DIP Episode 171 - USMLE Step 1 Cardiology Review Series 4 (and Podcast App Update!)

Okay, welcome. My name is Devine, I'm a resident. This is episode 171 of the Devine intervention podcast. And this podcast is going to be continued on a US Mly step one cardiology review series. I really want to try how to finish this series over the next few days. So I'm gonna maybe be focusing quite a bit on that and then some step two and internal medicine stuff that I have planned. And before I go into the podcast, I think I want to go ahead and mention something right. So, you know, I've got in a lot of requests for, you know, to try to get the podcast to like podcast apps. If you do a search for divine intervention podcasts, the podcasts are now available on the on Apple podcasts. They are available on Google Play podcasts and they also are available on Spotify. So essentially you have it in all those three avenues. So you should hopefully be able to access it that way. In general, though, the slides and what not for some of the podcasts, they will primarily still be hosted on the website. Okay, so let's go ahead and if you want to reach out to me again, you also reach out to me through the website or send me an email at divine intervention podcast to it and sdn.gmail.com. So let's jump right into it.

So what if you get an exam question about like a 25-year-old Ivy drug user and they tell you that this patient has, you know, like a whole host of Stullic murmur that's heard best at the left-stone border and this patient has had like fever for like a week and they tell you that this murmur was not present from the last physical exam and the, you know, the person's body temperature is like 101 and they give you like a CBCI. You notice that this person's white count is like 15,000. What's your diagnosis? So Ivy drug user, fever, new murmur, what is that? Well, I would hope you're telling me that this person has endocraditis, right? This person has endocraditis, right? So what really is endocraditis? And I mean like this person, if you really want to get a little closer, this person has a tricospid regurg, right? Tricospid regurg. I remember that when people have endocraditis and the Ivy drug users, the most common valve to be affected is the tricospid valve and the reasoning behind that right, if you really think about it is, if your Ivy drug user, I mean literally look at the name Ivy drug user intravenous. So injecting to a vein, where do the veins drink first? They drink to the right side of the heart, right? So the tricospid valve is the most commonly affected valve by endocraditis. In Ivy drug users, the second most common valve affected is the eotic valve in an Ivy drug user.

Although in general endocraditis tends to affect left-sided heart valves, a lot more commonly like 90% than right-sided heart valves. So what are the big things to keep in mind with endocraditis, right? So endocraditis is basically just as the term goes infection of the endocradium. The thing is that the vows of the heart constitute part of the endocradium, right? They are all lined by endocradium. So typically when people have endocraditis, it's the heart valve effects that you know causes a lot of the symptoms, right? And some big things you want to keep at the back of your mind, you know, a person that has that has endocraditis, right? Like if for example they give you like a very because sometimes right, the NV Me they just give you non-specific questions. And whenever they give you these non-specific questions, where they don't, you know, they don't give you too many hints, you know, they just give you like, oh, this patient has acute endocraditis, yada yada yada. And what is the most likely cause? My exam strategy, or I guess the strategy I teach people for those kinds of questions is just to pick the most common answer, okay? The most likely thing, right? So if you notice that a person you know over the last like week has developed endocraditis and you know they feel like crap and all that stuff, then it's likely stuff where, stuff where is the most common cause, very high, it's the most common cause of endocraditis, right? Acute endocraditis, right?

And then obviously they give you a question about a patient that has you know like like an IV drug user, obviously, obviously, obviously you absolutely want to think about stuff where is. If they give you a question about a patient that you know has had like a dental procedure, right? And then you did that over the last like three weeks, this person has not been doing well again, having fever, new murmur, yada yada yada, then think about strep viridans. In fact, this is a, you know, I guess a factor in not many people know, but actually strep viridans is the most like, if you take every like if you say, oh, let me count everyone in this world that has endocraditis, believe it or not, strep viridans is actually the most common cause of endocraditis. But in general on MDME exams, whenever you see a question on endocraditis, it's almost always acute endocraditis or IV drug user endocraditis, right? So whenever you see those things, think about stuff where is. So remember strep viridans, strep viridans, lots to cause endocraditis, especially in people that have you know, that have the endocraditis, and one thing I'll go ahead and mention is that stuff orias can cause endocraditis to people that already have preexisting like damaged valves, but they can also cause endocraditis in people that already have preexisting normal valves.

Not so is strep viridans, strep viridans almost always when it causes endocraditis, it causes it in people that already have like evolved with a quirk, right? So evolved with some kind of preexisting problem. That's actually a very subtle but very high yield point. You want to keep at the back of your mind for MDME exams. And then if they give you a question, what if they give you a question about a patient, you know, that has a, you know, let's say they just had a valve replacement like two weeks ago, and then they're having again like fevers and you know, the classic signs and symptoms of endocraditis, then the bug you want to think about is stuff epidermitis, okay? Staff epidermitis. The thing is when people will get prosthetic valves, remember if you get a prosthetic valve, you're supposed to be an anti-qualgulation for life, okay? So when a person gets a prosthetic valve, basically within the first two months, after they get the prosthetic valve, if they get endocraditis of that prosthetic valve, I really want you to think about stuff epidermitis. Remember, stuff epidermitis loves to form biofilm, so because it loves to form biofilm, right? It can cause endocraditis of, especially like on prosthetic valves, because prosthetic valves contain plastic, right? So they're very good for biofilm to attach to.

Now, if a person has endocraditis and they have a prosthetic valve and it's two months after they had that prosthetic valve placed, then you want to think more along the lines of stuff, okay? One thing more along the lines of stuff, or else, and the thing is once a person has endocraditis of a prosthetic valve, you need to replace the valve. There is no like, let's do this. I mean, they're still going to get antibiotics, where you're absolutely positively need to replace the valve. If not, the endocraditis will never resolve, okay? Now, what if they give you a question about a patient that, you know, they tell you that, oh, this patient has endocraditis and you know, they have a history of like inflammatory bowel disease, like Crohn's disease, or like, all sort of collitis. And then they ask like, what bog will most likely grow in the persons, because the thing is when a person has endocraditis, your first diagnostic step is always to grow blood culture, right? They can ask what bog will most likely grow in this person's blood. You want to think about things along the lines of like streb buvis, okay? So like streb buvis, or there's this streb buvis derivative called streb galoliticus. I already talked about this in one of my very, very early podcasts. So again, that's one of those big things you want to keep at the back of your mind, for example.

Although on the flip side, if a person, let's say a person getting a blood culture for whatever bizarre reason, and you grow like streb buvis from that blood culture, or again, streb galoliticus, then you want to think about that. You want to go ahead and perform a colonoscopy, not long afterwards, because there is a very strong association between streb buvis or streb galoliticus in the blood, and the presence of concurrent, like colon cancer or concurrent inflammatory bowel disease, like Crohn's disease, or like, all sort of collitis. Now, if they give you, you know, a question about a patient that, you know, let's say this person is in the ICU, and this person has had like, you know, like a CBC, like a central venous catheter placed for like, you know, days and days and days, and this person has endocraditis, again, like a new murmur, fever, yeah, yeah, yeah, yeah, then on that those circumstances, the thing, again, I really want you to think about these stuff warriors, okay? In general, once you insert like an IV line into the body, you increase the presence risk of a stuff warrior's endocraditis. So again, these are all big, high old things you want to keep at the back of your mind. And again, like I said, right, IV drug user, think about, like, try Cospy valve endocraditis, that's the number one affected valve. The euric valve is the second most commonly affected valve in, in endocraditis and the IV drug user.

But again, if you are taking all comers with endocraditis, the most common side of the heart that is affected is the left side. And the valve that is actually most commonly affected again, of all the cases of endocraditis is the mitral valve, okay? It's the mitral valve. Again, and most times when people have endocraditis of a valve, it tends to cause a regurgitant murmur, okay? It tends to cause a regurgitant murmur. So you typically would not see like mitral stenosis or tricospits stenosis be the outgrowth of a person having an endocraditis. It will almost always be like tricospit regurg or mitral regurg. Again, that is, again, you may say divine, you're being a little too detailed here, you're being a little too particular on distance. I promise you again, I've treated thousands and thousands and thousands of people probably over the last like two, three years. And then that's not counting like the decade before that, right? So I promise you these things are all very high for NBN exams. Although the tutoring I did a decade before that, because we'll maybe be like, hmm, how you're resident, there's 200,000 people for, no, that's for like a medical perspective. I've probably tutored more for like medical exams than I have for, I mean, sorry, for college exams, then I've done for medical exams, right? But again, I will strongly encourage you to keep these things at the back of your mind.

They are very important for the USMLE exams, because there's this trend with the current USMLE step one exam, where I don't know, I just feel like these days, on the USMLE step one, the exams are getting a little harder, right? They're getting a little harder. Like the MBM is beginning to take these like new paths and I'll maybe make a podcast about this down the line. They're beginning to take these new paths with the kinds of questions you're testing on step one. I will say that if you're comparing like step one and step two CK, because again, most times you know, they make pretty significant changes in the summer. I feel like step one has had almost like a complete makeover over the last couple of months. So again, just again, things to keep at the back of your mind. You should still use the classic resources, you'll still be successful with those, but again, just be a little smarter with your study in and actually just study harder pretty much. Okay, so how does endocratitis arise for the most part, right? If you really think about it and the reditis, typically the thing that happens is for whatever reason, a person will have like primary, he most taste like, you know, the person will have like some kind of like valve damage and then once the valve is damaged, you begin to expose, because remember, those valves are lined by endocardium, right?

