DIP Episode 244 - The NBME and Cardiac Valvular Disorders (+ Upcoming 2CK Course 7/11/20)

Okay, welcome. My name is Divine. This is episode 244 of the Divine Intervention Podcast. And in this podcast, I'm going to be talking about the Vavula disorders. I know I may have kind of talked about this little by little in like other different podcasts, but I don't think to have one podcast where I talk about the Vavula disorders because these are things that people often get wrong on MBME exams when they really don't need to, right? So I'm just going to talk about the things that are high, like essentially the highest deal to know with regards to these things, right? So, and again, many times they will give you like a classic presentation that you can kind of hang on to on these exams. And before I start, again, a lot of people have, you know, so far at least I keep getting a lot of requests like, oh, Divine, when is your next step to CK 10 hour course? So basically the next course will be taking place on the 11th of July. I'm just going to take place via Zoom. If you want to sign up, just send me an either a shripping a message through the website or send me an email at Divine Intervention Podcasts with an S at the end at gmail.com. Again, in the course, we cover about 600 to 700 concepts that touch on peeds, surgery, I am, Obeguin, Psychon, Neuro. So it's an integrated format for the exam.

And I make it like just one day because in one day I want to try to essentially like train you to also be able to keep your brain going for 10 solid hours, although we'll do it like four hours with a 12 break, four hours with a 12 break and then tours to round up the day. And we're round up with Psych. So again, if that's something you're interested in, just reach out to me. Again, I've run the course now three times and lots of people, people that have taken the exam and stuff, I've all gotten like really good feedback from it. So if that's something you're interested in, it's going to take place on the 11th, right? So, you know, there's a limited number of spots. So just send me an email, I'll give you some more information, you sign up. Once your maker is a vision via Venmo or Pay Pal or something, I will register you for the course and then you'll essentially have your support guaranteed. And the course takes place via Zoom so you can take it from pretty much anywhere in the world. Okay. So let's jump right into the volume of the soldiers. So what if they give you a question about like a 79 year old male and they tell you that this guy, you know, has been having like, you know, having all these syncopal episodes, having like shortness or breath that whenever when he's like mowing his lawn or he is doing something like physically demanding, he has like a syncopal episode or his syncopal episode or his thoughts having power, if you see stuff like that, right?

You definitely want to think about the Eodics the Noces, right? Notice, I didn't even bother telling you a systolic, dastolic, whatever. No, right? Just think about the Eodics the Nocesa on that those are circumstances, right? Think about the Eodics the Noces on that those circumstances. So what my, how does the Eodics the Noces classically present the thing is in an NV Me question, right? Many times they will present these things and throw in the audio. And the moment people say the audio, they begin to freak out. They are like, Oh, no, divine. How do I hear this? How do I listen to that? I don't know what I'm listening to. Blah, blah, blah, blah, blah, blah, blah, blah, blah. To be honest with you, at least in my experience, I feel like 80 to 90% of these audio questions, you can answer them correctly, very accurately, without even paying attention to the audio at all, right? Because if they give you an old guy with syncopal episodes, I will be shocked if there is any other thing it's going to be, other than Eodics the Noces. So as I'm introducing these different available pathologies, I will try to essentially talk about, Oh, this is how exactly how it's going to present on your test, right? So Eodics the Noces on your exam is going to be a person above 65, almost certainly above 70, right? That with one exception and I'll talk about that exception in a bit, right? That has all these again, like, engine all symptoms or syncopal symptoms or heart failure symptoms.

And you'll have that in the setting of like a point of maximal impulse, right? That is, laterally, displays, you know, that's kind of going towards the axilla, right? Because Eodics the Noces, right? It's a kind of pressure overload. So because it's a kind of pressure overload, you'll undergo concentric hypertrophy of the left ventricle, right? So again, old guy, the classic disease script, these things are disease scripts. The classic disease script for Eodics the Noces is old guy syncopal episodes, old guy syncopal episodes. If you keep that at the back of your mind, you're locked and loaded for this on an exam. Now, so Eodics the Noces, right? So let's say a few more things about it, right? So it's going to be heard best at the right in a personal border, right? And again, it may say, okay, divine. How do I, how do I try to know these things without memorizing it? If you remember from step one embryology, right? We know that the Eodir drains the left side of the heart, right? The Eodir drains the left ventricle, the Eodir drains the left ventricle. So essentially, if you really think about it, because the Eodir drains the left ventricle, remember that if you think back to the anatomical model of the heart, the left ventricle is on the left side of the body, right? But the Eodir goes all the way to the right before it then forms the Eodic arch, right? So the direction of flow is from the left ventricle up and right.

