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Okay. So I will just make a start now then um just in the interest of time. So my first point is to describe the structure and the function of the heart in relation to its electrical um conducting systems. So the first question is going to be what is the pacemaker region of the heart scope? This should be very basic revision for um case too. Um If I launched the polls actually, um sorry, give me a second uh huh. It electrical. Now, there you go. So I'll just give you 15 seconds to answer the questions. OK. Brilliant, nice. So answered too. That's going to be the sinal atrial note. Yep. And as you guessed that is indeed the correct answer. Um So a is the Aviane and not be for ventricle for the ventricles. And the delay of the impulse bundle of his is the pathway to get to the ventricles. Um bundle of ken is actually the accessory pathway. So that's your abnormal pathway that's involved in um conditions such as wolf Parkinson white and back in this bundle is the bundle that innovates the left atrium. Okay. Next one, um a patient presents with lightheadedness and palpitations that lasted an hour and E C G is performed and shows delta waves. So what is the likely diagnosis and what pathways responsible for this? Ok. Quickest be eight, another 15 seconds for this one. It's nice. Um We'll send out the slides to you. Um We'll send out a feedback form and you can fill in that. Um And you can access it from this app gold medal. So that would be involved in the feel about form as well. Okay, Britain. So the answer you've put down is see. So also um just for the not the positive, it's for Dom and Laura, if you guys wanna um answer us all, feel free to drop in the chat. Um Yeah. So um the answer is actually c perfect. So Wolf Parkinson White um and that will cause your slurred delta wave which goes upwards. Um That's because of the pre excitation of the ventricles. So on the E C G is gonna come up as some kind of electrical activity because of that pre stimulation. Ok. Brilliant. So, um this is just a very quick summary of the electrical conducting systems of the heart. It all starts off with your sinoatrial node. Um That's your pacemaker region, as you mentioned. Um So as I mentioned, um and the bargains model is what innovative your left atrium. So that will go that way. Um Primarily the rest of the conduction path ways to go to is a VM um through the international tracks, um which will also innovate the right atrium. So once that the A V N um your impulse will get delayed and after that, it will transmit down the right and left bundle branch is um and that will go towards your respective ventricles. Oh, and this is just a summary of the main facts and figures of your electrical contesting system. So I'll just run through it very quickly. So the sinoatrial node is the natural pacemaker. Um that's located in your rights uh atrium and that's responsible for your atrial contraction. Um It's 6200 BPM at rest and it's regulated by the autonomic nervous system. We'll get into this later on, but it's primarily vagus nerve for parasympathetic and the sympathetic trunk, which is what it says on the Tin Bachmann's model is responsible for your left atrial contraction and it's the main intra-atrial conduction pathway um bundle of his um that's the big pathway down towards the ventricles and it's made up the right and left bundle branch is um A V N is delay that impulse towards the bundle of his um and the trokendi fibers will innovate the myocardium itself. So the impulse would go from the endocardium outwards. Ok. Brilliant. And that was just a very quick summary of um that's so L2 is going to outline the physiology of the electrical conducting systems of art. So if we say um what is absent in the pacemaker region? Um Okay, what's report? I'll give you slightly longer for this one about a minute. Okay, brilliant. So the answer you've gone for is e potassium channels. No. Um The answer is actually be so we'll get into this later on but potassium channels will be present in most cardiac might most cells actually that has a action potential because you need the potassium channels to re polarize. Um And far sodium channels will not be present because that will give you your funny current and primarily is driven by calcium in your pacemaker region. Not sodium. Okay. Um What phases of cardio action potentials are in pacemaker cells? So you can watch the pool now give you about 30 seconds. Sounds of this one. Okay. Also um Sophia can you see you can't see the zoom thing on the left side of the screen, right? Just, just to check, right? No, we can't. Yeah, sorry. Thank you. That was a quick spoiler alert. Sorry. Here. The actual answer is a so it's gonna be 403 and we'll we'll go into why in a second. Um So um it all starts with phase four but yeah, we're going to y in a second. We'll just do these questions from them. Sorry, sorry, technical difficulties, right? So OK, just a quick presentation on this. So in the sinoatrial node, you've got the three phases I mentioned to phase four, phase zero and phase three. So in phase four, you've got your um H D N, which basically we'll give you your funny current and these are going to be permeable to sodium and that gives you your funny current because it's going to give you a slow uprise. And that, that's why I mentioned that there's no rapid sodium channels there. Um And this funny current is going to be spontaneous and around minus 50 millivolt is your threshold to trigger your transient type calcium channels. And that minus 14 millivolts that threshold is needed to trigger your l outside calcium channels. And this is what I mean by when I say it's calcium driven. So in phase four, um no sodium is involved in this because the pacemaker lax that far sodium channel and they've only got slow sodium channels. So you're influx of calcium is what triggers the deep polarization. Um And it is slower than other cardiac might sites as calcium is not as um fast at depolarizing compared to sodium. Um So in phase three, um you're all type calcium channels are going to close. Um and the potassium channels will open and this allows you to re polarize by expelling potassium from the cell just to talk about the A V note. Um So sympathetic innovation um will increase your conduction to the A V N and I will increase your slope at phase zero. No epinephrine will bind to your beta one adrenoceptor is to increase interest, cellular cyclic amp. Um One way to remember these adrenoceptor xyz if you think about B to one, um it's like one heart. So beta one, so one heart and beta two is for lungs. So beta two is like two lungs. Um So in terms of um drug therapy, so beta one is going to be um the target for beta blockers. So another thing is the process, the parasympathetic innovation is going to be supplied by the vagal nerve and this will decrease the velocity to the A V N. Um And therefore, it's going to decrease that slope, phase zero. Um This is our Colin will bind to your muscarinic receptors which will decrease that interest ended a cyclic amp um Over simulation of this will actually result in an A V block. Um And the A V notice a primary target for things like atrial fibrillation and atrial flutter, which I think Laura will go into more detail apart. Cool. So uh in terms of the actual rest of the cardiac wire sites itself, you've got the rest of your phases. So phase four, phase zero, phase one, phase two, phase three. So let me talk about this will always start a phase four. Um This is your true resting potential at 90 millivolts. Um And this is where your potassium channels will roll open and you're fast and sodium. So you're fast, sodium and calcium channels are all closed at this point. So um at phase zero. So this is what you see from the big spike up here, that's going to be a rapid deep polarization um at minus 70 millivolts. So that will be a threshold and this is when Axion potential will be generated. So at this point, the fall sodium channels will remain open and your sodium, your potassium channels were closed and this will cause a rapid rise up to about plus 10 millivolts and then that will be followed by phase one. So at this point, your transient outward, potassium channels will open and potassium will leave the intracellular space. And that will cause a small dip in your millivolts. And in phase two, you're going to get a little plateau and this plateau is caused by L type calcium channels opening and this allows calcium to um into the intracellular space. So um by balancing the potassium leaving and the calcium entering this causes that plateau because you've got an exchange of electrolytes, um they're both positively charged. So at this point, the cardiac myocyte is going to be in contraction alongside all the calcium that's entering the cell as well. We'll get onto that later on. But I think you must know from case to about um so not the case to PCS too. And in phase three, um your calcium channels are going to be inactivated and um the rectifier, potassium channels will open to cause that repolarization in. So that will bring you back to phase four, which goes you back which gets you to true resting potential cool just, just a bit about uh just about absolute. So the refractory periods, you've got two types, which is going to be your absolute refractory period and your relative refractory period. Okay. So your absolute refractory period is where no other actual potentials can be generated whatsoever. Um As the far sodium channels will be inactivated, um this is a protective mechanism to ensure blood is being pumped as efficiently as possible. Um And your relative refractory period is um is the fact that some points at, at some point some channels will be active, but the majority of them will be inactivated. And if a large enough impulse arrives and that action potential can actually be generated. So that is the principle behind it and your absolute refractory period, which generally is around here and your relative, it's during that phase of re polarization. Great. So um just a bit about cardiac minus like physiology and um also be a quick recap. So, um in terms of calcium induced calcium release, that's using extracellular calcium to generate more calcium release from the sarcoplasm reticulum and uh cardiac myocyte relaxation. This is the removal of that calcium from the intracellular space to terminate contraction. I'll go into this um in the next two slides. Mhm Right. So this might seem a bit complicated, but I'll talk through it now. So this is 0.1 So at this point, um an action potential will arrive and this will propagate towards the calcium channels down here through your t to booth. And that causes it to open and allow an inflow of calcium into the sub. And around 25% of the total calcium is derived from here. Um at this point. So in phase in phase two, sorry, in point number two, calcium will bind to your reality receptors. So you're are y are receptors and this triggers that calcium release from the psychopathic reticulum here. Okay. And a 20.3 um point three. So the calcium will then bind to your T N C components of the troponin. Um and