DIP Episode 165 - Comprehensive USMLE Step 1 Cardiology Review 3

Okay, welcome. My name is Divine, I'm a resident. This is episode 165 of the Divine Intervention Podcast. And in this podcast I have episode 165. I'm going to be talking about a cardiology for the US Mly Step 1 exam. Although to be honest, if you're struggling with cardiology for the Step 2 CK exam, this will not be a bad podcast to listen to. But basically this is going to be a cardiology review and this is going to be part three. This is a continuation of episode 154 which is part two. So let's go ahead and jump right into it. Now what if they give you a question about a patient that has a history of like Down Syndrome, right? And they tell you that, oh, you hear like murmurs in the patient's heart. What kind of congenital heart defect does this person likely have? Well, I hope you're telling me like an endocardial cushion defect. Remember, endocardial cushion defects are the most common heart defects in patients that have a history of a history of Down Syndrome, right? And hopefully you remember the other SQ Lite that associated with Down Syndrome, right? So Down Syndrome tends to be associated like like the Epicomphal folds, right? It tends to be associated with the single parmarachryce, right? Down Syndrome also has an association with like a Dordinal atregia, right? So if they give you a question about a kid, there has billions of them in and you see like the double bubble on imaging, or like a radiograph. You know they are dealing with Down Syndrome, Dordinal atregia.

And remember that that occurs from a failure of recanalyzation. And then remember that Down Syndrome is also associated with Anola pancreas, right? So again, that can actually also be a cause of billions of them in on an MBA exam with like chronic small bowel obstruction and maybe like even pancreatitis in a kid, right? And then one of the things you should think about Down Syndrome is like crash problems disease, right? Where we have like a colonic egonobiosis, so that causes like chronic constipation, failure to pass mechonium and things of that nature. So those are all how you think to keep at the back of your mind. I remember Down Syndrome is obviously a trisomy 21. And those kids remember Down Syndrome, they also have an increase risk of ALL, right? So ALL, remember this pneumonia, right? They all fall down, right? That's a classic pneumonia that's in many resources, right? They all fall down to help you remember that there's an increase risk of ALL in kids that have Down Syndrome. And then another thing you may also see with Down Syndrome on MBA Me Exams is you may also see the association with early Alzheimer's, right? Because remember the one of the genes that plays a role in the development of Alzheimer's disease on chromosome 21. So it's almost like the person has like a triple dose of the badness, right? So that can easily put them in trouble.

Now what if you get a question on the exam about a patient that presents with like severe, like tear and chest pain and it's redeating to the back? What are you thinking about on that those circumstances? What diagnosis are you thinking about? Well I hope you're thinking about the early dissection, right? The early dissection. Remember the early dissection is pretty bad. It has a actually pretty higher mortality. And I mean you have some classic ways it presents on exams, right? So usually you'll be a person that has like you know like severe tear and chest pain. Although sometimes they may not have like the severe tear and chest pain redeating to the back. Then we just have chest pain. But the thing is there are some other classic antecedents that your friends at the MBA Me like to throw on on exams in terms of oh this is how this stuff presents, right? So some ways they can present it so they'll have like you know the chest pain or you may see people have like differences in blood pressure between the arms, right? Because the thing is as you're having the dissection you may begin to have involvement of a subclavian artery so you begin to high pull perfuse one of the upper extremities, right? So you have those differential blood pressures in the arms. And then one of the thing you may also see is like widened media stina on a chest x-ray, right? So widened media stina that's a classic image in finding.

Occasionally they may even give you a person that has like you know like severe chest pain and they tell you that the person has a plural of fusion like a unilateral plural of fusion. If you see that that's another classic presentation of the audit dissection on MBA Me exams. And the thing is usually when the person has the audit dissection right, you know they'll usually give it like some kind of risk factor.

