DIP Episode 106 - ABIM/Medicine ITE/USMLE Step 3 Review Series 6 (Cardio 2)

Okay, welcome. My name is Divine. I am a PGY-1 transitional year resident. That's ultimately going into radiology. And this is episode 106 of the Divine Intervention Podcast. And this podcast will be another review for the ABIM exam. So like basically the medicine board exam and the internal medicine entry in exam right. And again, this is something that will potentially help a person studying for the USN Listet 3 exam. So I'm going to continue the theme of cardiology. If you notice I'm focusing quite a bit on cardio because that's like almost like 20% of the medicine board exam. So I'll kind of focus on that because it's usually again the area that maybe tends to give people more trouble than normal right. So I will basically try to finish that up before I begin to talk about the sessions sections or at least like talk about it in a very high in very high quantity. So let's just go ahead and jump right into it. What if you get a question about a young athlete that is like exercise in and then the athlete like kills over collapses and dies or something right. So what's your diagnosis for this patient? Right, that'll be hypertrophy cardiomyopathy right. And remember in hypertrophy cardiomyopathy right those people basically have like asymmetric hypertrophy of their interventricular septum right.

And the thing people don't realize is that if you're having hypertrophy right of your interventricular septum, the thing is the interventricular septum on its own when it hypertrophies it takes up space that is normally for the leventricular flow tract right. So that can cause a lot of problems right. Like it can basically cause issues where the leventricle can not eject appropriately. Another boss phrase you want to be able to I sort of like correlate with hypertrophy cardiomyopathy is this thing known as a systolic anterior motion so Sam. So systolic anterior promise is a very high ill boss roto remember. systolic anterior motion of the of the mitral valve of the anterior mitral valve a leaflet. So basically the thing that happens is because of that hypertrophy again one of the mitral valve leaflet excuse me is pulled towards the ventricular septum right. And again that basically causes like a dynamic leventricular flow tract obstruction right. And the thing is right so again classically in a young athlete and obviously you make the diagnosis with with an echocardiogram right.

And the thing is HCM your friends that write these exams they kind of like like these cardiac again another reason to like cardiology because it's one of those ways that they can sort of test to see if you actually understand what's going on right because the thing is the general thinking by the people writing this board exams is that they're like this are resident they are worked pretty hard so they just try to like learn the learning formation real quick and move on and they don't really like buckle down to understand what they actually learning right. So the thing is these questions right obviously I mean if you're good at memorizing and all that fine you do well on them. Well the thing is there also some of these questions where like if you have an understanding of the reasoning behind certain like findings right it makes analyzing these questions so much easier right like cardio questions people look at them they're like super nebulous but they're really not if you understand if you sort of understand the pathophys behind like certain things you as you're reading the question you basically see exactly through the whatever the test writer is trying to like get you to see right.

In fact there are many times that I'll read a cardio question read like the first half of the question and I pretty much know what they're going after right because it's like they give you all these data they give you this they give you this the data just like oh of course this is elevated this is depressed blah blah blah you know exactly what they're gonna talk about right because again you kind of have an understanding so I'll sort of try to give you some tips in that regard as we go along right so one area that I think is kind of like useful to understand to understand a HCM is to understand it in the context of differences with the other x the most is because they love to test those things on exams but the thing is and again I will try to explain this as best as I can so I don't give you a headache and just stick with me and sort of follow me along and you'll see that this problem subject there can be very easy to understand right but before I do that there's something I want to explain first let me explain certain maneuvers and what they do right so that when I start saying oh if you do this what happens if you do this what happens you'll make sense so one classic like provocative a physical exam maneuver that is described a lot on on these aboard exams is the valve solver maneuver right so if you valve solver right you're basically breathing against the closed out glottes right so that will raise your intra-thoracic pressures if you raise your intra-thoracic pressures you're compressing your SVC if you compress your SVC your venous return goes down right so if your venous return is going down your left ventricular volume will decrease because you're just not sending enough blood to the ventricons right so that's one thing you want to keep in mind now what if they give you a question and they describe the hand grip maneuver the thing is when you grip a person's h

and right you're compressing arteries you're compressing like they're radial artery they're on artery right remember those are arteries so by definition those are coming from the heart right so if you compress those vessels you're increasing after load right because it's like oh things that drain the heart you are squishing them down so the heart can not drain as well so after load is increasing when you perform the hand grip maneuver and think about it if you increase after load it becomes harder for the ventricle to get rid of blood so the volume in the left ventricle will increase okay now what if they give you a question and they tell you that the person a patient stands right so think about it when you stand you're basically pulling blood in your low extremities right you're pulling blood in your low extremities I mean think of a patient with like chronic venous insufficiency if that patient is in the hospital or you consult or through they're like raise the patient's leg up raise the patient's leg up they're saying raise the leg up right so that you can increase you can basically send that blood back to the heart so the patient stands right you're pulling blood in your veins remember veins are very good capacitance vessels so your veins will keep that blood if your veins keep that blood right your preload actually goes down so when you stand you actually decrease in preload so the volume of the ventricle especially like the left ventricle will be decreased in this instance because you're not sending them as much blood back contrast that with squatting if you squat on an exam right you're squishing those lower extremity veins when you squish those lower extremity veins you actually increase in venous return because by squishing those veins you are decreasing your capacitance and you're basically compressing the blood out of them and sending them right back to the