And remember that if you damage your valve and you know, kind of strip off some like the surface of the endocardium, you can expose like some collagen and that collagen can trigger primary hemostasis, right? And when you activate primary hemostasis, you have like fiber, you have platelets, that kind of hang around the valve. The thing is those things can serve almost like a sieve, they begin to trap like bacteria and all that badness and then those things can proliferate and then begin to cause even more damage to the valve. So the thing is with endocratitis, you may be like, okay, so if I suspect endocratitis, how do I make the diagnosis? Well, the thing you typically do is you get a blood culture first, right? So if, if no diagnostic test has been done in the Q Stem, the first thing you absolutely want to do on your exam is to get a blood culture. And then after you get the blood culture, you want to get some kind of echocardiogram. And likely on the MDM exams, they want you to get a trans-isophageal echocardiogram, a TEE, okay? Remember TEE is more sensitive than a TEE. A TEE, you do it on the surface of a person's chest, a TEE, you do it through the esophagus. Remember that the left atrium is the most posterior chamber of the heart and the esophagus is smacked up against the left atrium, right? So if you put an ultrasound probe in the left atrium, I mean, sorry, in the esophagus, you'll see like the heart chambers extremely well, okay?

So again, these are all high old things you want to keep at the back of your mind, for example. And again, like I said, classically, if a person has an endocratitis, they'll almost always have like fever on the exams, they'll have like a new murmur, they could be like an IV drug user. Sometimes they may actually give you like a rising creatinine in a person that has his stroke endocratitis because the thing is those vegetations and all that badness, they can actually begin to embolyze or and those vegetations sometimes the body may even form antibodies against them. And then you have like a vasculitis in the ring of the cells, okay? So you can get like a glomerulone, like a glomerulone fritis in the setting of an endocratitis. It's usually like an ephritic syndrome kind of picture. And then some other things you may also see in a person that has endocratitis, right? You can see things like, you know, you can see like the splinter hemorrhages, right? So you look on that person's no beds and you see like red, right? That's a splinter hemorrhage. That's like an embolyzation phenomenon again. One key thing to keep in mind is that these vascular vegetations, right, that people having endocratitis, they can flick off and begin to occlude vessels. And those like embolyzation phenomena can cause like strokes, for example, but it can also cause some classic things you may see on a physical exam. Like you could see like the splinter hemorrhages, right?

You could see like the janeway lesions, right? So because many times when people are studying for a step one, all they remember like, oh, what can cause lesions on the palms and so's. And then the only thing that you remember is that, oh, you drive a Kawasaki cars with your hands and feet. I will challenge you to maybe adjust that on the Monica little too. I drive janeway Kawasaki cars with my hands and feet to tell you that janeway lesions, it's not a rash obviously, right? But it's a lesion that you can find on the palms and so's. Same thing with in Kawasaki's disease, you also find a rash on the palms and so's. If a person has cocksaki a virus, right? So like hand-footed mouth disease, that can cause lesions on the palms and so's. And then re-ketsiari ketsai, the bug that causes rock-emounting spotted fever, that can also cause a rash on the palms and so's. And then secondary syphilis, not primary not tertiary. Secondary syphilis is also as well as the development of a rash on the palms and so's. So that's your differential for if a person has a rash on the palms and so's on in-baming exams. And then remember, and the thing is the janeway lesions are painless lesions. And again, they are rights from embolization or phenomena. And then there's like the osler nodes, right? The osler nodes, you tend to find them like on the finger pads, okay? You can find them like on the finger pads or your toe pads.

And the thing is one key difference between the janeway lesions and the osler nodes is that the janeway lesions, like I said, they are painless, the osler nodes are painful, okay? So that's a nice way to tell those two things apart. But the big thing you want to keep on the back of your mind, again, like these janeway lesions, these osler nodes, these splinter hemorrhages, they are all like embolic phenomena. And then another classic thing you may see, like on a physical exam in a patient that has endocraditis is something called a rough spot, right? So you basically do a fondoscopic exam. You see all these red in these people's eyes and in the midst of the red, you see like white dots. When you see that, think about a rough spot. The rough spot is actually from, again, almost like an antigen antibody complex phenomenon. Less so like an embolic phenomenon, right? So essentially most of the physical exam findings in people that have endocraditis tend to arise from embolic phenomena with one key exception, which is the rough spot. The rough spot, again, it's an eye-finding, right? Tens to arise mostly from just, it's almost like a mild vasculitis kind of deal where you have like antigen antibody complexes forming. So again, those are key key things you want to keep at the back of your mind with endocraditis, right? And then what are some nice ways your friends at the end being me can integrate some other stuff with endocraditis.

They can give you a question right about a patient that, you know, has endocrad, you know, has like a new murmur and this patient has like a hisch, like a Miller-Rash on physical exam. They obviously want to think about the endocraditis associated with lupus on the those circumstances, right? And remember that lupus can cause a kind of endocraditis known as the libman-sax endocraditis, right? So there's this nice cononic that many people use that SLE causes LSE, okay? I don't mean the London's, London School of Economics by LSE, I mean like libman-sax endocraditis. Libman-sax endocraditis is essentially like a sterile kind of endocraditis, right? So the person will also have vegetations, you know, on their valves, usually it's the mitral valve, but you know it's sterile, right? So you, if you do like a blood contract with people, you very likely not grow any bugs. And then one unusual thing you may occasionally see on MDM with endocraditis is you may see a person that you know maybe has like a malignancy, typically it's like you know some kind of like small bowel or large bowel malignancy, like colon cancer or like stomach cancer or something like that, like gastric cancer, right? And then they tell you that this person has like a new murmur and all that stuff. You want to think about something known as marantic endocraditis, okay? Marantic endocraditis.

The reason it's called marantic endocraditis is that it's essentially an endocraditis that does not arise because you have like a bacterial infection, but it arises from it's almost like a apparently plastic phenomenon that arises in the setting of certain malignancies. The thing is there are many malignancies that for whatever reason, like even like ovarian cancer, even does this a decent amount of the time, they will, you know, these malignancies will produce like mucin. And the thing is mucin is a very again powerful activator of of a hemostasis, right? So when you have like mucin secreted by these malignancies and then it kind of travels in the bloodstream. I mean, obviously if anything travels in the bloodstream, it's going to go by the heart at some point. As it goes past the valve, right? Again, you can activate hemostasis and then you form like some vegetations, right? So sometimes these things I even call like the non-bacterial thrombotic endocraditis because they don't arise from bacteria, right? But you essentially have like a thrombotic complex form on a person's vial, right? And the person again can have signs and symptoms of endocraditis. Yeah, and I mean, this definitely causes like pretty you know, pretty major morbidity and mortality in patients that already have a pre-existing malignancy. So again, one last thing I mean like endocraditis takes a ton of time to treat, right?

Like many of these people, you know, they'll have to get treated with like IV antibiotics for like weeks and weeks and weeks. Usually it's like six weeks, but that's more of a step to see gay concept. But the thing is because it's a chronic infection, believe it or not, endocraditis can actually cause anemia of chronic disease, okay? Endocraditis can actually cause anemia of chronic disease. So that's again one key high-old association. You want to keep at the back of your mind for endemic exams. So personally, I think of, you know, maybe set everything I want to say about endocraditis. Let me just mentally run through and see if there's any other key thing I'm forgetting. I don't know. I don't think I'm really forgetting much. I think I've said at least from my mind, I feel like I've said most of the high-old things that tend to pop up on exams with endocraditis. So what if you get a question about a patient and then they tell you that this patient, you know, like two weeks ago, this patient had like a sore throat or had like some kind of upper respiratory infection. And then they tell you that over the last two days, this person has been having like profound shortness of breath and that when you listen to the person's lungs, you hear crackles and then they tell you that, oh, that you perform some kind of, they may not even tell you this extra information, but if they do, like you should, I guess be thankful.

But they can, you know, tell you that this person, they get an echocardiogram and it shows like, you know, like massive biventricular dilution and the person's ejection fraction is like 20%. What's the diagnosis that you should consider under those circumstances? I hope you're thinking about myocarditis, okay? Myocarditis. Myocarditis, the classic, I mean, in fact, I will say that if a bug is the cause of a person's myocarditis, I don't think I've ever seen a different presentation than what I just described on any endemic exam, right? It will classically be presented by an operator in infection or sore throat and then the person will have like global cardiac dysfunction. Whenever you see that think about myocarditis, okay? Think about myocarditis, right? And the thing is for the myocarditis can actually, it's actually pretty bad, and you say, oh, who cares? It's just myocarditis. No, it's not just myocarditis. About half of the people that get myocarditis, they end up dying within like five years, right? So it's actually pretty nasty. I mean, it's one of these things that can essentially snatch a young person in the prime of their life for it. So it's just one of those things, you know, you don't kind of mess around with. Especially if a person is having like a severe shortness of breath.