that induces a change in t troponin T and that causes your cross bridge cycling to occur. So this is where the application of that plateau is quite relevant because at this point, all of this is occurring. So your cross bridge cycling okay. And finally, just to talk about the terminations of um contraction. So this is going to be the second phase of your cardiac action potential. And um there is a lack of calcium and this is where there is a lack of calcium sorry between the D H P and the Iran and receptor space. And that's and this will cause your calcium release to be inhibited from the S are. So the D H B and R Y R spaces um in this space over here. Okay. So, this will cause your cycle plastic reticulum, calcium ATPs and that's abbreviated to circle that causes it to be coupled with phosphor Rambam. And that will pump the calcium back into this cycle plastic reticulum. The other thing about circle is that it has a high affinity for calcium that becomes very saturated, very quickly. So um then calcium ATPs can pump calcium from the cell into the intracellular space. So extracellular space, but that that's over here. So circle will need a bit more help to get calcium out of the, out of the cell basically. So what happens is you get three sodium's in one calcium out. And um the potassium rectifier channels will remove any excess potassium from the cell. And calcium also completely unbinds um from T N C R E T N C and this will cause Tropomyosin to return to his original shape. Brilliant. One way to remember how which troponin calcium binds to is from T N C T N calcium. Basically cool. And the third learning objective is going to be outlining the mechanisms that contribute to the control of heart rates and rhythm. All right, very quickly. So, if I launched a pool now, um what is the marathon, what is the parasympathetic control of the heart and the heart trouble? We'll give you guys 30 seconds to answer this. Also, my sbs might seem a bit easy but they are all basically refreshers of um case two and pcs to um what my colleagues will be talking about is more in depth and we'll have more clinical retina clinical relevance, more relevant to you as to. Um but mine sort of is the underlying principle behind it, which is actually quite important as well. Um Yeah. Okay. Five more seconds. Ok. Brilliant. Right in the pool there. So everyone's gone for a and that is indeed the correct answer. So your vagal note um is the primaries, parasympathetic control of the heart rate and heart rhythm, the our back and my snot plexus. Um You wouldn't know about this until case. Um 14. So that's going to be uh involved in lower gi sympathetic trunk is what it says on the tin, so sympathetic and T wanted T four spinal roots. Um This will be actually the nerve roots for your sympathetic trunk. So it's not. Um but um what is the term to define the strength of contractivity of cardiac Myer sites? Okay. Nice. I'll give you guys five more seconds to answer this. Okay. Send it to that brilliant. So the majority of you have gone for B and that is the correct answer. I'll go into each of these definitions later on in more detail. Um But you know, we'll move on to the next one. So what is a term to define the rates of relaxation for cardiac my sites? We'll give you guys 15 seconds to answer this one just with the interest of time okay, we'll end it that brilliant. So all of you have gone for eight. That's correct. So that is Lucy Trophy. Sorry, this is. So what is the term used to define the rate of contraction in the cardiac myocyte? I think most of us sort out answer them. So it's actually Corona Tropea. Sorry about that. Um Yeah, so corona being time um that's one way to think about it and my sbs are all in the wrong order. Sorry about that. So um the term used to define the conduction velocity is going to be drama Tropea, right? Sorry about that guys. Um So in terms of what governs your heart rate and heart rhythm, um it's just a quick mention of the fact that the intrinsic pacemaker, XYZ the pacemaker region and that will set the pace for the rate and rhythm. So this is what starts off the external factors that will govern it is primarily the cardiac plexus which will contain the vagus nerve and the sympathetic trunk. Um the vagus is involved in the parasympathetic control. Um whereas the sympathetic trunk is involved in the sympathetic control of that. And that's just a diagram of what this um cardiac plexus looks like. Brilliant. So just a quick run through for this um you know, Tropea, that's going to be the force of your contraction. So positive in a trophy is a strong contraction and negative is a weaker contraction. Drama Tropea being the conduction velocity. So how quick um the impulse moves through the heart. So positive is faster conduction and negative is slower conduction. Um In terms of lucy Tropea, this is the rate of relaxation. So if you have a positive Lucy Tropea, it's more rapid relaxation. So faster filling of the heart, um whereas negative Lucy Tropea is slower relaxation is a slower dice that um corona trophy is going to be the heart rate. So positive is faster, negative is slower. So, so just a few uh trips and Corona trips to be aware of. Um So you're positive, I know troops are things like adrenaline nor adrenaline dobutamine whereas your negative inotropes, um and Corona trips will be things like phenylephrin and propanolol. Aw okay. Um Pressure volume, you oops, I'll just touch into this just in case um anyone's quite confused on this stuff because I know I was quite confused at the start, but they're much more simple than they seem. And you just need to remember that these are pressure changes within the ventricles alone. Um So we'll start with the diagram on the right then. Um we'll start from point A. So at point A, your mitral valves are going to open and this will mark the end of systole from here and the diastolic phase is just going to start off. So as the heart is relaxed and there's blood in the atria from the vena cava, um blood will then fill into the ventricles via that pressure gradient. And this will mark um at this point also marks the and systolic volume. So appoint be here that which is denotes the phase of diastolic filling. So in point see, um this is going to be the start of systole and at this point, the ventricles will be in to contract. Um note that the at this point, the pressure is um the pressure is basically enough to close the mitral valves when blood pushes against it, but there isn't enough pressure to actually supports the aortic pressure. Um therefore, in them. So therefore, the aortic valve will stay closed. Um So as the ventricles are contracting in this closed space, um the muscles are really contracting but they're not changing in length. So that gives you isotonic contraction. Um So your isovolumetric interaction as well. So in point D uh this will mark where the pressure is actually exert. Um the pressure exerted surpasses that aortic pressure and this is where your aortic valves will open. Um And this will cause blood to move into the a autumn. And at this point, um this will mark your sorry, this will mark diastolic BP. Um Actually, yeah. So what diastolic BP means is the pressure exerted against the aorta from the systemic vasculature. So, when the ventricle pressure exam, um surpasses this, that will mark how much pressure was against the able to at the start. And in e this would denote your ventricular ejection. And so point f this is where blood will leave to the rest of the body. And the pressure of the aorta is now greater than the pressure in the ventricles. So the pressure gradient forces the hills evolved to shut. Now, the pressure in the ventricles is still high enough for the uh microvalve to remain closed. But during this time, the ventricles will be relaxing. Um And at this point, um this will mark systolic BP because it's the pressure from the heart against the systemic vasculature. Um Because simplify that too, you know how much pressure is in the ventricles from systole essentially. Okay. Hopefully, that was clear enough if not drop me an email and I'm happy to clarify. So, in terms of inotropes, um inotropes are essentially what increase your contractivity. And there could be several factors to increase that. Um So the changes from positive in a trophy um to the pressure volume loop itself is that there will be a lower left ventricle volume at the end of system. E so there's a, there's a lower and systolic volume because if you think about it, if you increase that contractivity, more blood is going to leave. So when more blood leaves, your end volume is going to be lower, um and the changes from negative inotropes is going to be the complete opposite then. So there'll be more blood left in the ventricles as they've not all been ejected So that will end up in a, they'll end up with a higher end systolic volume cool. And this is just a diagram of what factors will increase in a trophy. I'll give you a read of this in your own time. And um in terms of preload, uh this will link back to the Frank starting law that you've learned in pcs to. So when you increase preload, this will increase the stretch in the cardiac myocyte. Um and therefore, they will be more active, the Meyer's and heads in contact with each other. And this will mean the contraction will be greater. Um And the increase preload will have the opposite effect where there is less stretch. So the contraction will be weaker. Um Just basically imagine a rubber band, the more you pull it, the greater the fling basically. And I'm not sure uh after load is to do with the systemic vasculature and its pressure against the water. So, uh if you think about it, if there's more pressure, pushing against the heart, you're going to need more left ventricle pressure to um to, to surpass that. Um Whereas if there's less after loads, if there's less pressure against the heart itself, you're going to need less pressure from the left ventricle to pump blood to the rest of the body. That's the basic principle behind it anyway. But um yeah, that's um that's it from my side. Um Just a quick whistlestop tour about physiology I think we'll pass to the more relevant people. So she's on the dome. He will take us through that. Yes. Yeah. Okay. Yeah. Thank you. And um it's very good presentation that's very important to know those basics next fundamental. So I'll share my screen now. Um Yes, I'll just be going over the arrhythmias sort part of case 12 and then I'll also be touching on the diuretics as well into slide share. Yeah. So our first learning outcome is basic explain the recording of electric cardiogram in relation to the changes in the cardiac cycle. So just to recap the cardiac cycle to start off with, as we know, it can be divided to systolic and diastolic phases. Uh systolic phases where we're contracting and diastolic phases where we're relaxing. Um And we spent about a third of our time in Sicily uh compared to 2000 in dietary. Um So the order is uh as you know, from first years, atrial Sicily, ventricular systole, then cardiac diastolic altogether. Um and the movement of blood through the heart itself is depend on