to the SVC and IVC okay so just something to sort of keep keep at the back of your mind so now you understand that let's ask ourselves right what are the classic ways or maneuvers because believe it or you may say oh divine this is too detailed I promise you it's not at least I certainly got the chance to take the medicine in training exam I will tell you that these maneuvers and like oh like oh the murmur gets louder with this gets softer with that I promise you these things are tested pretty frequently okay so if a person has and the reason they like to test HCM in the context of a eotic stenosis is because it has many similar findings but they are some salient differences right so for example if a patient has a hypertrophic or cardiomyopathy they will have like a mid systolic murmur right you have like the mid systolic ejection murmur you'll hear really well at the right opera sternal border right but the thing is in eotic stenosis right you know that that murmur radiates to the carotid in hypertrophic cardiomyopathy the murmur actually does not radiate to the carotid that's one key difference you want to keep at the back of your mind and then another thing is if you think about it anything that puts more blood in the left ventricle will make the murmur of eotic stenosis worse and why is that think about it if you put more blood in the left ventricle right that means the left ventricle has more blood that it can push forward through the eotic valve the stenost eotic valve and if you have that right the murmur will get louder because you are using that valve more now the thing is in hypertrophic cardiomyopathy right the thing is remember I talked about that buzzword where you have like the asymmetric septal hypertrophy and you have that's that's the stolic anterior motion of a mitral valve liflet the thing is basically the ventricular septum coming together with th

at mitral valve liflet is what constitutes the dynamic left ventricular outflow tract obstruction that causes many of the symptoms in hypertrophic cardiomyopathy so here's the thing whenever there is more blood in the left ventricle that actually separates that mitral valve liflet from the hypertrophied intraventricular septum so that will obviously make the murmur better it will make it not sound as loud okay so the key principle you want to remember because you like instead of memorizing this crap manover crap manover crap manover just remember the concept anything that increases the amount of blood in the left ventricle will keep the hypertrophied intraventricular septum and the liflet of the mitral valve apart so that will increase flow through the left ventricle outflow tract you are basically relieving the obstruction so the murmur sounds softer okay so anything that increases the volume in the left ventricle will make the murmur of HCM sound better okay it will sound softer it won't be as loud contrast that with eodics the notice where anything that increases the volume of blood in the left ventricle will make the murmur sound louder again because you're having more flow through that stenost eodic valve the thing is when you increase the volume of blood in the left ventricle you're essentially relieving the dynamic stenosis that constitutes hypertrophic cardiomyopathy again it's super important to understand this point right so if for example a person has like hand grip right if you have hand grip that will keep more blood in the left ventricle and if you keep more blood in the left ventricle the murmur of HCM will sound softer okay so again very important to understand very important to understand that right and remember I told you that in HCM the murmur does not radiate to the carotid so that's important to know and remember in eodics the notice you probably

remember this buzzword from back in the day like in Met School where they talk about like the the pauses provis a tardis right so tardis the word a tardis means tardis right like a kid that's coming late to school right so in eodics the notice you have like the delayed carotid upstroke right the thing is the carotid upstroke in in HCM is actually not delayed so again that's another difference that can sort of help you delineate between eodics the noses and hypertrophic cardiomyopathy on any of these exams now the thing is so how do you how do you treat hypertrophic cardiomyopathy right so classically on these exams you basically give them something that makes the heart go slower right because think about it if your heart is going slower right that means you'll have more time to fill if your heart has more time to fill you're increasing the volume of blood in the left ventricle if you increase the volume of blood in the left ventricle you are relieving that dynamic left ventricular outflow tract obstruction and that essentially fixes some of the problems you have in a HCM right so you can give like a beta blocker you can give a non-dihydroperidine calcium channel blocker right so like verapamele or deltaiazine because those slow the heart down so the heart spends more time in the astleine right so the ventricles are feeling because that's what happens in the astleine and then I mean that asymmetrical septal hypertrophy you can do like a like a surgical a myometany so you call cryotheraic surgery they chop up some of the persons are interventricular septumal though people tend to get like heart block after that happens or like a bundle branch block or something and then if they give you a whiff in the question that the patient has like a battery for me like like proxy like like VTAC happening every now and then right for those people you want to go ahead and place an IC