So it would make sense that since the flow direction is up and right, then an Eodics the Noces should be heard best at the right upper, sternoborder, should be heard best at the right upper sternoborder, right? And again, right? Classically, it's a systolic memory, right? It's a systolic memory and it relates to the carotid, right? And one buzz word you may hear on the test is Paul's Purpose Purpose E Tardis, right? So Paul's Purpose E Tardis, Tardis comes from the word Tardis, right? If you're a Tardis student, it means you are a lead for class, right? So that means the prison's carotid pose, you'd be like, huh? I can feel this person's heart pumping, but it's like, man, it's taking a long time for me to feel this carotid pose. That's what's called Paul's Purpose E Tardis, right? So those are classic things in the system Noces. Now, the buzz word pathophysiology behind the erotic stenosis, please do not forget this is that you have a calcification of the valve. The valve is calcified in a person that has erotic stenosis. That's one key thing to know. Another key thing to know here is that erotic stenosis, right? Again, it's a systolic memory, right? A personal border, but you can see it in a person that is younger on an in-beam example. So someone like their late 40s, in their 50s, like super early 60s, if you see people like that having erotic stenosis, you want to think about a bike-cost-periodic valve.

So you may say divine, why are these people getting their symptoms much earlier? Normally, the erotic valve has what? Three cossps, but a person that has bike-cost-periodic valve has two cossps. I just kind of think of it as less of your resident on busy service and you have three residents covering 100 patients, right? Versus two residents covering 100 patients. The two residents covering 100 patients who are under go-mawware and tear, right? So that person's erotic valve is under go-mawware and tear, under go-maw classification. So the person tends to have symptoms earlier. And please do not forget that bike-cost-periodic valve, right? That classically associated with erotic, I mean with a toner syndrome on an in-beam example, a toner syndrome on an in-beam example, right? So again, that's something you want to keep at the back of your mind, going into, going into tests. Remember, toner syndrome also causes a quotation of the erotic, right? And one of the thing with erotic stenosis, right, is, oh, what will increase the intensity of the murmur? The big thing you want to know here is that anything that puts more blood in the left ventricle, right? Or let me put it this way. When anything that makes you have more flow across the erotic valve will make the murmur intensity louder, right? So say, for example, if you give the person an infusion of normal sailing, right?

The apprylode is going to increase, the amount of blood in the left ventricle is going to increase, more blood will flow through that stenotic valve, right? So those people, right? Those people who have, we have a louder murmur, right? They'll have a louder murmur, right? Alternatively, right? If, for example, you crush your decrease after load, let's say you give the person an arterial diliter, right? An arterial diliteral decrease after load, so it'll be easier for blood to come out of the left ventricle. That will also make the murmur of erotic stenosis sound louder, right? That'll make the murmur of erotic stenosis sound louder. Okay. Now, how do you treat erotic stenosis, right? Basically, for those people, you need to go ahead and replace the valve. But if you need some kind of temporizing measure, you know, you can consider doing an intra-erotic balloon pump, but that's not something you would really go after on an immune exam. For the most part, if a person has an erotic valve problem, you need to go ahead and replace the valve, right? Go ahead and replace the valve. And remember, if you start having heart failure symptoms, you'll probably be dead within a year or two. So you're kind of like on the clock in that situation. You need to go ahead and replace those people's valves. Basically, from least bad to most bad, in terms of like, oh, I got to replace this valve is, angina is number one, syncopy is number two, heart failure is number three. Remember the word ash.

So angina syncopy and heart failure. If you study having heart failure symptoms, you need to replace that valve. If no, those people have a very high risk of sudden death. So that's something you want to keep at the back of your mind as you're studying for these exams, right? And then the next valve will have a problem, I think I'll go to is erotic regurgers, right? So erotic regurgers again, how will it present on an embankment exam? Essentially, the way this thing will present is these people, they will tell you that they have a murmur that so I'll tell you that 90 to 95% of the time on embankment exams, it's either going to be heard best at the left sternal border or it's going to be heard best at the left lower sternal border. And again, you'd be like divine, how does this make sense? Okay, remember what I just said for it, external system said that we have the left ventrilo on the left side of the body, right? The other takes off to the right and up and then forms the arch that goes downwards. So think about it, again, the direction of flow from the left ventrilo to the other is up and to the right. So if you are regurging, that means blood is going in the reverse direction. So that's down and to the left, right? So it should make sense that the murmur of erotic regurgers is heard best at the left sternal border again or left lower sternal border.