So the risk factor in like young people or they tend to be like you know like if you have some kind of like weird connectivity should disorder so like people that have like marfans, remember marfans is a chromosome 15 defect in febrile or the zomadouin anti-heritance or they may have like L-hasdanlos syndrome or remembering L-hasdanlos it's a defect in collagen some kinds of L-hasdanlos especially I think the vasculolus dandos is a defect in type 3 collagen right although there's some other L-hasdanlos that's also associated with a defect in type 5 collagen right so people that have like marfans, people that have R-hasdanlos, most conditions tend to be associated with a eurid dissection especially young people there are again many other connective tissue disorders even like by cosperiodic valve so they give you a question about a patient with a history of toner syndrome that's having like severe again chest pain, think about the eurid dissection right because my cosperiodic valve is a big risk factor for eurid dissection okay and my cosperiodic valve in addition to co-acquition of the eurid right at the two classic heart problems associated with people that have toner syndrome and then remember if a person you know has all these other things like tachyasus at a rightis or giants at a rightis those things basically anything that can cause an eurotitis so inflammation of eurotitis so like giants, celtaciasus, syphilis remember tertiary syphilis right tends to involve the eurotitis right because remember that in syphilis you in syphilis, t-palidoma especially in the tertiary stage loves to scrub the visor visorum of the like ascending eurotitis right so that can cause eurid dissection in that regard and then ankylosein spondylitis right arey so like runnathoid arthritis and cylosein spondylitis those things that all associated with the those things can all cause an eurot

itis and that can all trigger eurid dissection or the one thing you want to remember is that the biggest risk factor for eurid dissection is hypertension that is something that classically shows open exams especially on step two but the thing is they also begin to test these risk factors on step one so it's one of those weird things you want to try to commit to remember so hypertension is the biggest very high yield hypertension is the biggest risk factor for eurid dissection so what causes eurid dissection right so typically happens in people that may have like already have like an euric aneurysm of something of that nature but basically you have like a t-in the intima right remember right the eurid is a big large muscular artery right so it has the three layers has like the intima has the media has the adventicia so you have a t-in the intima when you have that t-in the intima blood will track along that tear and track through the media right track through the media right so inside that media you ultimately create like a false lumen what the thing is that false lumen as it grows and expands it can compress the true lumen of the eurid and then that can cause hypoprofusion of like the brain so people can get strokes in the setting of eurid dissection or you can like have the blood like track proximally to like the pericardial sac so people can get cardiac tamponac from eurid dissection that's one of the reasons why you can see a widened media sign on imaging or you can have like the dissection track back to like a coronary vessel remember your coronary vessel can arise coronary vessels they arise around the area of the eurid costs right so if it tracks back to your coronary vessels especially the right coronary artery that's probably the most commonly involved coronary vessel in the eurid dissection so if it tracks back to those coronary vessels right present can obvi

ously get my carcinem function and sometimes people can get like really body eurid pre-gurge from from a from eurid dissection so those are all things you can see right so that's why a eurid dissection is bad it's just the extension of the dissection that tends to cause many of the symptoms and then on the some unfortunate circumstances people can have like really body eurid dissection where it just extends extends extends extends extends extends and then your rupture the euric wall that's obviously terrible right because I mean most of those people don't survive it's just a bad situation all around so the thing is eurid dissection you want to be able to break it up into its two major types I mean there are many classification systems but the one you will likely assume you examine is the Stanford classification right and the thing is there is something called the Stanford A classification and then there's the Stanford B classification basically Stanford B means that it's only the descending order that is involved okay Stanford B just tells you that it's only the descending order that is involved but if the A descending order is involved in any way shape of form then you know that you're dealing with a Stanford type A dissection the reason you have to differentiate these two things is that there are differences in treatment right so like a Stanford type B dissection all you need is medical therapy right but a Stanford type A dissection you need medical therapy plus surgery okay so that's the key difference you want to lock down in your mind so you may say oh divine what do you mean by medical therapy the thing is if a president ever has the early dissection your first step in management and again if if you're like a second-year medical student I promise you you promise you this question at least 10 to 20 times before you graduate from med school but and this is like wh

