[User] Please transcribe this text

[Assistant] Think about having high pressure in this circuit, okay? Think about having high pressure in this circuit. When you push blood from the right ventricle out into this circuit here, right? When you push blood into it, it receives the blood.


[User] Please transcribe this text

[Assistant] Kind of as elastic, it accommodates it, and then it should recoil and push the blood out into the respective circulations, but some of it should come back down, and that's why we got those good old valves, to snap shut, and to prevent the backflow.


[User] Please transcribe this text

[Assistant] Imagine having such a high pressure system which is pushing down on you. So imagine I got this pressure on my back, right? I push blood out.


[User] Please transcribe this text

[Assistant] And then now I have all this pressure in the pulmonary artery. It receives it, it recalls and pushes down. When it pushes down, it pushes down with a lot of force and it snaps that pulmonic valve shut very hard. So again, high pulmonary artery pressures are going to shut the pulmonic valve very hard.


[User] Please transcribe this text

[Assistant] And that is going to produce that loud S2. And so you would see this in any condition where there's what's called pulmonary


[User] Please transcribe this text

[Assistant] Hypertension. And there's many different causes for pulmonary hypertension, right? That's past the scope of this lecture, but again, thinking about this can help you in your diagnosis. So you're very loud as two, more particularly like the pulmonic component, so you'll be listening more in that left upper sternal border maybe. You should be thinking about pulmonary hypertension.


[User] Please transcribe this text

[Assistant] But if you have a loud S2 and it's due to the higher pressures that are actually occurring within the aorta. So this would be hypertension. Nothing, nothing crazy about it, right? So you have systemic hypertension. We'll call this systemic hypertension.


[User] Please transcribe this text

[Assistant] So you have systemic hypertension. This is going to have your high pressures in the aorta. So the high aortic pressures.


[User] Please transcribe this text

[Assistant] When you push blood from the left ventricle into the aorta, the aorta is going to recoil and then it's going to


[User] Please transcribe this text

[Assistant] It's actually going to expand, accommodate that volume, and then recoil and push it down into the descending aorta, push it up into the branches off the aortic arch, all of that stuff.


[User] Please transcribe this text

[Assistant] And when it pushes some of these blood back down, it's gonna really slam that aortic semilunar valve closed. So it's gonna shut the aortic valve very hard.


[User] Please transcribe this text

[Assistant] And again, when that happens, it's going to get very loud.


[User] Please transcribe this text

[Assistant] That would be things to think about, right? You know, it could be other issues, you know, corrected aorta, things of that nature as well, but big thing is the easiest one to remember is systemic hypertension, okay? So here, loud S2's you think high pressure within the aorta, high pressure within the pulmonary artery. Boom. Roasted. Soft S2.


[User] Please transcribe this text

[Assistant] This is actually going to be an interesting one where, again, S2 is the closure of the pulmonic valve and the aortic valve.


[User] Please transcribe this text

[Assistant] Now, soft S2 is actually relatively difficult to hear with respect to the pulmonic valve just because pulmonary stenosis isn't a super common type of occurrence.


[User] Please transcribe this text

[Assistant] With the aortic valve, it is actually the most common type of valvular disease. So imagine somebody has aortic stenosis, right? Think about aortic stenosis and this valve is just super calcified, it is just fibrotic, it's sclerotic, it's super immobile and just doesn't want to allow any blood to be able to go through it. So it's ability to open,


[User] Please transcribe this text

[Assistant] Stinks. And it's ability to close stinks. It's not very good at being able to open or close. Now think about that.


[User] Please transcribe this text

[Assistant] Imagine the valve is like this, right? It's super stenotic and fibrotic, right? You got a small little space there.


[User] Please transcribe this text

[Assistant] You try to push blood through it, it barely opens and lets blood go out. And then whenever you want it to close, it only goes like this. It doesn't actually come close to one another and actually snap really tightly together very well. So sometimes you can get kind of a stenotic and regurgitotic murmur.


[User] Please transcribe this text

[Assistant] So again, imagine the valve is like this. It's very little orifice. You're trying to push blood open and it only opens up a little bit. And then when you close, it only has to close that small distance. So that's a short distance if it does close. And so in situations like that, this is where you may see soft S2s. So again, in this situation here with the soft S2, there may be a, again, less pliable


[User] Please transcribe this text

[Assistant] And because of that, if it doesn't close very well and it doesn't close with a nice force that you would like it to, is you think that if I go from here to here, that's going to give me a loud sound versus from here to here. So again, not closing well will give you that soft type of S2. And the condition that you would see a lot of this in particularly is going to be aortic.


[User] Please transcribe this text

[Assistant] Stenosis. You may see this in pulmonic stenosis, but it is way less common. And again, you can differentiate these by particular maneuvers, but also just location. Aortic, should be right upper.


[User] Please transcribe this text

[Assistant] Okay, we've talked about the S1, S2 hard sounds, we've talked about the changes in intensity of them, soft and loud. Now let's go into the S2 a little bit more, because what we haven't really talked about is that S2


[User] Please transcribe this text

[Assistant] There's two components that are easily able to differentiate. The aortic component, so the closure of the aortic valve and the pulmonic component, the closure of the pulmonic valve. And sometimes we can actually separate those sounds really well and they call that splitting.


[User] Please transcribe this text

[Assistant] So we should be able to talk about that now called the splitting of the S2 heart sound. Alright, so now we're talking about the splitting of the S2 heart sound. So this is an interesting concept.


[User] Please transcribe this text

[Assistant] Whenever you're listening to the heart, you hear the lub dub, lub dub, lub dub. Right, so S1, S2, S1, S2. And again, ventricular systole, ventricular diastole, ventricular systole, ventricular diastole. It's the whole concept.


[User] Please transcribe this text

[Assistant] But you know what's really interesting? Is that when you look at the dub component, the S2 component of the hard sound, the closure of the aortic and the pulmonic valve,


[User] Please transcribe this text

[Assistant] Sometimes there's certain ways and certain pathologies by which that heart sound actually for S2 can become split where you can actually hear both.


[User] Please transcribe this text

[Assistant] The pulmonic component and the aorta component. Separately, not as one entity or one particular S2 heart sound. And that is called the splitting of the S2. So this can be physiological and we'll take a listen here in a second, but what is the physiological split S2?


[User] Please transcribe this text

[Assistant] Alright, so whenever somebody is expiring, what is happening to the blood flow to their heart?


[User] Please transcribe this text

[Assistant] Well in this situation, whenever there's expiration, you got more blood flow coming via the pulmonary circulation.


[User] Please transcribe this text

[Assistant] Into the left atrium, and then when it comes into the left atrium, down into the left ventricle, you have more blood that's going to be filling into the left side of the heart. The left ventricle already contracts a lot faster, and it contracts with a higher pressure, so that's not going to be a problem. It's going to push blood out.


[User] Please transcribe this text

[Assistant] Via the pulm, I mean, into the aorta, out into the systemic circulation. And when it pushes the blood out into the systemic circulation, into the aorta, the aorta receives the blood during systole. And whenever it does that, it will recoil and smash blood out into the systemic circulation. Some will go back down towards the left ventricle and snap shut the aortic, the aortic valve.


[User] Please transcribe this text

[Assistant] The same kind of thing will happen but there will be less, there will be more blood flow onto the left atrium and during expiration there will be less blood flow into the right ventricle.


[User] Please transcribe this text

[Assistant] The right ventricle is a smaller pressure system. It takes a little bit longer to push blood out of it though, too. So, but since there's less volume of blood coming into the right ventricle, it's going to be able to pump blood out into the pulmonary artery.


[User] Please transcribe this text

[Assistant] Relatively easy, you can push it out, and then whenever it pushes the blood out into the pulmonary artery, pulmonary artery will receive it, recol- send it out to the pulmonary circulation, some will go back towards the right ventricle, snap the pulmonic valve shut.


[User] Please transcribe this text

[Assistant] Since this is kind of occurring in a way where you get more on the left side and less going on the right side, it actually causes the sounds, just because the left ventricle contracts really quickly, it causes the sounds to become very close to one another. It's very difficult to differentiate.


[User] Please transcribe this text

[Assistant] And so when you're actually looking at this on a graph here, so this is time, and we're looking at the S1 and S2 hard sounds, S1, this is S1, right, so that's the closure of the mitral and the tricuspid valve.


[User] Please transcribe this text

[Assistant] Then you have the period of ventricular systole until we get to the point where the


[User] Please transcribe this text

[Assistant] Aortic valve and the pulmonic valve closed. The red component here


[User] Please transcribe this text

[Assistant] Is the aortic valve. We're gonna put A2. So this is the aortic component of the S2 heart sound. And then the blue here, which is actually less intense. So intensity we could actually say is the Y axis.


[User] Please transcribe this text

[Assistant] Our pitch. This is your P2, which is the pulmonary component of the S2 heart sound. It'll come just a little bit after it.


[User] Please transcribe this text

[Assistant] And again, intensity wise, the A2 is higher intensity, a little bit louder than the P2. P2 a little bit less intense, a little bit softer than the, uh, the A2. But again, they're so close to one another that we actually can't differentiate them from being separate from one another. Here's where it's interesting.


[User] Please transcribe this text

[Assistant] During inspiration, what happens to the blood flow to the heart?


[User] Please transcribe this text

[Assistant] During inspiration, you get a lot of blood flow coming into the right side of the heart. Like a lot of blood flow. Cause what happens is during inspiration, what do you do? You take a deep breath in, your intratheorastic pressure decreases and you suck blood into the right side of the heart.


