump the pressure within the ventricle is so high that you're myocardium has to pump harder to generate a higher pressure. Dejected that out of the heart card that sounds complicated. If you remember your cardiac cycle, the reason that your heart can even pump blood out of your ventricle into the aorta is because there is a pressure difference. If you have a disease that's causing a pressure All the load on your ventricle. This means that you're ventricle has reached a higher pressure in order to pump out blood. Anyone think of any conditions that can cause pressure overload on the heart. Specifically the left ventricle, her memory, hypertension, thinking about the left ventricle here. 16 OSIs. Yeah, exactly perfect right on the dot guys. So if you think about it, anything that causes increased after loads is going to cause pressure overload quickly recap it after. You know, after Lord is the pressure against which you're ventricle has to contract to eject blood. So if your aortic valve is still nose or it's smaller, then it's causing the ventricle have a lot more pressure on a lot more work to pump out the same amount of blood through it. Similarly, if you have a high peripheral vascular resistance, do two hypertension again. Your heart has to pump against ah, higher pressure to get the blood up, and this causes pressure overload on your ventricle. In response to this, what can happen is that sock um ears can be added, are added in parallel with each other. Okay, so you get this concentrically I particular becomes thicker and fatter. And my card, it just becomes, like, thicker, basically, and this doesn't increase the size of the ventricle. But what it does do is make the walls thicker, and therefore, what you have is something like that looks like this. So on the left is a normal, normal myocardium where it's all Children are all normal sized. But do the pressure overload they hypertrophy become greater and size occupying more space? Um, and that's what happens. And so this is a picture of what it kind of looks like a course section. You could see a very, very thick left ventricle year. A problem with this you can imagine. I mean, you must be like Okay, um, has more muscle. Therefore, surely must contract better if it has more muscle and your right to certain extent. In the very beginning, it does. However, you must note that this concentric hypertrophy is not accompanied by a corresponding hypertrophy of your blood vessels. There, for some of the myocardium that's building up does not have capillary supply, and therefore it's not really doing a lot of really pumping. It's not really contracting and therefore just sat there occupying space, but it's not really pumping. Um, and we'll talk about the decompensated changes that happened. How are feeling in a second? That's one of the things that happened. The other thing, the other. What the other picture heart number three we saw is your volume overload. Volume overload is when there's so much volume in the ventricle that it just expands and expands, and because it expands too much, it's going to basically, really damage the sock, um, ears. And it's going to damage the myocardium, and it's going to make it like, wider and kind of like make it loose and baggy onda conditions that can cause this of valvular regurgitation or shunts. Do you think about it if you have mitral regurgitation, for example, where blood is coming in from your age? Um, two ventricle, but it's going back to the atrium. What's gonna happen is that eventually, over time, a lot of blood is going to build up your ventricle new atrium, and this eventually, over time is going to cause a stretch in. There is reversible Stretch on. In histological perspective, this is seen as stock premieres being added in series to make it longer as opposed to thicker. So whereas in Pressure Overlord, it was made thicker. But being out in parallel in volume overload, you get out in series and makes it longer. And, like, larger and bag, you're basically it's in this case, the size of the chamber itself increases. It just becomes bigger and baggy. Essentially. So he has the picture again for you to contrast. What pressure and volume overload look like? Um, yes, Great. Now let's talk about heart failure. The past, like what happens, is consequence of our trailer. So you did answer that question earlier. If you have heart failure primarily, the problem is that you have a reduced cardiac output. This is defined usually by the reduced stroke volume, right, and as a result, you get end organ damage because your end organs are not being profused and they cannot function. And therefore your body just is not coping. However, your boy doesn't give up this quickly. Actually, it's a bit of a fighter. Were all fighters on your body has many ways of compensating for this heart failure in the beginning, because it's not gonna give up on your heart that easily, and it's actually really impressive how this works. Let's talk about how your body is able to initially compensate for initial heart failure. We talked about the initial problem. The initial problem is you have decreased ventricular function. Left ventricular function. Okay, you have a decrease stroke volume and a decreased cardiac output. If you have a decreased Codec output, chances are your blood crashes going to plummet. It's going to be low. Okay, This is not good, because again, this