DIP Episode 154 - Comprehensive USMLE Step 1 Cardiology Review 2

Okay, welcome. My name is Divine, I am a resident. This is episode 154 of the Divine Intervention Podcasts. In this podcast, I'll be continuing my cardiology review for the USML Step 1 exam. I already have podcasts on cardiac pharmacology. I've already covered that in great detail. I do have a part one of this podcast. I believe it's episode 116, but I want to write this all the way through to the end, starting with this podcast. So this will be part two. So let's jump right into it. So what if you get a question about a patient that, you know, like three days ago, presented with chest pain, was found to have an MI, and then they tell you that all of a sudden the patient becomes unresponsive and that on oscutation of the chest, they tell you that you can be you cannot oscute it in heart sounds. The patient is profoundly hypertensive, has like rapid onset, GVD, and all that stuff. What are you thinking about? I would really hope you're thinking about something along the lines of like a ventricular free-water rupture. That's causing a cardiac tamponate. So obviously this is one high-yield complication of an MI. So let's go ahead and talk about these complications of an MI. So the thing is, MI is there are certain classic things they love to test on the USML exams.

So the one thing, one big thing they love to test, you see a person that suddenly dies like in the first few hours after an MI, the most likely cause of death under those circumstances is a very nasty ventricular rhythmia. Usually it's V-fib. In fact this is very high-yield to know. V-fib is the most common cause. Again very high-yield. V-fib is the most common cause of death within the first 24 hours after an MI. But the thing is after a person has an MI there are many many many many other things that can happen, right? Like they can have they can have like parachyditis, right? They can have parachyditis. It are happening like a few days. Usually it's within the first like three to five days or they can have parachyditis happening a couple of weeks after the MI, right? So the thing is the parachyditis that happens a few days right after the MI is called like acute fibrenosparachyditis, right? Usually it happens like one to like one to five days after after the MI sort of shows up. And remember that the acute fibrenosparachyditis, classic findings of parachyditis on an EKG, you see ST elevations everywhere, right? So like ST elevations in a non-vascular or you can see like a non-territorial distribution. And then in addition to that those patients tend to have like a diffuse PR segment depressions as well. So those are the two high-level things you want to keep at the back of your mind in a patient that has parachyditis.

They will have the few ST segment elevations and the few PR segment depressions. And then down the line like weeks after the MI, right? They can have I almost think of it as like a chronic fibrenosparachyditis. Although it arises from an autoimmune etiology it's known as a dressless syndrome. Essentially, right? If you think about it when a myocyte dies, right? The sodium potassium ATP is pumps stop working if they stop working, right? The cell swell, after the cell swells over time, the cell will explode. When the cell explodes, they release cardiac proteins into the circulation and your body can make antibodies against those cardiac proteins, okay? So that's why it takes a few weeks, right? Because you don't just make antibodies immediately, you encounter a given antigen, right? So the body makes antibodies against those antigens and that's how people get a dress dresser's syndrome. Again, dressless syndrome is a kind of fibrenosparachyditis, kind of like the one you have a few days after an MI. But again, it arises weeks later and it's from an autoimmune etiology. And then if they give you a question about a patient, you know, they had like a recent MI and then they tell you that the person becomes like suddenly like hemodynamicly unstable and they tell you that when you are schooltating the chest, you hear like a holosis stomach murmur of the apex and the patient like develops like a flush pulmonary edema.

I would really hope on that those circumstances, you are thinking about a papillary muscle rupture that is causing a mitral regurgitation. That's kind of like the big, big, big thing you want to keep at the back of your mind there. I mean, they can also like rupture the try rupture the papillary muscles and scrub the tricospid valve, where that is much less common. I would probably go more for the mitral regurgers with a holosis stomach murmur of the apex on NBM exams. And then you also want to again, patient again, suddenly becomes unresponsive, flush mitral regurgit, flush, pulmonary edema, really bad hemodynamic status and then they tell you that oh when you are schooltating the chest, you hear holosis stomach murmur like a harsh holosis stomach murmur at the left sternal border, they may say the left lower sternal border. I would really hope on that those circumstances, we are thinking about an interventricular septal rupture, okay, that is causing a VSD essentially. Again, these things all occur in the first few days after an MI and then the situation I described earlier, right where the person you know essentially had the signs and symptoms of cardiac tamponant like the backstriad where you have like the morphode heart sounds, the the hypotension and the sodium onset, the development of a GVD, that's cardiac tamponant from a ventricular free wall rupture.

The reason that people get that ventricular free wall rupture is because all the neutrophils and macrophages that are causing all those, put that inflammation, the sort of either way at the wall of the ventricle wall becomes very thin and that can ultimately cause a lot of trouble. If you just either way the ventricular wall, you have the free wall rupture and then the person gets into trouble. Alternatively, another thing you also need to think about and the thing is your friends at the MBM love you to be able to differentiate between these two things is a ventricular aneurysm versus a ventricular pseudo aneurysm, okay, a ventricular aneurysm versus a ventricular pseudo aneurysm. The thing is a ventricular aneurysm, right, it's just like a dilation of the wall of the left ventricle that happens in the setting of it's a dilation of the wall of the left ventricle that happens in the setting of so ventricular aneurysm, right, it just basically happens when the left ventricular wall dilates, okay, typically in the setting of like you know a few weeks after an M.I. And I guess you know what maybe let me let me take a small step back here and maybe try to parse this out because it's very high yield to remember not just for a step one but also for step 2 C.K. believe it or not. So the thing is the big things your friends at the M.I.

me sort of care about with these ventricular like aneurysm versus pseudo aneurysm is certain a few things here and there, right, so the first one is timing, right, the thing is ventricular pseudo aneurysms they tend to shop like of like less than two weeks after an M.I. versus a true ventricular aneurysm that tends to shop greater than a week after an M.I. I mean sorry so whoops what am I saying so ventricular aneurysm greater than two weeks after an M.I. Ventricular pseudo aneurysm less than two weeks after an M.I. Okay, so usually it's like three days to like 14 days after an M.I.