About 5% of the time on embankment exams, especially in a person that has really body erotic regurg, the murmur of be heard best at the right sternal border. So that's something you want to keep at the back of your mind on exams. I saw like a Reddit meme recently about the people's, like the back of people's minds getting like pretty huge, sorry about that, but don't worry, in a few years you'll be done with this whole USMELY process. Okay, so and I think, I guess let me think the people on the right as well for their support. You guys have been an amazing group of people and I hope to keep making podcasts like these are in the future, but back to this, right? So erotic regurgers, right? So again, if they tell you, if they say, oh, oscoticatory findings at the left sternal border are like so. You see it is like an adult. It probably doesn't even make sense for you to waste your time listening to the audio. It's almost likely going to be a erotic regurger. Another high probability thing you'll see in a question that tells you, oh yeah, this is erotic regurger. Is if they give you a presence of blood pressure is like 120 over 40. A blood pressure of 120 over 40 is not normal. I'll tell you that right now. It is not normal, right? Because essentially that person has a wide pulse pressure, right? Because a normal blood pressure of 120 over 80, right? The spread between the systolic and the stodid blood pressure there is 40, right? So normal pulse pressure is right around 40.

But if you notice that, huh? A person's pulse pressure is like 80, like an insane number. Oh, this person's blood pressure is 150 over 50. If you see that, again, don't waste your time reading the rest of like listening to the audio or whatever, it's going to be a erotic regurger. If it's a pediatric question, it could be a erotic regurger or a patent doctor's arteriosus. So again, erotic regurger is a systolic murmur, right? That is heard best at the left sternal border or the left sternal border about 95% of the time. 5% of the time in a severe case, it'll be heard best at the right sternal border, okay? And one of the things I think I want to see to you here is remember that erotic regurgers, right? These people tend to have some interesting physical exam findings, right? So they can have like the headbubbing, they can have the water hammer pulse, they may have like a hyper dynamic pulse. They'll have all those things. Those things all arise from the white pulse pressure phenomena. So you may ask yourself, okay, divine, can you explain this whole business with a white pulse pressure? Well, the thing is remember a pulse pressure is the spread between your systolic and your dastolic blood pressure. I'll say that again, pulse pressure is the spread between your systolic and your dastolic blood pressure, right? So what do I mean by that? In erotic regurg, the systolic blood pressure actually goes up. Why? I'm not explaining this in multiple podcasts, right?

So I'm gonna like not spend too much time on this, but basically your systolic blood pressure is equivalent to your cardiac output. Whatever happens to your cardiac output will happen to your systolic blood pressure. Your dastolic blood pressure is related to your systemic vascular resistance. Whatever happens to your systemic vascular resistance will happen to your dastolic blood pressure. So think about it. In a person that has erotic regurg, normally the in the normal individual, the left ventricle gets its preload from the left each. When a person gets has erotic regurg, they are getting their preload not just from the left each. But also the left ventricle is also getting preload from the other. So the preload overall is increased, and if you remember the Frank Stalin principle, as the preload increases, the cardiac output increases. So the cardiac output increases, the systolic blood pressure will increase. Now let's look at the dastolic blood pressure side of things. In the normal individual, blood in the other gets shuffled into one room. That one room is the rest of the body. I almost think of it as like, oh you have a hundred people and you put them in one room. But in a person that has erotic regurg, blood in the other can spread out to not just the right of the body, to the rest of the body. But it can also spread out to back to the left ventricle. So it's like you have two rooms available to deal with a hundred people. So you can put 15 each room.

So there is less systemic vascular resistance. It's like a functional decrease in systemic vascular resistance with your decrygurg. So if the SVR goes down, the dastolic blood pressure should go down. So you're seeing that the SBP is going up, the DBP is going down, so the pulse pressure should be wider in a person that has erotic regurg. In a patient, doctors' arteriosus, which again classically presents us like a continuous machine-like murmur. I'll just throw that in as a bonus. Remember in those people, why do they have a white pulse pressure against the same physiology? If you have a doctor's arteriosus, again, if you notice, let's talk about the SVP side of things first. So again, normally, the left side of the heart just gets feedstock from the pulmonary veins, right? You know, things that come from all right ventricle, pulmonary artery, pulmonary capillary veins, left feet from left ventricle, that's it. But now, in addition to that highway, a person that has a PDA, there is another extra source of blood from the other to the pulmonary arteries. So it's like the pulmonary arteries are essentially getting, be a preload from two sources. It's getting from the right ventricle and it's also getting from the other through the opined doctor's arteriosus, right? So again, overall, that's sending more blood to the left ventricle, more preload to the LV. So that means the left ventricle is seeing more blood, so the cardiac output goes up.

