DIP Episode 496 - Aortic regurgitation and some USMLE integrations

Welcome it's Divine. This is episode 406 of the Divine Intervention podcast. And to this podcast I'm going to be addressing the topic that I like to title demystifying Eotic Regrage. This is something I know I feel like I've seen a lot of questions from people in recent times on Eotic Regrage and the angels I mean people probably have is not probably many people have memorized the findings you know that people that have Eotic Regrage it's a nostalgic decrescendo marble her best at the left third intercostal space that may reach to the left floor left floor, the floor border blah blah blah blah blah blah blah. Fine. Many people know that of the top of their heads but there are many findings in Eotic Regrage that I feel like for quite a number of people do not make much sense. So every now and then I like to put out a podcast or two on topics that I've noticed that many a lot of people seem to be having issues with so that we can address them and you can fully understand it instead of just memorizing it. So I suspect there's something that anyone taking step one step to step three is going to benefit from. So what's the classic vignette for Eotic Regrage? Well they'll give you a question about a person typically this person they'll tell you that the person is having a shortness or breath the person may have signs and symptoms of heart failure.

But the critical thing you're gonna notice in the cue stem is that the person's stolly blood pressure is gonna be high and the person's that stolly blood pressure is gonna be low. So whenever you see a person that has a blood pressure of like 140 over 50 for example that's just a huge anomaly because if you think about it normally blood pressures for the average human being in a normal range should be about 120 over 80 the difference between those two numbers the number of the top and the number of the bottom is what's called pulse pressure. That range should be 40 but you see a person that's a blood pressure of like 130 over 40. The stolly blood pressure is higher than normal. The stolly blood pressure is lower than normal. The spread the difference between those two numbers is what's called the pulse pressure. So the pulse pressure widened it increases in the early pre-grage. So why exactly does that happen? Well if you think about it so this is me just going straight up into the pathophage of fence. If you think about it for a second here. Normally, normally if you look at the operation of the euric valve during systole the pressure in the left ventricle exceeds the pressure in the eur. So the euric valve is going to open. The blood is going to rush off from the left ventricle into the eur. Blood is being ejected from the left ventricle into the eur. Now over time as the europhils, feels, feels a blood. The pressure in it is going to rise.

That pressure in the eurote that is rising as it fills with blood from the left ventricle is the systole blood pressure. I'm going to say that again that pressure that builds up in the eur. As blood fills it from the left ventricle is the systole blood pressure that initial initial initial. And we're raised now where initial pressure in the eur. After blood comes out of the left ventricle is the systole blood pressure. But over time. So over time means after that initial rising pressure. Over time give it like a second or two. The pressure you then start seeing the eur. After it has filled is the systole blood pressure. That's the blood pressure. That's the blood pressure. So the thing is you may already begin to see that over time the pressure in that eur is going to build up build up build up. And then since the pressure in the eur is building up building up at some point it will become bigger than the pressure in the left ventricle. So you'll think that oh okay blood may flow back from the eurote into the left ventricle. But a normal person that does not happen because the euric valve closes. Again if you understand the normal physiology when I'm start bringing in the pathophase of the euric regurg and its problems you'll make more sense to you. So that's what's supposed to happen. The euric valve is supposed to close right as the pressure in the eur. It builds up and it exceeds the pressure in the left ventricle. But in euric regurg what exactly happens?

In euric regurg the euric valve is not properly closed. And it's not properly closed for many different reasons. The big thing if they ask you like oh what is one of the biggest risk factors for euric regurg on your exam? You want to think about dilution of the euric root. I'm gonna say that again you want to think about dilution of the euric root. So many cases we have no idea what's causing that euric root to dilute. I just gonna think of euric regurgers. Wow you have these valves inside the pipe that is your euror. But if the valve if the pipe becomes wider and wider like a bigger circle then those valve leaflets have been poured apart. Since those valve leaflets have been poured apart then they won't come together nicely. So blood can backflow into the left ventricle. Although in some other people though this euric root dilation we can see this in people that like very old people that have syphilis, the tertiary syphilis and the eurotitis. We can see it in osteogenesis imperfecta. Remember that's an Orozomodominant disorder collagen type 1 mutation. We can see this in people that have had euric dissection, put out morphine, people that have bishops, disease, or lasdano and kilosine spondylitis. Even in lupus we can find many of these people. And if you have reenasty endocratitis that torches your euror that can certainly cause that problem. So let's then go step by step and what happens. So think about it.