[User] Please transcribe this text

[Assistant] More blood goes into the right atrium and into the right ventricle. During inspiration less blood is going


[User] Please transcribe this text

[Assistant] From the left atrium into the left ventricle. So you're getting way more venous return to the right side of the heart. And you're getting less venous return to the left side of the heart.


[User] Please transcribe this text

[Assistant] Which side takes a longer time to be able to push blood out? The right side. Now you fill it with more blood. It's going to take an even longer time. So what happens is during inspiration, you drop the intra-thoracic pressure, and when you drop the intra-thoracic pressure, that causes increase in right-sided filling, and that prolongs the right ventricle contraction.


[User] Please transcribe this text

[Assistant] Inspiration. The whole purpose behind this is because whenever you take a breath in, you drop your intrathoracic pressure, sock blood into the right side of the heart, more blood on the right side of the heart, more volume that the right ventricle has to deal with, it's gonna take a longer time for the right ventricle to depolarize, contract, and push all that blood out.


[User] Please transcribe this text

[Assistant] What is not normal is when you have a wide split S2.


[User] Please transcribe this text

[Assistant] A wide split S2 is where you actually have the splitting of the S2. There's the splitting of the S2 already present. So you can actually see here that during expiration you have an A2 component which is audible.


[User] Please transcribe this text

[Assistant] Okay, during expiration. Okay, you have that differentiation factor there. You can hear that during expiration. During inspiration, something really interesting happens, right?


[User] Please transcribe this text

[Assistant] So, during inspiration, again, you get more blood to the right side of the heart, right? So it's the same concept. During inspiration, you're going to drop your introthoracic pressure, you're going to increase your right side filling, and you're going to delay right ventricular contraction.


[User] Please transcribe this text

[Assistant] And if it takes a longer time for the right ventricle to contract, it's gonna take a longer time for it to pump blood out of the pulmonary artery, a longer time for the pulmonary artery to accommodate that, a longer time for it to recoil, a longer time for the pulmonic valve to close. So it's gonna come later, way later.


[User] Please transcribe this text

[Assistant] So you see how it's split during expiration? It becomes even more exaggeratingly split during inspiration. So there is a splitting that's present during expiration and even a wider split during inspiration. Why? What is causing this?


[User] Please transcribe this text

[Assistant] Well, the reason why it's happening at expiration and during inspiration is that there's something already previously wrong with the right ventricle. There was probably something here previously.


[User] Please transcribe this text

[Assistant] Where the right ventricular afterload was already high and so it was taking a longer time for blood to get pumped from the right ventricle into the pulmonary artery. So what are some reasons why it would already take a long time and then you filling the ventricle with even more blood would even prolong the time even more. Right ventricular afterload is increased


[User] Please transcribe this text

[Assistant] There's a high right ventricular afterload. This could be due to pulmonary hypertension. If you have pulmonary hypertension, the pressure in here is higher. It's going to take a longer time for the right ventricle to pump blood out into the pulmonary trunk.


[User] Please transcribe this text

[Assistant] And if you have it get filled with more blood you're even gonna prolong that time even more. What if you have a pulmonary embolus?


[User] Please transcribe this text

[Assistant] Now you got a clot that's sitting here in the pulmonary artery, that's going to increase the pressure. Again, your right ventricle is going to have to take a longer time to generate enough pressure to push blood out. That's going to delay it, and it's going to be even worse during inspiration.


[User] Please transcribe this text

[Assistant] What else? What about pulmonic stenosis? If you have pulmonic stenosis, where you have a terrible pulmonic valve and it's really, really stenotic and it's not really wanting to open.


[User] Please transcribe this text

[Assistant] If it doesn't want to open, now your right ventricle is going to have to get thicker, it's going to have to work hard, it's going to have to generate more pressure to push blood out of the pulmonary, out into the pulmonary artery. That's time. And that gets worsened during inspiration.


[User] Please transcribe this text

[Assistant] What else? What if I, what if I actually cause delay of the right ventricle of the depolarization? So not only do I cause the afterload to be higher, but I cause the depolarization. You know there's the structures here. Your good old SA node. Your good old AV node.


[User] Please transcribe this text

[Assistant] What if I, what if I, what if I damaged my right bundle branch, and now it can't supply electrical activity to the right ventricle, so it takes a longer time for the right ventricle to actually depolarize? Oooooh, that would make sense, right? So what if I prolong right ventricle depolarization?


[User] Please transcribe this text

[Assistant] And if I have a right bundle branch block, it's gonna take longer for the right ventricle to depolarize, it's gonna take longer for it to contract, longer for it to push blood into the pulmonary artery, longer for it to recoil and shut that valve. Man, we good. But let's take it to the next level.


[User] Please transcribe this text

[Assistant] What if not only is this a problem with the right side of the heart, what if I took it to the next level and I said, what if my left ventricle depolarized early?


[User] Please transcribe this text

[Assistant] I depolarize that area, I cause it to contract early, I cause it to push blood out even faster than it already is doing. That's gonna separate it away from the P2. Right?


[User] Please transcribe this text

[Assistant] What would do that? What would actually cause this beautiful left ventricle to depolarize a lot quicker?


[User] Please transcribe this text

[Assistant] Okay, so I'm gonna put down, we increase left ventricular depolarization and we do that quicker or earlier.


[User] Please transcribe this text

[Assistant] Then I'm gonna have electrical activity moving through the left ventricle. Stimulating the left ventricle first.


[User] Please transcribe this text

[Assistant] And if it depolarized the left ventricle first, it'll contract early, push blood out into the aorta early, cause the aortic semilunar valve to close earlier.


[User] Please transcribe this text

[Assistant] This would be a condition where there's an accessory pathway running right into the left ventricle via the Bundle of Kent. This is a situation called Wolf-Parkinson's White Syndrome and we particularly call this Type A where the Bundle of Kent is located between the left atrium and the left ventricle.


[User] Please transcribe this text

[Assistant] So this is what I want you guys to remember, again, in patients who have widespread S2. They naturally have two, three things wrong. One,


[User] Please transcribe this text

[Assistant] Is the right ventricular afterload is high, causing them to take a longer time to be able to push blood out of their right ventricle.


[User] Please transcribe this text

[Assistant] The right ventricular depolarization is prolonged, taking a longer time for them to contract and push blood out of the right ventricle. In that situation, it's already gonna cause the P2 to come later, regardless of expiration or inspiration.


[User] Please transcribe this text

[Assistant] But, during inspiration, you bring more blood into the right side of the heart, you cause a larger volume that the right ventricle is going to have to deal with. So if they have a high afterload and they have a longer depolarization period, now it's going to take even longer time for it to push blood out. And that's going to cause that P2 to come even later.


[User] Please transcribe this text

[Assistant] The other situation, which seems a little odd, but it's kind of like a little extra one to think about, is what if I cause the, you know, I cause the left ventricle to depolarize a lot earlier than the right ventricle.


[User] Please transcribe this text

[Assistant] So that would kinda just go against this in a weird way. If I depolarize my left ventricle early, it's gonna contract earlier, push blood earlier, close the valve earlier, and so it might shift the A2 where it looks like the P2 was the one that was drifting away, but it was actually the A2 drifting away.


[User] Please transcribe this text

[Assistant] And so you can see that in this situation of Wolf-Parkinson's White Syndrome Type A. Okay.


[User] Please transcribe this text

[Assistant] Let's now move on to the next one, which is called the fixed split S2. So fixed split S2 is a very interesting one. So fixed split S2 would actually be where the splitting of the A2 and the P2 component during S2


[User] Please transcribe this text

[Assistant] Is the same distance regardless of your expiring or inspiring. It doesn't matter. It's the same distance. It is a fixed distance or separation or differentiation or distinction between the A2 and the P2 component. And it's not changing. So look at this. Look at this.


[User] Please transcribe this text

[Assistant] During expiration the distance here is the exact same as the distance here. That is weird. How can the A2 component


[User] Please transcribe this text

[Assistant] And the P2 component be the exact same distance during expiration as it is during inspiration.


[User] Please transcribe this text

[Assistant] Well that means that there has to be some type of communication between the heart. An abnormal communication that is equalizing a lot of the pressure and the transit time in and out of the heart. What kind of communication would that be?


[User] Please transcribe this text

[Assistant] I'm so glad you asked because it's actually called an atrial septal defect. So you know in patients who have something called a atrial septal defect.


[User] Please transcribe this text

[Assistant] During expiration, which side is actually getting filled more? During expiration, which side is getting filled more?


[User] Please transcribe this text

[Assistant] You should have left-sided filling. So during expiration, imagine there's the pulmonary veins here. You should get blood that's filling into the left atrium and down into the left ventricle. That's what should happen here, right? But, think about this also.


[User] Please transcribe this text

[Assistant] During expiration, you get more blood to the left atrium. Which side has a higher pressure? Left atrial pressure or right atrial pressure?


[User] Please transcribe this text

[Assistant] Left atrial pressure, left atrium, left side it always has higher pressure. So the left atrial pressure


[User] Please transcribe this text

[Assistant] Versus the right atrial pressure, you're going to have much higher left atrial pressures.


[User] Please transcribe this text

[Assistant] Even in normal patients, no matter what, than your right atrial pressures. This should be lower.


[User] Please transcribe this text

[Assistant] So because of that, where would the blood want to go? It has an opportunity to go down into the left ventricle. But it also has this other area where it can go where there's less resistance. Left atrium to right atrium, lower pressure system. It's easy for blood to flow from areas of high pressure to areas of low pressure. So where else can the blood go? It can go right into the right atrium. And then the right atrium is going to get filled with blood.