So I'm saying this, again, if you encounter this as a physician or resident or a med student in the future, for a person, you know, has had like a sore throat, like, you know, like a couple days or weeks ago, and then now they have like just really bad shortness of breath. One of the big things you want to entertain in your diagnosis, I mean, in your differential is myocarditis. And unfortunately, most times, there is actually no real treatment for it. You just kind of give supportive care. Again, like half of half of the people that have it, they have like complete recovery, no issue. But again, about another half, they have like, you know, pretty bad symptoms. And they may ultimately end up needing like a heart transplant and things of that nature. Thankfully, it's not as common as it's not as common as it shows up on, I guess, on endemic exams. So what are some things that can cause myocarditis, right? So viruses, right? If a person has myocarditis, it's almost always from a virus on endemic exams, right? So you want to think about things like a coxacchi B virus, right? That's probably the most common MDME exam cause. Even if it's not the most common in the real world, because adenovirus is actually a lot more common than adenovirus is a lot more common as a cause of myocarditis actually than a coxacchi B. But the thing is, again, almost maybe like 95% of MDME questions have seen that tested viral myocarditis, they almost always went after coxacchi B virus. Okay?

I mean, like even like, probably B19, right? That single stranded DNA virus, can certainly cause a cause of myocarditis. If they give you a question about a person that, you know, is from like South America or like Central America, and this person has like, you know, again, like the classic signs and symptoms that like the presentation I just gave of myocarditis, think about traipanosoma cruziac, okay? Traipanosoma cruziac. The thing with traipanosoma cruziac already is it causes chagas disease, right? And there is this, I guess, maybe like series of thoughts that I give people to try to remember the different things that can be caused by T-cruziac, okay? Traipanosoma cruziac. They'll almost always be some kind of central or South American association in the Houston. But the thing is, I think of traipanosoma cruziac as a thing that causes big problems, okay? It can cause a big heart because you'll ultimately cause like myocarditis leading to a dilithic cardiomyopathy. It can cause a big esophagus because it can cause something known as ecalisia, okay? Where you have failure of the lower self-adjusted filter to relax, right? And that'll cause a big esophagus with like, Plasica, Birds, Big Sign. This is something that I'll talk about when I give my gastroenterology podcasts. And then you can also cause something like a big, like a big distal GI tract, right? So you can cause like a hersupron's disease, right?

Because those are traipanosoma cruziac bugs, they can essentially destroy, they can essentially destroy like the ganglion cells that you find in the distal GI tract. And that can cause hersupron disease, right? So those are all things that can be caused by traipanosoma cruziac, okay? So again, these are all big big traipanosoma cruziac, you know, these are all things that can cause a big picture of things you want to keep at the back of your mind. Many fungi can cause a myocarditis. So more than like rare bugs that can cause myocarditis that are, okay, you know, occasionally it'd be known to pop up on NV Me exams, I think it's like Lyme disease, right? So like, Borelia Bognopri, that certainly can be associated with myocarditis, a dephemia, right? Like the toxin that is produced by dephemia, the liver or not, it can actually cause myocarditis, carbon monoxide, even like bite from like the black widows spider, that can all cause a, again, that can all cause a myocarditis. And then some drugs, right? Like they can give you a question about a patient that's on some kind of anti-cancer therapy. It's almost always a breast cancer patient on NV Me exams. And then they tell you that they have myocarditis, you want to think about like your trastuzumab, right? Remember, it's a monocloryl antibody against her too, okay? Trastuzumab causes a reversible dilated cardiomyopathy.

So typically, before you start a person on trastuzumab, you need to obtain an echocardiogram to get a baseline injection fraction, okay? So that the injection fraction begins to drop, you can then stop the drug. So, some other drugs that can also cause that myocarditis, again, leading to a like dilated cardiomyopathy sort of business, things like your anthrocycline, right? So like doxoo and donor-rebusine, remember those drugs, right? They're, you know, they're very good ion key, like they tend to like complex with ion pretty well, right? And that ion can precipitate something as the fentine reaction in the presence myocardium. And again, that can cause myocarditis, and then that can cause a dilated cardiomyopathy. And obviously, right, I mean, you should hopefully know at this point that you can prevent a dilated cardiomyopathy or the myocarditis, as she said, with taking doxoo and donor-rebusine by giving a drug known as dexrazoxin. Dex-D-E-X-R-A, dexrazoxin, Z-O-X-A-N-E, dexrazoxin. Dexrazoxin is an ion-kileter, so it essentially prevents the fentine reaction from happening. And that can again, hopefully help with preventing the myocarditis and the dilated cardiomyopathy that can accompany the use of doxoo and donor-rebusine. And remember, on like trans-tusium, that causes a reversible dilated cardiomyopathy. Doxoo and donor-rebusine cause an irreversible dilated cardiomyopathy, okay?

That's a subtle difference that again is not emphasized all the time, but it's very high yield to know for the purposes of the US Emily Step 1 exam. And then, if a person gets like radiation therapy to the chest or they have like lupus or they have like scleroderma, right? Or again, like Kawasaki's disease. Because remember Kawasaki's disease can essentially cause like a myocardial infarction, right? And when it causes that myocardial infarction, right? Whenever you have the schemia to the heart, it is almost always followed by dilated cardiomyopathy, okay? So again, these are all things that can cause a dilated cardiomyopathy. And the thing with triplanosomacruziac, because I wonder, this is not something that you know, they hit on too much on step 2ck, but it certainly hit on quite a bit on step 1, is like how do you like detect it, right? The thing is, the detection of triplanosomacruziac, the thing is there are many complex tests that you can do. But let me tell you what is necessarily high yield for you to know for the US Emily Step 1 exam. Just remember the word stigot. So what do I mean by stigot? Let me spell it, STI, G O T E S, okay? Just remember the word stigot. If you detect some kind of stigot, let's just look for the answer that says detection of some kind of stigot in the blood.

If you see that, you're pretty much on the right track with regards to diagnosing a to detecting triplanosomacruziac in the blood, because it has like many parts of its life cycle, it has like the amastigot, the triple mastigot, yada yada yada. And remember that it is associated with getting bit by the redovid bug, okay? That's again one of those weird annoying things that your friends at the NBM, you kind of want you to know for example. So the thing is, so if you know, if you suspect the present has a myocarditis, actually there's one more thing I forgot, they can give you a question about a patient that has a history of schizophrenia. And again, they have like the classic signs and symptoms of myocarditis. Think about clasping on the circumstances. Clasping, remember, it's a needypical anti-psychotic that is associated with igranolocytosis and hypercellivation. It's also one high old drug cause of myocarditis on NBM exams, right? So again, myocarditis, again like I said, you have like almost like heart failure symptoms, right? You have like the dysmia, you have like the chest pain, you have like mouth fevers. The thing is, as the heart begins to dilute, that can be actually begin to cause some pretty nasty arithmias, right? So you can have like bondo branch blocks, they can have like ventricular attack, like ventricular attack arithmias. And again, these people can actually have sudden cardiac death, right?

So that's one of those weird things you want to keep at the back of your mind with with myocarditis, right? And again, obviously you make the diagnosis with an echocardiogram. If you want to like delineate the exact cause, you can do something called like an endomaiocardial biopsy. And the thing is when you do that biopsy, typically the NBM will say that, oh, that you see myocardium and then you notice that interspersed amongst the myocardium, you are seeing like some lymphocytic infiltrates. If you see that, in an NBM exam, you absolutely positively want to think about some kind of myocarditis going on. So again, like I said, for the most part, supportive care, and then you hope for the best with the patient, but obviously the patient keeps the generic 10 and their cardiac output goes to crap, then you need to consider a heart transplant on little circumstances. And I guess one last thing I will go ahead and see here is that because people that have myocarditis tend to get like, because I mean, like I said, you get the you notice that both ventricles are like massively enlarged and diluted. Because the ventricles enlarge, that will kind of pull the mitral valve leaflets apart. So that can actually cause people that have myocarditis, you can actually get like the murmur of myotary regurgitation. Okay? Like mitral valve regurgitation. So again, that's just something you want to keep at the back of your mind for tests.

And again, these people tend to again, just pretty significant symptoms like it's, I've seen some patients with myocarditis and it's pretty dramatic. You can see people from that they were like completely healthy, completely normal, like two weeks ago. And then they are like in the ICU, like almost on their deathbed pretty much. So myocarditis is something you never wish, you never wish on anyone. It's actually a pretty, pretty bad thing to have. Now, what did they give you a question about a patient, you know, that has like, I don't know, let's say they had like a myocardial infarction like three weeks ago, right? And over the last like, you know, like two, three days, they've been having like pretty significant chest pain, right? And then they tell you that this chest pain is worse when they lie back and it's better when they lean forward, right? And then they tell you that as the patient is taking a deep breath, you'll hear like almost like a three-phase scratchy sound, right? A three-phase scratchy sound. So they may say that, oh, you're hearing the sound insistently, you're hearing the sound at the beginning of the astaly and at the end of the astaly, right? And then they may even give you an EKG and you'll notice that there is ST elevations everywhere in the EKG or PR segment depressions everywhere in the EKG. With all this information I've given you, what do you think the likely diagnosis is? This is paracarditis, right?

