DIP Episode 116 - Comprehensive USMLE Step 1 Cardiology Review Part 1

Okay, welcome. My name is Divine. I am a PGY-1, a Transitionary resident that will ultimately be going into radiology. This is the 116th episode of the Divine Intervention Podcasts. In this episode I'll be starting a comprehensive review for the USMN Step 1 for cardiology. I know I read study 1 for GI but again I've been getting lots of requests from people to sort of have a variation in subjects. So I'll just push out many things at the same time but again I'll ultimately complete each series. So let's jump right into it. So what if you get a question about a patient? The patient presents with chest pain on step one and then they show you an e-kitch on your CNST televisions and in two, three and AVF in leads two leads three and AVF. What's the artery that has been infarcted? I really hope you're thinking about the right coronary artery, right? Although remember that the most commonly infarcted artery, right? In the setting of an M is the left anterior descending artery, right? Remember the LED? The e-kiglies that sort of map to that are like leads V1 to V3. So I guess with that let's sort of talk about the coronary arteries, right? So you know that there are two main coronary arteries, right? There's the right coronary artery, there's the left coronary artery. Now the thing is the left coronary artery sort of gives off the left anterior descending artery, right? That sort of supplies like the anterior part of the left ventricle.

And then another branch of the left coronary artery is the left... Excuse me? Is the left circumflex artery? That supplies kind of like the side, so the lateral wall of the left ventricle and also the back, so the posterior wall of the left ventricle, okay? And then remember that your RCA, your right coronary artery, right? Supplies... basically supplies most of your right ventricle, right? And it also supplies like the inferior wall of both the right and the left ventricle, okay? It does that for the most part through the posterior descending artery. And then it's also very high you to know that your SA node and your EV nodes, right? The blood, so you're like your SA node artery, your EV node artery. Those classically come from... those classically come from the RCA, right? So if a person has like an RCA infarct, it can actually present as hardblock, okay? So that's just one of those things you want to keep at the back of your mind, for example, right? And then with this posterior descending artery, right, that I said, come from the RCA. It doesn't always come from the RCA in people, right? But for the most part, it comes from the RCA, like 85% of people have their PDA coming from the RCA, right? That's something called a right dominant circulation. If you have your PDA coming from the left circumflex, right? That's something called a left dominant circulation, right? Because the left circumflex is a derivative of the left coronary artery, right?

That kind of happens again in like 8% of people. But there's some people where they have like their PDA, like the posterior descending artery coming from the left circumflex and the right coronary artery, right? That's something called a coronary circulation. I mean, I always wondered, like, man, how can one blood, how can, how can two arteries give rise to one blood vessel? The thing is the PDA has multiple branches. So if some of the branches come from the LCA and some of the branches come from the RCA, that's what's known as a codominant circulation, that tends to accommodate like 7% of people. Now, the thing you kind of want to keep at the back of your mind is that. So I sort of talked about the distributions of these arteries, right? How the RCA supplies mostly like the right ventricle and supplies like the righty trim, right? And he also kind of supplies like the, like the interventricular septum, but like the posterior one third of it, right? And then like again, the S a new and the A V note. And then I talked about how the left circumflex supplies the side of the left ventricle, so the lateral wall and also like the posterior left ventricle, right? And then I already talked about how the L E B supplies like the anterior left ventricle. It has supplies the interventricular septum, right? So the L E D has like septal branches, right? In fact, if you have like an STL vision in like V1, V2, right?

That tends to be more of like a septal MI, but that's probably a little too much detail. But the money part of all of this is the papillary muscles, right? So the thing is the heart actually has five papillary muscles, right? I remember right there, the valve between the right inch of a right ventricle is the tricospid valve, the valve between the left inch of the left ventricle is the bicospid valve or the mitral valve, right? These would remember that is that you try before you buy, right? So tricospid on the right, bicospid on the left. The thing is of those five papillary muscles, we have three going with tricospid valve, so like the anterior papillary muscle, the posterior papillary muscle, the septal papillary muscle, but on the left we have two papillary muscles, we have the anterior lateral papillary muscle and then we have the posterior medial papillary muscle, those are both with the bicospid valve. The thing is the PDA, right? The posterior descending artery, supplies the posterior medial papillary muscle, but the L E D and the left circumflex both supply the anterior lateral papillary muscle. So the thing is if a person actually has an infarction and like a microindal infarction, the most likely papillary muscle to basically die or infarct, right? And the person will have like flush mitral regurgitation with that is the posterior medial papillary muscle because it only has one blood supply, only has supply from the PDA.

