DIP Episode 172 - USMLE Step 1 Cardiology Review Series 5 (Congenital Diseases)

Okay, welcome my name is divine. This is a piece of 172 of the divine intervention podcasts. In this podcast I will be continuing the US and the US step one cardiology review series. This will be series five and again I'll talk about some high-year things and just I guess one I guess housekeeping thing. So at the end of the podcast I will just review the Vovila pathologies again real quick probably like in like five ten minutes because I don't know it's just an area found to be hard for people to grapple with on MBME exams. So I will spend some very quick time at the end just talking about the high-year things that are tested with those and just move on just move on from that. So let's jump right into it. What if you get a question about a child right? And this child you know is the child of a mom that you know has you know maybe drunk a ton of alcohol or impregnancy and in the tell you that you hear a holosis stomach murmur and left-low sternobotor in this kid. What's your diagnosis with that? That's a VSD right? And obviously I mean a VSD is a bad thing. You know that you can ultimately progress to like you know things like at first I mean you will be like a left to right shunt but you know over time if you have like pulmonary hypertension you can then become right to left and then you have isomangar physiology and all that badness. So talk about that as you go along. So really for the both part I just want to you know kind of take a stab at the congenital heart diseases.

I think the big thing I want to try to understand with the congenital heart diseases is first you know kind of understand how fetal heart circulation works and then when I start talking about the different diseases most of it will kind of make sense and again obviously I'm not going to talk about all of them. I'm just going to talk about like you know like the big ones and then those big ones you know kind of then the you know the little ones where you need to know like one or two things about them I'll kind of talk about that. So how those normal fetal circulation happen right? So basically right the thing that happens is you essentially have the placenta that's where like gas exchange happens and then the placenta you know it's almost like it's like you have multiple tubes and then the form one tube that one tube is the ombicovene right and then that ombicovene so because sometimes you literally see an endemic exam questions really ask that what vessel in the you know in the in the kit right especially when a kid is in the utero has the highest oxygen temperature that's actually the ombicovene. So the ombicovene you know kind of sends blood that blood keeps going going going and then as it goes around the liver it takes a detour called the doctors venosis and then that that that doctors venosis right it ultimately forms in fear of an achyvo blood.

The thing is that the IVC blood for the most part it you know goes to the right atrium and once it's in the right atrium it goes through the fremenoval to the left atrium right and then from the left atrium obviously go to the left and trickle and go to the rest of the body. On the other hand blood that comes from the superior venerate and a kid the thing that really happens is that most of that but you know it goes into the right atrium from the right atrium it goes to the right ventricle so from the right ventricle obviously we're going to the pulmonary arteries right but the thing is from the pulmonary arteries will actually go through the doctors' ateriosis okay go through the doctors' ateriosis to the other and then his sort of goals continues down the rest of the other that way and you may say okay do my way doesn't he go to the lungs well think about it right.

A fetus most of his lungs are bifid and fluid so the fetus lungs the fetal lungs are kind of hypoxic and remember that hypoxia causes viso-construction right so that viso-construction essentially causes a really bad pulmonary it's almost essentially a physiologic pulmonary hypertension in utero right so the pulmonary pressures are too high so blood does not go from the pulmonary artery so like the pulmonary capillary is not what happens is blood goes through the doctor's ateriosis from the pulmonary artery to the other and then that blood from the other ultimately goes back to the placenta through the two pulmonary I mean to go back to the placenta to the through the two umbilical arteries okay so we have one umbilical vein and two umbilical arteries if you have one umbilical artery that typically has an association with having like other like congenital heart diseases and that doctor's ateriosis the thing is for the most part whenever you have hypoxic conditions having happening in a kid that tends to keep the doctor's ateriosis open which is which is you know good in some way because again like I said the hypoxia the relative hypoxia around the lungs of the fetus you know can keep the doctor's ateriosis open and the thing is the placenta also makes personal gland in e2 okay personal gland in e2 can also actually help with um you know it is actually the primary agent that helps you keeping that doctor's aterosis open the thing that ultimately happens is you know when a kid is born and you know taking a deep breath they go from hypoxia to you know more oxy they go from hypoxia to amoxia and then those no-moxic conditions you know will increase the production of caracolomins and that will cause a viso constriction of the doctor's ateriosis and it then becomes the ligamentum ateriosis and essentially the doctor's ateriosis closes so um so again everything you know goes

back to the through those two umbilical arteries to the back to the placenta so that you can repeat the whole cycle again and then remember right that you know after a kid is born like I said the doctor's aterosis closes um and then the foreman ovale for the most part right now you know the doctor's aterosis you know takes it a couple of days to close but for the most part the foreman ovale should really close within the first the first you know day maybe two days but usually the first day of life it should be closed because the high pressures on the left side of the heart should essentially slum it shut against the against the right side of the heart so it closes okay and remember that the foreman ovale becomes like the fossa ovale that's one thing your friends at the mbmi love to love to test stuff on exams so let's go ahead and you know jump to the congenital or heart diseases um the big thing you want to remember about these congenital heart diseases is just you know remember like because the thinnest right many people try to like memorize memorize memorize the thinnest memorization is not really gonna get you very far with these are congenital heart diseases to be honest because the thinnest most times the mbmi doesn't test your ability to memorize like crap with these are congenital heart diseases what the mbmi tends to test for the most part is they just see okay can you analyze like hemodynamic factors that may occur in a person that has a certain congenital heart disease right so those are again big things you want to keep in mind but I think before I start delving into them I think it probably makes sense to talk about some high-yield associations with the uh some specific congenital heart diseases right one thing you want to keep on the back of your mind if you remember when I think I may have you know in my genetic diseases podcast I may have talked about

hunting disease where I say that oh you know it's a trying to repeat the disorder or a zomodominant inheritance C.E.G trying to repeat chromosome four is all screwed up right I talked about how those trying to repeat disorders especially for the most part you know the things being inherited in an orzomodominant fashion and then I talked about how they illustrate certain genetic principles right so I talked about how they demonstrate the principle of anticipation right way you know as future generations of born the disease comes in a most severe form and it comes much earlier in life right so the thing is whenever a condition demonstrates a genetic principle that is something the endemic expects you to know right also kind of like the same thing with um with like uh um predatory and engolment syndrome right and how they you know talk about like genetic imprinting and um uniparental disomni right those are all high-yield things you want to know the thing is the genetic principle you want to keep at the back of your mind with congenital heart diseases is that most of them have more typhacterial inheritance okay most of them have more typhacterial inheritance most of the factor just means there are many things that it's not like oh like I mean yeah there's some you know disorders that you know want to one relationship with congenital heart diseases but really for the most part uh there's many factors that come into play like genetics or environment yada yada yada into uh having a person I have a congenital heart disease so multi-factual inheritance that's one thing you really want to commit to memory for purposes of the endemic exam right and then remember like uh uh uh of all the congenital heart diseases right a VSD you know it's pretty common it's probably the most common on endemic exams and remember that uh VS Ds they have an association with like infants of a diabeti