So this is solid blood pressure goes up, right? Now, from the that's only blood pressure side of things again, in the normal person, the blood in the other relaxes to the rest of the body. That's it. But now, it's not just relaxing to the rest of the body in a PDA, it's also relaxing through that doctor's arteriosus into the pulmonary artery, right? So again, it's like putting a hundred people in two rooms. So systemic vascular resistance is going down, so that solid blood pressure is going down, so the pulse pressure is getting wider. Again, your pulse pressure is getting wider. That's very high up to no for exams. So, the other preload again, white pulse pressure, hyperdynamic circulation of explained the pathophys behind the pretty much all those things, right? So again, those are just all things you want to keep at the back of your mind for exams. And the thing is, in the other preload, typically for those people, you want to treat them with something that reduces after load. Because if you reduce after load, then you will lessen the regurgitation, right? You will lessen the regurgitation because if there's less after load, the blood has more of a motivation to move forward to the rest of the body that move backward into the left ventricle. Okay, so those are the aortic pathologies, right? So, let's go to the mitral pathologies.

And again, I'm not necessarily going to talk about like every valve-village pathology, I'm just going to talk about the ones that classically shop on exams, right? So, let's assume they give you a question about a patient that, you know, had like an upper respiratory infection that resulted out on antibiotics like three years ago. But now, over the last two weeks, this person has been having palpitations and they show you an EKG and you see A-Fib, right? If you see this, I'll really hope you're thinking about mitral stenosis, right? Mitral stenosis. And again, remember, when do you feel the effects of mitral stenosis? You feel those effects when you are trying to feel the left ventricle with blood. So because the left ventricle is going through feeling in that process, it's going to be a dastolic murmur, right? It's going to be a dastolic murmur with an opening snap. I'll say that again, it's a dastolic murmur with an opening snap, dastolic murmur with an opening snap. It's going to be heard best at the apex. That's the good thing with mitral murmurs. Mitral murmurs are all heard best at the apex. Simple as that. They are all heard best at the apex, right? They are all heard best at the apex. So, mitral murmurs all heard best at the apex, right? So it will be a dastolic murmur opening snap heard best at the apex, right? So what is the biggest risk factor for mitral stenosis? Well, that's easy. That's dramatic fever.

That's why I give you this vignette about a person having an upper respiratory infection that resolved without antibiotic therapy years ago, right? So mitral stenosis, the biggest risk factor for mitral stenosis is dramatic fever. But you also see that this person has a fib. Why do they have a fib? They have a fib because they have mitral stenosis. Remember, the biggest risk factor for a fib is mitral stenosis, right? So if a person has a dramatic fever and he goes on treated and he develops mitral stenosis over time, because the left is contracting against increased amounts of resistance. So those people have dilution of the left ischre, which can again increase the person's risk of having an e-fib. And I would hope you're telling me that, oh, for this person that has a fib from mitral stenosis, if you're doing that chats-vask business that everyone says you should own exams, the only option available for anti-qualgulation for those people is warframe. Remember, warframe is what you use for a person that has valveula e-fib. If they have e-fib from a valveula problem, your only option is warframe. You cannot use a no-walk, like dabigatran or a pixaban or any of those things with these people. Now, so mitral stenosis again, that's the Lyck murmur opening snap credit best at the apex. And again, if you were to ask you about an arrhythmia, like, oh, what is the most common arrhythmia in people that have a histral mitral stenosis, it's going to be e-fib.