If the euric valve is incompetent which is always called euric re-gurge then there's going to be backflow of blood from the euror into the left ventricle from the euror into the left ventricle. So think about this with me. If there is backflow of blood from the euror into the left ventricle, how many places is the left ventricle receiving preload from? Just work with me here. How many places is the left ventricle receiving preload from? It's receiving preload from two places. Normally the left ventricle is only supposed to receive preload from the left euror. But when you have a euric re-gurge you're getting preload not just from the left euror, but you're also getting preload back from the euror. So since you have two places contributing to the blood coming back to the left ventricle, the preload of the left ventricle is going to increase. If the preload of your left ventricle increases according to the Frank Stalin principle, what do you think is going to happen to your cardiac output? The cardiac output is going to rise. That's the truth. So there are two things that are now emptied into the left ventricle. Normally in a normal person is only the left euror that feels the left ventricle blood. But now the left ventricle is being filled with blood from the left euror and from the euror. So it has two sources of preload. So overall the preload of the left ventricle is going up. So if the preload is going up, what's happening to your end-dastolic volume?

Your end-dastolic volume is also going up. Again, what does end-dastolic volume mean? End-dastolic volume just means how much blood is in the left ventricle after the left ventricle has been filled with blood. Normally the left ventricle is only supposed to be filled with blood from the left euror. But if blood is coming not just from the left euror from the loam but is also coming back from the euror, then it's going to be more filling with blood. So you're going to have an increase in your end-dastolic volume. So if you have an increase in your end-dastolic volume, what's going to happen to your stroke volume? The stroke volume is going to go up. Simple as that. If you put more blood in the left ventricle, then when the left ventricle is ejecting that blood from it, it's going to inject more blood than normal. So your stroke volume is going to go up. Remember if you have an increase in end-dastolic volume, the stroke volume should go up. That's pretty much like an application of the front-starling principle. More preloading the heart, more end-dastolic volume in the heart, bigger stroke volume. And obviously if your stroke volume goes up, your cardiac output is clearly going to go up. Because remember, your cardiac output is your heart rate multiplied by your stroke volume. If your stroke volume is shooting up, then obviously your cardiac output has to shoot up.

And as your cardiac output is shooting up, what do you think is going to happen to that initial pressure in the order? Remember I said pay attention to that already, initial, because that's your systolic blood pressure. If your cardiac output is shooting up, if the amount of blood that you're ejecting from the left ventricle is shooting up, then what's going to happen to that initial pressure in the order? Well, here's the thing. The initial pressure in the order is going to shoot up as well. Your systolic blood pressure is going to shoot up. Okay? Your systolic blood pressure is going to shoot up. Okay. So remember I said when blood gets into the order, the initial blood that gets in there, bonus, the, the, that initial buildup of blood is going to cause what we know as a systolic blood pressure. But we said that over time, like a second or two, whatever, I'm just making up those numbers, but just over time, the blood in the order kind of relaxes a little bit, right? That's what creates your systolic blood pressure. Remember, in the astaly, you have like relaxation of stuff. So the thing is in the order that blood that gets the initially over time is going to relax. That's what creates the systolic blood pressure. Normally, that blood only relaxes inside the order. That's the truth. Normally, that blood only relaxes inside the order. That's it. Inside the order, that's it. But when you have a yodic re-gurge, that blood has a bigger, wider space to relax into.

Think about it. Normally, it's just the yoder the blood can relax into. But now the blood can relax into the order. But the blood can also relax into the left ventricle. So it's almost like the blood has more room to spread out. Just kind of think about it. Let's say you're laying down on a twin size bed. But then someone gives you like a king size bed. When you have a king size bed, that is way bigger. You're going to have more room to relax. So normally, the yoder, that's where blood carry, oh blood gets into the order initially over time, just relaxes in the order. But man, when you have a yodic re-gurge, it has more room to relax because some of it can go back into the left ventricle. So since the yoder, the blood in the yoder has more space to relax into, what do you think? What exactly do you think is going to happen to your dastolibular pressure? It's going to go down. It's going to go down. It's going to go down. So think about it. We've defended and explained that the systolibular pressure goes up and the dastolibular pressure goes down. Since the systolibular pressure is going up and the dastolibular pressure is going down, what do you think is happening to the difference between those two numbers? The difference is getting bigger. That's why the pulse pressure increases. That's literally why the pulse pressure increases. Remember, pulse pressure is the spread between your systolic and your dastolibular pressure is the difference.