And then the thing is between a ventricular aneurysm versus a ventricular aneurysm the one that has the biggest risk of rupture is a ventricular pseudo aneurysm because the thing is a ventricular pseudo aneurysm has like a very thin wall and if you remember the law of Laplace I'm gonna talk about that in one of the podcasts but if you look at the law of Laplace where Laplace where it's like the wall tension is equal to like the pressure times the radius divided by the two divided by two times the wall thickness the thing is a ventricular pseudo aneurysm has a very thin wall but a ventricular aneurysm has a thick wall because it has a lot of scar tissue so because the ventricular aneurysm has a much thicker wall the wall tension is much smaller versus a ventricular aneurysm that has a very thin wall so that means the wall tension is a lot bigger okay so that's actually very very high yield to no one remember for the USMLE step one exam and then eventually aneurysm I mean they can this is just semantics but the thing is normally you'd expect the leventricular wall to you know sort of squish in during the process of assistedly but the thing is when a person has a ventricular aneurysm the eventual wall actually actually bulges out in the setting of when the leventricular is undergoing a systole the thing is these aneurysm I mean like the pseudo aneurysm obviously can rupture and then the person can get like cardiac tamponade like threatening bleeding die but the ventricular aneurysm right the things that can happen is you can have things like like arrhythmias happen that leventricular is kind of like echinetics all this cloth can form so the person can get a stroke and have issues with that though that scar right the scar tissue can serve as a very good night us for aneurysmia right so all those things can kind of happen I mean the setting of a ventricular aneurysm so I t

hink that's all I think I want to say about all I think I want to say about like things that can happen after an MI so I guess with that let's go ahead and go to the next being yet okay so what if you get a question about a patient you know this person comes in came in with like chest pain but the troponies were negative the EKG was on remarkable so this person you know they couldn't exercise right so they got like a pharmacological stress test and then they tell you that oh this person you know for the pharmacological stress test when the test was administered you began to notice like inverted T-weaves during the test and the patients that a completely no even more chest pain and then under those circumstances the ask like what concept is this question you know straight it well I hope under those circumstances you're thinking about something known as the coronary steel principle okay basically the thing that happens is when a person has cardiac is like if a person has like like a thrombotic disease in the heart right the thing is the part of the vessel that is thrombotic I guess the part of the vessel that is of the coronary vessel that is distal to that thrombosis dilates maximally dilates to its best best best effort to try to maintain proficient to that part of the to that part of the heart so the thing that happens is when you give a visual dilator right you can give a visual dilator like a denocene or like an adenosine derivative like a padenocene or a gadenosine or whatever those cause visualization I guess one other thing you can actually give is you can give a this drug known as dipiridomo dipiridomo it's a it's an antiplacillary agent but in addition it's also an adenosine diaminies inhibitor so by being an adenosine diaminies inhibitor it prevents the breakdown of adenosine so the person's adenosine persists so that can cause visual dilation so the thing is

when you administer that visual dilator the normal coronary vessels will dilate but the thing is the coronary vessels that already have thrombosis have dilated maximally so they have no abilities to dilate even more so the thing that happens under those circumstances is those vessels that are responding appropriately to the dilation of a dilator they would have a mob blood flowing through them and remember it's a fixed amount of blood that's still flowing to the heart under these circumstances so those coronary vessels that don't have thrombosis they dilates mob blood flows through them and because mob blood is flowing through them there'll be less blood flowing through the thromboster coronary vessel right because again that thrombose coronary vessel cannot dilate any further so effectively still in blood from that thrombose coronary vessel that's why it's known as the coronary steel principle it is used quite commonly in the performance of this principle essentially is used in the is used in the pharmacologic stress tests for a person having like you know like he would him would dynamically significant coronary artery disease and usually right these pharmacological stress tests you do it in people that cannot exercise for some reason okay although remember an adenosine based stress test will be contraindicated in a person that has like severe COPD or a person that has severe asthma because adenosine is a powerful piece of bronchoconstrictor so it can cause a lot of problems in that patient so hopefully that's something you understand very very high you to know for the USMD step one exam now what if they give you a question about a patient that has been you know like losing like has lost like 15 pounds over the last three months and this person has been having like a lot of like syncopal episodes and he tells you that at 90s having like you know these pretty bad fev

ers and that's two weeks ago he had this episode where he he could not move his legs for a couple of minutes and then he ultimately got better and then they tell you that oh when you're scooting the chest at the apex you hear like a plop sound in the astray what you diagnosis on that little circumstances I would hope you're telling me this person has a mixoma right does this is the classic patholomonic representation of a mixoma essentially a mixoma right is the most common primary cardiac tumor especially in an adult if you're thinking about kids actually the most common primary cardiac tumor in kids is a rabdom aoma that's usually found like in the setting of tuberous chlorosis it can kind of present very similarly like almost like a cardiac mixoma as well but the thing is cardiac mixomas right they tend to arise in the left atrium they tend to be pedonculated so they are usually like found on a stalk okay and the thing is occasionally the in fact many times they do actually cause an obstruction of the mitral valve so they can actually cause like problems with filling of the left ventricle okay so the classic detail is that oh this on our quotation you hear like a diastolic not systolic a diastolic plop sound it's a diastolic sound right because the left ventricle fills in the astray because there's almost like a ball valve effects that happens with the with the tumor so cardiac mixoma you hear a tumor plop on our quotation of the chest you'll be pedastolic plop right and again these people tend to have like syncopal episodes because they may have trouble with like left ventricular filling right so they may not be able to send enough blood to the to the brain alternatively you notice in the in the in the venietha I gave you I talked about the person you know having a situation where he lost feelings legs for like a couple of minutes and then got better the thing is