That's just a very nice roundabout means of testing that the biggest risk factor for e-fib is mitral stenosis. Okay, now, let's talk about the other mitral pathology. So what if they give you a question about a patient, you know, this person is like six-foot-five inches tall, right? And they tell you that, oh, this person has had like more, this person, you know, has like very poor wound healing and all that badness and they have hyperextensible joints and all that badness, right? You want to think about, uh, Elasdanlo syndrome, right? Elasdanlo syndrome. If they tell you that, oh, these people have this person has like a holosistolic murmur, right? Her best at the apex, right? What they may say that, oh, it's a murmur with a mitral stenosis, like, again, her best at the apex. If you see that, you want to think about mitral valve prolapse. The thing is, to be honest with you, mitral valve prolapse and mitral regurg, I essentially the same kind of murmur, but you have to be careful here. You have to be careful here. Essentially, the most, let me put it this way, mitral regurg is like the super boss. Mitral valve prolapse is a subset of mitral regurg. It's like a special case of mitral regurg, because the primary problem is that blood is going back from the left ventricle to the left teacher. However, your friends at the MDME realize that many people have this confusion, right? So they try to mess up your head with these things, right?

So we're going to compare these things side by side. They are both systolic murmurs, but usually pure mitral regurg is holosistolic. Mitral valve prolapse is mit systolic with a click, right? But there are some other things that they go after, right? Again, to try to mess up your head on these exams, but again, your head will not be messed up because thankfully, you're paying attention with the spot cast. So let's talk about mitral regurg first, right? So mitral regurg is just means blood is going back from left ventricle or left teacher. That's easy, right? So again, it will be a holosistolic murmur, her best at the apex, right? The apex is the fifth intercostal space in the mechlavicular line on the left side of your body, right? So basically, people that have mitral regurg, right? So essentially, what would make the murmur sound louder? Well, if you think about it, if you put more blood in the left ventricle, then there will be more blood available to regurgitate, right? I make the murmur louder, right? So see, for example, you do something that involves increasing preload again, given a person like normal saline, right? Or going from a standing to a supine position, that will increase your preload, that will put more blood in the left ventricle. So there will be more blood available at baseline to regurgitate. So the murmur intensity will get louder, right?

Or if you think about it, if you do the hand grip maneuver, when you do the hand grip maneuver, you're squishing on a person's arteries in their arms, in their hands. If you squish on those arteries, they increase in systemic vascular resistance, they are increasing after load. It will be harder for blood to get out of the left ventricle. So if the blood is like, oh, I cannot get out through the numeral, through the yoder well, oh, there's this other word available from me, through the mitral valve, it goes ahead, takes that mitral valve, so you have more regurgitation. So anything that increases preload, or anything that increases after load will make the murmur of mitral regurgitation sound louder, or make the intensity louder. Now, mitral valve prolapse, right? Mitral valve prolapse. What's the big thing with mitral valve prolapse? The thing is, mitral valve prolapse is a kind of regurg, but the thing that causes the regurgitation is because the valve leaflets do not overlap very well. So this is actually a critical part you want in partation to. The valve leaflets do not overlap well at all. But is there a way we can, on our own, make those valve leaflets overlap better? We can. And that method actually is if we put more blood in the left ventricle. I'll say that again, if you put more blood in the left ventricle for any reason, you will make the valve leaflets in mitral valve prolapse overlap better, and you will essentially erase the prolapse.

And if you erase the prolapse, you will erase the regurg. So guess what? Anything that puts more blood in the left ventricle makes the murmur of mitral valve prolapse sound less intense. That's very important to know. It makes the murmur sound less intense. It makes the murmur sound less intense, right? That's very important to know, right? So see, for example, you do something that increases preload. Now put more blood in the left ventricle. That will make the leaflets overlap better. If that happens, guess what? The murmur will sound less intense. It will not sound as loud. Same thing, if you increased after load, you did the hand grip or the person squatted or whatever. Again, that would increase the amount of blood in the left ventricle. You will have better overlap of those valve leaflets and the murmur will sound better. So I hope that's something that you keep at the back of your mind for these exams. So again, remember, anything that puts more blood in the left ventricle makes the murmur of mitral regurg more intense, but anything that puts more blood in the left ventricle makes the murmur of mitral valve prolapse less intense. Again, just very nice, very handy, nice, easy roads to keep at the back of your mind. Now remember, the Boswatt Pathofisiology behind mitral valve prolapse, right? Is that you have a mixometrist degeneration of the valve. I'll say that again, you have a mixometrist degeneration of the valve. Okay, now let's see.