en you SML exams class exams and all that stuff for president has the early dissection that has been confirmed your first step in management is always medical therapy with a bit of blocker okay it can be any kind of bit of blocker even a bit of law remember a bit of law is an alpha bit of blocker that is okay for for you got a dissection right so your first step is always a bit of blocker if maybe they really wanted to stretch your thinking on the exam although they really do this but if a bit of blocker is not caught in it right then one thing you can consider is to give like like a sodium nitroper site right it's like a powerful visual dilator again you cannot just give any visual dilator you can like say oh take hydrolyzing no giving hydrolyzing is actually is actually gonna worsen the patients outcome in a unique dissection so you don't want to do that right so first always give a bit of blocker always always always give a bit of blocker first that is extremely critical to know for the USML exams you give a bit of blocker first because the the reason you do that is there is like some physiologic mechanisms behind that but I feel like I have a lot of stuff to cover so I'm not necessarily gonna like jump into that today but essentially you don't want a person to have you want to minimize tachycardia as much as possible when a person has a unique dissection because if they have tachycardia that will increase the shear stress on the world of the order and that will worsen the dissection right so you don't want to do anything that will raise the patients or heart rate that's why typically you give a bit of blocker first right but if you're like oh you know what let me give a visual dilator like hydrolyzing or something even the nitroperside is acceptable if you give that first right now we'll call it a massive visual dilation right the way your heart responds to massiv

e visual dilation right through those a bar receptor mechanisms have described in other podcasts is you have like a reflex tachycardia and now worsen the dissection so you always give the bit of blockers first right and then if you're dealing with a type d dissection you can then also proceed with giving a going with going to surgery right so call vascular surgery or whatever and then they will hopefully be able to fix the problem now you already dissection right how do you like make the diagnosis again classically on imaging you'll see like a wide-edmine is thine them right but obviously you know you want to confirm it you don't just want to go on open a persons chest and do whatever right so classically for you already dissection you can do like a CT angiogram right that's usually the right answer on mbim exams you get a CT angiogram you'll show the dissection beautifully the reason that you do the CT angiogram is it will help you like evaluate oh is the cause of this patient's chest pain hearing dissection or something else right something else can mean like another acute aortic syndrome like an intramural hematoma or things of that nature or you can show you if the patient has a p or something really that's also causing the chest pain what if you know the patient is like crashing not doing well you can do an echocardiogram you can do like a tte although that's not as good as a te right so remember trans thoracic echocardiogram is not as sensitive as a trans asophageal echocardiogram right so it's not as great but usually you can do a tte on mbim exams and that'll be correct what if you don't see tte as an answer choice you can go with te okay trans asophageal echocardiogram those are all things you do when the patient is crashing but if the patient is not crashing patients relatively him with dynamically stable you can go ahead and get a ct angiogram that study do

esn't take as much time especially with the advent of these are really faster ct scanners so those are all big things you want to keep at the back of your mind with the aortic dissection again don't forget the biggest risk factor for aortic dissection is hypertension that is something that your friends at the mbim love to test a quite frequently now so now what if you get a question about a patient that has you know like a 75 year old guy and they tell you that he has passed out like two or three times while I'm going his lawn and the tell you that when I was quotation of the chest you hear like this is stolic ejection memory deep into the carotids what's your diagnosis that's your ex-denosis right that's your ex-denosis really for these heart murmurs questions right the I mean I feel like I have like some dedicated podcasts we have talked about like just murmurs like I think it's probably one of my earliest podcasts on this website maybe like episode four like right around there well there's this podcast where I go into like extreme detail on the physiology of murmurs and like the pathophys behind many of the findings it's a very it's probably one of the best podcasts I've ever made so if you know if you're interested and you really want to like deep deep into murmurs it's not a bad podcast to listen to but basically right this person has aortic stenosis right and the thing is really for these murmurs to be honest the big thing is you just want to remember is at this historic or the astolic right what's to different maneuvers due to these murmurs and again many of these things make perfect sense if you just kind of think about it many people just try to memorize a random crap what you don't need to do any of those right so just think is this is stolic or the astolic raise it her best and then you also want to again know about your different maneuvers right and the th

ing is for the maneuvers I think the smartest thing to learn with your maneuvers is does this maneuver increase preload or after load right because for most of the murmurs all you need to understand is if I increase preload what happens to this murmur if I decrease after load or increase after re-arayara what happens to this murmur so those are all kind of like the big things you want to remember with with your with your murmurs now one thing I want to go ahead and see is there's this thing called Carvalos sign right that can really help you with murmurs like if a murmur gets us included with inspiration you know you're dealing with a right sided heart murmur you can essentially like take that to the bank rule out many answers relatively quickly on nbm exams so if a murmur gets worse with inspiration that's one of those Carvalos sign that's classic for a right sided heart murmur because when you inspire her right what happens to your videos return your increase so if your videos return increases that would increase flow or flux through whatever right sided heart valve right so that would likely make the murmur get louder okay so again those that's a big thing of keeping in mind and then right you want to remember like we're certain murmurs I heard best right so like there's this one I mean there are many in the monics you may see you may see like the demonic apartment m like eptm or all physicians take money or I don't know just find whatever the money that works for you but basically in the right-up personal border you hear right murmurs best left-up personal border you hear pulmonic murmurs best left low-standard border you hear try Cosmic murmurs best and then at the apex right basically like around the ear where you should pop it the point of maximum impulse right that's where you hear my trauma merst best now the thing is that left low-standard border is also whe