[User] Please transcribe this text

[Assistant] Okay? And so it's gonna get a little bit more blood than it usually will.


[User] Please transcribe this text

[Assistant] During expiration, what happens to the Venus return on the right side?


[User] Please transcribe this text

[Assistant] The venous return on the right side is reduced during expiration. Because your intrathoracic pressure is generally going to be higher and it's harder to suck blood up into the right side of the heart. So during expiration there should be a reduction in venous return. So let's just actually represent that as just like one arrow.


[User] Please transcribe this text

[Assistant] Moving down from the right atrium into the right ventricles during expiration. So there is a reduction in right filling.


[User] Please transcribe this text

[Assistant] During expiration, that's a normal process. Lower reduction, there's a reduction in right-sided filling.


[User] Please transcribe this text

[Assistant] But there's blood coming from the left atrium via the atrial septal defect, increasing the fillings. So you got three arrows there. Okay? So three arrows there which are going to represent the splitting. So now if I have more volume of blood in the right ventricle, there's more volume.


[User] Please transcribe this text

[Assistant] More volume of blood in the right ventricle is going to take a longer time for the right ventricle to depolarize, a longer time for it to contract, a longer time for it to push all that blood out into the pulmonary artery. Pulmonary artery has to accommodate, it has to recoil and push the blood back down and shut the pulmonic valve closed. That's time it's going to take and the left ventricle is going to finish that before it. Alright? That's why it'll come later. But here's where it's interesting.


[User] Please transcribe this text

[Assistant] Into the left side of the heart. So there should be less blood that's coming into the left side of the heart.


[User] Please transcribe this text

[Assistant] Regardless though, left atrial pressures are going to be higher. No matter what, right atrial pressures are going to be lower.


[User] Please transcribe this text

[Assistant] You have less blood coming into the left atrium during inspiration. Less blood coming into the left atrium during inspiration. So maybe because of that


[User] Please transcribe this text

[Assistant] You're not gonna have as much blood to push from the left, there's still higher pressure here, so I can still push blood from the left atrium to the right atrium. But because I have less volume of blood coming from the lungs to the actual left side of the heart, I don't have as much volume of blood to donate to the right atrium. But I push a little bit over.


[User] Please transcribe this text

[Assistant] So now I push a little bit over and let's represent that with one arrow that I put some blood into the right side of the heart due to the ASD. Okay. So again, this is the ASD that we're talking about here, atrial septal defect. But during inspiration, during inspiration, what happens to the filling to the right side of the heart?


[User] Please transcribe this text

[Assistant] You increase the right heart filling. So now during inspiration, you should have higher right heart filling.


[User] Please transcribe this text

[Assistant] So more blood should come into, so you have inferior vena cava, superior vena cava. You're gonna have more filling here. And let's represent that. We only had one arrow to represent the right heart filling from, uh, expiration. During inspiration, you're gonna get more volume of blood.


[User] Please transcribe this text

[Assistant] And so you should have an increase in venous return to the right side of the heart. There's three arrows. How many arrows did I represent? I know it's not a matter of arrows, but it's the whole principle here. I'm getting, during expiration, more blood coming from the left side of the heart to the right side of the heart. And less venous return during expiration.


[User] Please transcribe this text

[Assistant] During Inspiration, I'm getting less blood coming from the left side of the heart and more blood that's being filled into the right side of the heart during Inspiration from Venus Return. But either way, the number of arrows is the same because no matter what, regardless, there's a communication between the atria that is allowing for this kind of, kind of equalization of right-sided filling.


[User] Please transcribe this text

[Assistant] But either way, the right side is going to take a longer time to be able to contract, a longer time to be able to push blood out of the right ventricle, into the pulmonary artery, a longer time for the pulmonary artery to accommodate that recall and snap the pulmonary valve shut.


[User] Please transcribe this text

[Assistant] And it's gonna cause it to come later than the A2. But it's a fixed distance. It's the same during expiration and inspiration because of the way the blood is moving across the left atrium to the right atrium during expiration and inspiration varies. And that's the cool part.


[User] Please transcribe this text

[Assistant] And the amount of blood that's coming into the right side of the heart during expiration and inspiration varies.


[User] Please transcribe this text

[Assistant] But they equal each other out in a way that it keeps the distance the exact same. How cool is that?


[User] Please transcribe this text

[Assistant] Alright, left ventricle contracts quicker, it's under more pressure, it's gonna push blood out into the left, into the aortic a lot quicker, close the aortic valve a lot quicker. That's a general concept that we've been able to pretty much assume throughout all of these splitting of the S2s. It's always come before the P2.


[User] Please transcribe this text

[Assistant] What if there's some situation where the actual A2 comes after the P2? That's odd, right? That would be really odd. That would mean that the left ventricle is taking a super long time to be able to contract and push blood out into the aorta.


[User] Please transcribe this text

[Assistant] So there's something that's causing the afterload, just like in the other situation where there was a wide split S2, there's gotta be something in the same situation where the left ventricle has a high afterload, it's having a difficult time pushing blood out into the aorta, or


[User] Please transcribe this text

[Assistant] The depolarization of the left ventricle is being delayed, or the right ventricle is being excited early. So just flip it, whatever it was for the wide split S2.


[User] Please transcribe this text

[Assistant] Into the aorta. So that would be one particular reason where there is a high left ventricular afterload. So there's a high left ventricular afterload. What would be particular situations for this? What if I have a good old stenotic valve here that doesn't want to allow me to push blood out? Aortic stenosis.


[User] Please transcribe this text

[Assistant] What if I have really high pressure in the aorta and it's not a big fan of me pushing blood out there? This could be.


[User] Please transcribe this text

[Assistant] Hypertension. So systemic hypertension. Or, what if there is a really tiny narrowing? There's a narrowing of the vessel in very congenital heart diseases where the aorta is actually co-arctate or has a little narrow stenotic point. Co-arctation of the aorta.


[User] Please transcribe this text

[Assistant] In these situations, it would take longer for the left ventricle to build up enough pressure to push blood out into the aorta because the pressure in the aorta is way too high.


[User] Please transcribe this text

[Assistant] Simple, right? Not too bad. And if that happens, it's gonna cause the actual A2 component to come a lot later. It's gonna come a lot later during expiration, and it's gonna come a lot later during inspiration. Okay, but we'll make sense of why maybe it's a little bit more during expiration. Don't worry, we gotcha.


[User] Please transcribe this text

[Assistant] Alright, next thing here, what would else be the other reason? The other reason is we said that the not only would be higher afterload, but the left ventricle is having a decrease. It's depolarization is coming later. It's prolonged depolarization. So we said that there also could be a prolonged


[User] Please transcribe this text

[Assistant] Left ventricle. So it's taking a longer time for us to be able to get the left ventricle to depolarize. So think about that structure stuff that we talked about before. Here you got your SA node. Here you got your AV node. Here you got your bundle of hiss, your right bundle branch, your left bundle branch. The left bundle branch is giving the electrical activity to the left side of the heart. What if I jack that bad boy up?


[User] Please transcribe this text

[Assistant] The last scenario here is that we said what if there's some type of like weird like ability to stimulate the right side of the heart faster for it to actually depolarize quicker. So what if there is a quicker depolarization


[User] Please transcribe this text

[Assistant] Of the right ventricle. So a quicker depolarization.


[User] Please transcribe this text

[Assistant] So if I have electrical activity that moves from the atria down into the ventricles, particularly the right ventricle, and then it can go back and excite the right ventricle and cause it to depolarize quicker,


[User] Please transcribe this text

[Assistant] If you were to component, that would be a situation where you have Wolff-Parkinson's white syndrome, but the rare type, type B, where the bundle of kent is actually associated between the right atrium and the right ventricle. Not a common one, but it's something to think about.


[User] Please transcribe this text

[Assistant] Alright, so that's the concept here. That's the reason behind this paradoxical splitting S2. Why the A2 component has to come after the pulmonic component. But let's see how it changes during expiration and inspiration. During expiration, what are you noticing here?


[User] Please transcribe this text

[Assistant] Oh wow, it's wider. It's wider during expiration. Let's think about why that is the case, my friends. During expiration, which side of the heart gets filled more?


[User] Please transcribe this text

[Assistant] The left side. So during expiration there's increase in left sided filling.


[User] Please transcribe this text

[Assistant] If I have more blood coming into the left ventricle, and it's already taking a longer time for it to de-uh, to actually contract and push blood out, it's taking a longer time for it to depolarize, what do you think that's gonna do?


[User] Please transcribe this text

[Assistant] And so that means that there's less blood that's gonna come into the left side of the heart, but there's still these issues where the left ventricle is under high afterload, or it's taking a long time to depolarize and contract.


[User] Please transcribe this text

[Assistant] But the big difference here is during expiration, there's an increased separation because you get more filling to the left side of the heart, which is gonna prolong the ability and the time it's gonna take for the left ventricle to push blood out because it also has these associated issues. Man, we're good. Alright, Absinthe Split S2. Absinthe Split S2 is another interesting one.


[User] Please transcribe this text

[Assistant] It's sometimes just called a single S2. It's where you get no splitting. Alright, so you should normally have splitting of the S2. But when you have no splitting of the S2, this is something that's very interesting.