And given the patient's history of a recent MI, right? And they tell you that it's like three weeks later, what are you thinking about? Well, I hope you're thinking about dressler syndrome, okay? Dressler syndrome. Remember, dressler syndrome is an autoimmune style paracarditis that tends to arise weeks after an MI versus the favorite of paracarditis that can arise days after an MI. So what is paracarditis, right? Paracarditis basically is where you inflame the paracardium, right? You have like inflammation of the paracardium and the thing is there are many things that can cause it. Most times we actually don't know, like the most common cause of paracarditis is we don't know, okay? But there are some other things and they will likely not give you the we don't know one on exams. Well, there's some classical, like high-value areas that your friends at the NVME kind of love to hit on tests, right? So the thing is there are certain bugs that can cause a paracarditis, right? Like mostly again viruses, viruses, viruses, viruses, they love to cause paracarditis. If a person has lupus, lupus has, in fact, paracarditis is one of the most common complications of lupus, believe it or not. If a person has rheumatic fever, right? Rheumatic fever can actually cause a paracarditis. If a person has chronic kidney disease and they have like body urinia, that can also cause paracarditis.

If a person has, again, like a recent MI or recent cardiac surgery, though although the paracarditis after a recent cardiac surgery is called like post paracardialidamine syndrome, but after a person has an MI again, they can have problems like a few days after the MI. That's like the Faberinal paracarditis or they can have issues like a few weeks after the MI. That's the autoimmune paracarditis known as Dressler syndrome. Again, it's not as Dressler syndrome. So if a person even gets like, you know, like meds, like you know, like cancers in the area like breast cancer, lock cancer, like leukemia, lymphomas, those can make a test the size to the paracardium and that can cause again a nasty, nasty, nasty paracardial effusion. In fact, if a person is beginning to have a paracardial effusion from like a metastatic malignancy, those people's rate of death within the next few like weeks to months is extremely high, it's extremely high. And then you're if again, like I've talked about the chronic kidney disease case, but one other thing that the MBM actually, MBM actually lives, likes that can cause a paracarditis, is people that have things like these like connectivity issues, diseases like lupus, like scleroderma, those things can all cause a paracarditis, right?

And again, the classic presentation is would be a person, you know, that has fever, you know, it would be like a mild fever, they'll have like the heart rate will be up, they'll have like, you know, like a tachycardia, and the chest will be positional, right? And so they'll have like the chest pain that you know, better when they lean forward, kind of worse in when they lie back because the precardium is closest to the chest wall on that those circumstances, right? And then classically, right, when you oscultate the chest, you hear like the paracardial friction rope, right? But the thing is the MBM exam, the, the friends at the MBM, they recognize that if they put the term paracardial friction rope, every human being will get the question right, right? So they don't, obviously don't do that anymore. These days, they'll see that, oh, you hear like a scratchy sound, what you can see that you hear three-faced sound like a systolic sound, early dust, lyridastolic and lidastolic sound on oscultation of the chest. If you see that, think about paracarditis and the thing is typically for person as paracarditis, right? If you get an EKG, you'll see like almost like global ST segment elevation and global PR segment depression. If the person has a paracardial effusion, they can actually have like a low voltage EKG, right?

Because that paracardial effusion kind of like, you know, serve is almost like a barrier between like transmitting the electrical activity of the heart to the EKG to the EKG leads, right? And when a person has paracarditis, right? Like the, what's it's an only to just mention? Come on, do I think. They may actually have almost like a cardiac tamponat stile presentation, right? They can have a cardiac tamponat stile presentation. Obviously, under those circumstances, you wouldn't, you know, maybe consider doing like a paracardial synthesis to relieve the pressures around those people's or paracardium. At least around the heart, right? That's like that fluid that's in the paracardium. And again, in terms of diagnostic testing, again, you get an EKG. If you really have to pick a diagnostic test on the USMLA exams, consider getting an echocardiogram for paracarditis. And you're really, for the most part, the reason you get the echocardiogram is to see if they have any fluid around the heart that may be hemodynamically significant. Now, with paracarditis, right? So how do we treat it? In general, your first line treatment for paracarditis is an end-set. For whatever reason, your friends at the end of the end of the like endomethocin on exams, if an end-set is not an answer choice, you can presume that steroid steroids are second line for the treatment of paracarditis. And then third line, we have a cochisin. Cochisin is a third line agent for the management of paracarditis.

And the reason that, because they make you know question about you, like, hmm, this person has paracarditis, why are they so hypotensive? The thing is, if a paracardial diffusion develops in the center of paracarditis, then that can essentially squish the heart, especially the right side of the heart. Because remember, the right side of the heart is more built for tolerance in like elevated pressures very well. So the thing that can happen is that if they build up so much fluid that they have like a cardiac tamponat, stalf situation, remember, cardiac tamponat has like the classic thread of like, of a hypotension, muffled heart sounds, and juggler Venus' distinction, right? So again, if that fluid encases the heart, it will squish the right heart real well, right? And when the heart, right heart is squished real well. Well, guess what? What provides blood that ultimately goes to the left side of the heart, the right side of the heart, right? So if an outblood is not making its way to the left side of the heart, the vision will become hypotensive. That's why. Second thing is, you'll also begin to observe this thing known as pauses paradoxes. Posaus paradoxes is essentially like a drop in systolic blood pressure by more than 10 millimeters of mercury with inspiration. The thing is, normally when you inspire, right? That lowers your intra-thoracic pressures, your Venus return increases, more blood goes to the right side of the heart.

And the thing is that right side of the heart, you know, like, especially the right ventricle because of that extra blood. So I'm describing the normal circumstance now because of that extra blood, you know, you kind of have like increased pressures in the right ventricle. That sort of like bulges the interventricular septum into the left ventricle, right? So the cardiac output for the left ventricle transiently decreases. So this is stably blood pressure, uh, translately decreases under those circumstances. So, um, that's the normal situation, but usually this is stably blood pressure with inspiration. It does not decrease by more than 10 millimeters of mercury. But if you have fluid around the heart, for example, in the setting of pericarditis, that's complicated by a pericardial effusion, then when blood gets into the right ventricle, the pressure is in the right ventricle a lot higher because you're not just having pressure from that blood that is in the right ventricle. That's already diminished, but you also have impressions from the fluid that's squishing the right ventricle. So that bulge, when the left ventricle, uh, when the right ventricle is like, you know, contracting or whatever, that bulge into the interventricular septum is exaggerated because there's not many places for the right ventricle pressure to dissipate to, right? Because again, there's all this fluid surrounding the heart that's squishing the heart.

So you have like a more pronounced bulge of the interventricular septum into the left ventricle. So you have a pronounced, a more pronounced decrease in systolic blood pressure because the left ventricle is not ejecting as much, right? And under those circumstances, you have a greater than 10 millimeter of mercury decrease or decrement in the patient's systolic blood pressure. That's what's known as pulses peradoxes, okay? It's just an exaggeration of normal physiology because you have fluid that's surrounding the heart that's especially compressing the right ventricle. Again, you may see divine, you're spending so much time on this stuff. Cardiology is just one of those like sciences that if you don't get down now, you're just going to keep paying for it in the future. You're going to pay for it on step one, you're going to pay for it in your third year, you're going to pay for it on step two, you're going to pay for it as an intern or a medicine resident or whatever, and then you're going to pay for it on your, like your board exams in the future and on step three, right? So just one of those things you don't want to neglect because you're literally going to save a patient's life if you understand cardiology. So that's why I tend to take my time with this cardiology podcast because again, I'd rather put out a good product than because I'm trying to hurry, I put out a garbage, right?

So at least that's the kind of promise I've made to myself that I will try to try to never do. So what are some things that can happen with with a pericarditis, right? Obviously, like you can build up fluid, you can go to like cardiac tamponat, but the thing is if pericarditis, if a person has like many recurrent episodes of pericarditis, one thing that can happen is you can actually have something called a constrictive pericarditis where all this inflammation around the pericardium is then accompanied by like the formation of scar tissue and then you can also have like almost like dystrophic calcification within that scar tissue. In fact, if you ever get a question about a patient and they show you like an image, they love like these pericarditis like associated images. If you get like a chest extra of a patient or you get like a chest extra of a patient and you see like white that's outlining the person's heart. Essentially, you can pretty much stop reading the question and pick the answer choice that says constrictive pericarditis, okay? You pick the answer choice that says constrictive pericarditis. If you see that, again, I promise you almost 100% of the time on NV Me exams, it's constrictive pericarditis. And the thing we constrictive pericarditis, right? Again, like most of the causes of acute pericarditis tend to cause constrictive pericarditis.