pressure, pressure, grade things. Um And if we're looking at the at the diagram here, um the heart valves open and respond accordingly. So, um if we follow in on here, we've got our actual contraction which is filling our last 20% of ventricular volume. And then when we have ventricular contraction, the pressure is is exceeding that the actual pressure and it's closing the mitral valve and the closure of the mitral valve and tricuspid valve gives us our first heart sound. That s one sound which is our love. Uh And then we have our eyes, a volumetric contraction which is what you alluded to earlier uh to the point where we exceed the aortic pressure. And the aortic valve opens and we eject the blood into, into the aorta. Uh and then as we're losing the pressure inside the ventricle, we then have the aortic valve closing. Uh and this gives us our second heart sound. So that's our dub s to sound. Um But I've included some notes uh with this slide for you sort of look over in your own time. So E C G leaves themselves. So we've got a 12 E T C G which is made from 10 electrodes and that sounds a bit weird, but we basically have um these two electrodes make up multiple leads. So we've got six chest leads. So um they are placed, we've got be one to be six, uh B one and RB two are placed uh next to the sternum in our fourth intercostal space on the right and left side. Uh We then have the four before it's placed in the midclavicular line in the fifth intercostal space. And D three is placed in between. We have the five in our anterior axillary line in the fifth intercostal space and the six in the midaxillary line on that side. And that's really important to remember for your, uh, whiskeys. Uh, in case they ask you to, to do an E C G. Um And then we have our three Lim leads. So they're placed um, uh, on, obviously on the limbs. Um, and we are using this Pneumonic here Riddle Green bicycle, which is really handy to remember where they go because uh they're colored red, yellow, green and black. So, uh we have our red leave, which is uh it was going on, our right shoulder are yellow going on our left shoulder, the green going on the left leg and then our Earthly, which is our black one going on the right leg. Um And then A V R A V L and aVF are basically created by having um to lead users reference electrodes, we take the average of those two leads. Um Let me create a reference and then we use the other lead to create sort of the direction in which we're reading through, which is exploring electrode. Um So we've got uh and then you sort of just remember those in direction just AVR to the right aVL to the left and then, and then aVF sort to your uh to your feet. Um And then, yeah, if we're thinking about are so justly, they are covering the horizontal plane of the heart. So if we think sort of, of our imaging when we've got transverse planes, this is, it's the horizontal planes coming out towards us. If you think, whether it's measuring the uh conduction through, then Arlene limb leads are sort of in our corona plane, there are in that frontal plane, which is, which is across the heart. Okay. So the E C G, because the anatomy of the heart, the the coronary artery is so predictable. We can use the E C G to um sort of predict the territories of the heart and uh the territories are supplied by certain coronary arteries. So we can use that when the E C G is abnormal to predict where the pathology is in which artery. So, um yes. So um this is something basically just need to learn. Um There's a few ways you can remember it. So if you think of your inferior leads, they sort of from the boot of the E C G. Uh sort of looks like a boot at the bottom. And I also learned replacement recently that someone's been using Sally as a way to remember it. So if you go from the start V one and V two, we've got S for septal, uh the three of the four A for anterior and then the five G six L and I can sort of convince you that the five G six and A B M one is sort of like a backwards L across and then we have I the inferior down the bottom. So, yeah, and then in terms of the sort of coronaries associated with these territories. So are anti receptor is going to be a left anterior descending. And as you can see in the diagram, that sort of does cover sort of anterior portion. And the the exceptions obviously inside um are lateral. Uh the territories are left circumflex and then are inferior territory is typically are right coronary artery because the inferior territory is sort of dependent on which um uh coronary gives rise to the posterior interventricular branch. And in 80 to 85% of people, it is from the right coronary. But in a small amount of people who are left cardiac dominant, they have it coming off the left circumflex such as something to be aware of. Um So yeah, now the E C G waveform you're familiar from this uh from before uh East years, basically just graph voltage against time. Uh And we have our P Q R S T waves um uh that form that and there's a diagram that sort of summarizes that, but I'm sure you already know that already. So um in terms of the E C G as well though, so the size of the inflections is sort of representative of the muscle mass. So H has got smaller in flexion because there's less muscle mass that that's being deep polarized. Whereas in the ventricle, you got a higher in flexion because there's more muscle in the ventricles, ventricles, the bottom got a key E C G point. So um a wave of the polarization towards our electrode is going to be a positive in flexion, whereas a wave of re polarization towards the electrode is going to be negative in flexion. So we're just gonna explain this really quickly here using the diagram the bottom. Uh I hope you can see my cursor. But um so at the start as, as you and explain, you got the S A node that's releasing a signal, it's going down the back and the bundle were having simultaneous contraction of the atria. Um And the overall uh sort of wave of deep polarization is coming down. So if we think in our lead to which is what this is uh this easy at the top is showing the electrode is down at the bottom here. So this wave of, of, of depolarizations going towards the electrodes if we get a positive in flexion, now the Q wave is always a bit that is kind of difficult to understand. So after we've gone through the A V node, we've had our pr interval, we then have uh the deep wave differences come down the bundle of here and into the bundle branch is now because the left ventricle is thicker than the right, we have more uh sort of deep polarization on this side and it comes towards the middle of the sector. So we have more deep polarization coming from the left towards the right than we do from the right to the left. So because of that, we have a net or deep polarization coming across and away from the electrode. So we have a small little uh small deflection um coming down for the key wave. And then because the overall uh deep polarization wave is coming towards the apex of the heart where the electorate is at the bottom, we then have a positive very positive spike in our, our wave. And then it comes down again to the S wave when we have the wave of the polarization coming up towards the uh sort of a Kinji system. And within that, as we know, atrial re polarization is hidden because the uh QRS complex is, is such a big sort of deep polarization. Uh It's sort of masks um the re polarization of the atria uh and then R T wave because it's really important that we don't have contracted muscle on top of relaxed muscle, we relax from out to in. So we re polarized from out in and that means that the wave of re polarization is going away from the electrode because a wave of re polarization toward the electrode is negative away of report uh re polarization away from electric must've positives. That's why the T wave is positive. I hope that makes sense. So E C G features in sinus rhythm. So just to go through this really quickly, so the sinus rhythm, we need a P wave followed by one Q R s uh pr interval must be normal. So for that to be normal, need to be between 100 and 2200 milliseconds, you have a regular rhythm. So if you use your, our uh our waves uh sort of measure the, the distance between them that should be regular and the rate should be within 60 to 100 BPM. And then I just put some sort of measurements for your uh in terms of TCG Pope, your small squares on what is normal. Um just down there. Okay. So it's just some S V A S. So uh Hamlin's revising the cardiac cycle and is recapping the causes of different heart sounds. She remembers that the dominant heart sounds heard on auscultation because by the closure of the heart valves, which of the following represents the closure of the aortic and pulmonary valves of the start eyes, volumetric relaxation. So just launched the cold in front. Okay, a bit of time. Okay. Yeah. So the majority, you've uh the correct answer which is um go for it, which is because it's s two. So s ones are try custard and our mitral S two is our uh aortic and uh pulmonary. And those are the key ones. Remember you got S three S four sound as well. They're like they're to do with the blood flow through the heart, hitting the, hitting the walls. I have included those in the notes but really just want to try with S one or two and S five. That's not sound okay. Next question. So a 55 year old female presents the emergency department with pain in her jaw and left shoulder as well as the nausea and vomiting. The E D reg suspects an M I as a top differential and uh request the CT, the CT shows ST elevation leaves be five and B six. The registrar determines that this patient has A C S and arranges immediate primary PCI which coronary vessels included in this PCS presentation. Okay. So just most of pool again. Okay. You OK. Again, yeah, the majority of your correct. So for this one, if you remember that weird Sally uh Pneumonic, it is the left circumflex. So be five and the six, we've got the 1 to 4 is going to be our left anterior descending which a few of you put and then five and six and then one and A B F are going to be um sorry A B L, they're gonna be your um left circumflex. Uh So next question, an E C G is a graphical representation of voltage changes in the heart. Uh The E C G waveform consists of P Q R S T waves which represent electrical changes occurring during the cardiac cycle. What does a Q wave represent? So it is okay. Uh huh. A little bit more time. Okay. There's a little bit of confusion on this one. So um maybe that explains to, well, we'll go back to the slide. So the answer this one is uh the polarization is be the polarization of the interventricular septum. We quickly go back to the thing. So um basically Q wave. So when we get to the Q wave, we've just come through the IV node and we're now in these left and right bundle branch is, and it's because the left ventricle is thicker than that of the right. There is more to depolarize on this side and I can't get my cursor. So it's more to depolarize on the left and that moves into the center of the septum. So you have a wave of deep polarization. It sort of predominant comes from right to left, which is away from the