c mom right like infants of the diabetic mothers they tend to have like they can either have like VS Ds they can have hypertrophy cardiomyopathy um I talked about that in the prior podcast and then um uh uh kids where they are you know mom consumed a ton of alcohol in addition to like the smooth field trauma and all that stuff they also tend to get VS Ds and then remember right rubella right so congenital ribellate syndrome has an association with like patented doctor satiriosis right so those like weird key high-yield associations you want to keep them at the back of your mind I mean like lithium lithium and epstins and nominee right where you have like uh itchialization of the right ventricle right remember that's uh that's a key association or if mom is taking like phenytoine for for you know like some uh seizure disorder that she has that can cause something called a fetal high-dentined syndrome right so that's one association when you keep in mind remember that when people have a lupus right when people have like children syndrome um those anti-ro and anti-lanty buddies they can cause they can cross the placenta and damage the conductance system in the fetus and cause like a third-degree hard block right so that's one thing you want to keep at the back of your mind even a line of disease can also ultimately cause a third-degree hard block um so again those are just again key associations you want to keep in mind um uh uh so I think you know those are probably like the big big big one side wall uh I'll go ahead and uh I'll go ahead and mention so and the thing is congenital heart diseases where you can kind of classify them as okay like are they cyanotic or a cyanotic that is probably the most common dichotomy that most people use uh when they are presenting this material to folks and I think it's a good dichotomy obviously the cyanotic congenital heart diseases bad

right because you're cyanotic right so you're not supplying enough oxygen to your organs and then the ones that are a cyanotic right I mean they're they're you know they're okay at first but they ultimately become bad because most of these a cyanotic congenital heart diseases be tend to be associated with like a left to right shunt initially what the thing is that left to right shunt can ultimately cause especially if you don't treat right that left to right shunt can ultimately cause um um um um pulmonary hypertension and then that left to right shunt then reverses and becomes a right to left shunt right because the blood uh when you have pulmonary hypertension the pressures in the right ventricle increase so that essentially reverses the shunt and then you then turn from an isanotic heart defect to a cyanotic heart defect right and that can ultimately to I mean that phenomenon is known as like uh isemanger complex right and that can ultimately cause cyanosis and once people get that those people usually end up requiring like you know like a heart and like a heart transplant for the most part so uh sometimes they even need like a heart long transplant which is obviously not ideal right now if you remember early in this uh like the podcast from last time right I said that when people have uh um um uh endocraditis right like I was talking about like the risk factors for endocraditis I believe one of the things I said is that when people have congenital heart diseases especially like the cyanotic ones that actually increases the risk of having an endocraditis so typically a classic mbm question may be a person that you know is getting like some kind of surgery and they have like a cyanotic congenital heart disease um usually those people especially the cyanotic congenital heart diseases not those people typically need some kind of antibiotic umprophilaxis before the su

rgery starts right so you usually give like some kind of penicillin-based compound like umpicillin or something like that that's actually something very high you do you want to keep at the back of your mind for exams and then I also said earlier that you want to make sure you are able to like analyze himodynamic factors with regards to these are congenital heart diseases on the USMELY exams one big one you want to keep in mind is think about it right like if blood is coming from the rest of the body right obviously it comes in through the vein akeva right it's like the SVC and IVC right comes in through those into the new comes in through those to the to the right side of the heart right the righty trip right and obviously that blood is deoxygenithead right I mean it's not unoxygenithead it is deoxygenithead it still has some oxygenating I mean the oxygenation is probably like you know like 75% are there about right so you know but the thing is if you think about it as you go from like uh SVC IVC to like righty tremorite ventricle the blood oxygen tension should be decreasing right and then when you get to the lungs the blood gets oxygenated and then it goes to the left side of the heart that's what should happen normally right but if for example they give you an nbmi question and typically you know they'll meet this question bizarre or you know try to scare you or whatever well these questions end up being like extremely easy if you know exactly what they're asking about but if for example you notice that a person's oxygen like blood oxygen saturation is rising as you go from the righty tremorite ventricle or as you go from like the righty tremorite ventricle to the pulmonary like arteries that's not normal right that tells you that they must have been some kind of intermiction of blood that is deoxygenithead and blood that is oxygenithead that essentially tells you

that the person has a left to right shot okay that's a very specific finding in left to right shots on nbmi examples on the other hand if they give you an nbmi example question I you notice that the oxygen tension is dropping as you go from like left to left ventricle or from like left to left ventricle to the other right that tells you that they must have been some kind of intermiction of blood between the right side of the heart essentially deoxygenithead blood and the left side of the heart oxygenithead blood right so that has brought down the oxygen tension so whenever you see a decrement in oxygen tension as you because you go between chambers like chambers on the left side of the heart that tells you that the person likely has some kind of rights to left shot again it means sound like a benign concept I promise you it's not a benign concept they love to actually test this stuff on the usml exams not just step one they also love to test the stuff on step two seeking and they love to test the stuff on step three and you likely also see this stuff a stuff a tested a tested on the shelf exams you're taking you're taking a third year okay so again these are all big things you want to keep at the back of your mind with tests and the thing is one thing that I guess I'll go ahead and mention what left to right shot I don't know for whatever bizarre reason this concept is not usually emphasized quite well actually I'll see maybe two concepts I want to talk about so this then for whatever reason is not you know typically emphasized quite well on mbim exams actually I take that back three concepts I want to emphasize this concepts I guess let me say what I want to say these concepts I don't know for whatever reason it doesn't just pop up on on tests common I not on tests not in resources commonly but I'm gonna talk about it right so I think my first exposure to this concep

t was probably like in BRS physiology something that kind of like modified my thinking on these are continental heart diseases right so here's the thing whenever a person has a left to right shot most times everyone says oh because of the left to right shot you know the right ventricle will be the right ventricle will be overloaded which is true right you know the right ventricle gets overloaded the person ultimately gets you know pulmonary hypertension right and that causes trouble but one thing you should actually remember is that when people have left to right shot that actually causes essentially like an eccentric hypertrophy of the left ventricle so you may see divine why is that the reasoning behind that is when you have a left to right shot right you're sending more blood from the left ventricle to the right ventricle that extra blood in the right ventricle you know you will go to the lungs that will cause like an increased venous return pulmonary venous return ultimately to the left side of the heart so because the left side of the heart is getting progressively volume overloaded right because it's just getting more venous return than it's used to that's an example of an a volume overload kind of situation right and that will ultimately cause a diluted cardiomyopathic from the eccentric hypertrophy so again that's one of those you know kind of like weird bizarre things you want to keep at the back of your mind that's the first that's the first thing second thing I wanted to mention is that when people have sanotic congenital heart defects I'm one thing that tends to happen in these people is they tend to have like polycythemia right because remember whenever a person has a sanotic congenital heart they're sanotic right so because they're sanotic they're in a state of hypoxia and there's this I believe it's transcription factor it's called like hefu and alpha i

t's like hypoxia inducible factor one alpha when a person is hypoxic that increases expression of the transcription factor and you begin to make more and more erythropoiten if you make more epoch right now obviously increase the oxygen carrying capacity of the blood this is a very nice way of friends at the beginning love to integrate cardiology with pulmonology right because the thing is if you know that because really kind of like the nice way to think about this is if you know that you're a sanotic right your hypoxic let's say you have 10 buses and those 10 buses normally they could carry 20 people each but now they can only carry 10 people where you're like okay if I still want to meet the same demand let me make more buses let me make 10 extra buses if I have 20 total buses carrying 10 people each they'll be able to carry the 200 people I was able to carry initially when those 10 buses I just had at the beginning carry 20 people that's essentially what happens so a reactive polycythemia classically arises in the setting of a classically arises in the setting of a sanotic concord genital heart diseases right so essentially in this kind of polycythemia you know the person's levels of epoch will be high so their epoch levels will be high and in addition to their epoch levels being high right you have very high levels of hemoglobin the reason I'm talking about this is you want to be able to compare and contrast this with polycythemia vera when people have polycythemia vera they will have you know like a crop ton of red blood cells so you know they'll have like a bit polycythemia but the thing is their epoch levels will actually be normal or low okay the epoch levels will be normal or low remember that polycythemia vera is one of those of my low proliferative disorders and it typically arises from like a jack-to mutation right again and then remember that there are ce