certain parts of this tumor can flick off and they can embolize to the brain and cause like mini strokes in a sense so that's something to keep at the back of your mind and then these patients they tend to have like you know like constitutional symptoms like fever and stuff because many times these tumors can secret cytokines like interlooking one and interlooking six that can cause fever like those big symptoms so those are key things you want to keep at the back of your mind although remember me you may say oh cardiac rhodoma is the I mean cardiac mixoma is the most common like primary heart tumor that is true but the thing is most like if you find a tumor like in the heart it usually arises from metastasis as against like a denover arising from the heart so that's one big thing you want to keep at the back of your mind most tumors that metastasis so the heart they go to the pericardium so they can cause like a very nasty a pericardial effusion so that's something again high you do want to keep at the back of your mind for the USM and his step one exam now what did they give you a question about a patient that has a history of head B and then this patient over the last like three months has been having like you know pretty severe episodes of abdominal pain has had a ton of weight loss and has like really bad hypertension and then they tell you that on our quotation of the lungs you don't find anything right I would hope you're thinking about like one of the vasculidities okay one of the vasculidities really the big one should be thinking about it especially since I gave you that his shrub head B should be polyadritis nodosa right it's like a medium vessel of vasculitis basically those people they have all this inflammation that happens and they ultimately destroy like the tunic amidea of like the amidium size vessels and they also destroy like the internal elastic l

amina of their blood vessels right it's a vasculidities right so it's a it's a vasculitis right so it's like powerful powerful powerful inflammation in the blood vessel when you have all those things happening ultimately you can those people can actually have like aneurysms right they can get aneurysms of blood vessels and those aneurysms can rupture right they can have like a rupture like they can rupture like a triple or something from polyadritis nodosa and that although P and technically those not have for the most part does not really affect the other it tends to affect more like branch points of the other like like the renal arteries is probably that's probably the most commonly involved and then you can actually affect like coronary vessels you can affect some of the vessels in the liver you can affect the superior mesenteric artery that's why the patient you know is having like abdominal pain from like the chronic mesenteric ischemia so those are things you want to keep at the back of your mind and then one higher thing you absolutely positively want to remember is that the way you can diagnose a P and is you can actually go ahead and do like angiography right you'll see like the you will see like almost like irregular structures in the in the lumen of vessels right from like the segmental inflammation that kind of that kind of occurs and you want to remember for sure that P and does not affect the lungs very this is like florida hyalutinopherexamps P and does not affect the lungs and because it's because it's a type of a vasculitis right for the most part you treat it with like steroids and cyclophosphamide that's the big big thing you want to keep at the back of your mind but really the kidneys are the most commonly affected and then you have like the heart and then they can have like liver like portal vessel involvement and they can have like GI involvement

right usually it's the super mesenteric artery that's a very high-old anatomic association you want to keep at the back of your mind for exams since I guess we're on the topic of vasculities right so don't forget like they can give you like a question about a kid and this kid has like you know like for the last like week or two they're having like pretty high fever like temperature has been 104 and then they tell you that this kid has like conjunctival injection and has like has like a rash on the palms and souls right under those circumstances you want to think about hopefully Kawasaki's disease remember Kawasaki's disease is one of those high-year things that causes a rash on the palms and souls that rash right remember it typically is typically on the palms and souls kind of like secondary syphilis and also like a cox the coxacchi a virus right that's something high you do want to keep at the back of your mind remember that Kawasaki's disease right the classic findings usually be like an Asian kid right and that Asian kid will have like conjunctival injection will have like the rash on the palms and souls will have like the unilateral anterior cervical lymphatic anapathy that's a big one you want to keep at the back of your mind and then they also tend to have like a strawberry tongue remember strawberry tongue is not pattern of monic for polyadritis no dosa you can also find it in people that have like scarlet fever right from a group H stripping infection right so that's a that's a big one you want to keep at the back of your mind and then they also like get like a dima of like their hands they can even get a dima of the gallbladder right so if they give you a question about a patient that has a history of Kawasaki's disease and then this patient has like red opacodron pain think about gallbladder high drops as the as the etiology of their problems and remember

for the most part you treat Kawasaki's disease with like a combination of IVIG and aspirin because these people can get like the vasculitis affecting the coronary vessels so with that they can actually get cardiac ischemia from all those from all those things right so those are big things you want to keep at the back of your mind with Kawasaki's disease and the next vasculinity is I'll talk about right if they give you a question about a patient that's a smoker and they tell you that he has like you know like like dark toes and all that crap you should really think about like burgers disease it's not bird it's not a burgers burgers disease is a IGA is like is a IGNF property this one is different this is burger so I don't know if I'm pronouncing it right but anyhow but it's like B.U.E.R.G.E.R.R.

like burgers disease sometimes you may see it on MBM is referred to as a thrombone jade subliterance it's a vasculitis that can happen classically I can almost promise you's gonna be a smoker on your exam and the thing is these people tend to essentially like the smoke a ton they get a vasculitis of the blood vessels they have feed their digits and they are low extremities so these people tend to have like ulcers on their feet nasty gangrene just dirty nasty spooky stuff they tend to have like the gangrene of their feet they tend to have like really bad renotes phenomenon so when they step out in the cold they can they are ischemia can be estentuiteta under those circumstances and really the only treatment for this disorder is just stop smoking you stop smoking it can go away what if you don't stop smoking it's gonna get bad and you're gonna lose your lips okay I guess that's the way you can try to I guess scare patients to make them sort of like stop smoking because I mean losing lips tends to be a pretty powerful motivator for for most people so the next vasculitis I guess I'll go ahead and jump to is what if they give you a question about like a 55 year old female she tells you that she has been having like a lot of pain when she tries to true and then she tells you that she has also had like some visual difficulty over the last 12 hours what is your next step in management for this patient I would hope you're saying to give like super high dose of cortical steroids I mean this person clearly has a giant cell at right is sometimes you may see referred to as temporal arthritis on ambient exams the big thing is once you suspect if you have any incline that a patient has a giant cell at right is give high dose cortical steroids and ask questions later okay if you try to do any kind of diagnostic testing first I promise you're gonna get that question wrong the very fir