electrode, which causes a negative in flexion. Okay. I hope that makes sense if it doesn't just Yeah, I can, it's uh just ruined that one. Whoops. Um Sorry, gone too far. Yeah. Anyway, you see a patient with an A C T H street small cell lung cancer haven't taken blood from the patient. Her results related uh she has hyperkalemia. You decide to do the 12 mg. Stay on this patient detect any cardiac complications. The city with the electrolyte environment. Where is the, the five league place in 12 E D C G? Um I didn't accidentally go too far in this one. So you should hopefully you'll get it, right. Okay. So a bit torn on this one actually. So um we're 50 50 in between C and D. Um And the answer to this one is actually D um just because so the mid fifth intercostal space, midclavicular line is your V is your V four and then D is going to be your V five and then it is your V six. Um Yeah. Uh And then last question for this one, a patient has presented the emergency. Can't plenty of new onset. Okay. Wait, chest pain and shortness of breath. Any studies performed which shows ST elevation in the inferior leads. Primary PCIS performed on the angiography shows that there is no occlusion of the right coronary artery in which vessel was the inclusion located. So question about cardiac dominance. This one. Okay. Okay. You barrels okay. Okay. So a few of you got that right. So the answer is this one is left circumflex if it will change because if we look at think back to our territories, um the inferior leads are sort of the territory that they supply territory that they represent is supplied by the prostate interventricular branch. And that can arise either from your right coronary or your left circumflex. So it's not going to be your right marginal because it doesn't come off of there. You're right. Main technically, maybe, yes, but because there's normal flow in the in the question stem that says there's no problem with your right coronary artery is, is not going to be this uh left anterior descending, is your anteroseptal diagonal branches come off of your left anterior descending. So it's going to be your left circumflex. Okay. So, the next learning outcome is described the path of physiology of common cardiac conduction abnormalities. So this is what the main chunk of the arrhythmia stuff. So, arrhythmias themselves are any disturbance of the heart's normal rhythm. You've got tacky arrhythmias, which is too fast. And as you said earlier, sinus rhythm is between 1600. So too fast, it's above 100 and radio arrhythmias which are too slow are below uh 60. Um And then in a, everything that uh the normal P Q R S T sequence is either disrupted or it's, it's uncoordinated. So it can be completely disrupted or just simply irregular. Um And in terms of the common cause is arrhythmias. We've got blocks coronaries. Um and fibrosis from previous MRI which is sort of the key ones um to know that there's a whole list uh of things. So yeah, so if you go into atrial fibrillation, um they like to access a lot. It's very high yield facts to know that E C T features of H fibrillation are irregularly irregular rhythm and that there are no P waves. So you can see that on the rhythm strip there, classification of atrial fibrillation. So it's divided in between paroxysmal, which is you get two episodes in less than a week per system, which is two episodes uh over the course of more than a week, um or any af that needs treatment to resolve. Um And then permanent is when you've got longstanding atrial fibrillation. And you can, it's sort of failed to be corrected by cardioversion. Uh and then af the pathogenesis of AF itself comes from pulmonary vein or offices. So basically, when you've got the pulmonary vein, you've got the excitable sort of cells of the uh the cardiomyocyte. And then you've got the pulmonary vein, which, which isn't excitable and that the division there, you've got sort of uh an increased chance of having um cardiomyocyte and things that aren't, um that's all more likely to give up ectopic beats. Um And that's basically what happens in A F. So you get uh pulmonary bein roots, you get sort of these ectopic beats given from these uncoordinated cells. Um So, yeah, and then there's just a nice little um uh acronym for causes as well uh actual flutter. So, uh atrial flutter has a, it's a super ventricular tachycardia, it's characterized by really rapid atrial deep polarization waves. Um And you can see this in that sort of pattern. Uh it's narrow QRS complex and it's got a regular rhythm. And basically what you get here is you get a re entrance circuit in the atria. Uh And you basically get a macro entrance circuit around the Tricuspid analyst which sends off multiple signal and um which, which depolarize is it a lot? But because you got the A VM, which stops that being transmitted to the ventricles, your ventricles keep a persistent rate. Um And in typical atrial flutter, you have a 2 to 1 ratio. So you get about 300 BPM of atrial uh atrial beats to 100 and 50 ventricular beats. So that's still quite a lot because normally you'd have a little bit of delay in between anyway, because you're sending off lots and lots of uh actual deep polarization waves. You've got a really high rate, um uh supraventricular tachycardia. This is sort of quite a tricky one to uh sort of remember really. Um You divide this into uh a V nodal reentry tachycardia, AVNRT or you've got a D reentrant tachycardia was a V R T and A B nodal reentry tachycardia. I've stolen this diagram from osmosis because it's quite handy. Um Basically, what you get is the IV node normally contains two pathways. You get slow and fast and the slow pathway has a sort of short refractory period. So it's ready to be deep polarized again quicker. Uh which you can see on the left here, where's the fast pathway has a long refractory period. So the two pathways then combined at the bottom normally and then it goes down into the bundle of hiss towards the ventricles if you can see this at the bottom. Um and then normally what you get is no recirculation. It just comes down nicely both sides and it goes to the to the bundle of his and intervention cols um that's because both pathways and they're a fracture period when the impulse get to the bottom. However, in typical or slow, fast AVNRT, what we get is too rapid, consecutive, actual impulses that come um come down into the IV node. And what happens is the slow, fast path, which which has a short refractory period is ready to be too polarized again quicker. So when the second impulse comes in, it comes down this pathway, it doesn't come down this pathway because it's still, it's refractory. But when by the time it gets to the bottom, it comes off down to the ventricles like normal. But this pathway is now open again because it's come out of its refractory. So it goes back up and then it basically just recirculates and it shoots off impulses to the atria and the ventricles and just keeps going around sending impulses in both directions which causes this tachycardia. And then in a V retention tachycardia, you weren't alluded to it. Um With the bundle of Kent, you have an accessory pathway which bypasses the A V node. And uh basically you um yeah. So this is sort of commonly associated with Parkinson White syndrome. So instead of having the delay uh that the A vineyard gives all these sort of signals to transmit it straight into the bench schools which can be really dangerous when you have, um, fast atrial rates because it gets conducted straight into the ventricles. So in terms of the E C G features, um, AVNRT because the, they're shooting off in both directions at the same time. Um, you something also, sorry, uh, the P waves are buried in the QRS complex. So you don't, um, you can't see your P waves whereas in a VRT uh you have pre excitation which you an alluded to. So because that you have these delta waves, you got the slurred upstroke and because you're coming in from this direction, uh this is against the sort of normal flow of the electrical conduction system. So it's slower. So that's why you have this sort of gradual depressurization before it shoots up because the impossibility through the IV node. So, yeah, and then quickly onto heart block. Um you have basically this is a V block, so it's different degrees of a V block. Um And um yeah, most common causes. This is idiopathic fibrosis, uh and also cirrhosis of the conduction. So in first degree heart block, you have slowed avian conduction. This is sort of classic in people with high vagal tones that athletes, um people who exercise a lot and also people that are just taking medications like beta blockers and in the E C G sort of a prolonged pr interval. Um in second degree heart block you have intermittent conduction through the IV node. So uh this can be divided to move it's type one and move it's type two. So in moments type, when you get a progressive lengthening of the pr interval until a Q R S is dropped. So as you can see in this diagram here, you got a short pr interval sort of normal here and then it gets progressively longer and then you drop A Q R S in move. It's type two, you have occasionally nonconducted P waves without progressive pr prolongation. So as you can see, you haven't got the PR interval stay the same and then you just get a drop to Q R S and then in third degree you have complete conduction block. So um yeah, for any reason, if you have a right coronary artery occlusion, you're not supplying your Avey note. So there's no synchrony between atrial deep polarization and ventricular depolarizations. Um And so you have, yeah, on the STD, you have atrial deep polarization waves separate to QRS complex is um and QRS complex is still happen because there is some automaticity still in the ventricles. So they create their own egg topics and then bundle branch blocks. You have left and right bundle branch. The last slide on everything is so with left bundle branch, basically, what you're guessing is um a problem that lives below the atria. So the P wave and the PR interval is normal. But because one of the bundle branch is blocked, you have a sort of different deep polarization of the inter interventricular septum. So this will create changes in the QRS complex. Uh And the key thing to remember for this basic for exams is William Morrow. Um So the left bundle branch blocks in William, you've got two Ls in the left on the V one you have W so it looks like a W will convince you of that uh in the Q R s and then in the six, you have the sort of M looking QRS. Uh and then on the right, you got marrow. So the two hours for marrow uh and it's just the other way around. So B one looks like an M and M V six looks like a W. Uh my house actually just came back from, from placement as well and said that when the consultants said that the right bundle branch block already handy way to remember it is that N V one, it looks like our. So I think could just about convince you that it also looks like an ar there as well. So sbs sorry, I didn't want coffee so much. Just throat's been really dry. Um So first one, so a 72 year old man was admitted yesterday evening following a myocardial