rtain cancers that can produce epoch in a pernioplastic fashion right especially like red cell carcinoma or like hemangio blastoma that has an association with the one hippo lendouts syndrome like VGL remember that's like a chromosome three issue that can also cause that that those tumors hemangio blastomas red cell carcinomas those can produce epoch in a pernioplastic fashion and when you produce that epoch in a pernioplastic fashion that can also cause a polycythemia okay so again these are all big things you want to keep at the back of your mind and then one last thing I want to say about polycythemia because again this is kind of like a new area the end being is beginning to take a lot of interest in is that polycythemia is actually a normal finding in newborns right because again being a newborn your long zone works so you're hypoxic for the most part if you're hypoxic again that will also cause a polycythemia so you may see like a newborn they're like man this newborns hemoglobin is really high that's normal it tends to normalize within like a few days two weeks okay tends to normalize within a few days two weeks that may also begin to give you some insiders to why newborns you know they can have like this like John this this like indirect type of urbiniemia um one of the reasons behind that is just newborns by default just from the hypoxic nature of the uterus right just being in uterus as they are trying to get rid of all those excess red blood cells they have right remember as you break down red blood cells they become indirect bilirubin right but the problem is the newborns UDP look coronal cell transfer is that helps with conjugating bilirubin you know has not fully developed that's why newborns tend to be a pretty you know pretty strong risk of having like an indirect hyperbibirubinemia and that ultimately causes John this for the most part you know they t

end to do well but if you're not doing so well obviously you want to consider things like phototherapy or if the herbivirubin keeps rising despite phototherapy you know you want to think along the lines of like a partial exchange transfusion those are things you tend to see like on a pediatric shelf and i'll probably talk some more about that when i do the gastroenterology reviews for the u.s.nl step one example but again i just thought i should you know kind of take that take that detour and talk about the polycythemia because it's a very very high your concept that tends to again kind of screw with a lot of people's heads on exempt so let's go ahead and jump to the first congenital heart disease right so the first one i want to talk about is a VS key right so you know VSD is a pretty common they actually the most common type of a congenital heart disease and one thing you just again and i'm not gonna again say every single little thing that you need to know about like every single thing that you uh i will say the things you need to know for exams i'm not gonna like gov the gov the reservation or anything like that but big things you want to keep out the back of your mind with VS Ds right they have this uh if you it's essentially like a problem where you essentially have a hole between the right right ventricle and the left ventricle right so the thing is not what should be in that hole right what should be like be there normally right it's the ventricular septum and the thing is the ventricular septum right remember it has two parts there's the membranose part right that's thinner and then there is the muscular part that is thicker right so there's the membranose part of the interventricular septum and then there's the muscular part of the interventricular septum again if you're kind of understanding that like oh membranose is thin muscular is thick and that should e

ssentially already tell you that the membranose part should be the part that has the highest association with uh with a VSD right so most VS Ds they tend to have that hole or that conduit between the right and left ventricles in the membranose interventricular septum okay so what are some things that have associations with VS Ds right so i've kind of talked about how uh you know in front of diabetic moms they can have VS Ds um fiddle alcohol syndrome has a biggest association with a VSD remember that uh people can also have like an interventricular septal rupture in the setting of an MI right so that's one thing that can cause like a VSD but i mean obviously you'll be in a VSD in a presented just had an MI ready you'll be you won't be a VSD that oh as you're coming right out of the womb no right it's something that you know who happened in an adopt and classically the presentation of VSD is that it typically presents us like uh like a holocistolic murmur right at the at the left lost an obordered right that's a big thing and again i already talked about some of the hemodynamic consequences of having a VSD right so again like i said if you see because the left side of the heart right has higher pressures than the right side right obviously the VSD blood will flow from the left side to the right like left ventricle to right ventricle that can ultimately cause a pulmonary hypertension right and that pulmonary hypertension can cause like a concentric hypertrophy of the right ventricle okay but again like i said when a person has a VSD there's more blood going from the left side of the heart to the right side of the heart to it's ace anodic at first right that more blood going to the right side of the heart will increase the pulmonary venus return to the left side of the heart so that will volume overload the left side of the heart so that will cause an eccentric hypertrophy

of the left side of the heart okay and that can ultimately cause a dilated cardiomyopathy right so whenever you see a person you're like this person has concentric hypertrophy in the right ventricle and eccentric hypertrophy on the left ventricle those people almost always have like some preceding left to right shot business going on okay and again remember that whole business i talked about with like oxygen tension like the oxygen saturation and the blood going on between right and right ventricle that's not so whenever you see that on an mbim exam the very first thing i want you to think about is that person potentially having some kind of some kind of a left to right shot okay and again remember vsd's if you don't fix them you can ultimately end up with with the isemanger complex and one of the weird thing you keep to keep in mind with vsd's right is like again where the murmur is heard best the murmur is heard best at the left lower sternal border okay so be a holosistolic murmur heard best at the left lower sternal border holosistolic murmur heard best at the left lower sternal border those are the big things you want to keep and sometimes instead of putting the word holosistolic on mbim exams you know they can call it like pancistolic pancistolic holosistolic it's all it's just two names for the same for the same thing okay and really for the most part most vsd's you know they tend to close on your own but you know if you don't close you've got to fix it with uh better fix it with surgery so i think that's what i'm going to say with vsd's i mean obviously if i just talked about a vsd you know i want to talk about an isd as well right so isd's um big things really there's a thankfully not much you actually need to know about a isd's what isd's the big things you want to remember you want to remember that uh the associate they would like a white fixed split of the

s2 heart sound i believe i've talked about that in a different podcast if i have not i will talk about it when i start talking about like ekgs and cardiac physiology yeah those things tend to be a little uh i would no want to talk about it here because i don't want to cause like a brain overload forever is listening to this podcast i'll talk about the mechanisms behind that in a different podcast that hopefully should come up sooner rather than later um so the thing is you know isd right classic white fixed split of the s2 heart that's like the big association and again now you have essentially because blood is because the pressures on the left side of the heart are much higher than the pressures on the right side of the heart ring uh blood will flow from the left leg to the right leg trim right and again now overload the right ventricle corresponding hypertension if left untreated for long enough the person can have a isd manger physiology i think maybe i was not repeating this isd manger physiology business and this whole thing of like blood like oxygen tensions are stepping up from the right e-tron to the right ventricle i think you should kind of get that point by now it's kind of like a common thing with any left to right shunt and the thing is uh with an asd right remember that down syndrome actually has an association with uh isroceptor defect the big thing i want to mention though with down syndrome is the most common congenitor heart defect and people with down syndrome is actually something called an endocardial cushion defect and endocardial this very higher than endocardial cushion defect is the most common congenitor heart defect that's founding kids with down syndrome right what the thing is kids with down syndrome they tend to also have isd's and the kind of so let me be let me say this straight there are two kinds of isd a person can have a person can