st thing you should do in a person that has giant cell at right is is to give them big doses of cortical steroids to stave of the inflammation so that they don't lose the vision because the thing that happens in giant cell at right is is you have like and I guess let me just preface this by saying the next essentially giant cell at right is and the next one I'll talk about like Takayasu's which I essentially like the same disease is just like different age ranges and those things are they are classified as like large vessel vasculolidities compared to the early ones I talked about where those were essentially like a medium vessel of vasculolidities so the thing that happens is with the giant cell at right is you have like infill like like the position of like macrophages remember macrophages when they sort of like bandy together they form like giant cells so you have the position of those macrophages in the walls of of arteries especially like the branches of the carotid artery or even the ophthalmic artery that's why these people can get can get a blindness if you don't treat this if you don't treat this pretty pretty quickly right so those are again very high your things you want to keep at the back of your mind and it tends to show up in females right so it will be highly unlikely that you have a question about a guy with giant cell at right is on the mbm exams it will almost certainly be a female and it will almost certainly be a female over the age of over the age of 50 if you see like a similar presentation but it's a female less than the age of 50 especially like a Japanese female like an Asian female you really want to I'm not saying all Japanese like I'm not saying all Asians are Japanese people but if you say like a Japanese person most commonly on mbm is or you see any kind of Asian person with giant cell at right is stelt symptoms and they are less than th

e age of 50 then under those circumstances you absolutely positively want to think about Takayasu at right is but let me hold my horses a bit and talk about the other key associations with a giant cell at right is it has an association with with a jaw clonication right so these people as they are chewing it hurts to chew another one you may see on an exam is Polymergera Romarica right where people have like proximal muscle like tenderness right like really bad proximal muscle tenderness their ESR tends to be elevated although you want to remember that these people tend to have like a normal creating kindness that is a common misconception amongst medical students that oh if a person has a Polymergera Romarica they will have a elevated a C key that is actually not always true okay that is not always true yes you can under some select circumstances but that is extremely rare and the thing is the way you treat Polymergera Romarica is again to give a corticosterates but unlike giant cell at right is that you treat with high dose corticosterates Polymergera Romarica you actually treat it with low dose corticosterates and really for the most part if you want to diagnose giant cell at right is the thing you do is you do a temporal artery biopsy you need to do like almost like a you need to get like a decent chunk of those people's or temporal arteries because the thing is the inflammation is not like like it's not like continuous all through the temporal artery you can have inflammation in one small part and then new inflammation and then inflammation and another small part and then new inflammation right so you don't want to like take a small tiny piece of the temporal artery and let's say the part you take a piece out of right does not does not have inflammation you then say oh you know what this patient doesn't have a temporal arthritis right actually a negative biopsy do

es not rule out temporal arthritis FYI so that's something big time you want to keep at the back of your mind so again Polymergera Romarica low dose corticosterates legit giant cell at right is high dose corticosterates okay those are big things you want to keep at the back of your mind with your test and then remember it's a key answer to this right is again pretty similar presentation although they tend to present more like upper extremities symptoms where like they may have like differences in blood pressure between their two upper extremities or they may tell you that you can barely feel a palpate of pulse in one of the upper extremities but again Asian female less than the age of 50 under those circumstances think about a Takayasu's arthritis it tends to affect like the other itself and branches of the other as well okay versus giant cell at right is that tends to affect the carotids and branches of the carotids like the ophthalmic artery so again those are big things you want to keep at the back of your mind and really the way you treat a Takayasu's arthritis flare is with with a corticosterates so that is all I'm going to see about that now what if you get a question about a patient that presents with a patient that presents with like you know like severe chest pain tells you that you know it's like on the left side of the chest reading to the jaw what's your diagnosis under those circumstances I hope you're telling me that this patient has an MI right and if you suspect the patient has an MI what's your first step in in diagnosis what do you want to do first I hope you're saying to get an EKG right and the classic finding on NV Me exams right it's like if a person has like a territorial ST segmented elevation right in like contiguous leads so let's say for example like two three AVF for right-sided infarct or like V5 V61 and AVL for and for circumflex infarct o

r like V1 to V4 for an LED infarct remember an LED infarct is the most common then under those circumstances think about an MI right go ahead and get that EKG check the troponing the troponing will be elevated remember troponing is actually the most sensitive although there is actually some literature that's beginning to dispute that but that's a loyal discussion that I don't think really adds much to what we're discussing right now but basically troponins on NV Me exams are the most sensitive for the diagnosis of of a myocardial infarction although if a person has a reinfarct so let's say they've infarcted and then let's say like three four days later they start completing like new chest pain and you want to try to diagnose a reinfarct the thing you don't know those circumstances is to measure the CKMB okay because the thing is troponing it rises within a few hours of an MI but the thing is it stays elevated for almost like two weeks right but if a person has a C if because the thing is right cardiac myocides die as well your CKMB is gonna rise but the thing is CKMB actually goes back to normal within like three days so the person has a reinfarction CKMB is actually better than troponins for the diagnosis of for the diagnosis of an MI the only reason that CKMB is classically described as not being like super specific for an MI is because CKMB can rise from death of like skeletal muscle you can also rise from death of cardiac muscle right so if you see like a CKMB elevation you can say for sure it's from a person's cardiac muscle versus it's from a person's a skeletal muscle right so that's something big you want to keep want to keep at the back of your mind for exams and the thing is right so again on EKG MI you see like the classic ST segment elevations if a person has a new left bundle branch block so a new left bundle branch block that also fits with the diagnostic

criteria for to say that okay this person's got a this person's got an MI and again CKMB is the best thing you want to use for infarction for the most part within again like two to three days it returns back to normal so if a person has a infarction you want to come from CKMB over troponins as your diagnostic agents and then another weird thing you miss your occasional an MBA means they tend to do this with like our questions involving MI is with you say oh what happens to the levels of troponin of CKMB of myoglobin and all that stuff myoglobin also goes up in the setting of an MI in fact having like a low or a normal myoglobin has a very high NPV so very high negative predictive value for MI's but this is really checked checked in the real world but that's just something to give out the back of your mind actually measuring the levels of myoglobin is actually pretty has a pretty high negative predictive value for the diagnosis of of an MI so those are all big things you know you want to give out the back of your mind and obviously the person is having an MI right you want to give them drugs like aspirin you want to give them like you want to give them like a statin you want to give them like nitrate for the chest pain although remember nitrate is a terrible idea for person has a right-sided MI really a right-sided MI your treatment is to give those people a fluids believe it or not right and then yeah so those are all the big things you want to keep keep at the back of your mind with that and since we're talking about an MI quick question what kind of shock will be found in a person that has an MI what kind of shock will be found in a person that has an MI if you have your scheme over cardiac muscles what kind of shock would you have I would really really hope you're telling me that the person will have a cardiogenic shock okay cardiogenic shock and again your differ