infarction which was resolved through primary PCI. He has since been feeling dizzy and extremely fatigued and short breath following from his E C G results. It is decided he needs a pacemaker. What complication is seen on the C G? I hope the E C G is big enough for you to see. So uh she needs to launch the pole. Yeah, I just have a go even if you don't know. So yeah. Okay. Keep yourself first time. Okay. So yeah, that's good. So the answer to this one is um is E so as you can see in the E C G that isn't uh slight change, okay. There's no sort of synchrony between the uh the HDL deep polarization and the ventricular ventricular wave. So this is author to be hard block. There's no uh synchrony opportunity. So next question is 62 old man presents the emergency department with a week long um history of intermittent dizziness. He reports painting the day before his ECG shows intermittently nonconducted P waves. There is no sign of pr elongation or shortening of the waves that are conducted. What was the most likely diagnosis? I know these questions are quite hardy cds are not very nice questions, but let's give it a go. Okay. That's good there. That's, that's um that's right. So this is, this is C so it's move, it's type two. Yeah, the intervals the same, the same each time uh got a random drops. QRS complex. That's perfect. Next question, Julia is an F we'll work on the Cardiac Awards. One of the questions on the ward, one of the patient's sorry questions. One of the patients on the ward has recently undergone an aortic valve replacement and she's been asked interpret his post operative E C G. Julia is aware that postoperative atrial fibrillation is a common complication from this procedure. So she makes sure to rule out the features A F R E C G first, which of the following is a typical feature of atrial fibrillation on an E C G. This should be a nice question for you. Okay. Yeah. Yeah. Yeah, that's great. Yeah. And we need to explain that one, that one step is a um no P waves. So A A is a tacky arrhythmia caused by the development of ectopic folk. I outside of the S A M. This causes the atria to be disproportionately more in comparison to the rate of ventricular contraction in the pathogenesis of atrial fibrillation. Where do these ectopic folk I originate from? So, uh really, really quickly, because I'm aware that I'm eating up quite a bit of time. Give you 15 seconds of this one. Uh the max. Okay. Um Yeah, I think a few more of you put s a note um than the right answers to S A note is not right. This actually comes from the pulmonary vein, right? So we sort of spoke about the uh the sort of boundary where you've got the, the vein and then you've got the sort of excitable cells, the cardiomyocyte. Um And in between that boundary, they're more likely to become um ectopic, make ectopic beats. Um So, yeah, and the last question for this 1, 15 year old boys presented to a general practitioner with complaints of experiencing uh palpitations and dizziness after taking a history and examination and E C G is requested, the E C G rhythm strip is strength below based on this E C G trace, which of the following conditions is most likely results. You know. There you go. I think easy question for you already. So yeah, majority of you open that answer that correctly. So this is uh wolf Parkinson white and you can see that because you got the slurred up straight. You got the delta wave uh which is really clear. Okay. So the last learning outcome is describing the role of the kidneys and salt water, home stasis and relating modes of action, two different diuretics. So the net from really quickly, there's a million, each kidney is comprised the corpuscle and tubules. Your corpuscle is your bones capsule and your uh your gra Marylise and the tubules divided into parts. You got the proximal convoluted tubule, leap of Henley, distal convoluted tubule and collecting duct and then the different parts of the tubal responsible for exchanging different studies. So with that in mind, we've got diuretics uh and they act on the kidney to increase the production of urine and they do that at different parts. Uh And basically, we're trying to eliminate water from the body. So people that have heart failure and stuff, they have a Dema uh and it's high blood pressures and things that we can use diuretics to reduce that. So the type of diuretic I'm going to quickly explain to you because I'm wearing, running out time is uh far as our diuretics leave acting and potassium sparing these your key ones, uh your carbonic anhydrase inhibitors or another form, which basically we sort typically use these for glaucoma in the form of eye drops. And then osmotic diuretics, you come across Mannitol in case 13, which is used for people that have raised intracranial pressure and they have uh increased, they've got a Dema in the cranial vault. So thiazide diuretics, they're very simple mechanism of action. They basically block sodium chloride uh co transporters. Uh Because of that, you've got more sodium chloride in the lumen, which means that water is going to stay, it's not going to, it's not going to be re absorbed because it's going to follow where the ions are. Uh Yeah, it's generally thought as well that it's not as effective in patients renal failure. It's generally thought that uh they're not as effective because there's more sodium absorption approximately. That's just a F Y I. Um The only problem with diabetics is because we are blocking this channel, we're going to increase our aldosterone sodium uh absorption. And because of that, we're going to be excreting more potassium. And that means and hydrogen, so we can get a hyperkalemic um metabolic acidosis as well. Um So, yeah, just to note the iron changes really important to know the iron changes with different diuretics. Mhm So loop acting diuretics, uh These are your really high potency ones. So your examples of furosemide uh it's you're sort of key one. Uh and they act on the thicker standing limb of, of the loop of Henle e that surprise surprise loop acting. Um And the thick standing limit is in permanent the water and it contains these N K C C to co transporters. So the mechanism action is basically, they block the chloride site on the N K C C to co transporters, which basically renders it useless. You can't transport the ions in. So you get more ions again in the in the urine which stops the water being reabsorbed because it follows where there's high oz morality, which is going to be in the urine. Um So we have low sodium, low potassium and low chloride again because we're blocking sodium absorption through this route. We increase uh the aldosterone uh way of sodium results as we do still absorb some sodium. But it also means were excreting more potassium and more hydrogen ions which increases our chance of getting a which can exacerbate hypokalemia and uh exacerbate any metabolic assay doses that we have alkalosis evening. Sorry. Um So it's also important to note that magnesium and calcium are excreted too because they typically follow these irons paracellular early because these ions are being resolved, they just get excreted. Uh And then um no, I didn't mean I did mean a hypokalemic metabolic acidosis, sorry for previous life because you're excreting. Um okay. So, potassium sparing diuretic. So um these are important, there's spironolactone. Um they're weak potency. Um but it's important to conserve potassium. Some patient's um uh as well. So um they are the only diabetics don't act on the Luminal membrane. They act through that aldosterone um mediated water resort option that I was talking about a minute ago. So the normal Axion about austin bone is that the regulate enact channels in the principal cells of the collecting duct. And this increases sodium reabsorption and then sodium is put into the blood in exchange with potassium and potassium is excreted. When we have, when we take spironolactone, we stop this process. So we conserve potassium and we also have sodium left in the urine. Um And then we create a diary sis uh these waters that that's the the iron changes that you see there. OK. Quickly. Then for SBA so, Susie is a 60 year old woman who was diagnosed with the hypercalcemia related to a parathyroid hormone screen tumor cancer, chemotherapy, a temporary treatment for hypercalcemia could include the administration of what I know I went through that really quickly, but give it a go if you can okay. Say um okay. Uh So the answer to this one is b because furosemide is a loop acting diuretic. So, because as I said earlier, magnesium and calcium are absorbed paracellular lee normally when you absorbed through the N K C C too, because you're blocking that channel, calcium and magnesium are released. So this is the way that we can reduce the calcium in uh in the blood, which the following drugs has a potent diuretic effect, a short duration of action and ax fight inhibiting the N A K C L transported in the Nephron. Same. Uh I'm gonna be a bit cheeky here. I've given the classic example. Um it's a bit mixed. That's all right. So this is a loop acting diuretic. So um I think I did put on the slide really the main one you use nose furosemide but triamterene is also a leap acting. Oh, no, sorry, got that wrong. If a critic, acid is also a leap acting diuretic. Um Yeah. Um A thiazide diuretics work by reducing sodium resumption from the renal tubules inhibiting N A C L channels. On what part of the renal tubules do thiazide diuretics? Concert that facts. Yeah, that's okay. Yeah. Yeah. This one is, it's going to be the distal convoluted. She will want to quickly move on to the the last couple questions, which is the following is drug with more, less antihypertensive effect as often reserved in patients that develop hypochelemia, response to taking another more potent diuretic typically. Don't again. Yeah. Yeah. Okay. So patient with hypokalemia, we want to be preserving potassium so we can put them on a potassium sparing diuretic. So the answer to that one is gonna be e um it's one I like to. And then last question add a bio, a 45 year old gentleman has presented complaining of right side. A groin pain, C T K U B is ordered bank AFMC as a renal calculus. You've got renal stone. Why would prescribing a thiazide diuretic be beneficial in presenting the incidence of nephrolithiasis having kidney stones in this patient in the future. Uh huh. So it's possible. Mhm Okay. Just have enough one in there. So yeah, yeah, those you can't. So you got it right. So it's be induced hypercalciuria. So the majority of renal stones are calcium based. Um So yeah, because they're reducing the calcium. Um You're in the less likely before. Okay. That's everything I think I did slightly run over. So sorry about that. Yeah, stop sharing. Okay. All right. So we'll hand over to Laura now. It will take us through um the third part. So, hello everyone. I'm Laura and I'll be going through cardiac arrhythmias, hemostasis and heart failure with all of you. So, first off arrhythmias, there are four main types of atrial arrhythmias. The first one is sinus tachycardia. This is a normal physiological state which is achieved during exercise. It