D right because that will sort of decrease the risk of having like studying a cardiac death and then you can also give those people like amoeo you can put them on amoeu的人 right to sort of like make them not have make them not have these bad bad bad rhythms although if I'm not mistaken amoeu the rune has actually not been shown to decrease the risk of sorting cardiac death in patients with HCR it's placing an ICD that has been shown to decrease decrease the incidence of a sorting cardiac death in as far as I remember if I'm remembering correctly I mean in a HCR so and then one other thing your friends that write these exams love to do with HCR is they love to talk about like things that you should probably avoid in patients that have HCR right remember I told you that anything that puts more blood in the left ventricle keeps that ventricular septum and the mitral valve leaflet apart so that relieves the left ventricle out flow tract obstruction guess what if you put less blood in the left ventricle that will basically worsen their condition right I mean I've just explained that like many many different times so you want to like not give those people diuretics on an exam right because again diuretics will dry you out that will decrease preload and that will make the condition worse right you don't want to give them a nitrate remember your nitrates are vino dilators so by dilating veins you decrease preload and that'll make the condition worse right I mean like I mean you heard the story or at least is working out hard or playing a game kills over and dies right I mean why do you think that really happens in HCR think about it right if you're working out what are you doing what's your skin doing you're sweating a ton if you're sweating a ton right you're basically decreasing losing volume by losing volume you're decreasing preload you're decreasing preload you're worseni

ng the left ventricle out flow tract obstruction because there's less blood in the left ventricle so that may like exacerbate symptoms and then be that that's why they tell people at HCR basically stop working out right so that you don't get into you don't get into trouble so I think that's all I'll say about HCR I mean for the folks that are taking step three the thing you may see tested that's above and beyond what I've mentioned now is HCR right it's allosomo dominant inheritance right so you should definitely try to know that and then I don't forget that it's it arises from mutations in like the myocene heavy chain like the beta myocene heavy chain that's like the classic thing be tend to describe on the exams and they be telling you that oh the dad died in a car accident or some like weird crap right at the age of like 30 the dad did not die in the car accident because he was like reckless on the road he probably had an arrhythmia and died on the spot okay so that's the classic history they give on these on these exams okay now since I sort of talked about like like trying to compare contrast to HCR and Eodic stenosis right because those are two like somewhat similar murmurs let me go ahead and talk about like just differentiating between mitral valve prolapse and mitral regurg right mitral valve prolapse and mitral regurg because those are two other murmurs that they love to compare and contrast with like oh what makes it sound better what makes what makes it sound louder what makes it sound softer so that you don't get into trouble on your test so the thing is again you don't have to memorize crap just remember the principle the thing is in mitral regurg if you put more volume in the left ventricle right there will be more blood in the left ventricle to regurgitate through the bad valve okay so anything that increases the amount of blood in the left ventricle w

ill make the murmur of mitral regurg sound louder okay now mitral valve prolapse in fact I wish I could make like a schematic but basically just think of it this way picture in your mind that you have like the mitral valve leaflets like the two mitral valve I mean right the mitral valve is called a bicospid valve for a reason it has two leaflets right so the thing is in mitral valve prolapse those leaflets don't overlap well right and because they are not overlapping well then you have basically like regurgitation okay so the thing is whenever you actually so here's the critical concept whenever you put more blood in the left ventricle those two mitral valve leaflets overlap appropriately they overlap the way they were created to overlap and if they overlap appropriately the regurgitation goes away so the concept is whenever you have more blood in the left ventricle mitral valve prolapse actually sounds softer contrast that with mitral regurg when whenever you have more blood in the left ventricle mitral regurg sounds louder because again there is more blood for regurgitation across the valve if there is more blood in the left ventricle versus in mitral valve prolapse where if there is more blood in the left ventricle you have like a monmaterial overlap of the two mitral valve leaflets so you have less regurgitation so the murmur sounds softer okay so again if you understand those concepts and then put it together with my explanation of like hand grip stand in squatting on all that crap you'll see that you can analyze like oh this will make the sound softer this will make the sound worse and blah blah blah right so think of it this way so say for example right you you do the valve salve them and over right if you do the valve salve them and over that will decrease preload if you decrease preload there will be less blood in the left ventricle and if there is less blood