means low organ profusion. So what's gonna happen as a result? Anyone Tell me, what is the first thing you think or physiologically in in a BP response? What is really important in your body that controls BP? Ross? Yeah. Ross board else before us. What detects the drop in blood pressure? Barest after is Yeah, perfect. Exactly. So this decrease in blood pressure is going to be detected by by receptors. Anyone remember where your bowel receptors are? Here's a got andi carotids Sinus. Yeah, I had to sign. This is the more important one. Exactly. Yeah, perfect. Cool. You guys remember load from last year. Great. Um, so great. So if you have a decreased BP your bowel receptors. They're going to know this. They're going to be like, Oh, we need to do something to get it back up there. First thing is going to do is that it's going to increase sympathetic outflow in order to increase about pressure. The way it does this, a sympathetic outflow is going to increase the contractility in your heart. This has to do with calcium concentration gel, my cardio, Um, and it's also going to cause peripheral days of constriction and venoconstriction. And these together, as you can imagine, will cause an increase in blood pressure. What your virus, after all, to do is they decrease the parasympathetic out flow to the heart. This obviously slows the heart. It's obviously usually would slow down the heart if you had increased parasympathetic your flow. But here you have a decreased percent that er flow, and this will in paradoxically, increase your heart rate. And finally, it's also going to stimulate 88 secretion. Can anyone tell me you were 88 acts? What is like where does ADH axe and how is it increased BP tables of kidney CD kidneys? Yeah, exactly. So it acts to re absorb water and if you re absorb water, you have more fluid in your body and that increases BP. That's what you get to. Therefore, this is one way in which, um, decreased BP in a heart feeling heart convert compensated for initially the other way it happens, is your kidneys. They themselves detect that there's less blood. So your kidneys are very sensitive to hyperperfusion. Okay, so what's gonna happen is that they're going to activate like you. Many of you already said the Brennan and you're tense and aldosterone system and this is gonna have a couple of weeks. Firstly, it's going to obviously take other securities off aldosterone aldosterone extra of increased salt and water absorption in your kidneys. Which internal increase that pressure and what it also does is angiotensin two is able to cause vasoconstriction in the periphery and that because in increase in blood pressure and therefore initially, even though your heart is failing, even though the cardiac output is smaller, your body is able to, like, initially, systematically compensate for this through these mechanisms. So I hope this makes sense. Let's talk about where this goes wrong. The problem is that as much as your body is able to compensate. When these competition mechanisms occur for too long, taken like basically fall off the cliff and go downhill and I'm going to show you how that happens, the first human happens is like we discussed is that you get assistant activation of Iran and agitated and add Austrian system. What's gonna happen is that because you have this because we talked about how there's now more razor constriction, there's more fluid in the body because more for is being absorbed in the kidneys. You have a higher BP. This is going to cause a pressure overload on the heart like we talked about earlier. And when the myocardium is stressed, it's way too stressed. As a result, when this happens for way too long, it's going to decompensate. If you guys remember the frank styling law from first year, what's gonna happen is that the certain extent when you end diastolic volume increases. This is really good because the reason contractility after a point when it's too much, it's going to basically damage the sacrum ears in your myocardium and therefore they'll stop working. They'll stop contracting and you for getting a decrease stroke volume all over again, and then it gets quite bad. Second, if you have again the increased feeling and ventricular pressures this is going to cause, either it's going to cause a backflow of blood. If there's way too much pressure and your heart is unable to pump all this blood, it has to go somewhere, right? So just go to go backwards on everything. The context. The left ventricle is going to go backwards the lungs and cause pulmonary edema. If it's in the cases, right ventricle is gonna go backwards to periphery edema in your legs, in your body, in your sacrum. Yeah, so that's another problem. That's volume overload as well on D. If you get the dietician off your ventricular walls, they've been caused to problems. First dialect. A shin of your ventricles reduces the pressure within the ventricles, which means that as you know what, because the entire cortex I could realize and pressure difference is this really going to mess things up in terms of pressure differences and make it harder to pump second. So if you have delectation along the valve annular, the valve annually is basically a fancy word for saying the region between the ages of the ventricles, where your mitral on tricuspid valves are. If this is dilated, this is going to basically damage the valves and cause