has a heart rate of greater than 100 BPM. And you'll see the full P Q R S and T complex. The second type is atrial flutter. This is caused by previous damage to the heart. You'll have a heart rate of greater than 200 BPM. And it's often described as having a C sore pattern. And what that means is that there'll be multiple complete p ways before each QRS complex. The third type is atrial fibrillation that's also caused by previous damage to the heart such as in an M I. Um this as a heart rate of greater than 300 BPM and is often described as being irregularly irregular in pattern. There are often multiple incomplete P waves before each QRS complex. The fourth types are re entrance tachycardias. This is due to the presence of an additional circuit within the A V node. Often in these E C G S, you'll see a retrograde P way because the signal starts from the navy node and travels backwards to the sinus node. So how are we going to treat it in atrial flutter? The first line of treatment is vagal maneuvers. This includes blowing into a plastic syringe or a carotid massage. The point of these maneuvers is to trick the barry receptors into thinking that you have high BP and then they will send the signal down to your heart telling it's slow down. The second line is I V A denison, you give them a rapid bolus of 6 mg followed by 12 mg followed by 18 mg. This however, is contra indicated in asthmatics. So give them verapamil instead also just a side note. Anything extra I add to these presentations is in the notes in the presentation. So when you get the slides, they'll all be there. So next atrial fibrillation, the treatment plan for atrial fibrillation depends on whether it's temporary or perm persistent. If it's temporary, the patient's will feel palpitations common at random times and then disappear. So for these patient's is recommended to give them a long term rate control. This is in the form of either a beta blocker or a calcium channel blocker. And then whenever they feel these episodes of palpitations coming along, you give them flecainide or amiodarone as the pharmacological cardioversion. And this will set their rhythm back into normal flecainide is given if you have structural, if no structural problems, and amiodarone is given, if you do have structural problems, if you have persistent atrial fibrillation, then it depends on whether it's stable or unstable. If it's unstable, you're going to give the patient an electrical cardioversion. But if they're stable, you need to take into consideration whether or not the thrombus might afford if the AF has only been present for two days, that's very unlikely. So give them therm a collage pickle cardioversion with again flecainide and am I ordering. But if it's been present for over two days. You have to exclude the chance of the thrombus is formed and you can do this with either three weeks of anti coagulation or you can do a transesophageal echocardiogram to check if there's a thrombus in the left atrium. All right, re entrance tachycardia is the only definite treatment for. This is radio ablation of the accessory pathway. Alright, onto ventricular abnormalities. There are three types of ventricular arrhythmias. The first type is ventricular tachycardia. This is caused by an ectopic site firing within the ventricles. There often described as broad complex QRS. There are two main types. You have monomorphic in which the Q R S are similar in height and polymorphic in which they're not similar in height. The second type is ventricular fibrillation. This is caused by previous damage to the heart again, such as M I and it will result in absolutely no P Q R s or T wave being seen. And the last one is Tosa deep Juan sorry, who if anyone's friends here who definitely butchered that, but this is caused by a prolonged QT interval. So this can be caused by a variety of courses. So certain medications or certain congenital abnormalities, put people at higher risk of this and you can see them on an E C G by their characteristic twisting waves. So how are we going to treat it? Ball ventricular tachycardia, anti arrhythmic medications are recommended. So this is amiodarone and lidocaine for ventricular fibrillation, electrical cardioversion is recommended and for tosa deep want you give IV magnesium sulfate. This is in order to stabilize the membrane of the cardiomyocyte. All right onto the second bullet point, chemo stasis, chemo stasis. The process of blood clot formation. It has two separate parts. Primary hemostasis is when platelets are activated as they, as they bind to the exposed collagen of the damaged vessel. And they, they, once they're activated, they stick together and form an unstable clot. In secondary chemo stasis, the damaged vessel triggers this coagulation cascade to take place which ultimately forms fiber in which stabilizes this clot. We'll go into more detail about the coagulations cascade. Now, so this cascade has three separate sections. Extrinsic intrinsic and the common, the extrinsic pathway takes place within the vessel wall itself. It's injury to the vessel wall causes the release of factor three, which in turn activates factor seven. The intrinsic pathway takes place within the blood itself. You have the exposed collagen which activates black to 12 factors. 12 activates 11, 11 activates nine. Both the extrinsic and the intrinsic pathway activate the key factor back the 10. This one will lead to the activation of the common pathway. Back to 10 turns prothrombin into thrombin and thrombin turns fibrinogen into vibrant, which is the main product of this entire cascade as this is what will stabilize the clot. The last bullet point art failure. So what are the symptoms of heart failure. If the left ventricle fails, blood flows backwards by the palm re vein into the lung. And that's where it accumulates and will cause problems. The patient will present with these symptoms. They have dysphonia, which is the shortness of breath, paroxysmal nocturnal dysphonia, which is when an individual wakes up at night, gasping for breath and orthopnea, which is when the shortness of breath is worse online, flat, but better in sitting or standing. If you have right ventricular failure, blood flows back via the vena cava into the body. And that's where it causes the problems. So the patient will present with these symptoms, they'll have pedunculated ocma, which is when fluid accumulates within the legs. And that's because gravity pulls the fluids down the body to the lowest point you have ascites, which is the accumulation of fluid within the peritoneum. And that's a pre existing cavity. So, fluid likes to accumulate there and you have an elevated JVP and that's due to the backflow of blood into the vena cava. So what types of heart failure are there? You have systolic and you have diastolic heart failure, systolic, heart failure is due to a over dilation of the ventricular walls. And this means that the ventricle is no longer able to contract properly in the clinic. You will see the S three sound and that's because the new blood entering the ventricle is smacking against the blood that's still in the ventricle from the last cycle and you'll have an ejection fraction of less than 40%. And that's because this over dilated ventricle is failing to contract in diastolic heart failure. You have over thickening of the ventricular wars and this means that the heart is unable to relax properly in the clinic, you will hear the s force out. And that's because the last portion of blood within the atria really has to be forced into the ventricle at high pressures because it's volume is now so much smaller. And this high volume, this high force of the blood flowing in causes a vibration of the quarter tendon. It that causes this s four sound. You'll have an ejection fraction of over 4 50%. Because in a diastolic failure, there is no problem with contraction. The problem is in relaxation. So how are we going to treat congestive heart failure for the pharmacological options? The first line is an ace inhibitor such as Ramipril and a beta blocker such as Bisoprolol. The patient should be on both of these medications but it's not recommended to start them at the exact same time. Both of these medications aim to slow the rate of the heart. So it isn't as overworked and will last longer. The second line are aldosterone antagonist. So this with the spironolactone and epileptic loan. These are both jarrett IX that remove fluid out of the body and will reduce the preload the heart and the third line our specialist medications, but you don't need to know the mechanism of action for these. All right. So these are these surgical options available to the patient in left ventricular reduction surgery. The fibrotic tissue is taken out in a cardiomyopathy. Last e the latissimus dorsi muscle is wrapped around the heart and is activated with a pacemaker. And in a myo splint, a splint is put through the ventricle to stop it from over dilating. And if the patient has really severe heart failure, the last option you can have for them is a ventricular assist device. That's an external machine that takes blood from the left ventricle and pumps it into the order with a lot of force, essentially replacing the function of the heart. Alright, onto a mini test. First question. A 58 year old man attends the emergency department with palpitations reporting a racing heart four days but denies any pre syncope or chest pain. Usually he's fit and well on assessment. His easy g reveals an irregularly irregular pack pulse, whether ventricular rate of 100 and five BPM, he's hemodynamically stable. What is the most appropriate management strategy? All right. Oh, sorry. That's why no one was answering. I hadn't given you the answers. Okay. So a give three weeks of anticoagulants before elective cardioversion be discharge them with a beta blocker. See, perform a transesophageal electrocardiogram before performing immediate electrical cardioversion. D start an intravenous heparin infusion before forming immediate cardioversion or E start oral, am I ordering? I'll relaunch the polls now. All right. So the answer to this was a, why is that? Well, in the question, it says the patient has an irregularly irregular pulse. This is a sign that they have a F, they have had a F for over four days and they're stable. So the management strategy for them is to check that they have no thrombus, which in this patient you're doing with three weeks of anti coagulation before cardioversion. All right. Next question. A 44 year old woman presents the emergency department with this near. She has been feeling intermittently dizzy and short of breath for the past two weeks. On examination, her pulse is 100 and 80 BPM. Her pulse, her BP is 100 over 66 miller meters per mercury. Her oxygen saturation is 98% on room air and her chest is clear. She appears well perfused. An E C G is obtained as seen below. And what is the most appropriate? My actual strategy? Okay. I hope we've had a good look at the E C G. So, is it a intravenous anti odorant, be intravenous? A tentative c intravenous um of museum D intravenous labetalol or E D C shock. The answer to this is