in the left ventricle mitral regurg will sound softer right because there is less blood in the left ventricle so there is less blood to regurg through the bad valve but if the patient has mitral valve prolapse they will have less blood in the left ventricle so they'll be very unfavorable overlap of the two mitral valve leaflets so the murmur will sound louder okay so that's the way to sort of keep those two those two straight okay so I think that's all I'm gonna say about those murmurs for now so I think I'm gonna go ahead and move on right so what if they give you a question about a patient that presents and he presents with like the classic orthotnia, paroxysimonoctynal dyspnea and we have like three plus a dima right you already know that and then they'll usually put like an S3 heart sound on an exam right if you see that I hope you're thinking about like CHF exacerbation right so how do you treat a CHF exacerbation right obviously if you're hypoxic for me you want to sort of like put them on oxygen right but the big big thing you want to do is lube diuretics right so like lube diuretics like feroxamide right that will sort of like get rid of get rid of some of those fluid remember your lube diuretics work in the kidneys and then because by basically by giving a loop right think about it you're drying them out to your decreasing preload so you're basically giving their their hearts a break for the most part and you're decreasing that a dima right like that pulmonary dima that's sort of like making their lungs wet and making it hard for them to breathe right to exchange oxygen efficiently right I mean another thing you can actually also do is to give like morphine you can actually help with some of the shortness of breath in fact they'll usually make it in a patient that has like really bad CHF that's like terminal so let's say like the AF is like 10% multiple read

missions the correct answer on the exam for those people can actually be morphine especially if they tell you in the question that they've been giving like lube diuretics and all that crap and then right don't forget like as clinical pearls don't forget to measure your eyes and nose see if you're net negative check their electrolytes remember if a patient is in CHF exacerbation usually give pretty heavy doses of l6 remember l6 can cause like hypochylemia and hypointrym and all that garbage so you want to sort of keep an eye on those patients are electrolyte right and then you want to do like daily weights and all that okay so I think that's all I'm gonna say I'm gonna all I'm gonna say about that so let's see what I was going to talk about yeah I've just gone for 21 minutes so yeah I think there's more stuff I can talk about okay how about I give you this case so what if they give you a question about a patient and the patient says like in the Q-stem it tell you that this patient has pleuritic chest pain right they tell you that oh when it takes a deep breath chest really hurts right but when he leans forward the chest pain sort of goes away what are you thinking about on the other circumstances I really hope you're thinking about a pericarditis right pericarditis right so remember a cure pericarditis usually presents with like your classic pleuritic chest pain gets worse in when you lie back gets better when you lean forward right and usually those patients will have a fever on an exam right and then they may tell you that on a scutitian you have like a friction rub right and sometimes people say like divine but people that have like I don't know like viral pleuritis right they will also have a friction rub so here's the way you differentiate those two things on exams right if they tell you that when the patient holds the breath the friction rub disappears then that

tells you that it has to be a it has to be pericarditis right because if you hold your breath guess what is not moving against each other anymore your pleur your pleur is not moving against each other so the pleuritis like friction rub goes away but it's not like when you hold your breath your heart stops beating right that doesn't really happen your heart will keep beating I mean if you hold your breath for long enough your heart probably stopped but it doesn't stop instantly right so your heart will keep beating so you still keep having contact between your pericardial leave here right so you keep having the friction you'll keep oscitating the friction rub right and then remember right on EKG right classically these patients with pericarditis they'll have like the diffuse st segment elevation they'll have the PR segment depression remember the st segment elevation is usually like pretty diffuse right so it's like you're like man this st segment elevation does not appear to be obeying any particular vascular territory when you see that think about a pericarditis right and again they may have like the fuse PR segment depression well let me tell you this classically on these exams they may not give you the diffuse PR segment depression you're looking for they may just give you like the PR segment depression in lead to having a PR segment depression in lead to on these exams like these are ABIM exams or like the MDME exams they are very classic for pericarditis so that's something to keep at the back of your mind and one thing I'll encourage you to do this is again just a clinical trial for patient comes in pericarditis it probably makes sense to go ahead and check the troponing don't just say oh the fuse ST elevation so they cannot be having an MI or something you don't want to get burned right I'm sure like they'll be a nice attorney they'll be willing to come and ext

ract some of your income so I will encourage you under the circumstances just you'll check a troponing just to make sure you're covering all your all your bases right and I mean I know that for the most part you know these guidelines that all if you are more than two hours away from a PCI capable center you should go ahead and give TPA if a patient has an MI the thing is if that's why you kind of want to make the right diagnosis of acute pericarditis because here's the thing for patient has pericarditis and you're like hmm ST segment elevations it's an MI and you give TPA you're good based like you basically increase the patient's risk of converting from pericarditis to acute cardiac tamponat and then you have a huge problem on your hands you can go from a situation where the patient can leave for a while to like dying instantly so I kind of want to be careful with that right so try to make the correct the correct diagnosis so how do you treat acute pericarditis right like you can give aspirin usually I'll say on these exams aspirin plus an N set is usually a pretty good pretty good choice another classic scenario they can present is they can present the person that is having like recurrent recurrent like they keep coming to the hospital for pericarditis for those patients you also still want to give the aspirin but the thing you can add is like a long course of a coach is in okay before people used to say oh steroids steroids steroids for a pericarditis but it does look like there's some studies that are coming out that actually show that steroids appear to increase a person's risk of recurrence of pericarditis so I will see that on these exams think more about like aspirin plus an N set for like the acute event and then if you're having like recurrent pericarditis like aspirin plus a steroid okay I mean sorry aspirin plus coaches in like a long course like maybe lik

e three months of coaches so that's just something to keep up to keep in mind and you usually give like the like the big aspirin doses right so like your like your M.I.