valvular regurgitation. And as we discussed earlier, this one cause volume overload and damage your heart again. If that isn't enough, as you can imagine. If you remember again, your competition mechanism was to cause tachycardia. Sympathetic stimulation. If this happens for Toula long, if you are to tachycardic for too long, you're going to spend way too much time pumping and not enough time filling. And there, for the amount of blood that is filled in your part is lesser because you're spending more time injecting rather than feeling. And you have a reduced heart output as a result. And finally, as well as you can imagine in a hypertrophied hot where you have more myocardium. Now you have more cells, a supply with oxygen. The oxygen demand of the heart itself has increased in attempt to compensate on become more contractor. Your heart is increased its own metabolic demand which initially spine. But it happens to extent where if the oxygen demand is so much is going to become a scheme IQ on can cause, um, I've on for the skin. It damaged your my cardio. Like I mentioned earlier. This is not a problem if you're on athlete, because when you're an athlete, you physiologically high part of your heart and this is accompanied by a hypertrophy of your blood vessels as well. And therefore, hypertrophy, tarts and athletes aren't usually a problem unless you get hypertrophy cardiomyopathy, which is the whole problem on its own. But I want talk about that today anyways, and the last decomposition mechanism going to talk about is the persistent levels off all these chemicals like and his hands are doing aldosterone and catacholamines, and they have their their in attempt to sympathetically stimulate your heart's. But over time, they can cause remodeling your ventricle of my cardio, um, and make it less contracts. I'll I'll make it less easy for to fill on barefoot cause, um, discarded output because it can't pump very well. So this is essentially synopsis of where things go Well, things go wrong. Sorry. And how it can basically tip you over the cliff on put you in like irreversible failure. So how does this manifest in patients who could quickly brush over the symptoms. What is the time? Me second, it's 8. 45. Really? Sorry, guys. I would be a script. It's possible to get you out of here by nine. I try, um symptoms, Houses manifest. So anyone tell me the general symptoms of heart failure that you can see in both types of heart failure? Dyspnea Okay, Dema PND candy is more left sided. Heart failure Generalized. Dema Yeah. Okay. Anything else? It'll charges of breath? Yeah, Okay. Something else? Something else that's really basic That has to do with less blood. Leaving out palpitations yet? Perfect. Something else? I'm thinking off dizziness. Yeah, exactly. A long landed is Nece pretty? Yeah, that's the one. Fatigue is literally like probably the number one presenting symptom off heart failure because it's just very obvious to notice for patients like I don't know what it is. And then bring your retired lately, and then you get all your swollen ankles and you have, like, a primary cramps When I listen to your heart and your lungs and then you capture basically, fatigue is a really big one. Um, so general symptoms you can get with both times of heart failure, fatigue, palpitations, exercise, intolerance and dizziness. The other ones you guys mentioned are really good the correct. But they are for the more depending on which side of heart failure you have. Let's talk about that. If you have left sided heart failure, what is happening? You are not pumping enough blood from your left ventricle, right? So blood is gonna go backwards, it's gonna go to your lungs and therefore you get pulmonary edema. Hum radio has a fancy way of saying your heart back flow of blood and fluid into your lungs. Um and this means that's gonna make it more difficult for you to bleed for you to breathe because it's going to cause a VQ mismatch within the, um, hum really tissue. Okay, I can talk about the path of this more specifically in more detail, but don't have the time for that to the unfortunately, but essentially, you get some edema and this obviously, because of the VQ mismatches, going to make it more difficult for you to breathe on, for example, think about it when you're lying down. Okay? When you're asleep at night, when you're lying down. Your venous return increases to your peripheries increases to your heart. You haven't increased venous return into your right ventricle and then into your left ventricle eventually, and basically because there's more fluid up centrally when you're lying down. This means that there's going to be more fluid in your lungs when you're lying down. And therefore these people would left sided heart failure. When they're lying down at night, they'll be like, Oh, you know what I get. I get really breathless at night when I'm lying down, Um, but then the minute they stand up in a bit in a couple of minutes, they'll see they're less breathless, and this is because when they stand up again, the fluid is going back down under their legs on do is less fluid in the lungs. This is related to pee and D. Um, pretty much this is pretty much very similar thing to PND, and these people PND basically have again breathlessness at night when they're asleep. Because blood fills up centrally on, they usually will complain. The way I pick