But the thing is, if they're giving you like a question about like an immigrant or whatever that has constrictive pericarditis, think about TB. TB is actually the most common cause of constrictive pericarditis in the whole world, okay? But again, most other like, like I'll say like in the US, for example, one pretty common cause of constrictive pericarditis is if a patient has like like you know like open heart surgery or they have like radiation to the chest for like breast cancer or something constrictive pericarditis can be like a sequelae from that after like the radiation therapy. And remember again, radiation therapy to like the chest to the head and neck is the biggest risk factor for thyroid cancer, especially popularity thyroid cancer. And the thing is when people have constrictive pericarditis, classically on physical exam, they will have like one of two things, right? They can have something called a pericardial knock, right? Because again, essentially the person's you know, left ventricle is kind of like hitting the thick end up pridle or pericardium, right? Those are that's one classic physical exam finding. And the classic physical exam finding in constrictive pericarditis is something known as Kusmaus sign, right? Because remember, if a person has constrictive pericarditis, then the left ventricle, I mean the ventricle is in general, just do not have a place to bulge into, right?

So because the left ventricle is having trouble receiving blood in the form of venous return, right? The person essentially has a dastolic dysfunction, okay? The patient essentially has a dastolic dysfunction. So the thing is in some cases when you're trying to like, especially like when you inspire, or I remember when you inspire, when the thoracic pressures go down, if those pressures go down, venous return would increase, okay? Venous return would increase. And if that venous return increases, okay? If that venous return increases, and you're trying to get that venous return to a right ventricle that has that dastolic dysfunction, as you inspire, you may actually have like reflux of blood back into like the SVC or the juggler veins. And that distension of the juggler veins with inspiration is what is known as Kusmaus sign because normally, when you inspire, you're almost creating like this like negative pressure effect and you suck blood into the right side of the heart. So the juggler veins usually collapse on inspiration. What if they descend on inspiration? That tells you that you're having reflux of blood right back from the right side of the heart to like the SVC and the juggler veins. And on those circumstances, you want to think about Kusmaus sign. That is a very specific finding for constructive pericarditis on MBME exams, on MBME exams. Again, all high-year things, you want to keep at the back of your mind for tests.

And then again, like again cardiac tamponad, again, the remember, you obviously want to do like a pericardial synthesis for that. Classically on imaging, you mean, sure you like a water bottle shaped heart on imaging, that's like the classic presentation. And again, if a pressure has cardiac tamponad, they may also have this thing called like electrical alternation, sony kiji. We have like very inamplitudes of the QRS complex. And if a pressure has constructive pericarditis, really, the thing you're going to do is you're going to get rid of the pericardium, you do something called a pericardial rectum on MBME exams. Okay. So I think those are all the high-year things I think I want to say about pericarditis. Again, I know it's, I know it may look like a main detail then I really try hard to keep this podcast on there an hour. But the thing is cardiology is just detailed and it's just higher. These are all of those things again, like I said, if you don't understand, you're going to regret for the foreseeable future if you're doing anything in medicine, even pathology. Probably pathology, I really need to understand the cardiology more than the regular like internal medicine or physician, for example. Okay. So I think those are all the things I'm just trying to run through my memory bank. Is Daniel the big thing I've not mentioned about pericarditis? And pericardial effusions and culturally pericarditis? Hmm.

I mean, there's some things with like the juggle of inauspulse, but I think those are more appropriate for, the more appropriate for another podcast. So I'll talk about those different podcasts. So I don't know the well, whoever is listening to this podcast. Now, I think maybe where I would end here is, let me just, you know, maybe go ahead and talk about the different cardiomyopathies, right? The different cardiomyopathies. So the thing is, the different cardiomyopathies are very high-youtu understand, to know actually, for exams, right? And there's three of them, right? There's like restrictive cardiomyopathy, there is hypertrophic cardiomyopathy, and then there is diethic cardiomyopathy, right? And though, like, remember that these are HD nomonic to help you remember from the least common to the most common. Restrictive cardiomyopathy is the most restricted. It's the most, is the least common kind of cardiomyopathy. Dylated cardiomyopathy is the most common kind of cardiomyopathy. So, you know, let's talk about the least common one first. So the thing is, restrictive cardiomyopathy, whenever you see it on exams, the big thing you want to think about is anything that can cause infiltrative disease in the heart, okay? Infiltrative disease in the heart. So like people that have like amyloidosis, right? In fact, amyloidosis, this is very high-youtu. Amyloidosis is the most common cause, very high-youtu. It's the most common cause of restrictive cardiomyopathy in the US, okay?

So amyloidosis, if a person has like some kind of fibrosis of the pericardium, if a person has like sarcoidosis, or a person has like, even like, like for example, if a person has like pumpase disease, remember, pumpase disease is glycogen storage disease type 2, okay? People that have pumpase disease, right? It's usually die of heart failure. The heart failure almost always arises from the dastolic dysfunction accompanying restrictive cardiomyopathy. The infiltrate is all that glycogen that is just staying hanging around in the lysosome because the lack of acid moltase to break down that glycogen, remember? Pumpase disease is called a glycogen storage disease, but if you really dig deep into pathophysiology, it's actually like a lysosomal storage disease in this guy, okay? It's a deficiency of the enzyme known as acid moltase. I believe sometimes that's known as alpha-1-4 glucose studies on amyloid exams, right? So people that have pumpase disease and die of heart failure, the die of a restrictive cardiomyopathy. People that have like the HFG mutation like hairadetry or macromatosis, they also tend to get restrictive cardiomyopathy, although remember that people that have hemochromatosis can also get a dilated cardiomyopathy. Hemochromatosis is one of those weird unusual causes of both a restrictive and a dilated cardiomyopathy. And then if a person has again like sluriderma, that can also cause a restrictive cardiomyopathy.

Now, why do people get symptoms in a restrictive cardiomyopathy? The reason they get symptoms is essentially they have like that stoic dysfunction, because all the stuff that's infiltrating the heart, right? Essentially makes the leventricular compliance just go down pretty much. And if the leventricular is not very compliance, then the person is going to get that stoic dysfunction, right? And again, classically, right, you make the diagnosis by doing like an echocardiogram, some people do like a cardiac like MRI, although that's kind of like an advanced, advanced imaging tool there. But yes, you can do like an echocardiogram and then you can do something called like an endomaiocardiobyopsy to figure out the exact cause. Sometimes people can even do like a cardiac catheterization to try to figure out what's going on because there's like some weird pressure-bredient things that cardiologists can actually measure in people that have restrictive cardiomyopathy. And classically on EKG, right? So if you remember, a few minutes ago, I said that a low voltage EKG is something we find in a person that has like a paracadelofusion or cardiac tamponat.

Well, another high-eofin on MBMA exams that can cause a low voltage EKG is restrictive cardiomyopathy because again, you essentially have these infiltrates within the heart and those infiltrates within the heart kind of screws you over, kind of screws you over and you get that low voltage EKG because again, you have like contractile elements in the heart and then you also have a contractile element in the heart. Okay? So that's like the big thing on restrictive cardiomyopathy. And one trick, I guess, I kind of give people that sort of helps them remember, remember it pretty well is just remember the term like roses. So the word like rose, right? Like R, that's restrictive and then Osses. The thing is most things that cause restrictive cardiomyopathy on MBMA exams, the ending Osses for some reason. Hemochromatosis, sarcoidosis, amyloidosis, right? So those are all things that can cause a restrictive cardiomyopathy. And really there's no big treatment, I mean, ultimately these people are going to degenerate and die if you don't get, if they don't get a heart transplant, that's just pretty, that's pretty much it. Again, I know it kind of sounds a color on my end, but yeah, there's just really no treatment, unfortunately for restrictive cardiomyopathy. Although there are some new fungled treatments that are coming out that may improve survival in maybe like in a few years, but again, it's not something I'm going to see on the end.

Those will probably not make their way to like first day for like a couple of years. So just go ahead and throw that out there, because I'm certainly aware of some treatments that are coming down the pike that may actually help on that these circumstances. I mean, like obviously for pressing has like restrictive cardiomyopathy from like an on the like a cause you know, you know, usually you're going to treat if you something don't treat you treat, right? So see for example, the person has like hemochromatosis that's causing a restrictive cardiomyopathy. Obviously you're going to do for the bottom of me too. You know, hopefully help those people with the with the hemochromatosis, but again, most cases of restrictive cardiomyopathy, nothing you can do. The patient's going to need a transplant at some point at some point in their lives, unfortunately. Now, so I've talked about the R and again, that R nomonic like oh like restrictive cardiomyopathy like the causes all ending osis, that rule also kind of works for like restrictive long diseases, right? Most causes of restrictive long disease, believe it or not, they all end in they all end in osis, pulmonary fibrosis, this osis, sacoidosis, asbestosis, pneumoconiosis, right? Those things all cause restrictive long disease. So now let's talk about HCM, right?