have something called a secondum isd okay a secondum isd and again i will talk about this austiom secondum austiom premium yada yada yada in again now again i'll have another podcast just on cardiac embryology yeah cardiology is one of the highest sales subjects you you can ever know in the usml step one exam so i'll again i'll have podcasts dedicated to that but basically right an austiom a secondum isd is actually the most common type of asd like like if you take five people with asd's four of them will have the secondum asd the thing is the premium isd is very very rare but if you ever find a premium isd that patient likely has down syndrome okay that patient likely has down syndrome that's again one of just those weird associations you want to keep at the back of your mind on exams and then remember that if a person has an isd right you we have a dbt that's bad because the thing is usually right when people think of a dbt they think oh you know this person is going to get a pe because essentially the thing that happens is you know the dbt will truck along the venus system go to the right side of the heart and then launch somewhere in the lungs and then cause a pe right you'll occlude a pulmonary artery cause a pe but the thing is when people have an isd they can have something called like a paradoxical embellish that's again a high-yield concept you want to keep at the back of your mind for exams because basically the plot can make a make its way from the righty term to the lefty term left ventricle and then cause a stroke that's what's known as a paradoxical embellish that's a classic pathonomonic endemic exam finding in people that have an isd especially that's why you can actually like some finds when people have like strokes and you're like man the stroke is kind of weird this person just had a dbt and they have a stroke one thing that cardiologists typically

do is they do something called like a bubble study under like echocardiography to kind of figure out if there is any unusual connection between the left side of the heart and the right side of the heart now the next congenital heart disease i'll talk about right this one is the one that says you don't like rebell right so like congenital rebellis syndrome or the metallic that this person has like a machinery murmur right like a continuous machine like murmur um if you see that right obviously think about a pda right again a pda for the most part uh remember the doctor satiriosus is a conduit between the pulmonary arteries and uh and the order right so the thing that happens when a person has a pda is that doctor satiriosus is supposed to close within the first few hours or days of life if it doesn't close you know you'll essentially have a conduit between the order which represents the left side of the heart and the pulmonary artery rich represents the right side of the heart right so it ultimately becomes like a left to right shunt um and again if you keep overloading the pulmonary arteries that can ultimately cause like a pulmonary hypertension and then that can cause um so you get the you know the person can get the pulmonary hypertension and then if they get the pulmonary hypertension they can ultimately get you know like right like right vent like isemanger physiology developed right because again they can have like right heart failure and all that badness happen and again like I said the big key associations we want to remember right uh congenitor rebellis syndrome and again anything that causes hypoxia in utero because again hypoxia this is actually a very high-yalthinitinal hypoxia increases the amount of first-aglandin e2 and you see divine why does that make any sense well think about it if uh if a part of the body is hy if the body is hypoxic right the bod

y will be like okay let me try to dilute the vessels that lead to this hypoxic region and it so happens that first-aglandin e2 is a vasodiliter right so if you're hypoxic you produce more of a vasodilite in agent like first-aglandin e2 and that will keep blood vessels you know maximally dilated so that more blood can flow through them to that hypoxic region so when a person is hypoxic in utero less like they have like respiratory distress syndrome for example right or a person has like some kind of sanotic congenitor had effect like tetragiophilol those things can all cause uh patent doctor satirosis again because that hypoxia increases levels of first-aglandin e2 uh and again like I said right people can have uh uh maybe I should take a small step back here not necessarily isamine and giraffesiology but it's almost like how do I put this it's almost like a derivative of isamine giraffesiology so let me talk about this real quick for a second right so think about it when a person has a p10 doctor satirosis and let me be actually through this in here you treat it with indomethacin right indomethacin you know it's a cox inhibitor cyclooxygenis inhibitor if you inhibit cox you decrease the production of first-aglandin e2 right and then your caracolamine system will be able to take hold swing and that will kind of constrict down the doctor satirosis and fix the problem but this tends to work mostly in premature kids or like within the first hours or like days of life if the person you notice like a doctor satirosis like you know like years into life or whatever you're gonna have to do surgery there's not much you're gonna be able to do with uh essentially indomethacin is not gonna do score for you at that point you're gonna have to do surgery so let me say something here the thing is when people have a doctor satirosis right like a p10 doctor satirosis I said that blood w

ill flow from the order to the pulmonary artery right now you know you can get pulmonary hypertension and all that badness happen here's the thing usually when people have these doctors satirosis right right usually arises after the subclavian artery that's usually what normal and aden kind of like goes with right you know you have this doctors at yours is below the subclavian artery so the thing that can happen is that when a person has a pulmonary hypertension from this uh you know this chronic pda the thing that can happen is the shunt can reverse from going like blood going from the order to the pulmonary artery to blood now going from the pulmonary artery to the yoder but the thing is the part of the yoder it goes to is the is the yoder that is distal to the subclavian artery so in general these people will actually not have any problems in the upper extremities remember the subclavian artery can now kick starts like the axillary artery the brachial right so like essentially the upper extremities are covered right so they may present this uh uh pda question to you as an in-gamey question we're a person has like san noses in their lower extremities and their a-san not again their upper extremities right so like oh the upper extremities look great the lower extremities don't look so great if you see that you really want to actually consider um a patent doctor satirosis like a chronic pda where these people now have like a reversal of the shunt and again there are sometimes that concept is known as a differential san noses okay differential san noses because like this person is well this person's operate like upper body looks awesome well this person's lower lower body looks not awesome whenever you see that you really want to think about really want to think about a patent doctor satirosis and associated a differential san noses because the shunt has a reversed now

the next one I think next congeneral defects I think I'll talk about right is like tetralogy of a little essentially I'll just tell you this right you'll be doing yourself a huge disservice if you're taking the u.s.siml step one exam right and you've not reviewed uh tetralogy of a more just one of those things that you're kind of asking for it if you don't know like they test the stuff all the time on step one all the time on step two ck all the time on step three and then the pediatric shelf exam they they eat the stuff up right so they almost always test the stuff on exam so it's just one of these things that if you don't learn it now you'll just essentially hunt you for the rest of you of your testic incurrier so basically what's the big thing with tetralogy of a low the way I can think about tetralogy of a low is I mean you want to obviously know the four findings right but the thing is the four findings uh and I'll probably uh uh make a slide on this that I will post when I talk about cardiac eye embryology but let me try to describe it in words if I can't right so basically the thing is the normal thing that happens is you know you have like the muscular interventricular septum that kind of grows from the bottom of the heart so just think of the heart as a box again this is not very accurate but you you'll get the point so essentially thing that happens is so think of the heart as like a square box right so just try to visualize it as you listen to this podcast think of the heart as a square box and then in the from the bottom of that square box you have like a stump that grows that's the muscular interventricular septum the thing is to uh you know kind of divy things up nicely to divide the right and the left ventricle nicely I've already talked about what's going from the bottom the muscular interventricular septum well something has to go from the top the me

mbranous interventricular septum and meets that muscular interventricular septum like up it must meet it like those two ends most approximating nicely I kind of think of it as like almost like a lock and key you want those to I mean if if a lock or a not aligned properly then they won't meet well and you won't have this nice interlocking mechanism so the thing is that when people have a tetralogy of flow the way I've always thought about the pathophys and you'll see that this is a very useful way to understand it is the way I've always thought about the pathophysiology is that instead of the that thing that's thin that's thin that grows from the top to meet the muscular interventricular septum like in like a in lock step the thing that happens is that thing that's supposed to meet it from the top instead of coming down and meeting the muscular interventricular septum it comes down to the right of the muscular interventricular septum the thing is when you have that happening when you have that thin coming down to the right of the muscular interventricular septum then you don't have that lock and key mechanism anymore and because that thing comes off to the right of the muscular interventricular septum you see that the interventricular septum essentially doesn't form properly so VSD develops that's one finding already in a person that has the tetralogy of flow right and because again that thing that grows from the top and again I will describe this better with a diagram that I'll post with a you know the later podcast when that thing comes from the top because it's growing to the right right in fact let me let me give you a little more background here the thing that grows down from the top and ultimately forms the membrane of the interventricular septum the meets up with the muscular interventricular septum is actually the aortico-pominary septum okay it's actually the

aortico-pominary septum so look at the name aortico-pominary septum that means it's a septum that divides the order and the pulmonary system right it divides the order and the pulmonary artery system essentially so the thing that happens is if this aortico-pominary septum comes down to the right of the muscular so it comes down to the right anatomically of the muscular interventricular you see that you have more space because you're essentially not partitioning things equally right because normally you want to come down right in the middle you give equal space to the pulmonary artery you give equal space to the other but when this aortico-pominary septum comes down to the right of the muscular interventricular septum you give a crap ton of space to the other a.k.a.