it up is if you are, if you suspect in some of the heart failure us and the question, How many pillows you used to sleep a night? Um, and the Benicar two or three on my card. You have a sleep upright, or do you always sleep like lying down like, No, I sleep upright a lot, and that is very characteristic appearance is because if they sleep lying down than they're really struggling to breathe because this is where we want fluid and therefore they try to compensate for this by sleeping upright, and therefore there's less fluid coming up to the heart. Um, right. So the heart failure you have back from the right side is the fluid is going to go back to your periphery, is gonna go back from the right side atrium going to go to your ankles, Um, on it's gonna go to your, um, gastric area as well. That's why you get gastric symptoms, because if it's if it's going too congested in your in the veins around your tummy and your legs and everything, you get symptoms related to those areas. You can assess how severe the edema is by checking for putting a demon starting from the legs and work your way up. He started the shin and then keep going up to their knees and the thigh on, Do you see until what? Like which part of their body they have a D motto when they tell you kind of how severe it is. Really? Um, yeah. So this is what I found. What? Pitting edema. You probably seen this in your cardiovascular exam. If you press down the shin for a couple of seconds and then let go and it leaves like a pit on this LDL is fluid in the same as well. And this is not only with half for that you can get this anytime you're feelin the legs, like if you had any injury, you get a demon, your knee, and then it goes down to your shin and causes fatigue. So how do you diagnose heart failure? Well, to be honest, you got heart failure is really easy for your exams because it is very much clinical diagnosis. If you remember these signs and symptoms that honestly will tell you the diagnosis and therefore in order to corroborate it was diagnosed this instead of helping it Teo, make you diagnosis, use BNP, which is a blood marker for beat beat beat a natural crap right on what it does. Is it basically secreted in your heart in response, the left ventricular strain. And so somebody's and heart failure specifically left side of heart failure. That means the left ventricle is under strain and they're probably going to be secreted a lot of BMP. And therefore, if you're already suspecting heart failure and somebody and you do a blood and you get a high bnp like right, yeah, I'm pretty sure this is left heart failure. Okay, so this is something you just kind of have to learn, which is the classification of heart failure. So the New York Heart Association has four classes into which you can divide any type of heart failure presents, okay. And the categories under which these air decided. Oh, how is what symptoms the patient complains off whether they able to do physical activity And if if so, how much are they able to do during the physical activity? Do the experience, any symptoms and how are they addressed is under these four categories. With that in mind, when someone tell me what NYU Jake last one symptoms off. Plus, one patient would love life with heart failure able to walk to the shops. Okay. Exertion dyspnea. Keep going. Use these four bullet points to kind of help. No symptoms at all, yet? No symptoms? Exactly. Yeah. No. Okay, well, normally wear a stretch, but yeah, basically, it's like almost Zika's negligible amount of heart failure. Okay, They have no symptoms. You don't have breathlessness. They don't have that. Since the night. They don't have, um, no complaining off. Like nausea or decreased appetite. That's due to the heart failure on they are normally able to able to exercise normally without no, with no limitation, no angina, no brothers is an exertion, and they're perfectly fine addressed as well. And they don't have any typical heart failure symptoms like palpitations or breathlessness. Um, so that one Can anyone tell me what class for is which is the other end of this breathless at rest. Okay, I think this is a dumb question. Oh, sorry. I look a question later. Sorry. Breasting dyspnea into my address to civilization. Yeah. Great. Come along. Those lines. Yeah. So what happens is if it's really bad, this is the worst possible thing. It's in the other end of spectrum. It's when you're serious symptoms. Even at rest, you can barely carry out any kind of activity. Whether it's walking from your room to the toilet, that causes breath that causes exertion that causes this near that causes chest pain. Any physical activity is is uncomfortable. And but even the symptoms of present even addressed the breathless at rest. Um, Andi, they have a demon. Things like that. This point you to really bad picture and the other two classes a kind of in the middle. I let you read this in your own time. But this is something you just have to memorize because you will get SPS on this. Right? So you could you talk about treatment? How much of each time? Okay, 10 minutes. We can do this. I'm not feeling this is half of the drugs, like by far the most. This is the best thing you could remember from this whole presentation. If you're over two things, one is the part of his charge of heart failure. Second is the drugs and how they work. So because it comes up in PT all the