ent types of shock right I mean if you're taking the USMLA exams and you don't know your different kinds of shock you're essentially asking for it right you likely lose a you know pretty decent a number of questions on your exam so you know you want to try to avoid that that's usually usually not a smart thing to do to just lose points and willingly so the thing is cardiogenic shock right what are the things that cause cardiogenic shock many things actually right so for person has like an MI that can cause cardiogenic shock for person has like a very bad hemodynamically significant arrhythmia like V-fab or V-tac or Torsada point or like nasty nasty a-fab that can also cause a cardiogenic shock if a person has like really like bad let's say like popular muscle rupture whatever that can also cause a nasty cardiogenic shock right so there are many things that can cause cardiogenic shock right and usually these patients on a physical exam or in the MBM question they'll tell you that the patient is like profoundly hypotensive they'll have like JVD they can have like you know like a whole climbing skin they'll have like pulmonary edema because fluid cannot flow forward right and again really for the most part of a person say for example they have like an M-I and it's causing cardiogenic shock you want to you know reverse colorize those patients you know little sooner rather than later that is really the only thing that would see those patients on that those are circumstances and in general right it makes zero sense to give people fluids if they have a cardiogenic shock right because they give them to those fluids the heart cannot handle that extra fluid so you're worsening the opponent or g-magnetic and back right so you generally do not want to do that really the way you manage cardiogenic shock is to give like a positive anotrop so you want to give a drug like a dubutamin

e right dubutamine remember it's a bit of an agonist so it would increase heart rate and it would increase a stroke volume because it's a it increases a cardiac or contractility you can also give a drug like Miorinone remember Miorinone is a phosphodistory inhibitor right and when you inhibit phosphodistory cyclic AMP rises in cardiac muscle the thing is a rise in cyclic AMP in cardiac muscle actually causes increased contraction contrast that would smooth muscle wear a rise in cyclic AMP at 3 causes smooth muscle relaxation okay so the thing is when you give Miorinone you are giving something called an I know dilator because it's a positive anotrop so you'll improve cardiac output it will improve your systolic blood pressure but at the same time because it's a PD PD in inhibitor right it will also cause for muscle relaxation so that will actually decrease after look so that will actually decrease your systolic blood pressure so for the most part people's pulse pressures widen when you're exposed to Miorinone Miorinone can be used to treat cardiogenic shock I mean I've certainly used it in clinical practice works extremely well and then other drugs you can use you can use the juxtaposition although that's not very common with most people but yes the juxtaposition also works pretty well for the treatment of a cardiogenic shock and the thing is unfortunately your friends at the USML they expect you to know certain hemodynamic parameters right in relation to the different kinds of shock right so see for example if a person has like cardiogenic shock what should be true of their cardiac output it should be low right your cardiac output should be decreased because the cardiac myocytes are not working well one way they can try to like mess with your head on an exam is instead of saying cardiac output you can see like cardiac index cardiac index is just like cardiac output d

ivided by your body surface area so the person has cardiac shock their cardiac index will actually be low as well right and the thing is like your left ventricular like endastolic pressures and endastolic volumes will actually be up okay because again the heart cannot pump on forward so because you can pump blood forward right you won't give up much insisted so a lot of the blood will persist in the heart so the left ventricular endastolic volume endastolic pressures all go up the thing is because the person's cardiac output has gone to crap right essentially because they have the cardiogenic shock the thing that happens is that blood flow is like very slow very tiny like they have like you know very diminished blood flow so the thing that happens is to try to like maintain blood pressures those people have like you know like this big cuticle means search and also right I mean you're obviously if you have cardiogenic shock your hyper profusing your afternoon material so you have an increased activity of the reigning angiotensin and adosterone system right so your angiotensin 2 will go up and your tensing 2 remember is also a powerful viso constructor and then obviously our dostor will also go up as well to help you reabsorb sodium at the level of the principle set of the collecting duct and water will follow alongside as well okay so those people the people that have got a ogenic shock their peripheral muscle resistance goes up and the thing is because tissues are like hmm blood is flowing very slowly and not seen enough blood those people's tissues tend to get like super super super super efficient at extracting oxygen so there is something called the mix venospo 2 the mix venospo 2 saturation essentially is the like O2 sat of the blood that's making its way back to the right each room it tends to be low in people that have a cardiogenic shock so those are all high-yie

ld things you want to keep at the back of your mind with cardiogenic shock and then what if they give you a question about a patient that has like really bad pattern of Fridays and this patient is profoundly hypertensive and you're giving this patient like a ton of fluid patient is not responding what kind of shock does this person have I hope you're telling me that this person has a septic shock right septic shock septic shock for the most part again you want to be careful although you know they care more about this when you're taking the USMLST2 CK exam but one thing you want to keep at the back of your mind is that you cannot see a person has septic shock until you've noted that they've not responded to fluid administration you need to administer fluids and a person not respond to that fluid administration to see that a person has septic shock that's very high yield to know for exams right and again usually septic shock usually for the most part happens in the setting of like a pretty you know pretty severe infection so septic shock pretty severe infection is what tends to cause it and if you think about it right when a person has infection right you have like this like endothelial cell injury and when you have endothelial cell injury one thing that happens is you begin to release all these because endothelial cells they stall like PGI to the stall like metric remember endothelial cells express a lot of like NOS right so like metric oxide synthase right so the thing is when you have like endothelial cell damage from the sepsis they begin to release all these powerful visual dialeders so actually in people that have septic shock they actually tend to have you know like pretty bad visual dilation so the systemic vascular resistance actually tends to decrease okay the systemic vascular resistance tends to decrease and to be perfectly honest the thing because if you thi