overriding a other and then you give very limited space to the pulmonary artery a.k.a.

pulmonic stenosis and the thing is when you have pulmonic stenosis it'll be hard for a blood to be ejected from the right ventricle so that will cause a right ventricular hypertrophy okay if you understand what I just explained you will never like to be honest with you I have never forgotten the four findings in tetralogy of follow because I just remember this constructing my mind right so just to repeat the four findings right ventricular hypertrophy pulmonic stenosis overriding a order okay and a VSD and again all these things for me perfect sense if you understand what I just explained so those are the big you know big four findings in a in tetralogy of follow and then what are some other key things you want to keep at the back of your mind with tetralogy of follow right so the thing is you want to you know be able to recognize like the classic tet spells okay so those tet spells they tend to arise you know when the kid is like crying or when the kid is sick because the thing is when you cry that actually like you know kind of works since the uh kind of works since the Sanosis right so you know that works in the Sanosis and then the key turns blue right that's what they call like the blue baby yara yara so you know the kid you know kind of turns blue but the thing is once the Sanosis uh well like Danny say oh so how do you relieve this tet spell well the thing that typically happens is when the kid squats that relieves the tet spell so you may say okay divine why does that help well think about it when you squat you essentially squish in on your vessels on the big vessels of your body and when you squish on the big vessels of your body because the thing is tetralogy of follow because there is the pomonic stenosis it's most it's a sanotic heart defect for the most part so it's a right to left shunt right so it's a sanotic defect because blood that is not going to th

e lungs is going to the left side of the heart and then going to the rest of the body so it's a sanotic heart defect so that right to left shunt is bad because it's causing sanosis so the thing is when you squat right when you squat you compress the big arteries of the body that will increase after load on the left ventricle when that increases after load on the left ventricle the left ventricle pressures will go up and when the left ventricle pressure go up that will turn the right to left shunt of tetralogy of follow to left to right shunt right so you go from a sanotic shunt to an a sanotic shunt and that's why squatting relieves the sanosis that's associated with tetralogy of follow now you see but divine these test spells like why do these kids become very sanotic when the when the when the cry well the thing is think about it and I mean you probably experiences the kid you know from crying I mean there's no kid that's not crying like if I keep cries and cries like really well cries almost like a self-induced valve solvent maneuver right and because if you notice if you like like if a pressing cries right like I don't know if I should try to model this or anything like that people probably get a lot from this but when a person like cries like right when you're taking air like when you're like you're crying crying crying crying crying like that phase where you're like letting out this cry that is essentially like raising your intrathoracic pressures and when those intrathoracic pressures rise guess what your venos return goes down and if your venos return goes down you have very little blood in the right side of the heart right so that word here sanosis because you just don't have enough blood that carries oxygen because you're already in hot water with having to deal with the right solution and then even that little right to left that this is giving you some litt

le oxygen even if it's not enough then you are not calling of that supply by raising your intrathoracic pressures and lowering venos return that's bad right so that's why crying or like severe illness just anything that you know please this a big metabolic demand on your body can trigger the sanosis classically known as the tetspel in an entitrology of phallone and really tetrology of phallone for the most part to you treat it with you know you treat it with surgery this is really not much you can do there actually I think it was a cardiologist at my alma mater that actually this you know kind of like discovered the procedure for fixing a tetrology of phallone but that's a story that's a story for another so again these are all high yield things you want to keep at the back of your mind with tetrology of phallone so yeah yeah I think that's all I want to say about about tetrology of phallone and again like I said fix you with surgery now one thing you maybe want to keep at the back of back of your mind another I guess high yield or congenital heart defect is a quartetion of the yoder right so quartetion of the yoder remember it has like a very big prominent association with like toner syndrome right remember toner syndrome those people tend to get like a partition of the yoder they tend to get by cosperiodic phall so that can cause the odics the noses and remember that those people also tend to get what is it called there's this reno problem they have hoshukimi right we're like the inferpals of the kidney you know they stiff used so they're kind of stuck under the inferior misinteric artery you know kind of increases the risk of like hypertension increases the risk of you know like just chronic recurring utis right again all high yield things you want to keep in mind for for exams so quartetion of the yoder right like the classic presentation is you know you may see l

ike a chest x-ray the person may have like rib notching right like rib notching that's uh in fact I think at the end I would uh go ahead and um in fact you know let me let me go ahead and talk about this right now right just some key like weird like imaging findings and some of these congenital diseases because they love to test this thing and then I'll actually say something that you know I kind of neglected to mention so if you see the mention of the name butchipped heart on an nbm exam okay so butchipped heart on an nbm exam I will strongly encourage you to think about tetralogy of phallol okay it just happens because the person has a red ventricular hypertrophy so butchipped heart think about uh think about a tetralogy of phallol and then if you see uh they tell you that oh this person's heart on chest x-ray um looks like an egg on a string right if you see like an egg on a string heart I would really really want you to think about a transposition of the grid vessels I'll talk about that shortly in a second so egg on a string heart think about transposition of the grid vessels um if you see rib notching on a chest x-ray right you really do want to think about a quartetion of the yoder um one weird thing you may also see the me tell you that oh the person's heart on chest x-ray you kind of see like something called the snowman sign okay the snowman sign kind of goes with something called t a p v r right so like total anomalous pulmonary venus return um that's like the biggest it's your snowman sign I think really those are the big ones you want to know I mean there's some other weird things you may see uh but this is this is more like for the interest of radiologists like there's like the similar sign and the goose next sign yada yada yada yada yeah those things are all things that uh uh there's more important for radiologists than uh than uh medical medical studen

ts so I think we will kind of like leave that uh I mean probably the only other one that's probably also kind of important is something called like the double density sign right so the double density sign it's classically something you see like in a person that has like hypertrophy of the left atrium uh uh like you know like your person has like a big diluted left atrium that tends to be associated with uh with uh double density sign but yeah I think those are kind of like the big signs you want to keep at the back of your mind and then maybe another one you may keep in mind is like the water bottle sign right where the heart looks like a water bottle again don't confuse this with bud shape heart the water bottle sign when the heart looks like a water bottle I want you to think about a person that has a large pericardial effusion okay large pericardial effusion or if they give you a question about a patient that you know kind of has like calcifications outlining the heart on a chest x-ray or chest CT that person has constrictive pericarditis okay that person's got a constrictive pericarditis again these are all high old things you want to keep at the back of your mind for tests so let's get back to the partitions of the uterus so I've talked about the association with uh with a toner syndrome right so what are some other things you want to keep with keep at the back of your mind with a partition of the uterus um the thing is there are actually two types of aortic paracetia right so there's the one that is pre-doctor and then there's the one that is pre-doctor and there's one called juxta doctor that one is very low yield it's highly unlikely to shop on any examine you see so I think I'll maybe only talk about like the pre-doctor and the post-doctor ones so the thing is the pre-doctor one tends to be found in kids right like in infants right like you know when the firs