time as well. So happy drugs. First line, you have a inhibitors or beater blockers. Okay. And these are given to anyone with suspected heart failure. Anyone Tell me, what's second line for heart failure? If a thing of it is a beta blockers are working, but they aren't quite being extremely effective. And you want to give them something else on top of it. What do you give them? Okay, what I had, you know, MRSA. Sorry. Calcium know quite nitrates. Nitrate is more. Not really. That's more for skin McCarty's 1000 channel blocker. No, no, not really. Um yeah. Yep. Diuretics yet perfect. Solid. And somebody said, mineral mineral, a cortical receptor antagonist that is right on target. So you get them at a dollar store antagonised. I'll talk about how these work in much detail in literally a second if these don't work. Uh, and it's quite rare that you prescribed this, but this is only by specialists, cardiologists who prescribed these drugs. You can also give third line drugs like these without describe later. But these are like really lot like last last option drugs on described by specialist only. So let's talk about a sin Hib. It does. Can anyone named me comin a stimulator that's used about pro Perfect. Yeah, this is the most even ramipril very common drug works by inhibiting the enzyme that converts. And you're tense and and your denting two. Okay. And your tension, too, causes problems in heart failure. It increases sympathetic activity. It increases the amount of fluid in your blood and therefore, is bad. I mean, in decompensated heart failure. And therefore, if you give someone grab a pro, it's going to inhibit the formation of angiotensin two and therefore inhibit angiotensin two is effects. Okay, so that is first line about video. Can someone now tell me? Oh, no. Well, see, a common side effect. Most common side effect that people complain about when they put on the Lipitor. A golf. And why did they get this cough? Great. The kind of yeah, but it's too much ready, kind and build up. That's really good. Okay. Um okay, So give you scenario. Patient comes in, you give them how you get you the heart failure on Do you prescribe them? Ramipril you send them home to come back in two weeks. They're like, I don't know what it is, Doc, but I'm really breathless. Um, how about brothers. Sorry, I'm coughing a lot. I don't know what it is. And what do you do? Air bees? Yeah, perfect. You give them and and you're tense and receptor blocker. 100 Sense in receptor blocker, which is basically works very similarly but does not produce the same side effects. In fact, it's arguably better. The only reason we don't use it routinely because it's more expensive. Okay, so an example of this is kind of start on losartan that that kind of the Crohn's airbase, and they work by blocking the angiotensin two receptor, and it blocks a very specific receptors and you're dancing Do normally binds 200 s and one receptor, and you're so Airbnb I can't starter are going to go and block the 81 hours. Okay, this list this leaves the 82 R's open. 82 hours are good. 81 hours are bad. Okay, if you have more 82 hours open because all the 81 hours are blocked. Um, this is going to encourage things like vasodilation in, and it's not going to allow as much aldosterone to be secreted, and things of that basically has an opposite effect to angiotensin one receptor, and that's when it's you. That's how it works. And then be two blockers as well. Okay on. Can't remember the most common beat of locker prescribed in heart heart failure with that role. Yeah. If you go on the cardiology world, literally everyone is in the socket like everybody it is just is second nature in the words everyone's on it. And as the most common, um, hum failure. And as you Connecticut imagine it works in your beat of one of your receptors in the heart. It is cardio specific, unlike unlike atenolol, which is not cardio specific and can cause, like Broncho spasm and stuff was separated, still causing extent of bronchospasm. But it's way more cardio, specific and therefore is indicated. Um, on D. Yeah, this isn't here, but anyone named me any side effects would be two blockers. You may not have reps tell us yet, but it just come on, PT, I am regard you okay? Yeah, Miles, some really side effect. Is it? Bradycardia Fatigue? Uh, well, okay. Cold extremities. Yeah, Exactly. Yeah, it's a broken constriction. Like I said earlier. Bronchospasm perfect. Also poor, poorly perfused refreeze. They get called extremities and stuff on bronchospasm. Does the do most common side effects? Yeah, Great. Let's talk with diarrhetics. Really? This is like my favorite, but it is and I presentations. Have you haven't been listening so far? Please listen to this because it will help you. And it will make things very clear because diuretics can be complicated. So let's talk about the kidney. The kidneys, very ambiguous. Organ on do it is like what's going on? Lot of iron spotting around. And it's hard to understand diuretics, as patients refer to as water tablets work on the kidney. So let's talk about a kidney, okay? And how did the absorption works primarily? Okay, first in your kidney, you have your glomerulus. Right? Lamela's is the primary points off filtration in your kidney. Okay? And this is where about 20% of your plasma gets filtered. Okay, So basic things, like most things like red blood cells and proteins