nk about a person's blood vessel right blood vessels are made up of arteriomes and then you have capillaries and then you have venuals okay so the thing that happens initially when a person has septic shock is that they have dilation of the arteriomes and if you have dilation of your arteriomes well unfortunately one thing that happens is that increases the speed of blood flow like through the things that are even downstream of the arteriomes so blood will flow really fast through the arteriomes flow really fast through the capillary flow really fast through the venual okay so the thing is that blood actually cycles right back to the heart fairly quickly and the thing is if blood is flowing really fast through a person's vessels then there is not enough time for oxygen exchange to happen across a capillary that is why the mixed venous auto saturation actually goes up in septic shock because the blood is just moving way too fast way way way way way too fast so tissues do not have enough time to extract that oxygen from the blood that is why in general in the setting of septic shock the mixed venous auto is elevated you may say oh Devon this is so low you to know I promise you have taken all the USMLA exams that if you're listening to this podcast you're probably planning to take I promise it's very high you to know for tests so systemic vessel resistance goes down in septic shock cardiac output actually goes up in septic shock initially initially okay cardiac output actually goes up in septic shock initially because remember I told you that the thing that dilates first is the arterial and when the arterios dilates right that would decrease the systemic vascular resistance so those people have increased cardiac output under those circumstances but the thing is as the septic shock progresses you will begin to dilate the venuals and if you begin to dilate venuals unfortun

ately the thing that will ultimately happen is that you will begin to pull blood in the persons are like more dependent regions of their body like their lower extremities so that can ultimately cause a decrease in cardiac output so initially there is an increase and this is the one they test like 99.9% of the time on the USMLA exams in people that have septic shock initially the cardiac output goes up okay but as time goes on like days after if the person has been in septic shock for a prolonged period of time over time the cardiac output will begin to decrease and the thing is if you are looking at the leventric or like the leventric or in the stoic volume leventric or in the stoic pressure those will all go down in the setting of septic shock right because again the afterload is decreased from the decrease the systemic vascular resistance so it's much easier for blood to empty from the leventric or so again those are all high ill things you want to keep at the back of your mind with septic shock and again remember on like most of the other kinds of shock where people have like cool clummy skin people tend to actually have like warm skin in the setting of septic shock again from the viso dilation right so you have heat cannot distributed across blood vessels and remember the drug of choice at least the pressure of choice for the treatment of septic shock is more of an efframe typically before you get more of an efframe you would have gotten like antibiotics you would have gotten a crop of fluids like almost like 10 plus liters of fluids to sort of like help the patients of blood pressure along and obviously you want to try to you know control the source of the infection by giving antibiotics or removing whatever plastic then you have in their body that maybe habarena infection and then if a person has you know let's say a person you know bleeds out like real good wha

t kind of shock will that be now obviously be hypervolimic shock right that the hypervolimic shock really the thing that's just happening is those people are losing blood volume greater than the body's ability to kind of like compensate okay so those people they'll have like decreased effective arterial blood volume right so because they have like a decreased blood volume right they will they're essentially like hypervusing the efframe material right so obviously the renal drens and adosterous system will kick into high gear and those people in general in general in general they tend to have you know increase the peripheral vascular resistance the cardiac output will be down right because obviously if you have like less blood in your in your vascular tree right then obviously you would not have as much blood going like venous return will go to the crapper and if your venous return goes to the crapper right your cardiac output will not be great okay and your left ventricular endastolic like voluminous and astolic pressures will also be decreased again because you are not having enough venous return and the thing is again if a person has hypervolimic shock their blood is kind of like you know flowing very slowly and very slowly because their vessels are all like constricted up right so the thing that happens is tissues again I like okay I'm not seeing blood frequently so because I'm not seeing enough blood or frequently let me extract as much oxygen as possible so the mixed venous auto saturation actually goes down pretty profoundly in the setting of in the setting of a hypo of hypo volimic shock and then the last one I guess I'll talk about that is you don't really tested that much with occasionally pops up on the exam is like neurogenic shock right so neurogenic shock usually it happens when a person has like severe brain injury or like severe spinal cord injury so yo

u essentially take the sympathetic nervous system out of commission if you take the sympathetic nervous system out of commission then the thing that unfortunately will happen is you have like a profound visodylle emission so that will lower the persons of blood pressure right because again if you take the systemic nervous I mean the if you take the sympathetic nervous system out of a commission then you're no longer producing you know enough catacolomines right so you will not have adequate viso constriction and you will think oh because these people are so visodylated the thing that you would expect to happen is oh they'll have like an increase in like like a like a compensatory attacky cardio to happen but actually that that actually does not happen because again remember for you to have that tachycardia actually happening it's sort of like it's sort of predicated on your sympathetic nervous system working as well as it should so the thing is if your SNS is you know it's not working out so well then you you cannot have that compensatory tachycardia so if you see a person that has like a decrease the systemic vascular resistance and they also have like greedy cardio you really want to think about a neurogenic shock on that those circumstances so again I know it's hard it's tough and all that but again these types of shock you really do want to make sure that you know you understand them pretty well because these are things that shop on the USMLA exams are taught not just step one step two CK step three shop exams you're meeting your third year this thing just tends to shop like way way way way way way too frequently and this podcast has gone on for 43 minutes so hopefully I will try to be done fairly soon I guess let me just talk about a few things real quick so how when do you see a person is hypertensive like what what is this systolic blood pressure caught off to

see a person is hypertensive it's more having a systolic blood pressure more than 130 millimeters of mercury for the systolic side of things it's having a systolic blood pressure greater than 80 millimeters of mercury I mean the thing is beyond that is like stage one hypertension where it's like from 130 or 140 systolic and greater than like 80 that's stoic and then there's like stage two hypertension where the person's systolic blood pressure is between like 140 like 150 systolic and greater than 90 that's stoic so those are big things you want to keep at the back of your mind the thing is hypertension right I mean like these I'm gonna talk see some more about this in a future in a future podcast but I've also kind of talked about a lot of this in my in my Rinal review videos or my guest podcast whatever it is but basically there are many things that can cause hypertension for the most part people tend to have like primary hypertension so sometimes you receive referred to as essential hypertension basically it means like no one knows what's causing that but the thing is they are certain like predisposing risk factors right so if you're African American if a person is like native American also he's panics you know they tend to have a pretty high rates of hypertension and I mean there are some things that can sort of like increase your risk of hypertension right so like if you you know too much weight so like too much fat if you're taking a crop ton of sodium or you know you don't exercise as much as you should or you drink a ton of alcohol or you smoke a ton these are all things that can cause hypertension right they are all like things you can change to decrease your risk of hypertension classically on the USML exams they tend to ask like they will give you like a bunch of like lifestyle modifications and ask which of the following is the best that most effective of