C in the E C G. If we go back to it, you will have seen the characteristic twisting which is normal for to Soliqua And for the Tucson upon the management option is IV like museum sulfate. All right. Question three, an 82 year old female is found to have heart failure with the left ventricular ejection fraction of 30%. Her renal function is normal and her uh BP is 100 and 65 over 100 and two millimeters per McCree. She's not taking any other medication. What combination of drugs would be the best initial treatment for her? All right, well done to everyone who said e that is correct. The patient has heart failure. So the first line of treatment for them is an ace inhibitor and a beta blocker. Okay question for a 35 year old man is on an acute medical unit with a new diagnosis of hypertrophic obstructive cardiomyopathy. He is on a cardiac monitoring and an emergency buzzes pulled after he is noted to become very tech Codec and E C. She shows a regular broad complex tachycardia. The patient has a G C S or 15, a BP of 123 over 81 millimeters per mercury. And he reports feeling well, what is the most appropriate management plan? Right. The answer for this was see IV, am I ordering? The question says that the HCG has a broad complex tachycardia which is a hint that the patient is in Viti and the treatment for V E T R anti arrhythmic medications onto the last and final question. Boldon's everyone has stuck through, by the way, a 32 year old female presents the emergency department after suffering palpitations and excessive sweating for the past 2.5 days. When question ongoing questions, she has no other symptoms but admits to consuming a large quantity of alcohol and coffee. Four days previously, she has a past medical history of COPD observations show that the patient is a federal with a respiratory rate of 22 breaths per minute, pulse of 73 BPM and a BP of 100 and 22/83 millimeters per mercury's and an oxygen saturation of 95% on air. Yeah. A 12 lead E C G is performed and shows she is an A F party. A version is contraindicated in this patient. For what reason? The answer is E and that's because the patient has been an A F for over two days and is stable. Therefore, you need to take into consideration the risk of a thrombus have informed. All right, thank you very much for everyone who listened and I hope it was helpful. Hi. Uh So I will go through the last part for today and I'll just share my screen now. But so like Laura said, thank you so much for staying under like this time right now. And congratulations again for staying up for this time. But yeah, today I'm Sonya and I'm a 30 A medic like the rest of them. And I, I'm sure that a few, a few guys also, 30 A medics over here as well as second your medics. So I will try to make my presentation a bit more for the s too as well as the PT. So everyone gets use out of it. So these are the learning outcomes that I will be discussing about today. And the first one is actually about the neuro humoral response in card in heart failure and how that's targeted for the pharmacological treatment. So before we start, I know it's been a long day. So I'll try to wake you up with an S B A and I am not sure how to launch a ball way. I think, I think there should be a pool now. Yeah. Yeah, I think most of you got no, the answer. This is one of the easier questions and yeah, the answer is B and this is the barrel receptor. So this is mostly actually for the 02 is present here because both chemo receptors and barrel receptors are actually present in the heart, but you need to know which one does what. So chemo receptors actually detect the low oxygen in the blood and they trigger the response from there. So when the patient's acidotic or hypoxic and they don't have enough oxygen, the other chemo receptors who will alert the brain. Whereas when there is a fall in blood pressure or is generally more cardiac kind of symptoms. You can just guess it as Paris scepters and then the others, I'm sure that you already know about, but you can also read them in your later time. So, starting off with the neuro humoral response and first and foremost, what does neuro humeral even mean that means neurons or like nerves and humoral means proteins or like hormonals and peptides and how that, how do they respond uh in heart failure? So uh they summarize actually the neuro human response and heart failure is mostly of two things which is a sympathetic nervous system and the Renan and your Denson aldosterone system. And both of them actually are very good for the heart in acute settings. Or basically if you have a patient coming in E D who's in shock or for case 17, and when you like the uh your two's, when you reach case 17, you'll know what the scenario was. But basically, when a patient comes by like unstable and very acutely ill, these responses are very good. But then after a while when they have like progressively, you know, the these systems are progressively being used, they actually harm the heart and they lead to like poor prognosis in heart failure. And I will explain that why. But the start off that I will explain water and in and your dense in a lost your own system is and this system literally in your do it took me two days, the entire two days to understand. So first and foremost, you have your heart and just imagine that this patient is having heart failure. So the heart is not being able like it's not pumping uh stretch. Uh And since the heart is not pumping, it is stretching. And since barrel receptor is actually a stretch stretch receptor, it detects that it, yeah, it detects that and sends a signal to your brain. Now, the brain will understand that the heart is actually pumping a lot. Uh it's stretching more to pump the blood and the BP has fallen. So now the brain will uh send the signals to your kidneys uh like specifically the Afrin arterials. And in the jocks, juxtamedullary apparatus of the kidney which will secrete Renan. And that is part of the first letter over here Renan along with the angio tencent or like protein from your liver will form your angio tencent one. Sorry. So Renan plus angiotensin from the liver will form angiotensin one. And now this angiotensin one will be converted into angiotensin two. And that will be done by the angiotensin converting enzyme. And why is that important is because your kidney is actually and the other parts of the body which are affected by the R R A S S system accepts only or angiotensin do not the previous forms. Just why the conversion of uh basically this step is that's why it's very important. And this is what's been generally targeted when you have a Cinna bitters or other kind of medications. So now what does angiotensin do? Uh, angiotensin two does. So it firstly, razor constricts and visa constriction will lead to high BP and that's good in acute scenting. But for patient who's having a chronic heart failure, it's going to affect the heart condition even more. And now they also increase the sympathetic drive. So they increase ways of constriction. Again, they also increase your heart rate. They also increase other stuff which is part of the fight and flight response and we'll deal with it. The next slide, they also release aldosterone and aldosterone also actually works similarly to angiotensin. But aldosterone works on the D CT of the clamor Euless and the angiotensin works on the P C T and they basically uh re absorb uh sodium and chloride and they secrete potassium along with water. And yeah, I lost run. Does it in PCT? So A D C D and angiotensin does that in PCT. And angiotensin will also stimulate your brain again to release A D H which will help the water be retained. But that leads to more edema in the body. So that's where in heart failure, patients', you have more pulmonary edema, peripheral edema because the water is just being retained inside the body. So that was my like me trying to give an explanation of the renin angiotensin. A lost your own system. I hope that made sense. So now the sympathetic system, I'm sure most of you know about it. So this is the fight and flight response and the sympathetic nerves are actually in the sub endocardium and they are mostly these kind of nerves. And if you remember you have another nose which are coming from the Vegas Note and those are the palace sympathetic nose, I think in s to especially these kind of questions do come up because they just like to confuse you. So just remember the vagal system in the heart is more for Palace empathetic and sympathetic notes, they generally should call a sympathetic nerves only. But uh so the sympathetic nervous system also has receptors in it like the other every other system and these receptors are January alpha one and alpha one to be to 12, which is why to like to stop this or like to reduce the effect of sympathetic nervous system. You have beta blockers which basically will block these receptors. So you're sympathetic nervous system will not go in short crazy and will also help in like other heart conditions like M I and heart failure over here. And since you're sympathetic nervous system also increases the heart rate, reduces blood, uh increases BP. It eventually also helps in stimulating the R A S A R A S system, which is the rain, an angiotensin a las alone. And I just explained why that is harmful. So it's basically both of these responses are good when the patient's unstable and acute. But over the long term, they're just going to make your heart beat faster. It's just going to increase your workload for your heart. And over a while, this causes the muscles to stiffen. So more causes of cardiomyopathy and valves being like, you know, not being able to function. So, regurgitation over there and other stuff and then it's going to cause um more edema and the peripheral edema is obviously you can see swollen legs and sacred where you can see the back of them will be kind of also swollen. But when this also caused pulmonary edema, the patient's also more likely to be short of breath. And what laura was explaining about how when patient's lie down in the bed, they are not able to breathe properly and they have to sit upright is all because of the pulmonary edema being than the body. And that is because of these systems. So which is why these are the systems that you have to control. Now, this should help your tree is also present over here. So I think most of you have uh like most of you have given the progress, just have realized that BNP or I, I can't actually I can't even pronounce it. So I'm just going to call it M MP. So these NP peptide or like proteins are or BNP level is very good to detect for heart failure. Generally when you have a high BNP level, uh your mind's like, okay, the patient's most likely to have heart failure. And why is that now? So BNP is basically like RNP is basically made in the heart and there are different types of it. It can be an arterial NP. It can be a brain, be an MP and it can be an N terminal pro pro be type nine, whatever NP hormone. And these basically are the counterregulatory hormones against the neuro human response. Or basically, you're rennin angiotensin aldosterone. So to stop those kind of things and