and all those kind of things that fluid out and you're left with this fluid that's full of, like, a lot of electrolytes. Basically this fluid and then going to flow into your approximate convert The tube. You okay? by the way, I'm talking about normal kinesiology here. Right, So this filled it Fluid isn't going to cause your p C t in your piece. Easy. You have sodium bicarbonate absorption and you also have a lot of just sodium on its own being absorbed. Okay, the PCT is where the majority of your sodium is reabsorbed. So about 70% of your sodium is reabsorbing the P. C. T. And this reabsorption is eyes Oh, a small tick. When I see Eisa, a smart take that means for every morning local of sodium is absorbed he also have a molecule of water that's absorbed and therefore you get a lot of water also reabsorbed in the p c t. Okay, then you move down to your loop of handy. So this is your descending You prepare only over here and now you have the loop of handy itself. Within the loop of handling is important to note that it is impermeable to water. Sorry, that's wrong. It is probably is very probable to order. So you know that is very prominent water and therefore water leaves. Okay. And the the reason that water's able to leave is because Thean surrounding interstitial environment in Lupus family is hyper small tick that means is very high in salute. And therefore, what is going to move from a region of high concentration Too low concentration on going to leave lots of water is last year. Then you have your distal convoluted tube you on your ascending loop of Henle e, which is over here, and both of these things are impossible to water. Okay, you are sending loop of Henle E on your on this accommodated to both employed with water. This means what I can't leave, but other things can. So importantly, you have a simple water over here in your ascending loop of Henle E, which removes sodium, potassium and chloride ions in the ratio of one is to want us to to, uh, this joint is about 25% of your sodium, which is still a very significant amount. It's really is quite a significant portion of sodium on d again. Just because sodium is leaving doesn't mean water can leave, because again, it's improbable. The water. This is an important Cymbalta in your DC See, you have a sodium and chloride Cymbalta. That room was seven chloride. This is a smaller proportion of sodium, but it's still important again. No water can leave, so at this point, a lot of sodium and potassium, mostly sodium and chloride, have been removed. And you have a lot of water remaining in your DCD at this point. You then move onto collecting ducts, right? The main transporting we'll talk about collecting duct is this one. It is a kind of it is an anti border, so it removes sodium, but puts back potassium and hydrogen ion in exchange. Okay, so it takes up sodium back into the body and throws out potassium and hydrogen ion. Okay, um and this is important to note because aldosterone works on this transporter. So aldosterone up regulates this more adult stroke means more sodium absorbed and more potassium excreted. All right, next thing is that I can imagine earlier you have all this water now in your duct, and this is removed in the collecting down. And this is where ADH added a radical more, packs it up, regulates the aquaporin in your collection duct and increases water absorption here. Um, now, couple of things to note about the aldosterone receptor thing here So this transporter depends on two things. One, if you have a higher concentration of sodium in your ducks flowing through this means more sodium is gonna be absorbed and more protection is gonna be throwing out, right? Can someone tell me what problem this can result in the point? How? What could this be a bad thing, Hypokalemia? Yeah, Exactly. Because you're throwing out more potassium and you see on this because hypokalemia that makes us what other problem can this cause Metabolic something? Yeah, Exactly. Better for the warts. Alkalosis. Yeah, corrective alkalosis. Because your age, Because your protons, which are acidic, are being removed. And therefore, the blood surrounding the kidney at that point is going to have less each plus there for going to be more alkaline. Take that. Acidotic Onda have just some that are you. Oh, see summary. Continue quickly. Okay. I can't roll with that. Side is. Anyways, um that's what wanted drugs. Unless you're diarrhetics work, you might have seen a slight already, but on furosemide works on this simple water on the ascending loop of Henle e. Okay, The furosemide is going to inhibit the reabsorption off sodium, potassium and chloride in the ascending blow up of heavily. If you have less sodium being removed and re absorbed into your blood, that means you have more sodium in the duct and therefore you have more water in the dark and never more water is going to be removed in the urine. A nephew was my books, far as I diuretics work on the sodium and chloride and Cymbalta on the distal convoluted tube. You, As you can see, this is only involved with me and we'll get 5% of your sodium, whereas the transporter and you're sending a loop of Henle was about 25%. And therefore that's like the more significant transport and have a few hours. A night is a lot more powerful than thiazide, but few hours, Um, I can also be nephrotoxic, and therefore sometimes they be used in preference