t like year or two of life uh that's the pre-doctor one and the easy way to remember that the pre-doctor is tends to be found in adults is that I mean sorry that pre-doctor tends to be found in kids the way to remember that is um kids come before adults right so pre goes before post okay so pre goes before post so that's the way I kind of remember most of these things so the thing is essentially this pre or post that I'm talking about essentially refers to the doctor's arteriosus people that have a pre-doctor quotation aka kids the quotation arises before the doctor's arteriosus people that have the post-doctor quotation they have this quotation arise after the doctor's arteriosus well why is this pre-doctor one I mean the pre-doctor both of them are bad to be honest both are bad but why is the pre-doctor one why is it broken down this way the thing is when a person has a pre-doctor a quotation of the order the thing that happens is that um the quotation is coming before the doctor's arteriosus so one thing that can actually happen is that these kids they can actually supply blood to the distal-yorder aka the yorta distal to the subclavian artery by effectively sending blood from the pulmonary artery although it's the oxygenated blood from the pulmonary artery through the doctor's arteriosus to the distal-yorta so that's how they can supply blood to the lower body okay only problem is when you have that quotation of the yorta just before the doctors it kind of screw right because that's essentially like a live ventricular outflow tract obstruction right so that can essentially cause that can essentially cause like like really bad heart failure in kids because essentially the blood in their live ventricle really has nowhere to go other than the proximal yorta which is bad right so that's just one of those weird high-yield things you want to keep at the back of your min

d with with the pre-doctor a quotation of the yorta and again like I said it tends to be found more in uh found more in uh in kids and the thing is of all the aortic quartetions the pre-doctor type is actually the most common type of quotation is like more than 50% of all aortic quartetions arising the setting of a pre-doctor quotation now the postdoctoral one um you know you tend to find it in adults but you can also again find it in kids because again right uh most aortic quartetion cases you'll see in your life are probably in kids if you see that all right so postdoctoral quartetion so the quotation occurs after the doctor's arteriosus right and occurs after the doctor's arteriosus so one big big big big big problem that you kind of see with this aortic quartetion the postdoctoral type is that these people have a lot of trouble sending blood to their lower extremities right so that is what essentially gives you like the classic presentation of aortic quartetion on mbm exams where a kid will have very high blood pressures like this kid you have like bad hypertension and then you'll tell you that this person like they present this in multiple different ways on mbm tests they may tell you that the person has high blood pressures in the upper extremities and low blood pressures in the lower extremities right if you see like a difference in the lower pressure of like 10 or 15 or 20 between the upper extremities and lower extremities that's not that's not normal right you're likely dealing with aortic quartetion on that those circumstances especially like the postdoctoral type now another way they may present that on mbm exams is because again they know that many people have memorized this what is it called many people have memorized this high blood pressures in the upper extremities low blood pressures in the lower extremities they know everyone has memorized all that

crap so one thing they are starting to do is they may tell you that the person has a radio femoral postally I'll say that again radio femoral or radio femoral postally where because normally right if you I mean you can even check this on yourself although I don't know how possible that is but if you touch your femoral pulse around your groin and you touch your radial pulse they essentially arrive at the same time what if you're like man I can feel my radial pulse and my femoral pulse is not like man it's ticking it's it's sweet sweet time to come if you see that then you really want to talk up you really want to think about a aortic quartetion on mbm is again because remember the radial artery is ultimately a derivative of the subclavian artery and the subclavian artery arises from the aortic arch before essentially every quartetion that that you see on mbm exams right so those people have good profusion of the upper extremities and awful profusion of their lower extremities right so that's one other way can present another way can present is they may tell you that oh this patient has like two or three plus like the hotel you present is like three plus like a radial pulses to tell you that this person's radial pulse is like really really high right and then you may tell you that pulses are barely detectable in like the brosalus pides or the posterior tibial arteries if you see that think about again quartetion of the yoder on mbm exams and the thing is if you see because many people are used to like oh like you know long term smoker has pain that is very bad in both legs and it's relieved after the person you know rests for a while and they're like oh this person has low extremity clodication of which smoking is the biggest risk factor the thing is if you see clodication in a very young person I really want you to think about quartetion of the yoder because again you'

re essentially high-po profusing your low extremity blood vessels and if you high-po profuse your low extremity blood vessels that can cause that can cause that can cause a low extremity clodication so again that's actually something very high yield you want to keep at the back of your mind on mbm exams okay so if you see clodication in a very young person especially a person that doesn't smoke or whatever think about think about a quartetion of the yoder right and the thing is these people tend to have hypertension for many different reasons right the reason they have a lot of hypertension is that one there's just nowhere for the blood to go right in the upper extremities right so I mean in the upper body because of that quartetion right so they have like upper extremity hypertension but underneath is think about it one of the offshoots of the descending yoder right it's really like the abdominal yoder is the renal artery right so people that have quartetion of the yoder they're not profusing the renal artery very well right so they're not profusing the renal artery the afrin arterial is not seen enough blood so the juxtaglomerulus cells begin to freak out and they begin to secrete a lot of renal right and again that will kick start the whole renal and jutez and our duster and system right and that will raise blood volume that will cause viso constriction and that will ultimately cause a hypertension okay that will ultimately cause hypertension and the thing is these people because they have such elevated pressures prior to the quartetion that actually that can actually cause I mean the upper extremity hypertension that you have can actually go ahead and cause the eurid dissection okay so eurid dissection is actually pretty common in people that have a history of euric quartetion okay that's actually a very high yield relationship you want to keep at the back of your

mind on the exams because actually the biggest risk factor believe it or not for eurid dissection is is a hypertension right and then another thing these people can also have they can also get like strokes from like sub-rocknoyed hemorrhage because again the pressure is proximal to the to the to the to the quartetion right like those pressures can involve the cerebral vessels as well because remember your carotids and everything they've all come off before the quartetion so the blood vessels in the brain right exposed to like very high pressures very very high pressures and those high pressures can kind of cause the formation of all these like barrier aneurysms and those kind of rupture and cause a sub-rocknoyed hemorrhage right remember the biggest risk factor for stroke is hypertension right so these like cardiovascular risk factors they actually kind of expect to know them for in-beaming exams so the biggest risk factor for stroke and aortic dissection the way remember that is sad right so like sad like SAD I hope none of you are sad but so stroke aortic dissection the biggest risk factor is hypertension and then a myocardial infarction a triple link so like an abdominal aortic aneurysm and and a clodication of the lower extremities the biggest risk factor for all those things is smoking okay those risk factors again believe it or not they tend to test them quite commonly on the USMLE exams okay so I think those are like the big things I want to say with the quartetion of the yoder but the one again I know I'm spending a lot of time on this and I apologize but one thing I also want to say is this is actually one area that the nbm also loves to pick off with regards to anatomical concepts okay they love to pick this off with anatomical concepts on the exam because the thing is I mean many people tell me like oh divine how do I remember how do I study anatomy for st