re you hear VSD really and that's also where you hear the murmur of hypertrophic cardiomyopathy pretty well and that's also where you hear the murmur of the oedic regurgurge pretty well right and you also be able to see divine the oedic regurgurge house that remember the the order takes off from the left side of the heart and goes towards the right side of the bud right like as it's going upwards to from the arch it goes towards the right side of the bud so if you think about it if blood is regurgitated blood is that means blood is flowing backwards so blood is flowing back from when it's king so it's flowing from the right side of up high to the left side down that's why it's heard best at the left low-standard border really for many of these murmurs if you just sort of track the flow the place is where they are heard best it kind of makes a lot of sense so those are big things you want to keep at the back of your mind with these murmurs and again these things like people you see people try to memorize or which murmurs as the stoic with murmurs are that stoic and you don't need to do that just analyze what the what that chamber of the heart is doing and you should be golden for the most part so the patient I talked about earlier clearly has the oedic stenosis if you see like a murmur in a person that's in their 70s on inbim exams almost like 99% of the time it's oedic stenosis in fact many times if they give you like they give me like the audio whatever's I don't even bother listening to those because the answer is usually you know like pretty obvious so person has the oedic stenosis right and remember the both were pathophysiology behind oedic stenosis is calcification of the valve so it's calcification around about beats if you're in your 50s or in your 60s or 70s it doesn't matter but one high-yield thing to remember is that the most common cause very high of the

most common cause of oedic stenosis before the age of 70 is a bicospidiodic valve okay but past the age of 70 you have like just the signal calcification and again remember a bicospidiodic valve has an association with toner syndrome that's one factoid I've already repeated multiple times and really yodic stenosis right the classic boss phrase right then you see that oh the person has a crescendo decrescendo then you see the person has a diamond shaped systolic ejection murmur radiating to the carotids right if you see that think about the oedic stenosis and again there's some other things you can see what the oedic stenosis right like you me see like the pulses prowess it try this and because again think about it right if you have a lot of trouble getting blood out of the left ventricle because you have a stonard evolve obviously that's going to go ahead and cause problems with getting enough blood early so like when you hear the heartbeat when you feel the heartbeat in you're like oh okay this person is is insistally right now when you are checking the carotid pulse like man it's taking a long time for this this carotid pulse is kind of taking its sweet sweet time right like it's like almost like tardy it's like remember the word tardy means late right so it's like late tardy pulse that's what that's what they call a pulse a parvasa itardus okay so that's a classic buzzword association with when you're extenosis and remember that the oedic stenosis right you can have like like there are these three things and I remember them with the pneumonia ash right they can have like angina so like chest pain from the oedic stenosis they can have syncopy right that's the esti can have a heart failure like symptoms basically the reason I give those three things is once you start having those sequelae from you I said I mean oedic stenosis you do need to go ahead and replace the v

alve because these people are very likely to die within a few months to like a year or two if cares not taking and obviously in order of back to worse right like if you have heart failure symptoms you'll be dead within a couple of months right if you have syncopy from a oedic stenosis you'll be dead within like maybe like a year right but if you have angina you'll probably be again be dead within like three four five years right so and a oedic stenosis you know really there's not many options available for you you just need to go ahead and now you need to go ahead and I'll replace the valve okay so that's a classic thing you want to keep by the back of your mind for the USML Es and again if you're thinking in terms of maneuvers right again the murmur will be louder if there's more flow through the valve right so if you increase pre-load right there'll be more left ventricular in that stalling volume so you have more flow across the sternonic valve the murmur will sound louder right but think about it if you decreased afterload that will also accomplish the same effect right because if you decrease afterload it will be easier for blood to flow across the oedic valve right so again that will make the murmur sound louder right on the flip side if you increased after look right if you increased afterload the gradient between the left ventricle and the the order will be diminished right and remember right you need the more gradient you have the more flow you have so if you have less gradient you have less flow so if you have less flow where you have less flow across the sternonic oedic valve and you won't have a sound a softer okay so again those are you know just easy quick high of things to keep at the back of your mind now what if they give you a question about a patient and they give you like the person's blood pressure is like I don't know like 150 over 40 and the pers