So I guess let me just talk about a few more special topics and then I think I'll be done, right? So these ones are just like one of pieces of information that you want to keep in mind for tests, right? So it will tell you that you hear a holocestolic murmur at the left-low external border, right? That's going to be a VSD on your test. So I remember VS Ds at the most common kind of congenital heart defect and again, it will start off asianodic, right? Because the left ventricle has more chiropractic than the right ventricle, right? So you have more flow from the left to the right ventricle, right? What over time with that increased load on the right ventricle, the pulmonary circulation, the present can develop pulmonary hypertension and then what was previously and left to right asianodic shunt becomes the left sanodic shunt, right? That's isemengar's syndrome. And then remember that an ASD, right, will present the buzzword on the test, will be like a white fixed split of the S2 heart sound, although if the MbMe wants to mess with you, hey, because they know every human being that has the job description, my student has memorized, oh, white fixed split, S2 heart sound, ASD, right? So these days, one thing they can do is they can tell you that, oh, you notice a split of the S2 heart sound on inspiration and expiration.

If you see that, that's basically them telling you that it's a white fixed split of the S2 heart sound, because normally the S2 heart sound is only supposed to split on inspiration. Why is that? When you inspire, you lower your intrathoracic pressures, that causes more venous return. So there is more blood on inspiration flowing through the pulmonary valve. So it takes the pulmonary valve a little while longer to close compared to the uric valve, but you're only supposed to observe that on inspiration. On expiration, you're not supposed to see that. That splits, that physiologic split is supposed to disappear on expiration. So if you notice that a person has an S2 heart sound, that is split on inspiration, that is split on expiration, that's not normal, that's an ASD, right? That's an ASD on an MbMe exam, that's an HRO Septo defect, and remember, ASD is the most common kind is the second um defect, but in people that have Down syndrome, a primal defect is a lot more common. That's high ill to know for tests, right? And another thing I think I want to mention here is, if they tell you on an MbMe exam that a person has a loud S2 heart sound or a loud P2, right? A loud P2, if you see that, that's cold word on an MbMe exam, for a person potentially having pulmonary hypertension, right? You want to think about that, as a person that potentially has pulmonary hypertension on an MbMe exam. So just again, good, nice, high ill things to keep at the back of your mind for tests.

And then, if for example, they tell you that A2 is coming after P2, so you're like, hmm, that's weird, the pulmonary valve is closing before the audit valve, that's bizarre. Whenever you see that, again, instead of memorizing a long list of like, oh, this causes this, this causes this, this causes this, this causes that, again, no. The smart thing I tell people is, learn the least amount of information that will allow you to control the biggest amount of knowledge, right? So the principle is better, that's why it's better to learn principles than to just learn facts, right? So what's the principle here? Whenever you have anything that slows down the depolarization of the left ventricle or slows down the closure of the audit valve, that can make A2 come after P2. So the pulmonary valve, you're like, yeah, it's closing before the audit valve. For example, if a person has a left bundle branch block, right? Or if a person has really bad erotic stenosis, right? All those things can all cause the erotic valve to have to close after the pulmonary valve closes, right? So again, all high-ealthings to keep in mind. And then I think one of maybe the last memories I would discuss is the murmur of hypertrophica cardiomyopathy, right? Hypertrophic cardiomyopathy, right? Again, genetic disease, autosomodominant inheritance. Oh, I'm sorry, I forgot to say that my trovaft prolapse radius associated with, um, real as down low syndrome and morphine syndrome. On NV Me exams.

And also people that have a history of psychiatric disorders. So, classically, MVP will show up in younger people on NV Me's. It's not really going to show up in an older person on NV Me exam. So, um, what is the big thing to know about HCM again? Autosomodominant disorder is going to be an athlete. Usually it's a guy athlete. It can happen in women, but it's almost exclusively men on NV Me exams, right? So it'll be a guy, like, think of a lepisod while he's playing sports or something like that, right? And the material that are all like an uncle died in like a car accident at 35, like some weird bizarre story. Basically, the uncle had a dangerous rhythm and died, right? So, while they were driving essentially, right? So, you know, autosomodominant disorder, it's a problem with like sacchonia proteins, right? What do you mean, say like, mayocin binding protein C, or dimisibiramayocin heavy chain, right? Those are all the mutations that can cause a, um, HCM, right? And basically, the member of HCM is actually heard best at the left lower sternoborder, okay? It is heard best at the left lower sternoborder and it does not read it to the carotids. That's very important, right? It does not read it to the carotids. It's a systolic ejection murmur, but it does not read it to the carotids. I'll see that again. It does not read it to the carotids.