lower in blood pressure the most effective measure in lower in blood pressure is weight loss that's number one the second one is actually the dash diet that's number two third thing is exercise that's number three four thing is decreasing your your sodium intake okay so just remember like WDS that's the way I've always remembered it like weight loss is number one diet is number yeah dash diet is number two exercises number three and then decreasing your sodium intake is number four in order of most effective to list effective with regards to lower in a person's blood pressure really if you lose weight that is the highest yield means of lower in a blood pressure and then really how do you diagnose hypertension right basically you make the diagnosis by essentially like saying okay on two or more occasions right so two or more do you record blood pressures that are greater than that cutoff of 130 systolic or 80-dastolic if you measure that like two different like so two blood pressure measure like two or more blood pressure measurements in two or more office visits right that essentially tells you that the patient has a hypertension and there are many many drugs that I used to treat hypertension I have discussed this in these in like extreme detail in our other podcast so let you go and take a look at those I do have a cardiac pharmacology podcast and again in my Rino videos and also like in future cardiology videos I will talk about like some things that can cause like secondary hypertension right so say for example right like if you take steroids right steroids have a permissive effect on the sympathetic nervous system they can certainly cause a hypertension and remember that steroids also have like some partial activity on the recordicoid receptors right and remember that are quite quite a lot of stuff right they can like cause sodium retention in the net front throug

h the principle cell they and as you're retaining sodium you retain water right so your blood volume will increase so your blood pressure goes up if you're taking OC Ps remember estrogen right has like a direct effect on blood vessels where it can make a person's blood pressure go up if you take an NS Aid remember NS Aid's inhibit cycloxygenase so that decreases the production of first a gland in if you have less post-agglending you have a ton of viso constriction so that can cause hypertension if a person is on a lantide depressant right like an SSRI or an SNRI classically on MDME exams the gum after the SNR Is right so drugs like vanilla faxino, duloxetino like melnasipran or they also go after like the the MEOI's right like your phenolzine or your trinocipromino or your isocaboxazid remember those MEO Is they can cause like nasty nasty hypertension if you consume like like a food that contains a tyrone so those things can all cause hypertension if you're taking because anything about if you're preventing the reoptic of like noripine for example right we essentially like making categories hung around more in circulation right so those can cause that can cause all those all those kinds of problems if a person is taking like pseudo fed right so like a fedrine or like pseudo fedrine those are alpha-1 agonist so they can cause viso constriction so that can cause a hypertension and then if a person is being treated for ADHD right without those stimulants again many of those drugs prevent the reoptic of like calicolomins right so that can also cause a hypertension remember they can give you a question about like a young female with resistant hypertension and they tell you that oh you hear brewery when you oscultate her flank on that those circumstances you should be thinking about fibromoscular dysplasia right similar presentation but like an old guy the metallic that okay lik

e old guy flanked flung brewery or the metallic that old guy for no-scopic exam you see you see something called like a atherovinus nichen so like a v-nichen that's like renal artery stenosis under those circumstances I really would want you to think about I really would want you to think about you know like like a secondary cause of those patients hypertension because remember again if you have renal artery stenosis of fibromoscular dysplasia you're not sending your hypoprophysine the atherin material so that will cause increased production of reining right so you're under-tensing to our doserone will all go up I remember under-tensing too is a path of his or constrictor our doserine increases the reabsorption of sodium at the level of the principal cell of the collecting duct right so those people have like you know reabsorption of a ton of fluid and then the blood volume will go up the blood pressure will go up as well right if a person has a feel chromosome tumor remember feels have an association with neurofibromatosis type one and also like the MEN2 syndrome right where again you have like this tumor in the adrenal medulla remember those at your right from neurocress cells be produced a crap ton of cadet colomines so that patient again can have hypertension if a person has like a con syndrome right where they have an adrenal adenoma usually it's an adenoma in the adrenal cortex that's secreting a crap ton of ourosterone right again I already talked about the rows of our osterone that will increase blood volume increase blood pressure right so those are all things that can cause an increase in blood pressure and the thing is if your blood pressure is chronically increasing and causing a lot of problems right like elevated blood pressure like hypertension is actually one of the biggest risk factors for end-stational disease in the US the other big one is diabetes

but really hypertension and diabetes there this is floorgy high you to know for exams those are the two biggest risk factors for end-stational disease in the United States and I will open to say probably in the developed world as well and the thing is over time right if a person has like you know like very nasty hypertension let's say they have blood pressure is like super super high and they begin to have like end-organ damage so let's say they have like headache or they have like elevated creatinine or whatever of visual difficulty then that's something that's known as a hypertensive emergency okay a pretensive emergency I breathe in emergency really can because by many things right so if a person is like on like you know like misses like the patients have had like these are classically I have like these patients in the ICU like a patient that has missed dialysis for a while that can cause like a florid rise in their in their blood pressures if a person has like these are vasculities like these are rapidly progressive agglomerulone afraid of these that can also cause a problems in the cause of hypertensive emergency of a person has like TTPHUS or like sclerodermal or kind crisis those can all cause like a profound hypertension on end-biming exams and really these hypertensive emergencies the drugs you want to use to treat them on exams you want to either use like a labeta law right or you'd want to use like an nitro-procide remember nitro-procide and cyanide toxicity you can also use some dihydroperidine calcium channel blockers like my cardiopine or clevidipine I am I promise you if you try to pick my febipine on an end-biming exam for hypertensive emergency you're gonna get that question wrong so pay attention here the only drugs you can use to treat hypertensive emergency is labeta law my cardiopine clevidipine and sodium nitro-procide that's it some people use l