So like I've heard from a cardiomyopathy, this one, the presentation already, if you get it wrong, on an exam, I'll try to take the exam, you know, go home and you know, kind of cry somewhere in the corner, it's a pretty classic presentation, pretty easy, right? It'll be a lot of things that, you know, that collapses during a game or something like that, right? Or collapses while they are working out, like a young person, right? I mean, this is literally the most common cause, very high illness, the most common cause of death in a, like, sudden death in a young athlete. And really, for the most part, what are some key things you want to know about hypertrophy cardiomyopathy? You want to know that it's in herithane and an orzomo dominant fashion, okay? And there are some classic proteins that tend to be mutated, right? So things like, mayorsine binding protein C, right? Or like the beta-mayorsine heavy chain? Those are the two classic proteins on NBME exams that I'm mutated in people that have thylitheta cardiomyopathy, right? And I mean, if they are asking about chromosomes, you know, like chromosome 11, like most of those gene mutations are like on chromosome 11, that give rise to a hypertrophic cardiomyopathy. Sometimes even, even, even, instead of even asking about those specific proteins I just mentioned, sometimes your friends at the NBME, they may just say that, oh, you know, this person has, like, what's the underlying path of physiology?

And the answer may be like, to choose something that says that they have a mutation in, like, saccomere proteins, okay? That's another thing you may also see on an NBME exam. And what are some classic things that happen that happen in people that have a hypertrophic cardiomyopathy? Well, some classic things that happen are things like, they may tell you that people that have HCM, I'm not going to keep seeing hypertrophic cardiomyopathy because I want to try to keep this short. But basically, those people tend to have like asymmetric hypertrophy of the intraventricular septum, okay? Asymmetric hypertrophy of the intraventricular septum. So you may see, hmm, the fun. Why do I care about that? Well, here's why you care. The reason why you care is for another boss freeze that I want to talk about. And it's this whole concept of SAM, okay? Not like Uncle SAM that, uh, uh, ticstax is every year, but more like SAM, standing for systolic anterior motion, uh, like systolic motion, like systolic motion of the anterior mitral valve leaflet. That's what SAM stands for, right?

So the thing that happens with SAM is that when you, when the left thing, when the person that, in the person that has HCM and you have like asymmetric hypertrophy of the intraventricular septum, during the process of systolic, the anterior mitral valve leaflet moves close to the intraventricular septum and it kind of causes like a very nasty obstruction, almost like, essentially like a legit left intraventricular flow track obstruction just below the aortic valve, right? So the people will have like almost very similar, like, almost like aortic stenosis, uh, like almost like, uh, same symptoms as a person that has aortic stenosis. That's the classic, uh, thing that happens that again tends to cause many of the symptoms in people that have, um, in people that have a hypertrophic cardiomyopathy, right? So, for example, they may give you an MDM exam question and describe a person that, oh, like this person is like in their 20s or like their late teens and they have like a systolic ejection murmur. Resist the temptation to pick aortic stenosis as your answer, okay? Resist the temptation to pick aortic stenosis as your answer, um, uh, because aortic stenosis on MDM exams is highly unlikely to show up in a person that young, okay? If you see an aortic stenosis like presentation in a person that is super young, like, you know, early 20s or late teens, the thing I really want you to think about is hypertrophic cardiomyopathy.

And actually, there's some key differences between the murmur of aortic stenosis and hypertrophic cardiomyopathy, that your friends at the MDM kind of expect you to know. Uh, so, uh, aortic stenosis, again, it's a systolic ejection murmur, same thing with HCM, right? But the thing is aortic stenosis, the murmur is heard best at the right of personal border, right? So like circling to a coastal space on the, like, on the right to the right of the sternum, it's not so with, um, with, uh, HCM, HCM, the murmur is actually heard best at the left sternum border, the left lower sternum border, okay? But the thing is sometimes your friends at the MDM for whatever reason, they may refer to the left lower sternum border as the left sternum border, okay? So those are all high yield things you want to keep at the back of your mind, for exams. And then, in aortic stenosis, people tend to have something called pauses, provis, eternus, right? So they will have like a delayed upstroke of the cruddy pulse, right? The thing is you don't, you don't actually do not observe that in people that have HCM. In HCM, you actually have something called like a bifid cruddy pulse. So you have like a small cruddy pulse and then you have a bigger pulse that follows up afterwards. Uh, shh, almost, almost at 55 minutes, yeah, I'm sorry, but it will take a while to explain the pathophys there. Maybe I'll talk about it in maybe like the full up or cardio podcast. Um, well, let's keep going, right?

And then the final thing is that the murmur of aortic stenosis tends to read it to the cruddy, okay? The murmur of hypertrophic cardiomyopathy does not read it to the cruddy, okay? That's again another high yield thing you want to keep at the back of your mind. And actually one thing that just dropped in my mind is, um, remember that if a person has aortic stenosis, right? Anything that increases prelude, right? Is going to actually make the murmur sound, um, louder, right? Because think about it, right? So let's say, you know, let's say you go from a standing to a supine position, right? So that will like get more blood from your legs to your heart, right? So that will increase your nose return. So that will like increase like the end-astolic volume, right? Or if a person is on, um, uh, if a person is, you know, like taking like a beta blocker, right? Or if a person is like, you know, like squat in or like they have like like a phospho handshake, those things all, um, um, maybe actually let me remove the phospho handshake thing. But if you squat or if you lie back or if you take like a beta blocker, right? Those things will all increase prelude because again, if you take a beta blocker, right? Your heart will slow down. If your heart slows down, you spend more time in the astaly, right? So your end-astole volume will be big, right? If you put more blood in the left ventricle, there'll be more blood to flow across the stenotic eotic valve, right?

So now make the murmur sound louder. Not so with hypertrophic cardiomyopathy. When a person has HCM, anything that puts more blood in the left ventricle, luckily make the murmur sound softer, okay? Because the reasoning behind that is when you have more blood in the left ventricle, that prevents that anterior mitral valve leaflet from contacting the asymmetrically hypertrophied interventricular septum during the process of systole, okay? So that's one actually, again, pretty high-o thing. You want to keep at the back of your mind with with ambinexept, right? So basically anything that ups your prelude will make the murmur of aelix anosis worse, anything that ups your prelude, I mean sound louder, right? Anything that ups your prelude will make the murmur of HCM actually sound softer, okay? And again, people, these people that have HCM, right? They tend to again, just kind of like young athlete passes out on the field and maybe dies instantly or whatever. I mean, they say like, why do these people die instantly? Well, they die for many reasons, right? Like, they have symptoms first and foremost because they have a gastolic dysfunction, right? They have a gastolic dysfunction. The, the, the hypertrophic, hypertrophied, not hypertrophic, that's wrong English. The hypertrophied left ventricle, right? Doesn't feel very well with blood, that's one. Two is that dynamic leventricleoflotract obstruction that happens below the euric valve.

Again, can essentially like, cordon or your cardiac output and if that happens, guess what? You have almost like signs and symptoms of like aelix stenosis, right? Like, you have aelix stenosis like symptoms. Like the person will have like, what is it called? Like, they'll have, come on, divine thing, they'll have like syncopy, they'll have like angina, right? But the thing that tends to like kill them, you know, pretty quickly, is that what is it called? Like, like really nasty ventricular rhythms, right? Because the thing is in that interventricular septum, right? Like they have like this like myocardial dyserate. In fact, keep that buzzword at the back of your mind, right? Like they'll say like, what would you expect on histology in a pre-patient with a hypertrophic cardiomyopathy? You'll actually find like, dyserade myocardial fibers. They're like kind of all over the place on histology. Those dyserade myocardial fibers, they can actually cause like some weird conduction defects, right? And the person can get like, v-thable, v-tack and die, okay? That is why in general when a person is, a person has a, a, a, a, HCM. The classic treatment is the hotel, you know, just stop strain on sex or size. So if you're an athlete, you know, stop athleticing pretty much. And then any drug that can tank your pre-load is bad, right? Any drug that can tank your pre-load, right? So like taking like a diuretic, for example, right?

Or taking like a, like a nitrate, like nitro per side, it's not a great idea for those people because that will cause venodilation, that will decrease pre-load. That will bring, if you have decreased pre-load, your endastonic volume will decrease. And that will bring that anterior valve, I mean, sorry, anteriorly fled of the mitral valve close to the asymmetrically hypertrophied interventricular septum. And that can worsen the living, tricholau flow tract obstruction. So in general, you give these people beta blockers because again, beta blockers, they will slow the heart down. If you slow the heart down, you'll have more time to fill, right? You'll spend more time in dastily. So the heart will feel, like, will fill with more blood, okay? And again, now prevent that dynamic LVOT that I just described a few moments ago, right? And then again, if these people are having like these nasty like V5, V attack arrhythmias, which again tends to cause like their death, you can, you know, put like an ICD in place, you can put like a defibrillator in your heart. And one of the usual thing that is tested more commonly on step two, what occasionally me pop up on step one is if you actually have a first degree relative with HCM, they do need to be like, let's say, let's say like, they give you a question about a patient with HCM. Every first degree relative has to be screened with an echocardiogram because again, remember, it's autosomodominant inheritance, okay?