to bend the guys. I'd like your attics Onda. Finally, you have, um, you have your spironolactone spironolactone is going to act on. Um, sorry. Second, spironolactone is going to inhibit aldosterone. It's going to antagonize out Ostrom, and this means that there's less sodium being re absorbed, and there is more potassium staying in the body. Okay, this can cause hyperkalemic because less potassium is being removed, and it's going to cause most of most more sodium to remain in the kidney. If there's more sodium remaining in the ducts, that ultimate is that more water is going to remain the duct and therefore more water is removed from the body. However, this isn't a very significant amount of sodium that's being reabsorbed, and therefore it's not very powerful. Therefore, spinal action is usually used in combination with either a thiazide or furosemide. Finally, third line drugs are digoxin, which is a It's a different all school drug, Um, has lost of toxic effect, which is why it's not used very much anymore. It's used in old people, and people who are quite sedentary don't exercise very much. There's lots of evidence to say that when if you're under doctor, then you're quite active. It actually doesn't really have much of an effect on your not really sure why, that is, I think you know it's one pump. I'm not really sure feel free to Google it, but it's using old or so dentree people, and it has lots of toxic side effects. So I would, um, memorized some of these for the sake of pt Other third line drugs that are extremely specialist very rarely prescribe. You get IV abrading on. So you control your cubital valsartan You confuse up in your own time. Not gonna go into them now for the time. Oh, great. It's 10 past nine. Okay, um, I'm not gonna give you any longer, but basically a whole section on thrombus formation as those his drugs. Um do people want me to go over this, um, or to be the one to go to SPS. I've got about four s p s. I know it's really late and you must be really tired. Please go over it. Thrombus I'd say I'm just going to talk about virtualized. Try at and talk about The fact is affecting post on vacation, and I called the anticoagulants. Keep going. Okay. Cool beans. Why so thrombus formation? Uh, we all know that thrombus is bad, because if your promise you can get lodged and cause a stroke, it can cause clots and other organs on mean. This causes ischemic damage to those organs and can cause failure. Basically, office organs. But how is it from. How do these throbbed? Thrown by form in the first place. There's a thing called virtuals triads that basically lists three factors that determined or kind of predict the likelihood off the formation of a thrombus. Can anybody named these told, please? Stasis yet? Perfect. Two more hyper coag later state yet perfects. Yep. And I think in your Yeah solid. Yeah, exactly. Perfect. So the first thing is hyper card ability. What does this mean? This means if anybody is in a state where they're more likely to have the coagulation factors upregulated, this means that more likely to form a clot because those chemicals are regulated. So okay, if, for example, you have platelets that I have a tendency to are the eight each other more than the regular person, this means your hypercoagulable if you are have x increased exposure to things like east region. For example, if you're pregnant or take the old contraceptive pill, this also increase your chance of forming clots because of the surgeon. Cancer is a hypercoagulable state on, and because it increases the, uh, coagulation factors and makes you have a regular, the other thing is endothelial damage. Okay, anytime a tissue in your body is damaged, it's going to secrete side kinds and cause an inflammatory response and in from to response usually involves the release of clotting factors. And therefore, if you have endothelial damage due to oxidative damage or because of like October and flowing vessels, this can cause inflammation and lead to the release off clotting factors that can cause clotting. Thirdly, if you have venous Stasis, what this means is that if you're in a situation where, um, the blood in your in your in your vessels are kind of stuck there and they're not flowing, this means that the blood is just going to circle on its own with in that one area. And this can cause a clot to form because it just can cause, like blood to circulate within itself on discount cards. A lot. Ah. Example of this is if somebody has, like a varicose veins where there's a lot of blood just sitting in their veins on, do not really moving on. Disk is a big risk factor for formation. Lots. The way to remember this is with this, um, acronym. He's virtue. Oh, so he's virtual HPI hypocritical Ability IV and the damage and be for venous Stasis. And now let's talk about what kind of things in a person can predispose you to developing thromboembolism. I use the acronym thrombosis, which makes it easier. He's the travel. Anyone traveling on a flight their legs are down, placed on a statin is sitting still for a long period of time. On this can call Stasis, uh, and therefore cause a clot to cause a DVT uh, deep vein thrombosis in that cough's have a card, a motor there or contraceptive pill pregnant if they're old. If you have cancer, if they have to, um, Ophelia, if they're beasts, Onda if they just had surgery. Because sheriff surgery people