on they tell you that this person has been having like has a histro like that lifted a cardiomyopathy or the metering this person has a histro like aortic aneurysm what kind of murmur are you thinking about this is clearly aortic regurgers right I mean the blood pressure like again many times when you get this audio questions on the USM Ls again I typically I will say that you can almost always answer them correctly without even listening to the audio so typically my trick is again to look out for key things right so a blood pressure of 150 over 40 it's kind of weird right so this is not very normal right so that's something you likely see in the oedic regurgers right and that thing I'm referring to is a white pulse pressure white pulse pressure is pathonomonic for aortic regurgers although I know that murmur it's pathonomonic for an endemic exam is a beaten doctor satiriosis okay so if you see like a white pulse pressure in a kid that's likely pda if you see a white pulse pressure in an adult it's likely likely aortic regurg and one thing just kind of dropped in my mind so let me go ahead and talk about it so I don't forget so remember that I said that for aortic for aortic stenosis right the boswapathophysiology you want to remember is a calcification of the valve right for aortic dissection which I just mentioned a few minutes ago the boswapathophysiology you want to remember is cystic medionicosis okay cystic medionicosis sometimes you may see cystic medionic regeneration right and then another classic boswapathophysiology your friends at the mbimilovii to remember is the boswapathophysiology which I'll talk about shortly but my trovoproleps I want to remember it makes some of us degeneration okay you may see divine we are human factoring these words from I promise you these words are very high-yield words to know on exams so so aortic regurgers right again white p

ulse pressure together with a pretend doctor's arteriosus right so you may see okay what causes aortic regurgers essentially anything that can widen the aortic regurgers will cause aortic regurgers right so for presenias like again essentially many of the risk factors for aortic dissection are kind of like the same risk factors for aortic regurgers right so like again bicosopid aortic valve tertiary syphilis, tachyasus, giant cell all that stuff right and there's some weird things that like weird physical exam findings that your friends at the mbimilovii to run exams right so then you have like a head bobbing right so people may have like head bobbing and you have like the quinky pulse so the medallion that oh when you look at the anelbed or you puppy the anelbed you can see like pulsations or the medallion that they have like a water hammer pulse really many of these physical exam findings they arise because the patient has a white pulse pressure so you may see define what causes the white pulse pressure in aortic regurgers well not rocket science actually so the thing that actually causes the white pulse pressure is if you think about if a person has aortic regurgitation right first thing that happens is obviously it's a dastolic memory right so the classic description is oh it's a dastolic bluing memory right so dastolic bluing memory so the thing that happens in aortic regurgers is that blood will flow backwards right from the order to the left ventricle during diastin right so the thing is think about it if the blood that is supposed to be packed in the order during the astolyth some of it has made its way back to the to the left ventricle that means the amount of blood in the order in the astolyth will be diminished so if that's diminished that means that your dastolic blood pressures go down right so that's totally blood pressures go down for that reason now th

ink about it if more blood is flowing back to the left ventricle what happens to the left ventricular endastolic volume with the next run of the cardiac cycle it goes up right so the left ventricular endastolic volume goes up and if that goes up that means if you're again thinking in terms of the frank starling a mechanism right if your left ventricle endastolic volume goes up that means you have more blood to eject with the next systolic bit of the heart right so those people's astral volumes will be higher and that will raise systolic blood pressure so essentially if you notice in a person that has a early dissection the systolic blood pressure is rising the dastolic blood pressure is decreasing right so that will obviously widen the pulse pressure right because hopefully remember that pulse pressure is the difference between systolic and dastolic blood pressures so it's that widening of the pulse pressure that is responsible for many of the physical exam findings you have because especially like those water hammer pulses it just really arises because you have like an increased level ventricle endastolic volume from the regurg right so your stroke volume goes up a ton so your cardiac output goes up quite a bit so your systolic blood pressure increases okay that's what causes many of those physical exam findings you observe in in a eotechal regurgitation and then what if they give you a question about a patient that's from like a developing country and this patient has this patient has you know like has a history of like like an upper respiratory infection that was not really treated kind of resolved on its own and then they tell you that oh you are now hearing like a dastolic murmur at the apex right and maybe the person has like an irregularly irregular interval on an ekegi right hopefully on that these circumstances you're thinking more along the lines of um mitro