[User] Please transcribe this text

[Assistant] You know, a patient who has very, very terrible, and I'm talking about like the most severe type of aortic stenosis where their valve is so stenotic, the dang thing doesn't even want to move at all and allow blood to go out. It doesn't want to allow blood to go, uhm, out at all. So it's super, super, super stenotic. Like think about the most severe case of aortic stenosis. So in severe,


[User] Please transcribe this text

[Assistant] Severe cases of aortic stenosis where it's super-impliable. It's very, very immobile, so severe.


[User] Please transcribe this text

[Assistant] Aortic stenosis. Super, super calcified, fibrotic, not pliable, very immobile. When I wanna push blood,


[User] Please transcribe this text

[Assistant] From my left ventricle out into the aorta. Right?


[User] Please transcribe this text

[Assistant] You'd think about this a little bit. You'd say, oh man, wouldn't that really increase the afterload? It definitely could. But here's the thing.


[User] Please transcribe this text

[Assistant] You have to have two components or you have to have an actual closing of the valve. You need a closing of the valve to actually produce an aortic component or a pulmonic component. So you would think, oh, wouldn't this just kind of like, you know, be the same thing as a paradoxical splitting of the S2 where it would come later? It would if you actually could hear that sound. That's the key thing.


[User] Please transcribe this text

[Assistant] So imagine you push blood up from the left ventricle into the orda. The orda has to accommodate it.


[User] Please transcribe this text

[Assistant] In a situation where that valve is so immobile, so fibrotic, so calcified, not pliable whatsoever, you have blood come back, imagine hitting that valve and the thing doesn't even do anything. It doesn't even close. Normally if you have some type of aortic stenosis, there's some pliability that'll actually at least snap shut and give a sound.


[User] Please transcribe this text

[Assistant] But if that thing is so fibrotic and so, uh, calcified to where you come back and cause blood from the aorta to push back down, to snap it shut, it doesn't even move, it doesn't snap together, you're not gonna get any hit of the aortic valve leaflets, no vibrations that are gonna cause a sound.


[User] Please transcribe this text

[Assistant] And so this severe aortic stenosis in these patients, they have no like actual true closure.


[User] Please transcribe this text

[Assistant] of the aortic valve. And so, because of that, all you're gonna hear


[User] Please transcribe this text

[Assistant] Is the P2 component. So all you'll hear for these patients is the P2 component. You won't hear the aorta component. If it were to be there, it probably would come later like a paradoxical splitting of the S2.


[User] Please transcribe this text

[Assistant] Because it's going to increase the left ventricular afterload. But, if you can't actually have the valve close and give a sound, you're not going to get any splitting of the S2 and no actual A2 component in comparison to the P2 component.


[User] Please transcribe this text

[Assistant] So this is a big thing to remember, very, very severe aortic stenosis, where there is very, like, fibrotic,


[User] Please transcribe this text

[Assistant] Aortic valve. This is where you would see this. Okay, my friends, we've covered all the splitting of the S2. This is a beast. So let's go ahead and test your knowledge quick. So let's test your knowledge. Let's take a look at these and being able to point them out. That's going to help you guys to really kind of like recap what we talked about because it was a lot. I'm not going to lie. Alright, so we take a look here. Expiration, inspiration is represented by the E and I. Okay, you take a look here. P2 component. Why is the P2 component early? Normally it's always supposed to be what? A2 component early. But the P2 component came early.


[User] Please transcribe this text

[Assistant] And it's more distance during expiration. That was the weird one. What was that one called?


[User] Please transcribe this text

[Assistant] This is the paradoxical splitting of the S2. So don't forget that one. Paradoxical splitting of the S2 is where the P2 comes early or comes before the A2 and there's an increase in the distance or splitting of the S2 during expiration. Alright, take a look at the next one here.


[User] Please transcribe this text

[Assistant] Expiration, inspiration. During expiration, okay, the P2 is coming forward. It's coming, I'm sorry, the A2 is coming first. So if the A2 is coming first, that's normal. There's no paradoxical stuff there. That rules that one out. The P2 is coming later, which is good. But look at the distance.


[User] Please transcribe this text

[Assistant] The distance between these is pretty much the same. It's about the same distance. So because the distance between these are the exact same, if it's a fixed distance during expiration inspiration, that would be, which type of situations?


[User] Please transcribe this text

[Assistant] That would be the fixed split S2. Okay? So with the paradoxical, that was high left ventricular afterload, a longer period of left ventricular depolarization, or early excitation of the right ventricle. For fixed split, it had to be a what? Atrial septal defect. Okay, we come over here.


[User] Please transcribe this text

[Assistant] We have expiration inspiration. Again, we have our A2 first, which is good.


[User] Please transcribe this text

[Assistant] We have our P tube, but it's actually like fused with it. So we have like no true splitting during expiration. During inspiration we have splitting.


[User] Please transcribe this text

[Assistant] Well that had to be the only one where it's actually like, again, close together during expiration. That's normal, there's no actual pathology there. And during inspiration it actually causes the splitting to occur. That has to be the physiological split. So we'll put physiological. So this is the physiological split.


[User] Please transcribe this text

[Assistant] Last but not least, we take a look here and we only have one of these big ones left here. Expiration, Inspiration. Again, you have your A2 coming first.


[User] Please transcribe this text

[Assistant] And you have your P2 coming later. They're split no matter what.


[User] Please transcribe this text

[Assistant] During expiration there's a little split and during inspiration there's even more exaggerated split that's actually present here. That means that there has to be some type of pathology occurring that's causing the right ventricle to be under higher afterload, a prolonged period of depolarization, or the left ventricle is depolarizing quicker and earlier.


[User] Please transcribe this text

[Assistant] Absent Split S2 just because I feel like this is actually the most important ones to take away.


[User] Please transcribe this text

[Assistant] Alright, we tested your knowledge, we nailed it, we crushed it. Let's now move into the next part, which is the S3 and S4 hard sounds, which are extra hard sounds. Alright, so let's now talk about the next thing, which is the extra hard sound. So we've gone through the location. We talked about S1, S2, loud, soft, S1, S2. We talked about splitting of the S2 hard sounds.


[User] Please transcribe this text

[Assistant] There's an extra types of heart sounds that you need to be aware of that you can sometimes hear physiologically, but it also could be pathological. And these are your S3 and S4 heart sounds. Okay, so S3 heart sound.


[User] Please transcribe this text

[Assistant] The way that I want you guys to quickly understand these extra heart sounds is we have to briefly go through some of the parts of what's called ventricular diastole. There's, there's actually three phases in it. So during ventricular diastole, we have it represented here. So again, let's actually remind ourselves here.


[User] Please transcribe this text

[Assistant] This big black chunk here is going to tell me, here, I'm actually going to test you. This is, this black bar here is representing the closure of the mitral valve and the tricuspid valve. Which sound is that one? S1. I know you guys all said it good. Okay, then we have here,


[User] Please transcribe this text

[Assistant] This is the closure of the aortic semilunar valve and the closure of the pulmonic semilunar valve. This is the S2. Good. And then, again, we go back into


[User] Please transcribe this text

[Assistant] S1. So if I were to test your knowledge here, from S1 to S2 is the period of ventricular, systole,


[User] Please transcribe this text

[Assistant] And then from S2 to S1 is the period of ventricular diastole. So ventricular systole is when the ventricles are contracting, injecting blood. Ventricular diastole is where they're relaxing and receiving blood. Simple, right?


[User] Please transcribe this text

[Assistant] So between S2 to S1 is where you're gonna hear these S3 and S4 heart sounds. So they're only considered to be diastolic types of extra heart sounds. That's important to remember. You do not hear it during systole. You only hear these S3 and S4 heart sounds during diastole. But in order to understand where we hear them, we have to have the different periods here. Okay, so this is what's called the


[User] Please transcribe this text

[Assistant] Early diastolic filling, which is the pink color here. So we'll write that down here. This is the early diastolic filling. So early.


[User] Please transcribe this text

[Assistant] Okay, rapid entry of blood into the heart. Okay? Remember that, early diastolic feeling is when there's rapid entry of blood into the heart.


[User] Please transcribe this text

[Assistant] The next one is the purple. This is called the MID diastolic filling phase. This is called MID.


[User] Please transcribe this text

[Assistant] Diastolic filling phase. This is where there is a slower entry.


[User] Please transcribe this text

[Assistant] That's sitting and waiting there to flow into the ventricles. This is your


[User] Please transcribe this text

[Assistant] Early diastolic filling. It's rapid because it's just waiting in the atria to flood down into the ventricles. All of the blood that is in the channels here, like the superior vena cava,


[User] Please transcribe this text

[Assistant] Infervenicava and some of the vessels outside of the pulmonary veins here.


[User] Please transcribe this text

[Assistant] These are going to rush in after the blood from the atria dumps in. So this would be your mid-diastolic feeling. It's a little bit slower, but it's usually from the channels that are coming outside of the atria.


[User] Please transcribe this text

[Assistant] And then last but not least, if there's any remaining blood that's sitting in the atria at the end of ventricular diastole, the atria contract and push down the remaining 10 to 20% of the blood that's sitting in the atria. And so this is actually called the late diastolic filling, but we actually call this the atrial kick.


[User] Please transcribe this text

[Assistant] So this is called the atrial kick. So this is when the atria actually contract and push remaining 10 to 20% of blood.


[User] Please transcribe this text

[Assistant] Into the ventricles. Okay, so that's important to remember.


[User] Please transcribe this text

[Assistant] The S3 heart sound only occurs in the rapid phase of ventricular filling. So this is in the early diastolic filling. That's why it's really important. So S3 would only really occur in which one of these phases? It would only occur here in the early diastolic filling. So this is going to be your S3.