are like a mobile bed for a long time. And again cause blood Stasis if they're smokers. Because obviously, as you know, smoking is a very significant cardiac risk factor. Consummation of plotz sickness. Cool. This, I think, may have talked about this the child Vastic a lot harder that has Let's go. This basically help you determine whether somebody needs to be on anti coagulation in order to as prophylaxis for thrombus formation. Um and this is like this is quite actually used every day on the ward. Like you calculate somebody Chad score to tell and has bled school to see the need to be put in a big sea bands or other anticoagulants for prophylaxis. So you can go over this new meantime, I would memorize this table because you get SPS on it. So, um, I'm not gonna go over all anticoagulants and and the platelets and realizing drugs. But this is a very rough road shot to show you, Um, how the dividers. Because in my head, my first love this I was like, there's so many drugs and they also like to do the exact same things, Like how they different. This lotion should hopefully help you, like, divide things on, tell you like what is class and what, And to make your life even easier because I'm a bit of a legend. I am going to share with you my personal anticlotting drugs notes that I made repeat E and this is he some supp like every single like drug. The mechanism of action when they're indicated the common most common side effects on bone There contraindicated. Um, I made this flow chart thing I use and have memorized for PT on D. I will put this on there on the slide. So when you get slides, you can look at this and make your notes on this because this everything in each new and I use, like, pasteurizing other things to make this. So it's It's a It's a reliable source, I'd say. Um, great. That was thrown formation and coagulation. Anyways, um, here's some SPH. Um, making a k two large thumb. That's right. Fab. Thank you. That's let's let's crack on versus really quickly. Okay. This is a very kind of question you would I would predict would come up in your s to exam. Um, they're like they're, like, this kind of stuff lot. Okay, I'm going to stop it. There was a time, actually, we get least 20 of you to have all that. Yeah. Perfect. Okay, solid. Uh oh. Wait, You were doing well then. Okay, The answer is last three. And the reason for this is that if you look at on the classification that we saw earlier, um, in order to be class as a class, do you have mild symptoms? Ah, slight limitation. Physical activity, but you're usually okay at rest. And you have some, like, regular symptoms during physical activity. You look at the SBA. Simon has has exertionally symptoms. He's okay, addressed. And he has other symptoms as well. Uh, chest pain and things like that. And that puts him in class three. Okay, next. Next. SBA. So I have recorded how many people on said the thing in. So I'm making Have you? You recorded the percentage of people that answer the previous question right to tell? No, I haven't ordered it from this from Okay, nor is give a rough estimate. I know there's more people for beat and see. Um, can you remember? I think it was about 60. 40 60 40. Okay, cool. Oh, um Cates and more people to will be great. Okay, We can stop it there. Uh, okay, my guess is 93%. 90% but it be great. Yeah, correct. Perfect fit. Stuff. Guys, I think I think Meg mentioned isn't her talk is well, we spoke rights familiar. Um and yeah. So if you just look at my notes for the anti clotting drugs and then has negatives of action, if everything's just memorized that, um, on D of SBA. Okay, solid 79%. Really good stuff, guys. Great. Yeah. So be so. When? And he's in a better, um, they come back and they have symptoms like a cough, a dry cough. Then you switch them to an angiotensin receptor blocker, which is what? Losartan or, um, kind of start center. Okay, last one. Sorry. Just this is just the reference slide which has that information on it, right? This one is I haven't talked about this today on I put this in and purpose because I didn't have time to go over this on the talk today. But it's definitely something you should go on your own time. I didn't really learn. This is the last minute, but it's actually it's really important. Especially your skis. So I would learn it. Um, just a couple more people would be nice. Yeah, You don't know it. Guess it don't know about it. Okay. Great. Perfect. Okay. Um, unfortunately, um, but the answer is B. I don't have time to explain why it is B, but I know that geeky medics has a very, very nice resource. That explains exactly what each way, vis. And this is what I used to learn. It also very nice YouTube videos out there. That's really, like a hard It takes about a half hour to learn, and I would learn it. Yeah. Anyways, that, um, complete your presentation, guys, thank you so much. I put the slides up for you. Please send a few back form. Really appreciate that. Thank you for coming today. Any questions at all? If you could ask us now. Also, please sign up for our office, Keesey. 2 to 1 session as well. Um, you really benefit from it? It's great. Great fun. Yeah. Yeah. Thank you. So, no, that was a great talk. When we apologize running over today, everyone there's a lot to cover with. The rhythm is a heart failure. Um, but we hope the session was used for nerve. See, the recording will be going up and I put