So again, just one of those weird high yield things you want to give out the back of your mind, same thing with like the MEN syndrome for like MEN2 A and 2 B, you do need to, it's an autosomodominant disease, you do need to screen first degree family members for the same disease. And I mean like, yeah, HCM like some people do like alcohol ablations and all that stuff, but they probably won't go there on MBM exams. But again, I promise you, you need to know as much as possible. Like, if this is probably one of the most commonly tested concepts on the USML exams, hypertrophic cardiomyopathy. And the presentation is very similar every time, but the thing is, the reason the MEN2 A lost the test is it's a topic that they can literally make like 30 or 40 different questions from like literally, I can write like 30 different HCM questions from like many different dimensions, okay? So again, these are all things you want to keep on the back of your mind. Remember again, use beta blockers for treatment, don't give these people like diuretic or whatever because the reason I keep harping on this, don't give these people diuretic is people that have HCM, they can have like heart failure symptoms and your first temptation will be too. Let's give this person a diuretic to get rid of the volume. No, don't do that, right? Diuretic, even positive I know tropes, right? So drugs like dejuoxin or drugs like like myrenone for example, they're not ideal for people that have HCM, okay?

Because again, if you contract the heart a lot, that would decrease the endastolic volume and if you decrease the endastolic volume, again, that would worsen that dynamic level of ventricular outflow tract obstruction that is below the diuretic valve as I've described again multiple times already. Now, the last type of the last type of cardiomyopathy I guess I'll talk about is a diluted cardiomyopathy. Again, there are many things that can cause diluted cardiomyopathy. Basically, let me make this easy for you. If you remember many of the things I talked about as causes of myocarditis, those things can all cause diluted cardiomyopathy. If you remember, when I was talking about myocarditis, I kept harping on diluted cardiomyopathy, right? But some other things I guess I did not necessarily mention is things like alcohol, right? So people that have alcoholism, right? Remember alcohol would deplete your vitamin B when you're thiamine, or population, right? So that can cause a lot of problems, right? That can cause like a wernicic or socoph, right? Because again, of the thiamine, deficiency, and remember, if you have a thiamine deficiency, right? Guess what? Your pyruvy hydrogenous complex is not going to work anymore. And your citric acid cycle, your TCA cycle, also is not going to work anymore. So if those cycles are not working, guess what you're not making? You're not making ETP, and that can begin to cause problems with your myocardial.

That is actually the mechanism behind wet berry berry, okay? That is how people with just chronic alcoholism can develop a wet berry berry. Wet berry is essentially diluted cardiomyopathy in a chronic alcoholic. So again, all high-y things you want to keep at the back of your mind. I've talked about many drugs, and sometimes they may give you, although this is more prevalent on step 2ck, they give you a question about a patient that has, you know, that is like postpartum, right? Remember women that are postpartum, they actually can also get like cardiomyopathies because pregnancy is like a state of um, if I open this kind of warmth, I feel like I'll have to, okay, whoever is listening to the just podcast, I apologize. I know this is 63 minutes already, but there is just like so many good MBME ideas that are just dropping in my brain as I'm giving the podcast. So my apologies, right? But let me maybe talk about some quick pathophys here. I was going to extend this a little. Okay, so the thing is pregnancy, right? The way the body adapts to pregnancy is that it increases blood volume by like 50%, okay? It increases blood volume by like 50%, right? So like a pregnant woman may have a total blood volume of almost eight liters while she's pregnant. Let me see, hmm, why does the body do that? Well, here's the thing. The reason the body does that is because the body knows that in the presence of delivering a baby, right?

I mean, if you've ever done a no-be-gyner rotation, you know that essentially when a woman is delivering a baby, at least some of the deliveries I have seen, I mean, I thankfully got in a chance to catch the catch babies during at least one very mobile guy rotation at med school. The thing that can happen is you know, blood everywhere, right? A lot of blood, a lot of blood, a lot of blood, right? So the thing is the body tries to prepare for that blood loss during the process of delivery, but just open the person's blood volume, okay? So the thing is pregnancy. It's like you're living in a like a nine month state of volume overload, okay? Because and then this is me essentially taking a sidebar here, right? I'm taking a sidebar because I want to maybe integrate another concept that is actually fairly common on the USMLA exams, right? The thing is when we're exposed to chronic volume overload, that actually causes some changes in the wall stress of the myocardium and those changes in wall stress activate certain mechanoreceptors and those mechanoreceptors are tied to certain patterns of gene expression, okay? Those mechanoreceptors are tied to certain patterns of gene expression. So the thing is when you kind of like alter the gene expression in those myocardium, you can begin to like lay down like you can see, oh, how do I deal with this increased stress? Well, you can decide to start laying down like new succomere, right?

And the thing is you can lay down new succomere in different ways. In some cases, you can lay down new succomere in series, which is what happens when a person is exposed to chronic volume overload, like what happens in pregnancy, right? So that can actually cause like a diluted cardiomyopathy because the thing is when your heart is exposed to like just chronic increases in volume, right? So like in a person that has like eotic regurg or a person that is pregnant, right? That can dilute the ventricles and when that dilutes the ventricle, I mean that can cause stress on the ventricle and that stress again, like I said, it will alter gene expression and the person will begin to lay down a succomere in series. When you lay down succomere in series, you are essentially like not making the cardiac succomere interlock appropriately, right? So that ultimately cause something called a systolic dysfunction, okay? That will cause a systolic dysfunction. You may see some people refer to this as heiferif or heart failure with reduced ejection fraction, right? So this is what happens when you have chronic volume overload, right? And remember that volume overload tends to be associated with an S3, not S4, S3 hurts out, okay? Contrast this.

So anything that puts more volume in the ventricle like pregnancy or eotic regurgitation, that can cause a, that can cause a, you know, again a volume overload that will cause a diluted cardiomyopathy, which again is one of the reasons why women that are parry-partum. So there's this thing called a parry-partum cardiomyopathy. It's a kind of diluted cardiomyopathy that happens either just before you deliver a child up to like six months after that child has been delivered. So again, those are all big, again, high yield things, again, I know it's kind of annoying, but those are all high yield things to understand for in baby exams. Well, since I talked about volume overload, I think it probably behooves me to talk about pressure overload, okay? Pressure overload. So the thing is, when a person is exposed to chronically elevated pressures, right? So say for example, a person has like eotic stenosis. Remember, eotic stenosis does not, like, put, it doesn't put more blood in the left ventricle. It just means the left ventricle will have to work harder to get blood out, right? That's a different kind of overload. That's not a volume overload. That's a pressure overload, okay? And when people have pressure, like a pressure overload situation, that again will alter certain, like, stress, like, wall stress factors in the myocardium. And that will again alter gene expression, and these people begin to lay down new sacrameres.

But on like the volume overload situation, where you lay down new sacrameres in series, in the pressure overload situation, you lay down new sacrameres in parallel, right? Because think about it. This actually makes perfect sense, if you really think about it. The thing is, when a person is chronically exposed to lots and lots and lots of volume, it would make sense that you'll want to physically increase the cavity size of the left ventricle to be able to handle that increased volume, right? So that's why a diluted cardiomyopathy tends to come after chronic exposure to volume overload, right? But contrast is with pressure overload. When you know that you have a stenotic lesion in front of the left ventricle, like eiotics stenosis, for example, then you know that, oh, I'm not necessarily trying to deal with higher volumes. I just need to push with a greater amount of force to get this blood through the stenotic eiotic valve. Well, the way you can exert more force is to just become more muscular, right? I mean, think about it. If you go to the gym and pump iron for days and days and days on end, you should be able to lift heavier and heavier weights over time. That is essentially what happens to the heart when it is subjected to chronically increased after load, for example, in the setting of hypertension or in the setting of eiotics stenosis, right? So to generate those extra pressures, you alter your gene expression and begin to lay down new sacrameres in parallel.

The problem is when you lay down new sacrameres in parallel, your left ventricle becomes big and buff, but that also takes away some of the cavity size. It's like you are trading the ability to handle more volume for the ability to generate greater force, okay? So because you are able to generate greater force, the cavity size of the left ventricle decreases and that causes a dastolic dysfunction, okay? That causes a dastolic dysfunction. That is something you may classically see referred to as hip-pif or heart failure with preserved ejection fraction. And hip-pif tends to be associated with an S4 heart sound, not the S3 heart sound that is characteristic of volume overload and dilated cardiomyopathy. So I really, really, really hope the stuff makes sense. This is an I just described. I promise you, it's floridly high-youtu-no for all the USMLA exams. And if you're going into internal medicine in the future, the loved attendance loves to pimps students on this stuff and they love to pimps students on this stuff as well. Like med students, residents, they love to pim them on this. And then this stuff shows up quite commonly on the medicine like intruding exam and the medicine board exams. Again, I know this because I put a lot of internal medicine on residents. So again, high-youthings want to keep on the back of your mind. So now that I've gone off of this sidebar, let me go back to my dilated cardiomyopathy and hopefully I get to the end of this podcast. Whoops.