And just like we have pauses, parvase, itardus, ureodixtenosis, with, um, with, with, with, with, HCM, we have this thing called pauses bysphirians, right? You basically have a bifidiotic pulse, right? This is something I kind of need a diagram to explain, but I don't really have the time I need to run to something, but you have pauses bysphirians, you hear like a bifid, uh, bifid pulse, right? That's classically as you know, HCM. And again, HCM, right? Again, many people are like, oh, define what will make the murmur sound louder and what will make you sound softer? Uh, what is this long list I need to memorize? No, don't memorize the long list. Again, there is this thing that you've probably heard of known as sound, right? What does sound stand for? Right? It stands for systolic anterior motion of like systolic motion of the anterior mitral valve leaflet. Basically, that anterior mitral valve leaflet, because the interventricular septum is huge in a person with HCM, that anterior mitral valve leaflet causes its own left ventricular outflow tract obstruction. So it's almost like blood that is living the left ventricle needs to pass two hurdles. One, it needs to go through that anterior mitral valve leaflet, and then two, it needs to go through the actual euric valve. That is like the cleft's nodes version as to why you get a bifid euric pulse or a bifid pulse in a person that has, that has a hypertrophic cardiomyopathy, right?

So you may be like, okay, divine, is there something we could do? Because really, if you got that anterior mitral valve leaflet out of the way, then the murmur would not sound as intense. Because essentially, if you get it out of the way, then blood is much easier to flow out of the, out of the left ventricle. And so how can we do that? We can do that by increasing the amount of blood in the left ventricle. So again, instead of been raising a long list of stuff, you just need to look at the scenario they give you and ask yourself does he put more blood in the left ventricle if he does? Then the murmur of HCM is going to be less intense, right? So again, anything that increases preload, no more saline infusion, going from standing to a supine position, blah, blah, blah, blah, all those things, right? We'll cause the murmur to be less intense, because they'll put, in Chris preload, they'll put more blood in the left ventricle. But again, if you increase afterload for some reason, right? Again, they'll put more blood in the left ventricle, right? So they'll be less blood like having to flow through that nasty, nasty thing, right? So again, ultimately, they'll reduce the intensity of the murmur, right? So again, just all key things to keep at the back of your mind here. And we treat HCM on examinees with beta blockers, right? Because if you give those people beta blockers, your heart will slow down. Well, if your heart slows down, then you have more time for that stoic filling.

If you have more time for that stoic filling, Sam will go away, right? That's, and Jeremiah Trova will leave there will stop causing problems, right? And everything will get better, right? And again, usually for HCM, they test it more in the context of preload, increasing maneuvers. The afternoon, increasing thin is actually a lot more complicated than I'm letting on, right? So I'll see the big one you want to take away is if you increase preload, put more blood in the left ventricle, now make the murmur of HCM sound less intense. Now make the murmur of HCM sound a lot less intense. So I guess, you know, if a person has the early dissection, right? Don't forget, right? The Bosworth Pathophys there is a cystic medionic process, cystic medionic degeneration of the other. And again, remember, it's found that people that have like syphilis, right? Like tertiary syphilis, so people that have like marphins and drum stuff like that, right? Also people that have the early downloads, right? They can also get a early dissection. So let's see, is there any other big thing I want to talk about? Any other thing that comes to mind? Okay, I guess if a person has carstenoid syndrome, I mean, you probably remember like a tip snowmanic, but carstenoid syndrome like tips like tricospidian, syphilisian, syphilmonextinosis, those are the common valvella problems in people that have a carstenoid syndrome.

And then remember, if a person is an IV drug user, if they have endocraditis, it's going to go after the it's going to go after the the tri-costal valve first, right? Because again, if you have an IV drug or a littering, injecting drugs into veins, where do all the veins in the body drain into the drain into the right side of the heart, right? So it makes sense that that's the that's the valve they'll kind of hit up first. And then don't forget that murmurs, right? We investigate them with echocardiograms, right? So what are the murmurs we investigate? If it's a systolic murmur and it's three or greater, right? So a three over six systolic murmur is investigated, right? But one over six, two over six, you don't really care, right? So three over six we investigate. Any systolic murmur, one, two, six over six doesn't matter, we investigate. If a murmur is symptomatic, we investigate, right? And if it's holosis, stolic, typically we also try to investigate on an NV Me exam. And then in the pediatric realm, if they're giving you an NV Me question, and you're describing a murmur with a lot of like musical qualities, that's going to be something that's benign, right? Like don't don't freak out, just re-assure the parent and send the patient home, right? So if they say like, oh, this thing has like a musical quality or something of vibrating whatever, that's going to be a benign murmur in a pediatric, in the pediatric population on an NV Me exam.