If you subtract your dastolibular pressure from your systolibular pressure, that's literally your pulse pressure. That's literally your pulse pressure. So what are you going to see on physical exam? Because many people memorize all these crazy things like carigans, balls. Yes, that's a funny knee-yodic regear. It's like a big upstroke and collapse of your pulses. Again, that's something that happens. If you understand what I just explained, you understand exactly what that happens. Now, what that means? Or you see like this, they will say sign. Where the person's head is bobbing as they have it, each heartbeat. That's because of the white pulse pressure. To be honest with you, many of the physical exam findings in your dachshund are white pulse pressure phenomena. That's the truth. They are white pulse pressure phenomena. Or you hear of the water hammer pulse. Again, it's a white pulse pressure phenomena. So you're just going to keep that at the back of your mind. Over time, if we're kind of extending this knowledge a little bit and then I'll wrap this up because I want to be a short podcast. But over time, if you think about it, this your dachshund kind of becomes problematic. Maybe like why? Well, all that excess blood that keeps coming back to the left ventricle is going to cause volume overload. The volume overload with the left ventricle is going to ultimately lead to eccentric hypertrophy.

When you have that eccentric it's so basically you're adding your sacramir in series this time because you're having to deal with all this extra volume. So you're trying to increase the cavity size of the left ventricle. You're going to have eccentric hypertrophy. It's going to cause an S3 heart sound. Ultimately, it leads to heart heart failure. You're going to get in trouble. Now, one common thing that people get on the exam says, oh, how do you differentiate acuteodic regurg from chronic acuteodic regurg? Well, here's the thing. The way you differentiate those two is how studying do the asymptoms start. People that have acuteodic regurg, the asymptoms are going to start pretty suddenly. That's why it's called acuteodic regurgitation. Well, chronic acuteodic regurg, these people may barely have any symptoms for or sometimes even years. But then over time, they didn't start developing symptoms. That's the simple easy way to differentiate those two. Usually when a person has acuteodic regurg, they're going to have like floric pulmonary gema that develops very quickly because all that blood regurgitating back into the left ventricle regurgitating to the, you know, there'll be less emptying of the left echelon to the left ventricle over time and then the fluid will just back up into the lungs. So you're going to have an increase in hydrostatic pressures within the pulmonary capillaries and you're going to get into a lot of, a lot of trauma pulmonary gema.

And also, another thing they can do with the acuteodic regurg, again, these are just bonus points that you should know for your exam. They can easily make an arrow question out of the acuteodic regurg. So let's walk through a few hours rapidly and then we'll, I guess maybe before we talk about the arrows, let's talk about treatment because on the arrows to be the last part we stop on. That's like the high yield super awesome part. So obviously I love physiology. So basically you can treat your acute regurg just replace the valve, especially when the person is beginning to kind of going to heart failure symptoms, you want to go ahead and replace the valve. That's kind of important. And then you can give them the, you know, the heart failure drugs, give them the heart failure drugs, right? Like beta blockers, you can give them isinehameters and what not. But I'll say if you really have to pick a drug on your exam, just focus mostly on isinehameters. Beta blockers, you know, for years where like, oh, you got a yodic regurg, we can give you a beta blocker because think about it, which makes logical sense, right? If you have a yodic regurg, you take a beta blocker, a beta blocker is going to slow down your heart. If you slow down the heart, what's that going to do to your mastolic filling time? Well, it's going to increase. So you're basically slowing down the heart. So it has more time industrially.

So you're going to have more time for the regurgitation to happen, which is not ideal, right? But the thing is, as you're going to see when we get to the outer part of this, there are certain neuro hormonal changes that happen to a person's heart, when they have chronic acute regurg, that beta blockers can actually really help with. But if you have to pick only one drug to treat the yodic regurg, pick an asine inhibitor or a 100-tensing tourist after a blocker, that's certainly going to help. So those are kind of like the big things. But beta blockers, again, back in the day, they were contraindicated, but these days, especially when you have like, aortic regurgers, it's kind of causing heart failure symptoms. Beta blockers are not always the worst idea in the world. I'll just kind of see that. Okay, but again, if you have to pick one drug, pick an asine inhibitor. So let's go into the questions. But again, overall, you want to go ahead and replace the valve, simple as that. Now, what happens to your preload in your re-agreage? We've talked about this already. Your preload is going to go up because the left ventricle is being filled from the lefty trim under the ear. Okay, what happens to your endastole volume? Again, it's going to go up because your preload is going up. We've talked about that. What happens to your cardiac output? Well, it's going to go up because your preload is going up. Your endastole volume is going up. We've talked about that.