dose basically okay and I mean what are the classic patients that get pericarditis on these exams right so commonly it can be like a post viral right so they have like a viral respiratory infection and then they get pericarditis afterwards right so that's something that can cause that don't forget if they give you like an immigrant or a person like from some developing country think about TB right TB can cause pericarditis in these are people people that have like these are autoimmune diseases well I guess you can call them connective tissue diseases so like I don't know like lupus or like rheumatoid arthritis scleroderma they can all have pericarditis right and then if a patient has like radiation therapy to the chest right so like for a lymphoma right that can increase the risk of like pericarditis radiation is known to cause like peritis pericarditis remember right having a radiation to the chest is the biggest risk factor for thyroid cancer right like especially like papillary thyroid cancer on these exams so that's just something like a side piece of knowledge you want to keep in mind remember right you remia right so they can give you like a renal patient with pericarditis think about you remia's the cause remember you remia can also cause like bleeding because if you have a normal platelet combo your platelets don't work well because remember right uh uremia sort of makes platelets unable to degranolita appropriately so that can sort of like increase your risk for like a bleeding like a coagulopathy also um uremia right sort of makes your white blood cells not degranolita appropriately so that's why renal patients are kind of like a high risk for infection okay because your white blood cells basically don't work right and then don't forget right under classic scenarios like uh like a post-mi patient right so especially an mi patient that gets like a cabbage rig

ht so like a post-pericardia to me a syndrome right after like open heart surgery people can get pericarditis with that and then also mi remember like your dressless syndrome right like the autoimmune pericarditis uh you again treat that with like an insect aspirin the the works right so um it's another immune pericarditis tends to shop like a week or two after the mi event right you can even shop up to six weeks later so think about dressless syndrome as another cause of of a pericarditis right and then um remember that if a person has like long-standing pericarditis or like repeated episodes of pericarditis right they can go from acute pericarditis to like something called constrictive pericarditis right constrictive pericarditis and the thing is um constrictive pericarditis is really bad but the thing is um constrictive pericarditis it's usually pretty easy to make the diagnosis so how I mean the way you let me think about it right that that's why I kind of like a test print because it's kind of like logical the thing is if you really think about it how can they make a constrictive pericarditis question hard the easy way they can make it hard is to write the question to look a lot like restrictive cardiomyopathy right so really the big thing you want to know about constrictive pericarditis is how can I differentiate this crap from restrictive cardiomyopathy right because the management is kind of different right so you want to make the right diagnosis and another reason you want to make the right diagnosis is so you don't feel your exam right so that's probably a nice uh adeda um motivation there right so remember if a person has constrictive pericarditis you can reverse it with a pericarditis to me right so get rid of the pericardial sac and the patient will be fine first is restrictive cardiomyopathy where you're going after um like a heart transplant right and s

o let me just try and differentiate some of these things for you and then i'll tell you like some things that are kind of specific to um to constrictive pericarditis right so the thing is i already talked about the causes of pericarditis right restrictive cardiomyopathy you want to think more about like infiltrative disease as the theology right so the thing is here is a trick uh use quite successfully on many exams anything that ends in osis so osis like osis anything that ends in osis causes restrictive disease of the heart and lungs okay that's like a nice trick there like think of um like i don't know like restrictive lung disease right sarcoidosis causes restrictive lung disease pulmonary fibroosis causes restrictive lung disease if you look at restrictive cardiomyopathy right look at the causes amyloidosis amyloidosis is actually the most common cause very high you to know that is the most common cause of restrictive cardiomyopathy right but other things that can cause restrictive cardiomyopathy sarcoidosis hemochromatosis right uh here are the trig fibrillastosis right those things all end in osis right they all cause restrictive cardiomyopathy and then in constrictive pericarditis right so there are some key things you want to keep in mind right so those people can have something called like kosmol sign right um so kosmol sign right it's uh basically like uh when a person has like an increase in jvp when they take a deep breath when they inspire okay when they inspire right this is something that you um see a lot in our constrictive pericarditis on exams right and we think you can see divine know why is that well think about it if you're inspired right what happens to intra thoracic pressures intra thoracic pressures go down so if you're if your intra thoracic pressures go down it's like your your right ventricle right atron will be more accepting of blood rig