ep one if anatomy is clinically relevant it's typically something you want to know for tests and I mean thankfully I've you know made a decent number of anatomy podcasts for step one that you can review and I will make even more in the future right but typically with these different podcasts I mean for like the different systems I will also be talking about like the high-year relevant clinical anatomy so one thing I'll go ahead and say is a quartetion of the yoder has some very nifty but high-year anatomical relationships so the thing is obviously people especially that have this post-doctor quartetion they get a send blood in some way shape or form to their lower extremities right yeah I mean they just I mean you can't like say I'm not gonna give my lower extremities blood so the thing is the body begins to develop some collateral systems like some collateral or circulatory systems to kind of keep your lower extremities perfused one big one you want to remember is the collateral circulation between the superior pigastric artery and the inferior pigastric artery right so here is the thing right if you're looking at a person's ear like I said this post-doctor quartetions they tend to arise after the doctor's arteriosus the doctor's arteriosus for sure comes after the subclavian artery right so the thing is all the vessels like like you have like your briculous ethalic artery given off first and then you have your left common corroded and then you give off your left subclavian so all those vessels are given off before the quartetion even if it's pre-doctor they are all given off before the quartetion so the thing that happens is your subclavian artery one of the branches of the subclavian artery is the internal thoracic artery okay the thing is as the internal thoracic artery descends in the thoracic cavity on both sides of the sternum the name changes at some point esp

ecially when it's like like essentially like traversed I think the diaphragm and the name changes from internal thoracic artery to superior epigastric artery the thing is when a person has a quartetion of the artery because again there is still more than adequate blood flow in the subclavian artery some of that blood will be shunted towards the internal thoracic artery and then into from the internal thoracic artery it will be shunted to the superior epigastric artery which is essentially just the name change of the internal thoracic artery once it like gets into the abdomen the thing is that superior epigastric artery can form a conduit with the inferior epigastric artery and it so happens that the inferior epigastric artery is a branch of the external iliac artery right I remember the external iliac is one of the terminal branches of the descent of the abdominal iliac artery okay so that can then you can then have like retrograde blood flow in the external iliac artery to supply derivatives of the abdominal ayur and also the lower extremities so that's one high yield anatomical association you want to know the other anatomical association you want to know is that um um there is this conduit that also develops between the intercostal arteries right there's the conduit that develops between the intercostal arteries um the thing is uh there the anterior intercostal arteries and then they're the posterior intercostal arteries the thing is the anterior intercostal arteries they are branches of the internal thoracic so really for these aortic quartetions or just think the easy way to remember this is that all roads go through the all roads go through the internal thoracic artery right so the anterior intercostal arteries are branches of the internal thoracic artery so the thing is um uh when again you have ample blood flow in the subclavian artery because of the quartetio

n you have more blood flowing into the internal thoracic artery and then you have more blood flowing into the uh from the internal thoracic artery to the anterior intercostal arteries and those anterior intercostal arteries they actually establish conduits with the posterior intercostal arteries it so happens that those posterior intercostal arteries they tend to arise more from like the descending order so they tend to arise more from the parts of the order that are distal to the quartetion right so this is why people that have aortic quartetion they tend to have like rib notching because remember those intercostal arteries this is actually another high-yield anatomical relationship to remember those intercostal arteries they sort of run in a neurovascular bundle at the lower margin of a rib um or I guess if you're looking at it from a different perspective you can see like the upper margin of an intercostal space okay remember the lower margin of a rib is the same thing as the upper margin of the space between ribs aka the intercostal spaces um remember they love to test that in the context of oh if you want to put a chest tube or something uh in what in which direction you want to go in the intercostal space you want to go above the rib or below the rib obviously you want to go above the rib right because that's the most inferior part of the intercostal space so you avoid the neurovascular bundle if you do it above the rib where I mean if you do it uh if you do it below the rib so you want to go above the rib you don't want to go below the rib you go below the rib well all the best right because you can puncture one of the intercostal arteries cause a life threatening a bleed and then the present can die you don't want that right so um in general right um those intercostal arteries they run in the neurovascular bundle again below the rib or the which is the same th

ing as the upper margin of the intercostal space so the thing is uh those intercostal arteries because they have like more blood flowing them right that increased blood flow those vessels become more pulsata and those pulsations begin begin to like wear away the bone um like the ribs essentially right so that's why you get like those rib notches sometimes you can cause something called the three sign on a on a chest x-ray right those are all classic findings in people that have quartetion of the yoder and really again quartetion of the yoder it's only surgery that's going to help you there's really not much you can there's really not much you can do there um and then I guess maybe so i'll just go ahead and say this right now the spiel i wanted to do on uh on uh like the quick hits on the vows i'll have to do that in another podcast i mean obviously i'm already over an hour here but i'm gonna be done uh very uh shortly the last thing i think i'll go ahead and talk about right like um i'll just see like one or two quick things about these remaining or continental hard defects uh there's really not much here to know about transposition of the grid vessels um you just want to think about it as you know problems with like the yodicopommenary septum remember the yodicopommenary septum is derived from neurocrest that's a high-yield thing to know for exams and essentially the thing that happens is it's called a transposition of the grid vessels well what are your grid vessels your grid vessels are your yoder and your pomenary order the thing that happens is normally your yoder comes off of the left ventricle and your pomenary order comes off of your uh right ventricle right and um the thing that will cause this um transposition is when you have like problems with like the appropriate twisting of your or like switch like turning of the yodicopommenary septum again i'll talk ab

out all this the path of physiology behind all the stuff in uh in the cardiac embryology podcast that's another i'll say probably of all the embryologies to know the u.s.

m.l.

exams neuro embryology cardio embryology and ge embryology is probably the highest yield that you want to keep at the back of your mind on tests so you know if you have problems with like the spin or the turning of the yodicopommenary septum that's essentially what causes a transposition of the grid vessels so when you have this transposition the pomenary actually arrays from the left ventricle and the yoder is from the right ventricle and that's bad right because think about it if the president has like a complete transposition let's say like the right ventricle sends blood to the yoder the yoder will send blood to the rest and and again it's right ventricular blood right so that's the oxygenated blood they're sending that the oxygenated blood into the yoder they'll send it to the rest of the body that would the oxygenate the blood some more and then the blood will come back through the um through the svcivc to the right side of the heart go to the right ventricle and then come out through the yoder again that's bad i mean that's obviously not very compatible with uh does not compatible with life pretty much um so you have like one closed deoxygenated system for the right side of the heart and you have one closed oxygenated system for the left side of the heart that is again not very compatible with life so usually for kiddies to be born with a transposition of the grid vessels typically they will have like some kind of thing that is maintaining communication between the right side of the heart and the left side of the heart so you can have some mixing of blood if no there's no idoskis ever get born right so you know they'll need like an asd or a vsd or pd to keep those things open so with that said there's a very actually classic usml exam question it may give you a question about like a kid that you know this kid is born and this kid you know the abgas course where