to stop the effect of sympathetic and R S, uh the heart will release these uh proteins basically, which is why in heart failure when these symptoms, like these systems are going crazy, these hormones are formed and they try to regulated and generally for, especially for progress just if you have anything which is greater than 100 that's abnormal for BMP. And actually NP, this one is actually more specific. So at times people will ask for both BNP and this one, but both of them are actually generally good. And if you have that and if you want to investigate more, you can also ask for A and P. But generally you're going to see these two in progress test. So now I have an S P A and I will try to relaunch the pole. Yes. So you have Mister Jones who is a 78 year old man and he suffers with congestive heart failure. He has been prescribed ace uh innovators as one of his medications was the mechanism of actions of ace innovators. Generally, such a mechanism of actions for drugs are very, very common. So just make sure you're kind of thorough with them. And I think most of you have actually answered and most of you put it as b which is correct. Just remember that's converting and your tension one to do not the other way around. And I gave that explanation, but it was not written. So when you guys get these slides, everything will be written over here which will actually help, it will help you. And you can also Google this book or like website. I'll list my references also this, I think website had a very good explanation of the this pathway and I have another question for you. So MS Williams has started Ramipril for her left ventricular failure. Unfortunately, she developed a dry cough. So the G P has decided to change your medication to something else. What medication can they give and stuff Ramipril. So firstly, you need to know what is Ramipril and what will work similarly to that and what can they give? Yeah, I think actually one person did choose be, but most of you got it as a and that's correct. B is also I can understand why you went to be. But actually um dry cough is a very, very common side effect of a senna baiters. So when you have like, I think Laura also went through this, so be you do give beta blockers, so you're not wrong. But if um like ace inhibitors are like a Cigna bitters and if a senna bitters are not tolerated, for example, the patient comes in complaints about side effects and dry cough is the most common side effect. You can give an ARB which is nothing but Candra certain. And if you look at the running angiotensin aldosterone system, if ace is not there blocking the angiotensin two receptors is going to do the same effect as an ace inhibitor would have done, which is why you're going to use them. And yeah, I think Laura went over this. So probably I will not repeat. But I think secondly, for second years over here, uh knowing about a senna bitters is important. Yeah, I'll be probably or you just need to know that if the patient's are logic or you can't give them a senna bitters, you will give them A R B and B to blockers. Yeah, I'm sure you guys know and for the other drug that you need to know about is the jocks in. Otherwise I think these ones even I didn't know before I gave the presentation. So you don't have to stress about it. Another bowl for you actually another has beer for you. So Barbara present presented to E D with confusion irregular heartbeat and visual disturbance. As an F O F Y one on call you panic and you realize this might be due to an overdose of a drug that binds an inhibit the sodium potassium A T P S in the cardiomyocyte, which drug is he referring to here. But I think most of you have answered for like half of your countered, but I'll end the ball and it is a split between flecainide and the digoxin and just to confuse you guys, which is why I put flecainide. But the answer is the jocks in and why is that? Uh it's because digoxin is the sodium potassium A T P is in cardiomyo sides and these symptoms of confusion, irregular heartbeat, uh and visual disturbance kind of go with hypokalemia and hypochelemia and those kind of symptoms. And just understanding the picture is most likely to be the jocks in and the toxicity of the digoxin. And that's why I was telling the second years and actually even for PT to Oreos knowing the digoxin and why like how harmful it can be. It's very important, which is what actually most patient's are not given this drug until and all this, they are like very advanced in heart failure actually. So I I also uh mentioned one more point over here, especially for the 30 years. So you generally have New York heart scale or like heart uh basically a classification of heart failure. And if the patient's generally in the mild to moderate kind of stage of heart failure, you generally give them a sand beta blocker and Dietex obviously to remove the fluid. And as I'm sure both the previous students have explained, but only when the patient comes to a very severe stage or according to those classifications to like stage C or D or three or four, you start giving them these drugs and the digoxin is pretty much the very last one you give just because it has a very narrow toxicity therapeutic index and it can be really toxic. And if you do give a drug to a patient, like if you do give the jocks into a patient, you have to make sure that you monitor their heart functions, the kidney functions and basically the electrolytes in general and ask them how they're doing because it can be really toxic as, as I mentioned a lot. So yeah, it works by inhibiting the uh sodium potassium A T P S. And also it stimulates the parasympathetic response, which is why it helps in heart failure. And which is why it helps in other conditions like a failure and atrial flutter or any other like um irregular heartbeat. But um yeah, parasympathetic again, remember it was the vagal response and these uh symptoms are very of like very much of uh digoxin and it's toxicity and hypo uh Kalemie A hypernatremia and acidosis is very common. And I think at times they can also give you an E C G and ask you to understand what's happening. So just remember about, just remember if you hear the jocks in, probably it might be about it and the management of it would be through this drug and you of course, have to correct the arrhythmias because hypochelemia itself can cause a lot of problems to the patient. So that was, that was the first learning outcome. If you have any questions, just let me know and uh we'll move on to the second learning outcome, which I'll try to like kind of go uh oh, age can cause heart disease is and why is it that older patient's are generally having heart diseases. So just basically understanding the epidemiology of heart failure is the more older people that is generally the over the age of 65 are more likely to have heart failure and more males than females. And more generally the race of like African and Asian people than the Caucasian people are likely to have heart failure. And if you look at the physiology or like what exactly happens when we get old is basically that are connective tissues, firstly, are getting more harder and like more rigid. And that's why your arteries can also become more rigid as well as um your valves can get calcified. So they have hard time moving and all of these conditions can lead to different kind of heart problems. And that eventually can lead to heart failure. And of course, because of the like walls, thickening and stiffening, you can have high BP and high BP is not good to have anyways because it can cause stroke. It can cause Trumpers to form in literally everywhere in the body and a lot of other conditions. But I think mostly it's like the muscles are also getting weaker. So you have more chance of like the heart being not able to pump. Do you do many reasons and then thickening of those muscles also causing problems in the stroke, volume, cardiac output and then eventually basically leading to heart failure or the failing of all the organs. Uh This is another s be for you. I have X ray for this. So probably you guys can just take a few seconds reading the question, I'll come to the X ray and then show you guys. So um as BS of Katie, a 59 year old female who presents to a G P after experiencing orthopedia since or basically, that's worsening of short of breath when you lie down since a few uh months. Her past medical history includes type two diabetes and hypertension. Her social history is that she smokes 15 cigarettes in her day. The G P decides to take a chest X ray and ask you to interpret what condition does Katie have? And this is your chest X ray again, give you a few seconds to look at this and then go back to the answer options. Yeah, I think that should be okay. These are the answer options. If you want me to go back to the X ray, just let me know by either putting in the chat or um, muting yourself if you want. I think people are struggling to answer. So probably I'll go back to the X ray. Okay. I think three of you have answered and you have gone with pneumonia, which I can understand why. But basically this chest X ray was supposed to show uh cardiomegaly as well as like white area with her, which was like more signs of pulmonary edema, which you will find in congestive heart failure, which is why the answer was it. And again, focusing basically on age, I will not go in detail. But as you get older, you have more like more other co morbidities, which is why you also more likely to get heart failure. And these are also like all the risk factors which you can understand. And I think the first one always is age, that's why age can cause heart disease is. And the last learning outcome was like benefits of non pharmacological treatment. And I think this is the last SBA I have. So 53 year old man comes to the cardiac clinic for a follow up exercise for follow up uh stress exercise actually. And the doctor explains the physiological changes in heart while exercising, which statement, accurate story describes the pulse pressure of the patient. So it just has more on cardio physiology and more for it. I still really. Yep. I think most of you got it and correct its D and pulse pressure. Uh if you didn't know would be systolic minus diastolic pressure. And the fact is that can affect the pulse pressure are like the less working iota or less compliant iota, which would be because of advancing age or it can or like any increase in stroke volume and exercise can increase in stroke volume, which is why stroke volume will change this systolic pressure. And therefore this has gone down, this has most likely remain the same. So your pulse pressure has actually changed basically. And uh this is I think more important for uh s to people like like uh or do people because even though you could actually use your common sense and understand it, but it's just trying to understand these physiology, ease and these formulas just why in the end I kept like uh like a list of the formulas that were important for cardio cardiac physiology. And yeah, I hope that's helpful. That's the end if you have any questions, let me know right now. If not just email me.