stenosis right remember the biggest risk factor for mitro stenosis stenosis is a rheumatic fever okay the biggest risk factor for mitro stenosis is rheumatic fever they love to test that on exams um and remember that mitro stenosis is the biggest risk factor for a fib so the most common murmur I mean the most common erudmia in a person that has a history of a history of a mitro stenosis is a fib right because the left e-tron will obviously dilute if a person has a e-tron right so the thing is when a person has a mitro stenosis right um they tend to have again like dilution on the left e-tron where so that can cause a fib and the thing is as the left e-tron actually dilutes you can actually begin to compress the esophagus because remember right the left e-tron is like the most posterior chamber in the heart and literally like the esophagus is like smucked up against the left e-tron so the thing is whenever a person has like left e-tron enlargement that can actually go ahead and compress the esophagus right and the person can have this phasor from that right and another clinical query to it that is that is why we do something called a te that is why a te is more sensitive than a te te right because the transits of a g-like ocardiogram you're like smucked up right because you're literally putting the you know the ultrasound probing the presence of the esophagus right so the thing is you are like smucked up against the the left e-tron wall right so you know it works it works it works pretty well that's why it's more sensitive so that's I guess something to keep at the back of your mind and again I already described this if you increase preload right again in my in my cardiac in one of those in fact I'll reference those podcasts in the comments like in the description of this podcast when I'm fairly certain is one of my early podcasts on this website I describe like the d

ifferent maneuvers like again the pathophys behind those and how the like modulates these cardiac murmurs so I will make reference to that when I'm when I'm writing like the comments below the podcasting but in generally if you increase preload right or you decrease afterload right that will make that will make although really for microstenosis they tend to test it more in terms of like increased preload if increased preload there'll be more flow across the stenotic valve and again the murmur of sound the murmur of sound louder and then what if they give you a question about a patient and they tell you that oh that you hear like a holosis stomach murmur at the apex right this is obviously a mitral regurg right and mitral regurg for whatever reason on nbm exams they love to put in women that are recently like pregnant right that's one thing when you keep at the back of and then remember that mitral regurg can also be caused by like if you're like a person that has like a recent mi and the ruptural of those papillary muscles right that can cause a mitral regurg and if for example a person has like a history of like dilithic cardiomyopathy that can also cause mitral regurgert right because when you have dilithic cardiomyopathy the left ventricle kind of dilates and if you dilates right you will essentially pull the mitral valve leaflets apart right and that can cause mitral regurgert so that's one of just those like weird bizarre things you want to keep at the back of your mind on exams but again mitral regurgert right it's a holosis stomach murmur heard best at the apex and the thing is the murmur actually increases in intensity when you have an increase in preload right and also when you have an increase in afterload right so we have an increase in preload or an increase in afterload that'll make the murmur sound louder right and that should hopefully make sense becaus

e if you have more blood in the left ventricle that will have that would essentially give you more blood to regurgitate backwards right so anything that increases preload will put more blood in the left ventricle anything that increases afterload right will prevent blood from leaving the left ventricle so there'll be more blood in the left ventricle so you have a louder murmur so again those are all things to keep at the back of your mind for tests and I guess a closely related a murmur is like mitral valve prolapse mitral valve prolapse reading the classic we will present right they'll describe like they'll tell you that this person has like like a murmur with like a mit systolic like right and again typically it's in found in people that have all these connectivity should diseases like marphans or like alas danlos right or people that have like psychiatric disorders okay those people tend to have a mitral valve prolapse on mbm exams right so those are just all like again weird bizarre things you want to keep at the back of your mind on tests and then um mitral valve prolapse again I have described the pathophysiology in a different podcast but I'll just give you the Cliffs Notes version here but basically whenever you have more blood in the left ventricle the murmur sound softer because the prolapse of the valves is decreased by putting more blood in the left ventricle so actually if you increased preload or you increased afterload that will actually make the murmur of mitral valve prolapse a sound a softer again I've described this in many of the podcasts so and again I'll make reference to those podcasts in the comments section so I don't think I'm gonna like just keep a bit in the bush here and again so mitral valve prolapse so let me just go over these murmur descriptors real quick right so you're at the stenosis crescendo decrescendo systolic ejection murmur he