grays at birth and then they tell you that within a few hours of birth or like the second day usually it's like within the few hours or like the first few days of birth this kid then suddenly becomes like profoundly sanotic profoundly hypoxic profoundly hypotensive if you see that and be asked for the next best step in management your next best step in management from the usml exams is to administer a drug known as our prostadil okay our prostadil usually write these questions with like very little in the world of clues but this thing is like I promise you like if you're a medical student listen to this podcast between now that you're listening to this podcast and the time you graduate from medical school you'll get at least 10 questions on this one concept I'm about to talk about so essentially the thing that happens is that you have your next step in management is to give those people our prostadil which is a prostaglanding e1 analog right it's a prostaglanding e1 analog there is an you give that is if I let me explain the reason why those kids have those symptoms in the first place there is in those kids have those symptoms in the first place is what must have likely happened is that those kids they must have had um some kind of really bad sanotic heart defect that did not get expressed because they may have had like like a conduit a shunt causing mixing between causing mixing of blood between the right and the left sides of the heart like a pdf for example that you know mask in that sanotic congenital heart defect but the thing is once you get born that pdf begins to close and if that pdf that will then on mask the sanotic congenital heart defect those kids have okay so the thing you don't know those circumstances is you give our prostadil which is a pdf one analog and that would essentially dilate those um dilate those um dilate the keep the doctors at aerosols

open so that you can buy time before you go to cardiac surgery essentially again I promise you this thing is ridiculously high you know like again he tested all the time on step one on step two ck and the pediatric shelf in third year so again all big high u things you want to keep at the back of your mind and remember the egg on a string appearance of the transposition of the grade vessels and like obviously right you're gonna do surgery for that and then I mean the total anomalous of pulmonary venous return I talked about this in the context of the of the snowman sign on imaging right I remember essentially uh I mean look at the name it tells you essentially all you need to know total anomalous pulmonary venous return that means the pulmonary vein is returning blood to the heart in an anomalous fashion normally you're supposed to return blood to the the pulmonary vein is supposed to return blood to the lefty trim but if you return blood to the righty trim instead that's what happens in tp vr there are like many types of tp vr but that's beyond the scope of our discussion and you very likely don't see that tested on your exams and then remember right to try to copy that tree share right um this can essentially happen where you know you you essentially have no communication between the righty trim right ventricle again remember this is not very compatible with life so the only way a kid will try to try to copy that tree share can get born is they need an ASD and they need a VSD they need both to live essentially the thing that happens is well actually they can probably do fine we just then we just an ASD because that blood in the righty interim will go to the left each room and then from the left each room it will go to the left ventricle and then from the left ventricle it will go to the aorta and then maybe it can go through like the pulmonary artery um I mean throu

gh like you know left ventricle to the order and then maybe it's through a doctor's at your sister pulmonary artery but the classic teaching and the thing you will likely see on an MBN exam is that a kid will try to copy that tree share typically means an ASD and a VSD to be born that ASD will help you go from the right will help the blood go from the righty trim to the left ventricle and they I mean start from the right each room to the lefty trim and then the VSD will help the blood go from the left ventricle back to the right ventricle so that that blood can then go from the right ventricle to the pulmonary artery and then get oxygenated okay so those are the essentially the big shunts you need um in a person that has a tricospita atreasia and then the last one I'll mention is like tronco satiriosis this one the biggest decision I want to remember is essentially these people again have issues with the eorticlep pulmonary septum so essentially like the order of the pulmonary artery are really not divided there is like one common vessel that leads out of both sides of the heart which is obviously not a good thing right it's it's a sanotic defect because we essentially have a mixing of blood and remember that tronco satiriosis has a very high-yield association with the djorch syndrome right remember djorch syndrome arises where you have problems with the development of the third and the fourth farngale pouches again these are all high yield with your friends at the mbimi lofting degree these concepts on exams so um anomonic I maybe can give you is that all these sanotic heart defects they all tend to start with the letter T okay the else tend to start with the letter T um so I think I'm gonna you know go ahead and stop here one thing I'll say is uh you know if you're a mess student you know set off going into your third year it probably makes sense for you to also lik

e watch my piz video my piz video I talk about these are congenital heart defects from a piz perspective like a piz shelf perspective because they have some other nuances to this to these are congenital heart defects that again they don't seem to for whatever is in the emphasized in many resources so I sort of talk about them in terms of like all like increased pulmonary venous markings and all that I mean pulmonary arterial blood markings and all that stuff but that's more for third that's more for like third year but if you want like a clinical treatment and this year second year medicine you can just find the part of my piz video um where I talk about uh where I talk about the congenital heart defects um and then meditate things from them so as I do at the end of every podcast um I do offer one or one to you know for many exams step one step two ck step two cs step three uh pre clinical medical exams 30-ish off exams um and then if uh I do this usmly booster course right where it's like 10 hours for step two ck and step three or 20 hours for step one where if you're like at the end of your day the period or you know you're you're like okay I feel good about my knowledge base let me have someone put everything together for me in a very short period of time that's what that course is essentially for and basically the thing I do in that course is I teach you it's a Q&A format it's clinical vignette for the most part what I talk about and it's very rapid fire questioning but we touch on a lot of like the high yield most no concepts for the usmly exams when we do when we do those things so if you're interested again reach out to me that through the website or send me an email at divine intervention podcasts with an s at the end at gmail.com and then um I also do this thing that I call on you do not do in where if you're like a first second or 30 a met student I can teac

h you teach you for your like essentially to do it for your different exams like that exams you take in met school but as I'm to do for those exams like your block exams your shelf exams also to do for your upcoming uh usmly exam right and again the vast majority of people have done this with you being like very successful and then if you're if you're like a met student applying to like residences so like an iris application uh ira like yeah like an iris up or a collision and applying to met school so like an amkassap and I do offer like one or one like advice in coaching um like mock interviews personal statement writing um editing your application rec letters and things like that those are all things I can I can kind of help out with um so if that's something I'm interested in uh especially if you're an international medical graduate I feel free to reach out to me and then um if you're a medicine resident I need you to for like the medicine and training exam or the abi and board exam I do offer also offer a one or one tutoring for that um yeah I've definitely tutored a medicine resident so yeah there's you if that's anything you're interested in feel free to reach out to me for that um and then if you have like a college body that needs a tutoring for like gen camp okam physics biochem histology physiology again I offer tutoring for all those things so uh I'll continue this cardiology business again I feel like cardiology will probably end up being my most detailed step one podcast because there's just so much in cardio and the thing is cardio unfortunately it's just one of those things that I cannot just breeze through giving you like oh this is higher this is higher I actually need to explain because the thing is if you don't have the like cardiology is one of those things where if you memorize it you you you'll not get cardiology questions right on the USMLA exam

it's something you kind of need to understand so that's what I'm thinking like the extra time to you know putting that investment of time so that you actually understand what's going on so have a wonderful rest of your day I'll see you in the next podcast God bless you thank you

The umbilical vein.

The foramen ovale (becomes fossa ovalis).

Endocardial cushion defects.

Paradoxical embolism (allowing venous emboli to cross into the systemic circulation and cause stroke).

Differential blood pressure/pulse between upper and lower extremities.

Patent Ductus Arteriosus (PDA).

Renal artery stenosis/hypertension.

VSD, overriding aorta, pulmonary stenosis, and right ventricular hypertrophy.

Total Anomalous Pulmonary Venous Return (TAPVR).

Multifactorial inheritance (a combination of genetics and environment).

Post-ductal coarctation.

Squatting (increases SVR, reversing the shunt).

Ostium secundum defect.

The neurovascular bundle runs along the lower margin of a rib; therefore, chest tubes should be placed above the rib to avoid injury.

VSD, overriding aorta, pulmonary stenosis, and right ventricular hypertrophy.

Total Anomalous Pulmonary Venous Return (TAPVR).

Multifactorial inheritance (a combination of genetics and environment).

Post-ductal coarctation.

Squatting (increases SVR, reversing the shunt).

Ostium secundum defect.

The neurovascular bundle runs along the lower margin of a rib; therefore, chest tubes should be placed above the rib to avoid injury.