[User] Please transcribe this text

[Assistant] Three heart sound. That is important to remember. Okay? The other thing that's important to remember about the S3 heart sound is not only does it occur during the early diastolic filling time, we should understand why it occurs during the early diastolic filling time and what kind of actual normal things can cause it to occur and what kind of abnormal things can cause it to occur.


[User] Please transcribe this text

[Assistant] Okay, first thing is let's talk about the physiological reasons for this. So the physiological reasons for having


[User] Please transcribe this text

[Assistant] An S3 is that you just have a high amount of venous return or a high type of compliance of the ventricles. So there's a high compliance of the ventricles.


[User] Please transcribe this text

[Assistant] So what kind of situations would you have high like venous return where there's lots of volume of blood? But it's a normal situation. Pregnancy. And pregnancy that generally these patients have to have a larger volume of blood because they have to have enough blood to pump throughout their body and the baby's body.


[User] Please transcribe this text

[Assistant] And so pregnancy is a pretty common reason as to why they may have a higher amount of venous return and generally their ventricles are a little bit more compliant to accommodate all of that volume of blood.


[User] Please transcribe this text

[Assistant] You know what else? Young athletic individuals. Where they have good venous return and very good contractility of their ventricles, they're very healthy and so they're naturally compliant. And so young athletes also tend to be a very common patient population.


[User] Please transcribe this text

[Assistant] Now you can see these physiological S3 hearts down due to their increase in venous return. So if you have a good venous return into the right ventricle or a good venous return into the left ventricle, during the early phase of diastolic filling,


[User] Please transcribe this text

[Assistant] That is one reason, and also if the left ventral can accommodate that and allow for that blood to flow into it, that's another reason. Now why does this actually happen?


[User] Please transcribe this text

[Assistant] Imagine the blood flowing down into a lot of blood, either high venous return or having a large space for the blood to actually enter in. When that happens, blood can run down here and it can actually kind of go through this like turbulence.


[User] Please transcribe this text

[Assistant] And when it runs through this like turbulent type of process, it can actually give off a certain type of heart sound. Cause that's really one of the reasons for heart sounds and heart murmurs is turbulence of blood flow.


[User] Please transcribe this text

[Assistant] So imagine right when the atria allow for blood to flow from the atria into the ventricles, a rapid volume of blood flowing down is going to create a lot of turbulence within those ventricles and that's going to give off a vibration which is going to come into the chest as the S3 heart sound. So that's the reason why. It's due to rapid ventricular filling within compliant ventricles.


[User] Please transcribe this text

[Assistant] Or a rapid venous return into the actual ventricles.


[User] Please transcribe this text

[Assistant] That's physiological. What are some pathological reasons for an S3?


[User] Please transcribe this text

[Assistant] So pathological reasons is really kind of going to the same kind of concept. It's not really like a high venous return. It's not really a high compliance of the left ventricle. It's usually due to excessive left ventricular dilation.


[User] Please transcribe this text

[Assistant] So the left ventricles are like super dilated and in that way they're very compliant, they're very floppy, they can accommodate like, imagine having a big old like ventricle that blood can rapidly flow into.


[User] Please transcribe this text

[Assistant] And so what are situations where you have large amounts of very, very large left ventricles? This could be seen in situations like aortic regurgitation, mitral regurgitation, you can see this in what's called dilated cardiomyopathy, and you can see this in what's called systolic heart failure.


[User] Please transcribe this text

[Assistant] In these situations you may see commonly a patient with a S3 heart sound.


[User] Please transcribe this text

[Assistant] The next thing to think about is not only were you here during the early phase of diastole, so right after the S2, it's due to rapid ventricular filling creating a turbulent flow.


[User] Please transcribe this text

[Assistant] Physiological cases is pregnancy, young athletes. Pathological cases is left ventricular dilation. Aortic regurgitation causes a lot of blood to stay within the ventricles or flood back into the ventricles so they get a large volume, they dilate. Mitral regurgitation, you pump blood from the left ventricle into the left atrium, it comes back down to the left ventricle, it gets volume overloaded, it dilates.


[User] Please transcribe this text

[Assistant] Dilated cardiomyopathy is within the name. There's dilation of the left ventricle. And it's a systolic heart failure. It loses its contractility. And its contractility decreases. And so the actual ventricles kind of balloon up and become more like large. And this can be seen as a systolic heart failure. Where you get heart, the heart actually gets congested with blood.


[User] Please transcribe this text

[Assistant] In these situations, you want to understand two things. When you're listening to this actual heart sound, it's really important to remember that the pitch, the S3 heart sound is a very low pitch.


[User] Please transcribe this text

[Assistant] And so because of that it's not, you can, it's easier to pick it up with, there's two parts of the stethoscope. You know there's the diaphragm of the stethoscope and the bell of the stethoscope. The bell of the stethoscope is actually good for being able to pick up lower pitched types of heart sounds. So because it's lower pitched it's better heard with the bell of the stethoscope. That's an important thing to remember.


[User] Please transcribe this text

[Assistant] Okay, and the second thing that you want to remember here is not just this, but when we listen for this one,


[User] Please transcribe this text

[Assistant] Usually it's more common on the left side of the heart. Left ventricle. And so when you actually put a person in, you can listen at the left lower sternal border, like around left fifth intercostal space, mid clavicular line, like near the mitral area. But if you put a person on their side, what's called the left lateral decubitus position,


[User] Please transcribe this text

[Assistant] It brings the mitral valve closer to the actual chest wall. And when blood is rapidly flowing from the left atrium into the left ventricle, it's really close to the heart. You can actually accentuate those murmurs, uh, this S3 heart sound. So it's actually heard very well in what's called the left lateral decubitus position.


[User] Please transcribe this text

[Assistant] That's something I really, really want you guys to remember for this, okay? Alright, we talked about the S3 heart sound. Early rapid filling is when it's gonna occur. Doing it right after S2.


[User] Please transcribe this text

[Assistant] Again, it's going to be due to some increased volume of blood moving into the ventricles. A rapid ventricular failing creates turbulence of blood flow. It can be physiological in cases of high venous return, high compliance, pregnancy, young athletes, or excessive left ventricular dilation like aortic regurg, mitral regurg, dilated cardiomyopathy, and systolic heart failure. It's low pitch, best herb with a bell, and again,


[User] Please transcribe this text

[Assistant] Left ladder decubitus position is the best position to actually hear this in. Okay, let's talk about S4.


[User] Please transcribe this text

[Assistant] Alright, so S4 heart sound. This one's a very interesting heart sound as well. Okay? So again, go back and remember, what did we say? There's what's called S1 closure of the mitral and tricuspid valve. And again over here we just have another S1 closure of the mitral and tricuspid valve.


[User] Please transcribe this text

[Assistant] When S1 starts, until it gets to S2, is the onset of ventricular systole. Ventricular diastole is going to be, again, onset of that is going to be triggered by the closure of the aortic valve, which is the A2 component, and the closure of the pulmonic valve, which is the P2 component, but together we just call these the


[User] Please transcribe this text

[Assistant] Once S2 starts from that until we get to S1 is ventricular diastole. There's three phases I told you I want you guys to remember. The first one, which the pink one, was the early diastolic filling time period. Early diastolic filling. And I just want you to remember a big term rapid filling of ventricles. Then you have the mid diastolic filling phase. And again, this is the slow filling. It's really the conduits from the vena cava and the pulmonary structures.


[User] Please transcribe this text

[Assistant] Okay, so the atrial kick is basically going to be when the atria push blood


[User] Please transcribe this text

[Assistant] Down, about what remaining percentage? About 10-20% of the blood is pushed down.


[User] Please transcribe this text

[Assistant] Into the ventricles. And this is due to atrial contraction. Because the atria has to contract and push that blood down.


[User] Please transcribe this text

[Assistant] So if we were to think about that, where would the S4 heart sound occur?


[User] Please transcribe this text

[Assistant] Well, the S4 heart sound is actually going to be whenever the ventricles are really stiff, very, very tough, and difficult for them to actually feel properly. And we'll talk about what reasons that can happen. But in the S4 heart sound, the problematic issue, the phase, is actually going to be within the atrial kick component.


[User] Please transcribe this text

[Assistant] So within the S3 heart sound, it was during the early diastolic filling was the actual issue.


[User] Please transcribe this text

[Assistant] And patients with an S4 heart sound, it's during the last phase of ventricular filling, the atrial kick phase. And so when we actually listen for an S4 heart sound, it's actually going to occur in this last part here. So this would be early, mid,


[User] Please transcribe this text

[Assistant] So you can already tell the difference between S3 and S4. S3 would be early diastole.


[User] Please transcribe this text

[Assistant] Alright, so the question that we have to ask ourselves is, why is this atrial kick becoming more intensified? It basically is the reason. So that's kind of what's happening is that there is an increase in the atrial kick. So let's actually write that down. In this situation, the reason why this patient is having this S4 heart sign is there is an increase in the atrial kick.


[User] Please transcribe this text

[Assistant] And the reason for the atrial kick is that there is an increase in the left atrial hypertrophy.


[User] Please transcribe this text

[Assistant] So that, that bad boy is getting, it's working out, okay. It's working out, it's working hard, it's getting thick, hypertrophic type of left atrium can contract harder and generate more force and increase the intensity by which blood is flowing from the left atrium into the left ventricle. That sound when after the left atria contract and squeeze blood down to the left ventricle,


[User] Please transcribe this text

[Assistant] As to why this left atrium decides to go, you know, Arnold Schwarzenegger and get super jacked up. What would be some particular reasons of why that would happen?