ard best at the right of personal border relating to the carotids popus privacy tartus right mitral valve prolapse right so murmur with a mit systolic clik right heard best at the apex in a person with a connectivity should disease or a psychiatric disorder on mbm exams right mitral stenosis present with a histroveromatic fever right dastolic murmur heard best at the apex the person may have e-fib right the person may have this feature from left-exceling largement and subsequent a compression of the of the esophagus right and then um um and mitral stenosis right they'll describe like that stoic moment opening snap right so that's mitral stenosis so I've talked about mitral stenosis mitral regurg is just holosis stoic murmur heard best at the apex with regition to the accelet right those are again these are all like the classic descriptors that they open occasionally me put on exams although in my experience your friends at the mbm are beginning to you know like shy away from doing that on tests a meodic regurg regurg will again be like the dastolic murmur dastolic blowing murmur heard best at the left-low strontal border and again the patient will have like a white pulse pressure and you'll have all these like weird physical exam findings like head bobbing water hammer balls quinky balls um like there's like this durezy and all that stuff but those are all things you want to keep at the back of your mind and again I have like a very big treatment of the pathophys behind like the manoeuvres and the murmurs in a different podcast and again I'll point you to that in the conclusion so as I do at the end of every podcast right I mean if if you're a meds today you you're taking any exam I like it to do for that exam so like step one step two ck two cs step three preclinical meds school exams 30-a-shelf exams um if you're a medicine resident like the medicine boards um like

the medicine training exam ebi and board exam i tutor for all those um and then I do this longitudinal tutor infant that I've talked about at nasim at this point where if you're first second of 30 a-match today i tutor you for like your shelf exam so like your class exams but at the same time i tutor you for your upcoming USML exams and again that has been wildly successful people have and then I do those booster course right where it's like 10 hours for step two ck and step three and 20 hours for for step one where again if you're at the end of your dedicated period or you've uh all you know you've covered the material and feel good about your knowledge base it's like a quick period to put everything together in a Q&E format where we essentially go over like a lot of the high-yield stuff you'll likely see on your exam i would i do that on a one-on-one basis and then if you need coaching right for like um if you're medicine or plant a residency so like an ira application or a college student applying to med school so like an amcass application i feel free to reach out to me like personal statements rec letters editing applications mocking reviews those are things i'm extremely good at most of the people have worked with have much that their first choices um and again i've been on the admissions committee of a top two med school for like a year right so again i have a ton of experience reviewing thousands and of high-quality applications so that's something you're interested in either send me an email divine intervention podcasts with an sdn.gmail.com or you can just reach out to me through the website and i'll catch an email from you so have a wonderful rest of your day um i will continue this cardiology series god bless you and i'll see you next time thank you

Hypertension.

Wide pulse pressure, head bobbing, water hammer pulse, and Quincke's pulse.

The murmur will become louder because there is more blood volume available to flow across the stenotic valve.

Angina, Syncope, and Heart Failure symptoms.

Endocardial cushion defects.

Medical therapy with a beta-blocker to minimize tachycardia and reduce shear stress on the aorta.

Wide pulse pressure, head bobbing, water hammer pulse, and Quincke's pulse.

The mitral valve due to generalized calcification (though bicuspid valve is common <70).

PDA, duodenal atresia/colon atresia, and increased risk of ALL.

Type A requires immediate surgery in addition to medical therapy; Type B only requires medical therapy.

Diastolic rumble at the apex, with rheumatic fever being the biggest risk factor.

Increasing preload or decreasing afterload.

Wide pulse pressure, head bobbing, water hammer pulse, and Quincke's pulse.

The mitral valve due to generalized calcification (though bicuspid valve is common <70).

PDA, duodenal atresia/colon atresia, and increased risk of ALL.

Type A requires immediate surgery in addition to medical therapy; Type B only requires medical therapy.

Diastolic rumble at the apex, with rheumatic fever being the biggest risk factor.

Increasing preload or decreasing afterload.