ike phenodopam but that's not a very popular option on end-biming exams because that drug is kind of falling out of fever because all those things you read about that oh it can maintain renal profusion bloody bloody blood that ends up not really being true at least a lot of studies have shown that that is essentially like not a thing so those are big things you want to keep at the back of your mind the thing is some people this is a classic question I get from people like to really say oh divine so what is the difference between hypertensive emergency and hypertensive urgency the thing is hypertensive urgency usually the those people's blood pressures are like super elevated is usually like more than like 180 systolic or 120-stolic but they don't have signs of end organ damage that is the key differentiating feature between hypertensive urgency where you have no end organ damage and hypertensive emergency where you do have end organ damage so those are things you want to keep those are things you want to keep at the back of your mind for tests so I'm thinking should I end here if I think I've talked about a ton of stuff you know what let me just round up with let me try to keep this on there like an hour yeah this cardio reviews just tend to be on the long side because it's a ton of stuff in cardio right it's like almost like 5% of the first day book but the thing is I don't know for whatever reason your friends at the MDME they love to test the things that happen like that you can observe like histology wise after a person has after a person has an MI I'll just talk about the high points like the big big things you want to know you need to know for purposes of the example the thing is within the first day after an MI some things you can observe right so you you tend to see like you know like swelling of the cardiac myocytes because again the sodium potassium ATP is p

umps have field right so if the sodium potassium ATP is pump fields then ions will go down the ingredients into the cells so that'll cause cell swelling so the thing is when the cells swells you begin to see like these like like undulating myocytes sometimes people call them like wavy myocytes and then you may also see this known as a contraction bands really the contraction bands just occurs because when a person has necrosis right they begin to release all this calcium intracellularly and that calcium can cause like contraction of a cardiac myocytes right so you see like those are contraction bands are on histology the thing is within like one to three days right you begin to see like coagulation necrosis you begin to see like neutrophils right that's like the big big time you see neutrophils within like a like a day to three days like a ton of neutrophils you'll find the coagulative coagulation necrosis and then really like after like three days right like three days to like two weeks that's where you begin to see like a ton of macrophages you can also see some neutrophils but I will tell you that really for purposes of the USML exam think more about macrophages as being from three to 14 days after the first like from one to three these things more about the neutrophils right and because you see all these macrophages that is why typically you would observe that all these badness like the ventricular ferroir rupture or the interventricular septal rupture and all that garbage those tend to happen like within three to 14 days after an MI and then granulation tissue as well as something again you find within this three to 14 day period for the most part after 14 days the thing you're beginning to see is like fibros tissue right so like a ton of scar tissue so again yes they all these like you know like super specific details on like the stuff that people try to memoriz

e and all that crap but to be perfectly honest with you for the most part if you just sort of keep these high points in mind like they want cell swelling so they want cell swelling contraction bands they want to three neutrophils right the three to five I mean the three to 14 macrophages granulation tissue and then two weeks after or more scar tissue like fibros tissue those are kind of like the high points that should help you get like maybe like 99% of the morphology questions that you get on that you get on the USML exams so I think I'm gonna go ahead and stop here as I do at the end of every podcast I do offer like a tutor essentially for most things you'll ever see in med school so like your pre clinical exams 30-ish-off exams USML is step one two CK two CS and step three and then if you're I've talked about this longitudinal tutoring I offer out nose and wear I tutor you throughout like your med school like let's say your first or second year I tutor you for your class blocks but at the same time I tutor for step one so that when you get your dedicated period you feel like super super ready and then essentially and then I tutor you during the dedicated period really the people that have done this longitudinal tutoring with they've been like super wildly successful on the USML exams and then if you're a medicine and applying to like residency so like an era's application or a collection and a plan to med school so I'm and I'm just up I've worked with hundreds even of thousands of people on this stuff I have experienced like you know like editing personal statements writing personal statements letters of recommendation mocking reviews editing applications I do offer all those things so if you interested in any of those feel free to reach out to me and then I should also mention that if you have a college buddy that needs tutoring for like Gen Cam, O Cam, Physics, B

iochemistry, Histology, Physiology I do offer one on one tutoring for all those things so I wish you all the best I hope you've gotten something from this podcast I will pick up from here next time so have a wonderful rest of your day God bless you thank you

Ventricular fibrillation (V-fib).

ST segment elevations in a non-territorial distribution and diffuse PR segment depressions.

A holosystolic murmur of the apex (mitral regurgitation).

Pseudoaneurysms occur $<2$ weeks post-MI; True aneurysms occur $>2$ weeks post-MI.

High-dose corticosteroids to prevent irreversible vision loss.

Conjunctival injection, rash on palms and soles, and unilateral anterior cervical lymphadenopathy.

Adenosine-based vasodilators (due to severe COPD or asthma).

Hypotension, Jugular Venous Distention (JVD), and muffled heart sounds (Beck's Triad).

Polyarteritis Nodosa (PAN).

Emergency involves signs of end-organ damage; Urgency does not.

Nicardipine or Clevidipine (Calcium Channel Blockers).

Weight loss.

SVR decreases (vasodilation); $\text{SvO}_2$ is elevated (due to fast blood flow/poor extraction).

GCA affects temporal arteries and branches; Takayasu's typically affects large vessels, often involving the aorta and its major branches.

Neurogenic shock (due to loss of sympathetic tone).

Hypotension, Jugular Venous Distention (JVD), and muffled heart sounds (Beck's Triad).

Polyarteritis Nodosa (PAN).

Emergency involves signs of end-organ damage; Urgency does not.

Nicardipine or Clevidipine (Calcium Channel Blockers).

Weight loss.

SVR decreases (vasodilation); $\text{SvO}_2$ is elevated (due to fast blood flow/poor extraction).

GCA affects temporal arteries and branches; Takayasu's typically affects large vessels, often involving the aorta and its major branches.

Neurogenic shock (due to loss of sympathetic tone).