[User] Please transcribe this text

[Assistant] Well, let's think about this. What if I have a very, very stenotic valve? I got a valve here that's being pesky and doesn't want to open up and let blood flow through. So I want blood to naturally go from my left atrium into my left ventricle.


[User] Please transcribe this text

[Assistant] But this valve is restricting that process. It's superfibrotic, and now because of that, my left atrium is gonna have to get thicker, stronger, because it's gonna have higher left atrial pressures. When it has higher left atrial pressure, it'll increase to what's called left atrial hypertrophy. So that's that process there.


[User] Please transcribe this text

[Assistant] And then when it has that left atrial hypertrophy, whenever it comes time period for it to go ahead and contract, look how thick this bad boy is, it's going to generate more force to push blood down into the left ventricle. And that's going to give that, that atrial heart, atrial kick intensification, which is going to give you the S4 heart sound. So what would be particular reasons? One of the reasons would be mitral stenosis. Mitral stenosis.


[User] Please transcribe this text

[Assistant] Alright, what's another reason? Another reason this can occur is imagine this left ventricle. Your left ventricle is super hypertrophic.


[User] Please transcribe this text

[Assistant] So you have, so now it's going to be the opposite situation here. So you have, let's actually do this in a different color here. So you have increased left atrial hypertrophy. So there's other reasons why this can occur. One is because of the mitral stenosis, right?


[User] Please transcribe this text

[Assistant] But the other reason this can occur, this left atrial hypertrophy, just to have a different component here to explain it.


[User] Please transcribe this text

[Assistant] Is now, imagine that the pressure inside of the left ventricle is really high. So high left ventricular pressures.


[User] Please transcribe this text

[Assistant] So meaning that it's difficult, the left ventricle pressure is really really high. If the left ventricle pressure


[User] Please transcribe this text

[Assistant] Is really high. That means that the atria is going to have difficult times of being able to fill the actual ventricles. Because again, we want pressure whenever blood flows from one direction to another, we want it to go from areas of high pressure, areas of low pressure.


[User] Please transcribe this text

[Assistant] When the ventricles are relaxing, so we can actually call this what's called


[User] Please transcribe this text

[Assistant] The left ventricular in diastolic pressure at the end of diastole when they're supposed to be relaxing, their pressures are higher.


[User] Please transcribe this text

[Assistant] And we'll talk about reasons why these pressures would be higher. But if it is higher, that means that the atria, they're generally lower pressure systems.


[User] Please transcribe this text

[Assistant] In order for the atria to have to be able to push the blood down into the ventricles against this high pressure ventricle, it's gonna have to bulk up.


[User] Please transcribe this text

[Assistant] And so what happens is this high left ventricular end-diastolic pressure leads to the left atria having to hypertrophy.


[User] Please transcribe this text

[Assistant] Because they're gonna have to jack themselves up to generate higher pressures so that they can push the blood down into the ventricles down a concentration gradient. Imagine the pressure in the atria is like 20 and the pressure in the ventricles during rest is 50. Can you push the blood down that direction? No.


[User] Please transcribe this text

[Assistant] So then the left atrium has to jack its pressure up enough that it can be higher than the pressure in the ventricles to push blood down.


[User] Please transcribe this text

[Assistant] So that's what it does. The high left ventricular and diastolic pressures cause the left atrium hypertrophy and that's going to intensify that atrial kick. What are things that increase the left ventricular and diastolic pressure? Because that's the issue. This could be due to...


[User] Please transcribe this text

[Assistant] Hypertension, because if you have high pressure out here in the aorta, the left ventricle has to thicken to push blood out into it to generate more force. If you have aortic stenosis,


[User] Please transcribe this text

[Assistant] Aortic stenosis, you have a very stenotic valve. You have to cause the left ventricle to get thicker and stronger to generate enough force to push blood through that small little opening in the stenotic valve. Right?


[User] Please transcribe this text

[Assistant] These could be particular reasons. Another one is imagine you have like a fat septum that's occluding blood flow through that small area. And now you have to generate enough pressure to push as much blood as you can through that little narrow area.


[User] Please transcribe this text

[Assistant] Cardiomyopathy, ischemic cardiomyopathy. This is a condition in which they have multiple infarcts of their heart. And whenever they have infarcts, they replace that damaged myocardial tissue with fibrous tissue.


[User] Please transcribe this text

[Assistant] And if they can't open up and actually distend and accommodate blood, the pressure inside of them go up. And that's gonna cause, again, the left atrium to have to bulk up to increase its pressure when it hypertrophies, when it contracts.


[User] Please transcribe this text

[Assistant] And it creates a large S4 heart sound.


[User] Please transcribe this text

[Assistant] So this could be particular situations to remember and think about. Okay.


[User] Please transcribe this text

[Assistant] Next thing I want you guys to remember, just like the S3 heart sound, for the S4 heart sound, the other thing you need to remember is that S4 is low pitch.


[User] Please transcribe this text

[Assistant] So what would be easy to hear this with? The bell. Listen with the bell of the stethoscope. And then again, the other thing is that it's actually going to be best heard in the left lateral decubitus position because you get that left side of the heart mitral valve closer to the chest wall. Okay?


[User] Please transcribe this text

[Assistant] Let's test your knowledge, let's see if you guys understand this now. So you have a patient, let's say that you're listening, again, the left outer decubitus position, you're listening with the bell of your stethoscope. When you have them in that position, you hear a low-pitched type of heart sound, really in the early phases of diastole, the early phases of diastole.


[User] Please transcribe this text

[Assistant] When you hear this, you know that the patient is pregnant or you know that they're a young athlete or you know that they have causes of left ventricular dilation. You would say this is rapid ventricular filling due to a very compliant left ventricle or dilated left ventricle. Ooh, that is a S3 type of heart sound. Then I have another patient.


[User] Please transcribe this text

[Assistant] I'm listening with the stethoscope, particularly the bell of the stethoscope. I'm listening in the left lateral decubitus position. It's a low pitch murmur. When I hear it, I'm thinking, ooh, this is actually what phase of diastole? Ooh, this is the late phase of diastole, right before the onset of S1. If that is the case, I know that this has to be due to some type of


[User] Please transcribe this text

[Assistant] The big thing to remember is S4 heart sounds are always considered to be pathological. S3 heart sounds could be pathological or physiological.


[User] Please transcribe this text

[Assistant] Now that we've hit this home, let's talk about a couple extra additional heart sounds that you can hear during systole, diastole, or throughout systole and diastole.


[User] Please transcribe this text

[Assistant] Let's now move into some additional types of systolic heart sounds. We obviously know S1. We know S2. The changes in intensity in the S1 and S2. We know splitting of the S2. We know the extra heart sounds S3 and S4. Is there anything else that I can possibly hear, Zach?


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[Assistant] Yeah, we still have to do a lecture on murmurs in the future, but yeah, there's actually a couple extra types of sounds that could be present in Sicily or in diastole or even throughout the entire Sicily and diastole that we actually have to know for your exams or for the clinical scenarios. So first things first.


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[Assistant] And systole, you can actually get something called ejection clicks. Okay. So you can get something called ejection clicks. That's an important one to remember. So with ejection clicks, what's actually happening is we're going to take two particular vessels. Here we have our pulmonary trunk, which we're taking from here. And here we're taking the aorta, which we're taking from this position.


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[Assistant] In the ejection clicks, this is obviously occurring during ventricular systole. And ventricular systole would be the onset during what part?


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[Assistant] Would it be right after S1 until you get to S2, or would it be from S2 until S1? It'd be from S1 to S2. So we know from here to here for S1, and again here's the other S1, and this is S2, which is the A2 component and the P2 component, from here to here, I know is ventricular systole. So the ventricles are going to be contracting on the left side,


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[Assistant] You're contracting on the right side and pushing blood up to the pulmonary trunk, pushing blood up into the order.


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[Assistant] If we were to really zoom in on that and see what's actually happening, it's really interesting. So imagine the right ventricle is pumping blood up here into the pulmonary trunk.


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[Assistant] When it pumps into the pulmonary trunk and you have a patient who has what's called a pulmonary stenosis, they got a really stenotic valve here. Okay, so this is a patient who has what's called pulmonic stenosis. They have a very stenotic pulmonic valve.


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[Assistant] When you push blood into them, their valves are very, very fibrotic, sometimes even calcified. It's difficult for them to open, right? That's the whole problem. It's difficult for them to open and allow forward flow.


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[Assistant] So what happens is, they actually do something really weird. I'm gonna draw this with a dotted line. They actually kind of like do something called a bowing. They kind of bow. So imagine they're in this position. You push blood into them. You want them to snap out this way. You like them to go like this, close to the actual wall of the vessel. But instead, imagine them like this and then bowing.


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[Assistant] When they bow, here's the opening, here's the opening, this is what actually happens. They actually go from this position like this to this. And when they do that, every time you contract and push blood up into them and they bow, it creates a clicking sound.


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[Assistant] So going from this position where they're like this to bowing like this. This is called a bowing.


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[Assistant] of the valve, that's going to produce a very distinctive clicking sound and that can be heard during pulmonic stenosis. So again, imagine it like this. Here's your valve like this.


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[Assistant] Okay, here's the opening. You want blood to flow through here, right? When you want that to happen, you want this valve to open like this. But instead what happens is it actually does something like...


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[Assistant] This. It bows. So it goes from this position to this position. And that bowing is enough to be able to produce a clicking sound.