So I think I'm going to go ahead and stop here. I, I guess my life lesson for today is how to keep calm in the midst of a storm, right? How to keep calm in the midst of a storm, right? So what do I need by that? The thing is, many times in life, right? You potentially experience situations that are very not great, right? And sometimes in life, it may be like, just you are just being smashed from every angle. I mean, I have certainly had those experiences a few times myself, right? It's like, man, it's like, it's like I'm being dragged in every single direction, right? The thing is, if you're going through that hurt in your life, the first thing I encourage you to do is to calm down, take a step back, right? And just ask yourself, what is the biggest thing I need to solve, right? Because there are some things that are out of your control, but there are some things that are well within your control. So the thing is, don't let yourself get paralyzed by that. There is usually something you can do in that tough situation. If they, if it's something that's out of your control, don't waste your time on it. And really, to be honest with you, don't waste your time worrying about those things because guess what? Those things you're worrying about, you're increasing your cortisol levels, you're making yourself more unhealthy, you're just suffering, right?

So the thing I encourage people to do is when you're in a stormy situation, first, take a step back, just sit down and try to think rationally ask yourself, what are the things I have control over in this situation, right? What are the things I have control over in this situation? And try to then begin to one by one, make a list. There is nothing like having because one of the things that puts people in trouble when they're in a chaotic situation is they feel like their life has no structure. Well, there is a way around that, right? Now what is the way around that? The way around that is essentially to try to structure your life in some way, shape or form. That's why it's important. In a time of chaos, the best thing you can do for yourself is to have a plan. If you have a plan, then you know exactly what you need to do in that situation, right? You know exactly what you need to do in that situation. So I will encourage you, make a plan, what are things I have control over? Work on those things, right? Work on those things begin to knock out that plan one by one, one by one, one by one. And as you knock those things out, you begin to see that even if you are not feeling it then, right? Because again, you cannot necessarily feel your way into action or you need to act your way into feeling. You just keep working on things you can control. You begin to notice that over time, that stormy situation, you begin to assume dominion over that situation, right?

And the final thing I'll say is, I mean, I mean as many of you that listen to this podcast can probably tell, I'm a Christian, whenever I'm in these tough situations, I just pray and I just try to go to help me. At least for me, I found prayer to be very effective because it's almost like sharing those deep things that are going through my mind with another person that cares about me. So please, you know, these podcasts exist on Apple podcasts, they exist on Spotify and on Google Play and also have a You Tube channel and also have a Word Press website, it's devineinterventionpodcasts.com, right? So please, if you could subscribe to these media, leave good feedback, leave good comments, spread the word at your Met schools or whatever. I would really appreciate it. The more traction, we get the better. And if you have any questions, again, you can email me through the website or you can send me an email at devineinterventionpodcasts with an SID end at gmail.com. So thank you so much for listening. God bless you. I'll see you next time. Thank you.

Elderly patient, exertional syncope/dyspnea, and a harsh systolic murmur at the right upper sternal border.

MR murmur increases with increased preload or increased afterload; MVP murmur decreases with increased preload or increased afterload.

A fixed, wide split S2 heart sound that persists throughout inspiration and expiration.

Atrial Fibrillation (A Fib).

Dramatic fever/endocarditis (e.g., following an upper respiratory infection) and chronic rheumatic heart disease.

Endocarditis; the Tricuspid Valve (right side of the heart).

Diastolic murmur with an opening snap, heard best at the apex.

Because it is a valvular source of A Fib, and oral anticoagulants like dabigatran or apixaban are contraindicated due to high bleeding risk associated with valve pathology.

Increasing preload (e.g., giving normal saline) or increasing afterload (e.g., hand grip/squatting).

MR intensity increases; MVP intensity decreases.

ASD (Atrial Septal Defect); Primum defect.

Potential pulmonary hypertension.

Tricuspid Valve Stenosis/Regurgitation (or general valvular involvement).

Diastolic murmur with an opening snap, heard best at the apex.

Because it is a valvular source of A Fib, and oral anticoagulants like dabigatran or apixaban are contraindicated due to high bleeding risk associated with valve pathology.

Increasing preload (e.g., giving normal saline) or increasing afterload (e.g., hand grip/squatting).

MR intensity increases; MVP intensity decreases.

ASD (Atrial Septal Defect); Primum defect.

Potential pulmonary hypertension.

Tricuspid Valve Stenosis/Regurgitation (or general valvular involvement).