ht so you're preload your venus return should increase right and the thing is that increase is brought about because when you take when you inspire you are decreasing your venus ret your decreasing your intra thoracic pressures your right atron right ventricle is relaxing your jogular veins should basically collapse with inspiration right because it's like oh you are decreasing the pressures in that system because the intra thoracic pressures are down but think about it if a person has constrictive pericarditis your right ventricle is no longer compliant because guess what's happening it's being like basically like it's like it's like there's stone like it's like you've basically like cemented your ventricle awards right so your right ventricle is not compliant so even if you inspire that decrease in like pressures in the right side of your heart does not happen so that in your body is like oh I just this person I just inspired so let me bring more blood to the right side of the heart but it's like the blood gets there and because your right ventricle is not compliant it has nowhere to go so your jvd your jv like pressure actually increases so if you have an increase in jvd on inspiration that's close mall sign that's the pathophysiology think about constrictive pericarditis or you examine and then in constrictive pericarditis if you're also looking at the jvp like tracents you'll get like the x and the y descent like a rapid xy descent I will talk about the pathophysiology behind that at the very at the tail end of of this podcast and then another classic thing they will show you is they can show you like a chest x ray or show you like a cut scan of the chest and you see like white around the heart those are calcifications right so if you see those calcifications around the heart you can probably pretty much stop reading the question it's constrictive pericarditis ju

st be can answer related to it and move on and then they may tell you that oh when you're scooting the chest you'll have like a dastolic like knock like a pericardial knock sound okay that's pretty classic again for constrictive pericarditis you hear the knock because again it's like you've cemented the borders of your heart right so think about it I mean try to knock your thighs I mean I'm knocking my thighs right now you can barely hear anything but if you're knocking a table you can hear that if you're like knocking like something that's hard like calcified pericardium you hear that pericardial knock sound and then I mean another sneaky way they can try to test you on this is instead of showing you an image where they show you like calcium or like white around the ventricles the images show you that oh the me show you like the pericardium being thick if you see like a thick pericardium also think about constrictive pericarditis the thing is usually on imaging you should not be able to measure at least by like your eye it should not be able to measure the width of the pericardium if you're able to measure the width that tells you that the pericardium is thickened think about constrictive pericarditis on that those on that those are circumstances and then another thing you kind of want to think about it's like this finding like this is how they can basically make a constrictive pericarditis question like really hard right they can basically give you pressures in all the four chambers of the heart right and maybe like what are they going after here this is something you really want to think about if you have equal pressures or they tell you that oh there's equalization of pressures in all the chambers of the heart in diasteli okay in diasteli the first thing you want to think about is constrictive pericarditis another thing you should also think about on exams is a ca

rdiac a tamponat right you can have those issues again because again think about it in diasteli right the heart is supposed to be able to relax right and remember that in diasteli you're basically feeling the ventricles from the atria so you may see divine come on who cares if the pressures in the four chambers of the heart are all equal in diasteli and boohoo what's my problem there let me explain why that should be a procre- a consideration for you think about it remember for you to be able to have flow you need to have pressure differential right like things flow from high pressure to low pressure so guess what if the pressure in your right atrium is the same as the pressure in your right ventricle and there is no pressure differential guess what happens to fill in of the right ventricle it doesn't happen if your right ventricle does not feel hmm I don't know maybe you won't be sending blood to your lungs if you don't send blood to your lungs you get hypoxic right and then you run into a lot of trouble so that's why cardiac tamponat and the constrictive pericarditis are not necessarily a good thing right so um uh those are the two conditions on these exams that are classically associated with equalization of pressures in all four chambers of the heart are during the astral um so you may say okay divine if these two conditions have those that the same finding how do I differentiate between them right so the thing is if a person has constrictive pericarditis they will have like that rapid x descent on a joguila venosa pressure atricin um but if a person has um um cardiac tamponat they will have like an absent x descent so that's the way to sort of differentiate those two and the thing is the reason people that have constrictive pericarditis they tend to have like more right-sided problems is if you really think about it right the right side of the heart at baseline h

as lower filling pressures than the left side so if there is something that is compressing the cardiac chambers the right side is going to fill it more because it just has less ability to resist anything compressing it from from the outside okay so I think that's all I'm going to say about a constrictive pericarditis but I feel like since I've said a lot about like this joguila venosa pressure tree since let me just go ahead and um like in like four or five minutes just real quick go through like the key things like keep a thought like basically go through like the jvp tree since and then go over like keep athologies that are associated with them right so you may do you necessarily need to understand this for these exams no to be honest with you but the thing is if you understand them cardiology questions become like layups I mean if you're a basketball fan you want to you know what a layup is basically if you see a cardiology question if you really get like the venus cardiology is one of those fields where if you really understand the physiology the questions are like a joke because like regardless of how hard they write it you can sort of read through whatever crap that the person that wrote the question is trying to thread you right so let's you can skip this part if you're like uh just memorize stuff and move on that's fine but uh if you want to kind of understand just give me like four or five minutes of your time and I promise I'll make it uh make it worth your one right so let's talk about like I guess like the chemistry of a jvp right so in a jvp the first thing you want to think about is the a wave right and your a wave it basically arises from it's like a pressure increase in that you see your jogger veins right from your right it from contracting right so if your right it from is contracting think about it right your it's your pressures will go up if your p