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[Assistant] Same kind of concept can happen here with aortic stenosis. So here we have our left ventricle. We're trying to push blood up through the aorta. We want to push it up through the aorta. We want this bad boy to open. What would realistically we want it to look like this? We want it to open like this so that blood can easily flow out.


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[Assistant] But in a patient who has aortic stenosis, that valve is not good at being able to open like that. And so instead of it opening like that, guess what it actually does? So imagine here again, we have a patient who has what's called aortic stenosis. They're going to get this bowing. So imagine here we have our


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[Assistant] Aortic valve. We want it to open like this, but it doesn't. Instead, it actually bows.


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[Assistant] When would I hear this clicking sound? I know it's during ventricular systole. Is it during early to midpoint or is it from mid to late point? Because that's really the two points of where this can occur. And that's a good question.


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[Assistant] This clicking sound which you may hear in these patients could actually occur in the early to mid point. So we're going to call this the ejection click. And again, there could be the pulmonary or there could be the


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[Assistant] Aortic component of the ejection click here just to make it look cool. We'll put ejection click. And this is representing


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[Assistant] The clicking due to the stenotic aortic valve or the clicking due to the stenotic pulmonic valve.


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[Assistant] So you would hear this in the early to mid point of ventricular systole. And the other interesting point is that usually this merm, usually this precipitates a murmur.


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[Assistant] So whenever you bow the valve, blood is going to try to flow through that bowed valve and there's going to be a lot of blood that flows through and then less blood. And then again, that creates this weird type of murmur here, which we're going to represent here in black. This is going to produce what's called a crescendo.


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[Assistant] De crescendo type of murmur that you would see with pylonic stenosis and aortic stenosis. That's one of the big things. Why am I mentioning all of this? Cause we're gonna talk about this in murmurs.


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[Assistant] Well the big thing to do and understand here is that this can be somewhat different from another type of clicking sound that you can hear during systole.


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[Assistant] This is actually due to mitral valve prolapse. So you know the patient who has what's called a mitral valve prolapse. They also call this Barlow syndrome, floppy valve syndrome, a lot of different reasons for it. But usually what happens is there is a weakening of two tissues here. There's maybe weakening of the


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[Assistant] Cordae tendine, due to connective tissue defects, right? So this can sometimes be associated with what's called Marfan syndrome. It can sometimes be associated with Ehlers-Danlos syndrome. So there can be weakening of that cordae tendine, which helps to anchor down the leaflets. Alright, so those are weak. They're not holding on to the leaflet. Now the leaflet's just kind of like, you know, jiggling around. It's floppy. Alright?


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[Assistant] The other situation here is that you can develop something called mixomatous degeneration of the


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[Assistant] Mitral valve leaflet. So now this leaflet is all degenerated and actually weak.


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[Assistant] And so now imagine pushing blood against that leaflet to snap shut. It's super weak type of leaflet and you don't have a strong chord A tendon a anchoring it down. When you actually contract and push against that leaflet, it's going to bow upwards. And so what actually starts to happen here is it starts to look something like this. It'll actually bow upwards into the left atrium.


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[Assistant] And when it bows upwards into the left atrium during ventricular systole,


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[Assistant] When it goes from this position, so let's have some action. Let's imagine here I have like a dotted line. It was like this originally. Okay, it goes from here to here.


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[Assistant] From that position where it was in normally, during ventricular systole, when I'm trying to push blood out of the heart, it actually, this valve is supposed to close. It's so weak because of the weak cord a tendinitis or the weakened valve leaflet, it bows into the left atrium. That right there, that bowing of the mitral valve produces a clicking sound.


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[Assistant] But the question is, is why, uh, where would this actual clicking take place? Would it occur in the early phases to about the mid phase? Would it occur in the mid to the late phases? That's a great question. And this actually tends to occur more in like the middle to later systolic phases. So this would be your mitral valve prolapse type of click.


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[Assistant] Okay, and then here's the other interesting thing. So again, what would this be associated with? Mitravov prolapse. It would be the chordae tendonae are weak. Or it would be the leaflets are weak.


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[Assistant] And because of that, whenever ventricular systole occurs, it bows that actual leaflet inwards, which creates a clicking sound. When that happens, now think about this valve here. So get rid of this one.


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[Assistant] Well actually here, we'll keep it just for representation. We'll keep it there for representation. But.


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[Assistant] Imagine now that leaflet is bowing up there. Is it gonna be able to nicely click with this actual other valve leaflet? No. And so blood can easily regurgitate back into the left atrium. And so this may also produce an associated


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[Assistant] Murmur that you can hear as well in the later phases of systole.


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[Assistant] So one of the big things to think about for aortic stenosis and pulmonic stenosis is these ejection clicks occur in the early systolic time period.


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[Assistant] Mitrobop prolapse occurs in the mid-systolic time period.


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[Assistant] Aortic and pulmonic stenosis are associated with a crescendo decrescendo murmur and mitral valve prolapse is usually associated with a mitral regurg, kind of a holosostolic murmur. It may have a little crescendo fashion to it, but it's usually in the later phases and there's maneuvers that we can do to change that. And we'll talk about that in our heart murmur lecture. But these are the things that I want you guys to remember. So extra clicking sounds that you can hear is


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[Assistant] Prostatic valves. So I want you guys to also remember that if a patient has something called a prostatic valve, it's actually normal for them to have


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[Assistant] A clicking sound. We actually want to hear that clicking sound during S1 and S2. So in patients who have something called a prosthetic valve, it is important


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[Assistant] If at some point a patient has a prosthetic valve and the click is absent, we know that there could be a potential prosthetic valve malfunction. So there's three scenarios that I want you to remember. Clicking types of extra heart sounds. This could be aortic stenosis or pulmonic stenosis, so just those stenotic lesions.


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[Assistant] These are the things I want you to remember. Now that we've talked about those, let's talk about some additional heart sounds, particularly diastolic heart sounds that I want you to remember. So what are these additional heart sounds? We talked about the systolic ejection clicks, aortic and pulmonic, we talked about mitral valve prolapse, early,


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[Assistant] It's gonna be the aortic and phylloxinosis, mid, mitral valve prolapsed, and if it's prostatic valve, you should always hit the click. If you don't, it's a prostatic valve malfunction.


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[Assistant] Additional diastolic heart sounds that I want you guys to remember is particularly these things called opening snaps. Okay, they're called opening snaps.


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[Assistant] And so this actually happens particularly in patients who have mitral stenosis or tricospid stenosis.


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[Assistant] So you know what happens is during diastole blood is supposed to flow from the atria


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[Assistant] Into the ventricles. That's what's supposed to happen, right? Ventricles are supposed to be in a relaxation state. They're supposed to be opening up and allowing for blood to rush into them. So this is called ventricular diastole.


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[Assistant] And to understand diastole, we have to go through the heart sounds again. This is S1. This is S2. I'm sorry, S1, S1. Alright, this is the closure of the mitral valve and the closure of the tricuspid valve, S1. This is S2, which has the A2 component, which is the closure of the aortic valve and the P2 component, which is the closure of the pulmonic valve.


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[Assistant] Ventricular diastole starts from S2 until you get to S1. That's ventricular diastole. So.


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[Assistant] What happens is during S2 to S1, I'm gonna hear some type of opening snap is the whole thing I'm talking about here. This extra heart sound. We already talked about the S3, the S4 heart sound that we can hear in this. But now there's another additional heart sound that you can potentially hear.


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[Assistant] And this is the opening snaps. So opening snaps are usually due to two situations here. One more commonly is a patient who has something called mitral stenosis. Okay, we'll talk about that here. The other one is a patient who has something called tricuspid stenosis.


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[Assistant] So what happens is they have these fibrotic valves. Super, super fibrotic calcified valves. Both of them. They got fibrotic valves. Right?


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[Assistant] And these fibrotic valves don't really want to open very well. But blood is supposed to move through these valves and into the


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[Assistant] Ventricles, right? The left ventricle and right ventricle respectively.


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[Assistant] What happens is, when you want to push blood from the atria, so let's say here's the atria, down into the ventricles, you want to push blood from the atria down into the ventricles,


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[Assistant] What you have to do is generate a high amount of pressure. And when you increase the pressure inside of the atria to push blood down into the ventricles, it's enough that it causes these valves to just quickly create a little snapping sound because they're under such high pressure to push them open that it quickly snaps.


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[Assistant] So imagine it like this, right? So imagine I have this valve here. Imagine I have this valve and I'm trying to push, push, push, push it.


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[Assistant] The moment it clicks open just a little bit, even if it clicks open a little bit, that's going to produce an opening snap sound. So that moment that these click open, it creates something called an opening snap.


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[Assistant] Okay, that opening snap can be heard and we have to know where exactly would we particularly hear this. Well it's going to happen right in the beginning of diastole.


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[Assistant] So let's actually draw this in here, let's do it in black here. We're gonna say that right here I'm gonna have a opening, I'm gonna represent with OS, opening snap. That is that sound due to the mitral valve or the tricuspid valve popping open from the high pressure in the atria trying to push down into the ventricles. Here's the big thing that you can see and associated with this.


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[Assistant] When the blood flows down through that, imagine it like this. I'm generating as much pressure as I can, I pop them open. Once that thing has opened up enough, a ton of blood is going to flow through that. And it's going to be


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[Assistant] As you'll see like this opening snap and then a high pressure of blood flowing through, but it's going to be decreasing over time.