So again, I really feel about for reference listening to this. Sorry. I know this has gone on for much longer than I plan to go with. But this is a very, very high-youted podcast. And it's something I'm really hoping will serve you very well as you're preparing for your USMLA exams. So again, dilated cardiomyopathy, I've kind of said many of the big things about it. People that have like, you know, like acromegaly or like gigantism, right? The most common cause of death in those people is cardiovascular disease. You almost always die from, again, dilated cardiomyopathy. So again, it kind of presents, again, classic signs and symptoms of, like almost like a myocarditis, like presentation, right? And you make the diagnosis when an echocardiogram, these people will have like systolic dysfunction. The ejection fractions will all be down. It will usually be less than like 40% on an MDMA exam. And I mean, the treatment is, you just give them like heart failure treatment, like you give them like the beta blockers and ACE inhibitors and the outdo sooner receptor antagonists. But again, if those don't work, then you need to consider a heart transplant for these people pretty much. So I think I'm going to go ahead and pause here. I mean, there's one more topic I wanted to talk about to kind of like round this out so that I know that I know that I am done. Okay, let me just talk about this last topic. You'll probably take like two minutes and then I'm done here.

But basically, right, what if they give you a question about a patient that, you know, has like hypopigmented macules on the skin? And then they tell you that this patient has like, you know, like he's having like heart failure, stout symptoms, like, you know, like a US-3 heart sound or whatever. And then they tell you that they perform an echocardiogram and then they see like a mass in the heart. What are you thinking about? I hope you're thinking about like a rabdom ayuma, right? Essentially, the thing I'm telling you with the hypopigmented macules on the skin, I'm essentially making reference to tuberous sclerosis, right? So tuberous sclerosis. Remember, tuberous sclerosis, right? It tends to cause like again, like these ashy-leaf spots. And you know, these people tend to have like some weird like tumors, right? So they can have like hematomas in the brain, they call them those like tubers. They can actually have this a brain tumor known as SEGA, like sub-ependymal giant cell astrosyptoma, right? And then they can have like the renal angiomyolipomas, right? And then these people can also have like certain cardiac tumors known as rabdom ayomas. That's what I'm referring to in this Q-step. And then remember, another thing that's also common in kids with tuberous sclerosis is that they can get a seizure disorder known as a West syndrome. Sometimes it's known as infantal spasms.

And the thing is your friends on the MDM they kind of expect you to know the classic EEG finding with West syndrome. It's known as a hyp saratmia, okay? So that's just one of those annoying things you want to, you know, sort of lock in the back of your mind. And really this rabdom ayomer, it's a hematoma, like essentially what, like many of these things that happen in people with tuberous sclerosis deform hematomas in different parts of the body, right? So the cardiac rabdom ayoma, believe it or not, is actually a hematoma. And really, if you see like, you know, like you see like tumors and all that stuff around the heart, the thing you really do want to think about is a meds, right? So meds are more common than primary cardiac malignancies. So meds, because again, if you see a person, you know, they have like like a lung cancer or something. And then you see like another like tumor like in the heart, it's most likely a metastasis. And most times those tumors tend to be associated with like pericardial effusions, right? But if you're, you know, thinking about like primary cardiac tumors, one of the one you see on NBM exams, especially like a tumor like in the left atrium, I'm thinking about a mixoma, right? An atrial mixoma. Atrial mixoma for the most part, it's benign. Well, the reason that it's dangerous is that some parts of the tumor can flick off and then embolyze to the brain and cause a stroke, okay?

So the classic presentation on NBM exams, it will be a person that has, you know, has been having like, like, B-style symptoms, like weight loss or like a fever because actually the mixoma believe it or not can produce like interlooking one. So that can cause like a fever. It can produce like TNF alpha and cause like, you know, like B-style symptoms, right? But, um, it'll tell you, okay, this person is having like, you know, like, has, had like stroke-like episodes, has had like syncopal episodes. And then they tell you that on the quotation of the chest, you hear like, like a dastolic plop sound. So plop, PLOP, a dastolic plop sound at the apex. If you see that, you absolutely positively want to think about an atrial mixoma, right? The thing is, indastually, the thing can actually cause almost like signs and symptoms of like mitro stenosis, right? Because the tumor tends to be pedantulated. So it tends to move, like when blood is trying to fill the left ventricle. That's why it's classically described as a dastolic plop sound on a scutation. And obviously the way it should be is you, you know, you remove the tumor and you can make the diagnosis by doing a TEE. Again, remember, almost 90 percent. I think actually it's greater than 90 percent of atrial mixomas in the left atrium, right? So again, you want to be in a chamber that is smugged up against the left atrium like the esophagus. That is right.

A TEE, a trans esophageal echocardiogram is the diagnostic test of choice in figuring out that a person has an atrial mixoma. So they think I'm going to go ahead and stop here. As I do at the end of every podcast, I do have a one or one tutoring for a ton of exams, right? So step one, step two CK, step two CST, step three preclinical medical exams, 30-ishelf exams. I do this thing called longitudinal tutoring, where if you're like a first second or 30-ish student, I tutor you for like your block exams or your shelf exams, but at the same time I tutor you for like your upcoming US Emily exams. And again, the vast majority of people have done this with you've been like super, super successful on the US Emily exams. That's one thing. Next thing is I also offer that like these booster courses for the the US Emily exams. So like it's like 10 hours for step two CK, step three, and like the internal medicine like entering an exam with a lot of board exams, but it's 20 hours for step one because step one just has a crap ton of material. So basically this is something that's ideal for the end of a person's dedicated period where when they feel like you know the knowledge business is pretty good. And essentially the thing that happens is that in a Q&A format, I will put things together for you. And my Q&A will be like from an MBME context Q&A. I kind of put it like most of the higher concepts for you together in a very short time period.

Again, most people have done this with they've found out to be extremely helpful. You say, oh divine, this was like the big boost I needed at the very end of my dedicated period to score me, those extra points on my exam. And then I also do like one-on-one like advice scene, or I guess you can call it like coaching for like if you're like a medicine applying to residency so like an era's application, or a college student applying to a med school so an AMCA's application. I can help you with things like personal statements, rec letters, editing applications, mocking reviews. And then the final thing is if you're medicine resident, I have prepared for like the ABIM board exam or the internal medicine in training exam, or you're a college student and you're student for like Gen CAM, O-CAM, Physics, Bio CAM, Histology, Physiology, I'd offer tutoring for all those things. I mean you can probably tell from these podcasts that I really love tutoring. And again, as I said at the beginning, you can now find these podcasts on three podcast apps, Apple podcasts, Google podcasts like Google Play essentially, and then Spotify. I have all those on them. And as I add new podcasts, they'll be updated automatically on those apps. Although I will encourage you to also look at the website, you can actually download the podcast from there as well. And if I post slides for a given podcast, it will be on the website, not on these podcasts apps, unfortunately. So have a wonderful rest of your day.

Again, my apologies for this podcast, thinking essentially like an hour and 20 minutes, but this stuff is very high yield. And I feel like I covered a crap ton of topics. This is probably like maybe almost like, I will see I probably covered like 15% of the first day cardiology chapter in this one podcast. So I think you should find this to be useful. And again, remember that I have like three other podcasts in the series. And then in addition to that, I actually have like a cardio cardio farm podcast. So all the pharmacology you ever seen first like first date cardio, I've essentially covered all those in separate podcasts. Just again, go back, look on the website, you'll find those. So I will see you in the next podcast, have a wonderful rest of your day. God bless you. And I really do hope that the leakers bid the worst tonight. See you next time. Thank you.

The tricuspid valve.

Streptococcus viridans.

A diastolic "plop" sound at the apex.

Dilated Cardiomyopathy (DCM).

Kussmaul's sign.

Diuretics or vasodilators (e.g., nitrates).

1. Splinter hemorrhages (embolization); 2. Janeway lesions (painless, palms/soles); 3. Osler nodes (painful, finger pads).

Amyloidosis and Sarcoidosis (or Hemochromatosis, or Paget's disease).

AS murmur radiates to the right sternal border; HCM murmur is heard best at the left lower sternal border.

Trans-esophageal echocardiogram (TEE).

ROSES (R = Sarcoidosis, O = Amyloidosis, S = Sarcoidosis/Scleroderma, E = Hemochromatosis, S = Storage diseases).

Coxsackie B virus.

Rhabdomyoma (a tumor/hematoma).

1. Splinter hemorrhages (embolization); 2. Janeway lesions (painless, palms/soles); 3. Osler nodes (painful, finger pads).

Amyloidosis and Sarcoidosis (or Hemochromatosis, or Paget's disease).

AS murmur radiates to the right sternal border; HCM murmur is heard best at the left lower sternal border.

Trans-esophageal echocardiogram (TEE).

ROSES (R = Sarcoidosis, O = Amyloidosis, S = Sarcoidosis/Scleroderma, E = Hemochromatosis, S = Storage diseases).

Coxsackie B virus.

Rhabdomyoma (a tumor/hematoma).