ressures go up you'll sort of see like like an increase in pressure or like a pulsation in your jogger vein right so that's the big thing you want to keep in mind so what are the pathologies of the a wave that you may want to keep in mind for these tests right and you may tell you that this patient has no a wave or he can show you a jogger vein of spulse where there's no a wave like a flattening of the a wave if you see that you want to think about a fip right because remembering a fip you don't have like a coordinated like atrial squeeze so if you don't have a coordinated atrial squeeze um your you're basically not contracting well as a right it as like a right it from right so your a wave will disappear because the a wave is significant like signifies contraction of the of the uh right it from now what did they tell you that the patient has giant a waves giant a waves so the thing is think about it if the right it from needs to generate more force than is required for um to move blood from the right it from to the right ventricle right the right it shall a wave should be bigger than normal right so think about if a patient has like tricospit stenosis for example that can cause uh that can make the right it from have to work harder to send blood forward so you need to generate more force with like contraction right and that can that can cause like the giant a wave now another thing you may see they really want to mess up your mind on test is the canon a wave right so the canon a wave is basically an a wave that because nobody the a wave sort of like has a gentle up slope and then a gentle down slope but if you see like an a wave that basically looks like a like a straight triangle like goes up and down abruptly um that's what's known as a canon a wave that basically happens when your like your right it from is contracting when like the tricospit valve is closed shut

right so what's the classic scenario with that on exams that will be like a third degree AV block um right remember then the h and the ventricles they're they're not they're basically not talking to each other anymore so the right it from can be contracting when the right ventricle is contracting which is not what is supposed to happen right so uh that's the situation where the right it from can contract against like a closed tricospit that's what will classically cause the canon a wave on on these exams now the next thing that sort of comes up is like the c wave right so the c wave um basically the thing is after the right it from contracts you know sends blood to the right ventricle the tricospit valve then closes right and while the tricospit valve closes right the right ventricle is contracting we remember the right ventricle does not begin to eject into the pomonic system um um um immediately um when the tricospit valve closes right I mean if you remember from med school whatever you probably remember this whole concept of iso volumetric contraction uh the thing is like I sort of think of it as like the right ventricle kind of like warming up before it sends blood to the pulmonary um pulmonary um the pulmonary arteries right so um the c wave is the next wave it basically happens when the tricospit valve and uh and the pulmonic valve is closed right so the right ventricle is contracting as the right ventricle is contracting uh it will try to like blow back some blood to the right it from well the tricospit valve is like closed shut so it's like the tricospit valve will like blow back into the right it shall like cavity or like lumen if you may so that will transiently raise the pressures in the in the right atrium and that's pretty much all you need to know about the c wave now the x descent so the x descent um it's actually like a blood pressure decrease I mean l

ike a right atrial pressure decrease so remember I said that I just said that oh for the c wave the the tricospit valve is closed the pulmonic valve is closed the right ventricle contract you have a blowback of um of blood and as you're having that blowback of blood that bluster like slaps against the tricospit valve when it slaps against the tricospit valve um the tricospit valve sort of bulges back into the into the right atrium when your bulges back into the right atrium that transient derises the right atrial pressures now the thing is what then happens when the pulmonic valve opens right when the pulmonic valve opens all that pressure that has been building up from the right ventricle kind of like warming up is sort of dissipates because there is now like an open route for the blow through the pulmonic valve to like the lungs right so the thing is that tricospit valve that bulged back when we had the c wave it will now bulge into the right ventricle and if your bulges into the right ventricle then that's like lowering the pressures in the right atrium right lowering the pressures in the right and when you lower those pressures in the right atrium right the right atrium kind of relaxes and is more willing to accept blood and as it's accepting that blood obviously right blood will leave your like your internal joguula vein right so you have like a decrease in pressure on your joguula venosa pulse right so um the thing is if you do not see any x descents right that tells you that your atria is really not relaxing as it should right um so that can happen if for example um something bad happens where your tricospit valve is incompetent right so like a tricospit regearge uh if you have a tricospit regearge instead of the itchers to be relaxing it's accepting some blood back from the right ventricle so that can cause like an absent um um exa descent but another thing yo