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[Assistant] This is actually called a decrescendo diastolic type of murmur that you can see associated with. It's like a rumbling sound. We'll talk about that in more murmurs. But that's one of the big things to think about here is again, mitral stenosis and tricuspid stenosis. You hit this opening snap right after S2.


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[Assistant] And when you'd be like, oh, how do I differentiate this from S3 and S4? Well, you would hear the snap.


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[Assistant] And then you'd also have an associated diastolic rumble after that. That's one of the big things to think about.


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[Assistant] So what is this called? The pericardial knock. Son of a gun. So the pericardial knock is a really interesting one. You see this particularly in a condition.


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[Assistant] Uh, called constrictive pericarditis. So what does this do to? It's do a condition called constrictive pericarditis.


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[Assistant] Excessive amounts of fibrosis, uhm, of the pericardial cavity. When there's lots of fibrosis of the pericardial cavity, think about this. This is during ventricular diastole, right? So your ventricles are supposed to be filling with blood. So if they're supposed to be filling with blood, they should be relaxing.


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[Assistant] Trying to relax, right? But they got this rigid pair of carbons that's blocking them from relaxing. And blood's supposed to move into the ventricles from the atria.


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[Assistant] And a patient who has constrictive pericarditis, when the ventricles want to relax, imagine them trying to relax and then just being stopped by a ridge of pericardium. So they're only going to get a lot of blood flow coming into them during the early phases of diastole. And so it's going to fill the ventricles up really, really quickly, and then boom, they're going to stop.


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[Assistant] So there's going to be a sudden rapid flow of blood into the ventricles because they're going to have at least some space, but it'll rapidly flow into them. The ventricles going to try to expand to allow for more blood to come in, but then they're going to be hit by like a rock solid paracardium. They can't expand anymore because they can't expand anymore. There's a sudden cessation of blood flow and that produces this paracardial knock. And again, since it's occurring during what phase? The early diastolic filling time. Where would I see it? Right here in the early point, right around the same time as the opening snap.


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[Assistant] That would occur right here in the early phases of diastole.


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[Assistant] But would there be an associated murmur after that? No. And usually if you compare this to something like an S.


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[Assistant] Three hearts and you'd be like, oh, how do I tell the difference? It might actually be very difficult. Technically, the pericardial knock is a little bit higher pitched.


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[Assistant] In comparison to an S3 heart sound, which was a lower pitch. So you may not be able to hear, uh, this when you put the bell of the di- uh, bell of the stethoscope on in comparison to S3. So that's some of the things to think about. Okay, we got the pericardial knock, and we got the mitral stenosis and tricusposinosis producing the classic opening snap. So you can hear ejection clicks during systole in addition


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[Assistant] Right? You can hear opening snaps and diastole, or a pericardial knock. The last one that I want you guys to remember is something called a pericardial friction rub.


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[Assistant] So pericardial friction rub. So this one's really interesting, so you can see this in patients who have what's called pericarditis.


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[Assistant] And in pericarditis, there's an inflammation of their visceral pericardium and their parietal pericardium. And whenever the ventricles are going through their periods of contracting and then relaxing, contracting and relaxing, contracting and relaxing, we're just going to keep doing this, contracting and relaxing, it causes the visceral layer and the parietal layer to rub up against one another.


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[Assistant] And whenever that rubs up against one another, it produces like a velcro kind of like ripping apart or scratching type of sound that you can hear in all phases of systole and diastole.


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[Assistant] So if I were to actually listen to this, and again, this is not just in the actual ventricles. You would actually, cause again, this also surrounds the atria too. So you would hear this during the atrial systole. You would hear this during ventricular systole and ventricular diastole. It's actually called a triphasic. So sometimes we call this triphasic heart sound. Because okay, let's think here. This is S1.


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[Assistant] This is S1, which is the closure of the tricuspid and the mitral valve. This is S2 with the aortic component and the pulmonic component that are closing.


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[Assistant] If it's continuous, that means it has to happen throughout all of this tire process from ventricular systole and ventricular diastole. Right?


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[Assistant] So, throughout this time period of ventricular systole, I'm going to see this scratching type of sound here. Okay?


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[Assistant] Then, after that, I have S2, which starts the onset of diastole. So ventricular diastole, I'm going to have all of this scratching sound. Remember I told you there's one more thing, and that's when the A3 are in, systole.


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[Assistant] So during atrial systole you may also hear like this scratching type of sound on top of that. So this represents a triphasic scratching sound that you can hear during ventricular systole, ventricular diastole, and atrial systole.


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[Assistant] Ninja nerds, we done did it. We done covered a beast of a topic and that being heart sounds. I hope it made sense. I hope that you guys enjoyed it and as always, until next time.


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[Assistant] And I'm like, the only one at school who doesn't have a car.


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[Assistant] Dad, I love it. It's awesome. Can we get this one please?


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[Assistant] I don't know if we should buy that house. It's perfect for us, but it's so expensive.


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[Assistant] Today we're going to discuss conclusions, and conclusions for many people are the hardest part of a writing project. I know for me, I have a lot of trouble with conclusions. Even in these videos, at the end of some of the videos, I've been like


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[Assistant] Stuck with how to end the video, like in the beginning of the video I could say hello, I could talk about what we're gonna do in the video, but at the end I almost


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[Assistant] The reason conclusions are hard for people is uhm, very practical, I think. People, by the time they're writing conclusions, they might be up against a deadline and just don't have time to adequately devote to the conclusion. They might also feel a little bit tired of their writing project. They've already said everything you want to say in a writing project, and so what do you put in a conclusion?


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[Assistant] People also have questions about how to start a conclusion. They don't know kind of how to signal to readers that it's time to move into a conclusion, so they'll revert to a phrase like in conclusion or


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[Assistant] To conclude. And, and sometimes in some contexts that's okay.


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[Assistant] And a final aspect of conclusions that's hard for people is to decide how long a conclusion should be.


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[Assistant] Sometimes there are paragraphs, sometimes there are a couple paragraphs, uh, it kind of depends on the context in which you're writing. But the important thing to remember with conclusions is that they're really important. They're the last moment you have.


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[Assistant] The purpose of conclusions in general includes the following three aspects. To recap what has been said. Some busy readers, even if you hook them in the beginning as best as you can and even if you're


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[Assistant] So, well renowned and respected in the field that people generally hang on every word you say, uh, even still some busy readers will


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[Assistant] What's the purpose of you having written this argument? What do you really want readers to take away from it? Think about why it's important. What's significant?


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[Assistant] What do you want me to do with it? And so this is your chance in the conclusion to share that with people. And then finally a third element is to point towards future directions.


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[Assistant] Scholarly writing is an ongoing conversation. What you say, you hope.


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[Assistant] Other people are going to take away and do other stuff with. So what are some possible ideas, right, for either future areas of inquiry or new areas of application or things you didn't have a chance to cover or study or research for this? You can point your readers in some of those general directions.


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[Assistant] And with the final sentence of their paper. Final sentence is really important. It's the last words that people will read.


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[Assistant] Here's Coyle's sentence. More stars, Clifford says, are on the way. And I would say that this is an example of Coyle saying that uhm,


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[Assistant] It's kind of a hopeful, right? It's pointing to the future. So all kinds of more stars are up and coming. It's also the giving away.


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[Assistant] The, that final spot to, to Clifford. So that was a choice that Coyle made to kind of offer another writer that final, final moment in his essay.


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[Assistant] You can do this. This is important. This is why it's significant. And here's Tarnas and Toufiash.


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[Assistant] Despite the difficulty in pursuing research with experts, the studies undertaken in domains such as sports, medicine, and aviation during the past decade show the promise of the expert performance approach.


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[Assistant] And so here too, we have another example of future directions.


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[Assistant] I'm inspiring you, I'm inspiring something, something beyond what I have written.


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[Assistant] And also talking about the difficulty in pursuing research. So if I were a researcher, I would take that as kind of a challenge, right? So let me think about the difficulties. Let me name some of the difficulties. Let me work on this problem.


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[Assistant] Here's his signal that he's moving away from the body of his essay to the conclusion. For most people.


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[Assistant] I can imagine him kind of thinking that readers are going to take a breath. This is the beginning of a new paragraph.


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[Assistant] This is an alternative to him having written


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[Assistant] In conclusion, or to conclude, which would have been another choice he made, but I think this is a smoother version.


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[Assistant] For most people, work is hard enough without pushing even harder. Those extra steps are so difficult and painful, they almost never get done. That's the way it must be. If great performance were easy, it wouldn't be rare.


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[Assistant] Which leads to the possibly the deepest question about greatness.


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[Assistant] Which suggests, already, he's talked about stuff that's really important, but here, this is really it, right? And as a reader, this shows me, oh, I really need to listen, I'm so interested to hear what the deepest question is.


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[Assistant] They understand very little about where that behavior comes from. And here we have,


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[Assistant] Some experts. So again, we're still using experts in the conclusion.


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[Assistant] The critical reality is that we are not hostage to some naturally granted level of talent. And I would say at this point that Colvin is moving to do that kind of work of inspiring.


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[Assistant] His readers or a call to action of some kind, right? Like a rallying call. We can make ourselves what we will. Strangely,


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[Assistant] Maybe we can't expect most people to achieve greatness. It's just too demanding. But the striking liberating news is that greatness isn't reserved for a preordained few. It is available to you and to everyone. And here, that's like kind of the inspiring final ending.


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[Assistant] Uh, those workers who have been marked as essential. Can you comment on how this would impact, you know?


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[Assistant] I think so, uh, and we have another question, I believe, uh, if that can be queued up, uhm, which is?