What happens to your pulse pressure? It goes up. Why? Because again, your cerebral pressure is rising. That cerebral pressure is dropping. So it's going to raise your pulse pressure. Okay. Now, what happens to your re- what happens to your levels of reigning when you have your euricrigurge? Well, I want you to think about that. Think about it. If you have a euric, because normally the blood that gets into the other is supposed to flow forward in the other into the organs of the body, your kidneys and whatnot. But when you have your euricrigurge, that is not all that blood that is forward flowing. So if it is backward flowing. So you're going to be profusing the renal arteries very well. No, you're not. So your juxtapglomerular cells are going to freak out. So you're going to make a lot of reigning. As you make more reigning, right? So your reigning is going to go up. Guess what? Your endotensial one is also going to go up as well. As your endotensial one goes up, your endotensial two is going to go up as well. And as your endotensial two goes up, what's going to happen to your industrial levels? Your industrial is going to shoot up as well. So those are the lab values, right? So they may even give you some other labs like, oh, do you expect their potassium to look like? Well, they're going to have hypochylemia. Because again, when your dose run is high, you're going to excrete more potassium from the kidneys. You're going to have hypochylemia.

What would you expect the ACB status to be? Well, you should expect the metabolic alcoholosis because again, when you have high our dose theorem, our dose room is going to cause you excrete hydrogen ions. As you excrete many hydrogen ions, that's going to cause you to have a metabolic alcoholosis. So you're going to have a hypochylemia that have a metabolic alcoholosis. So again, remember, your recreateers can cause secondary hyper, our dose to run is in. Again, you can just see the many different ways they can go with these concepts. Okay. So I think I'm going to go ahead and stop here. Again, I have these, I have a review courses that I offer if you're interested. Again, I love to explain battlefield phase. I love to make integrations. I love to, you know, my review courses are not lecture based. They're all problem sets. And then I have some helpful tables. I also make available to you. But I have a course starting on first step one, order with step three, I have a test eating class this Thursday. I have a bio stats class on four hour class on Friday. Then I have a social sciences quality improvement ethics, you know, healthcare systems, communications and professionalizing class on Saturday. And then for people taking step two, I have a 20 hour course next week. And then we're going to take in step one in the second week of January, God willing. I do have a 25 hour class. If you're interested in many of these classes, shoot me an email.

I'll give you more information, although also meet a podcast recently. I get called December classes. So just check that out. It talks about my December and January classes. And then I'll throw in on one tutoring for all the USM in the exam. So I have these podcasts on Apple Google on Spotify. I have a You Tube channel. So check that out. You can see the videos I've made on there. And then I have another website called divine interventionlifelessons.com. Every week, I post like two podcasts. Actually, there's an Apple podcast associated with that. People go perspective address a life lesson. So if you're interested in any of those, just check those out. But again, I think just listen to this podcast. And I'll see you in the next one. Bye.

A decrescendo murmur best heard at the left third intercostal space radiating to the apex, and a wide pulse pressure (high systolic, low diastolic).

The backflow of blood from the aorta into the left ventricle during diastole causes rapid runoff, drastically lowering the diastolic aortic pressure.

According to the Frank-Starling principle, increased preload leads to increased end-diastolic volume and subsequently increases stroke volume and cardiac output.

Tertiary syphilis, aortic dissection, osteogenesis imperfecta, or connective tissue diseases (e.g., lupus).

Hypokalemia and metabolic alkalosis, due to secondary hyperaldosteronism resulting from volume overload/increased renin.

Acute AR presents with sudden onset of severe symptoms (e.g., flash pulmonary edema); Chronic AR develops symptoms slowly over years.

Wide pulse pressure (high systolic and low diastolic).

Aortic dissection, osteogenesis imperfecta, or connective tissue disorders/endocarditis.

It leads to volume overload $\rightarrow$ eccentric hypertrophy (dilatation) and eventually S3 gallop.

Hypokalemia, due to secondary hyperaldosteronism caused by increased renin release from renal perfusion.

Increased cardiac output and volume overload activate the RAAS system $\rightarrow$ high aldosterone levels cause hydrogen ion excretion (metabolic alkalosis).

Acute onset of severe symptoms; Chronic development over years.

Wide pulse pressure (high systolic and low diastolic).

Aortic dissection, osteogenesis imperfecta, or connective tissue disorders/endocarditis.

It leads to volume overload $\rightarrow$ eccentric hypertrophy (dilatation) and eventually S3 gallop.

Hypokalemia, due to secondary hyperaldosteronism caused by increased renin release from renal perfusion.

Increased cardiac output and volume overload activate the RAAS system $\rightarrow$ high aldosterone levels cause hydrogen ion excretion (metabolic alkalosis).

Acute onset of severe symptoms; Chronic development over years.