u can think about is if a person has like a prominent ex descent the thing is when one thing that can cause like a pressure tracing to be more prominent is if things happen abruptly right so i sort of think of it this way right so let's assume you're driving on the highway right and you see like the police like a mile ahead of you because you have like x revision or something like that you can slow down gradually over large distance right so the people in your car will be like oh you're such a good driver you're slowing down gradually right well let's assume you see a police officer like a police car and you see them like measuring the speed like i don't know like 300 feet away from you and you try to like decrease your speed you hit the brakes abruptly and your your vehicle just sort of like comes to like an abrupt stop right so the thing is that happens when you're like stopping your tracks over a very short distance so the thing is if a person has constructive pericarditis um when blood hits the right ventricle it hits it like very abruptly right um because it's like the right ventricle is not very compliant so because you're having that just abrupt like is like you're stopping the blood in the right ventricle like abruptly in its tracks that can basically cause like that relaxation of the of the like the right ventricle like contraction and sending blood out through the pomonic valve that sort of makes that process like end quicker than you expect so your x descent because it's like oh normally things are gradual no it just happens quickly so you have a prominent x descent kind of like the same thing actually happens with the y descent as well but i'll talk about that in like a minute because there's one thing that happens before you have the y descent and the thing that happens before that is like your v wave right so your v wave is basically like um an increase

in your right it your pressure that just happens because now you're having like venus return right so more blood is coming to the right it from like your ventricle and all that crap right so obviously if blood is being dumped in the right it's that will increase the pressures in the right it's the classic thing that you can test is if a person has like a giant v wave right so giant v wave that'll happen if more like more blood than normal it's coming back to the right it's right so again if you have like like try cospery regurg right it's like the h right it from is accepting blood from the svc abc but is also accepting blood from the right ventricle right so that'll cause like a giant like a giant v wave and then the y descent basically happens when you're having like like ventricular dastily right so blood is filling the right ventricle from the right it from obviously as blood as blood is filling the right ventricle from the right it from the pressures in the right it from will decrease right so it would like sort of empty and that will decrease the pressures right so you have like a decrease in pressure that's your y descent it's called the descent right because things are going down right so the thing is think about it right if a person has like a cardiac tamponad right in cardiac tamponad right because think about if your right it from is empty with blood it should relax but if your right it from is empty but there's still all the pressure from the outside because there's fluid around the heart right your right it from will not be able to relax right so that relaxation that should happen that y descent that should happen sort of disappears so you have no y descent in in a cardiac tamponad but again if you remember when I um when I said that if you have like tricospits stenosis right it's like if you have stenosis is like yeah you can let blood out of the right i

t from where you are letting it out at like a slower pace than normal because there's just like less room for the blood to go through the stenoster tricospit valve that can cause like a more gentle y descent if you may and then remember constrictive paracaditis like that abrupt crap that happens right if you have like a large like a prominent abrupt y descent think about constructive aparicaditis um on that those are circumstances so I know this was a lengthy podcast but really I promise if you understand this it will just make analyzing many of these cardiology questions a lot easier and then so I'm gonna go ahead and stop here so I'll put you out of your misery but as I always say hopefully you've gotten something from this and I do offer one on one tutoring for all the USMLA exams so step one step two CK two CS step three the complex exams um the preclinical med school exams the third issue of exams uh my do actually tutors on people for the medicine boards and uh uh medicine in training exam um and then if you have like a colleague or acquaintance that is in college and studying like biochem, okem, gen-cam physics, um histology, physiology, alpha one and one tutoring for all those things as well um and then um if you're preparing an application right so let's say you're a med student applying to residency so like an ERAS app or college student applying to med school so an AMCAS app I don't offer like one on one consulting for those so like preparing applications, personal statements, mocking interviews, stuff like that um I also do that one on one I mean all the people I advise this past cycle they all matched because I've actually been on like the admissions committee of a top two med school um for a whole year so I've shifted through thousands of high quality applications so I know the things that can basically like help you put your best foot forward so I will

see you in the next podcast have a wonderful day and uh I guess have a wonderful night because I'm actually going to bed right now it's almost a midnight I gotta go to the ICU tomorrow so I'll see you in the next podcast, sleep well and God bless you thank you

The hand grip maneuver (compressing radial arteries).

Hypertrophic cardiomyopathy (HCM) murmur.

Increased LV volume makes MR louder, but makes MVP softer (due to better leaflet overlap).

Calcifications around the heart, diastolic knock, equalization of all four chamber pressures.

Oxygen supplementation and loop diuretics (e.g., furosemide).

Cardiac tamponade.

Constrictive pericarditis.

Amyloidosis.

Amyloidosis, Sarcoidosis, Pulmonary Fibrosis (or Hemochromatosis, etc.).

Diffuse ST segment elevation and PR segment depression.

Intra-thoracic pressures decrease, leading to increased venous return and causing the Kussmaul sign (increased JVP with inspiration).

Sudden cardiac death in young athletes.

Dressler's syndrome (autoimmune pericarditis).

Amyloidosis.

Amyloidosis, Sarcoidosis, Pulmonary Fibrosis (or Hemochromatosis, etc.).

Diffuse ST segment elevation and PR segment depression.

Intra-thoracic pressures decrease, leading to increased venous return and causing the Kussmaul sign (increased JVP with inspiration).

Sudden cardiac death in young athletes.

Dressler's syndrome (autoimmune pericarditis).