Contrast this with the anterior lateral papillary muscle that has supply from the L E D and the LCX. It's actually very high to know these pieces of trivia. I know you're like, hmm, the Vindy sounds super loyal and I promise you it's not, right? It's one of those things that they love to test on exams. So I guess the next thing we can talk about is how exactly those blood flowing the heart, right? So again I'm kind of setting the stage here for the pathologies we're going to be talking about later, but how exactly those blood flowing the heart, right? So blood, right? I mean let's say from the rest of your body you have the oxygenated blood. That the oxygenated blood, right? Flows, infargell me just make this even easier for you. Basically, others by definition take blood away from the heart, things by definition return blood to the heart. Okay? If you remember that you'll be good and for pretty much everything, right? So you take all this the oxygenated blood, right? And you have like your SVC, IVC, bring it back to the rest, bring it back to the right atrium. Your IVC usually brings blood from like the lower extremities, your visceral organs and all that stuff. Your SVC tends to bring blood from like the head and neck, right? From the face and stuff like that. So if for example you have like a lung cancer that compresses the SVC, right? A person can have something called SVC syndrome, right? An SVC syndrome will cause like the facial engorgement and all that stuff, right?

Usually I raise this with lung cancer and things of that nature. So you have the SVC IVC, they bring the oxygenated blood back to the heart, right? And then that blood flows from the right atrium through the tricospit valve to the right ventricle. Remember the tricospit valve is the most commonly involved valve in endocratitis and an IV drug user, right? Because again, remember, if you inject, if you're an IV drug user, they don't say I a drug user, IV drug user. If you're an IV drug user, you're injecting blood into a vein and the vein drains to the right side of the heart, right? So the tricospit valve is most commonly involved in in endocratitis in IV drug users, right? And then from the tricospit valve, you have blood flow to from the right atrium to the right ventricle. And then from the right ventricle, blood flows through the pulmonary arteries. Remember, arteries take blood away from the heart. So blood flows from the pulmonary arteries to the lungs. Now, also looking at that right side, right? So what if they give you an exam question about a patient that has like episodes of bronchospasm and they have like flushing and they have like all this diarrhea and then they tell you that you are hearing like murmurs in the left upper sternal border and at the left lower sternal border, right? Hopefully you're thinking about carcinoid syndrome, right? Remember carcinoid syndrome, you have a tumor that's producing serotonin.

Remember carcinoid syndrome is high yield from many perspectives, right? But the first, the reason that it's kind of like relevant to the cardiac discursion here is that carcinoid, right? Usually, it doesn't cause any symptoms, right? Because the liver has the ability to metabolize it. But it metabolize the serotonin. But if it goes to the, if you have meds to the, to the liver, right? And the liver can no longer metabolize it. So those people tend to have like, so that serotonin can make it away from the liver to the right side of the heart, right? The left side of the heart usually doesn't see carcinoid symptoms because the lungs have the ability to metabolize serotonin, right? Remember, the lungs have a lot of metabolic activity. I mean, even under tensing, converting enzyme is found in the, in the lungs. So carcinoid's heart disease, whenever carcinoid causes valve-village problems, it causes right side-village problems for that reason, right? And classically, I cause it like tricospid regurg, which you can call trite. So it causes tricospid regurg and pulmonic stenosis, right? But then, much easier with a remember that is just remember the term tips. So tips, right? Tricospid insufficiency, remember, I'm not that name for regurgitation, it's insufficiency. So tricospid regurg, so tricospid insufficiency and pulmonica stenosis.

And then that blood, when it gets to the lung from the pulmonary arteries, it gets, it gets oxygenated in the lungs and then it flows back to the heart through pulmonary veins, right? Flows back to the left ear trim. And then from the left ear trim, the blood flows through the bicospid valve. Remember the, remember the bicospid valve has two cusps, it's also called the mitral valve, right? Or the left ear trim, tricolo valve, if you may, right? So flows through the bicospid valve to the left ventricle. And then from the left ventricle, it flows out to the other, right? Remember, the other has multiple kind of sites to it, right? So the other has like the ascending the other, we have the aortic arch, we have the descending yoder. And I hope you sort of can remember the branches, right? Of your yoder, right? So on your first branch that comes off is the bricosephalic artery, right? The bricosephalic artery gives rise to the right common carotid and the right subclavian, right? And then after that, you have the left common carotid come off. And then after the left common carotid comes off, you have the left subclavian come off, right? And again, all these things, I mean, if you remember my vascular anatomy podcast, that's one of those podcasts that you'll be doing yourself a great service. If you don't listen to before you take literally new US Emily exam, especially like step one and step two, and also your surgery shelf, and also your neural shelf to a limited extent, right?

So there's some key things you kind of want to know about the arch, right? So I just talked about how the right common carotid, so the common carotid artery, right? Comes off of two different things. So on the for the right common carotid artery, right? It comes off the bricosephalic artery, which comes off the early carch, versus the left common carotid artery that directly comes off of the arch, right? But the thing is your common carotid arteries, when they are traveling in the neck, they actually travel in something called the carotid sheath, right? They travel with like three other things, I mean two other things, right? So you have the common carotid artery for starters, right? And then you have the IGV, the internal jogger living, and then you have the vigorous nerve. Now, the thing is the internal jogger living, so if you're sort of looking at your carotid sheath as a circle, the carotid sheath is just kind of because remember, there's a lot of like real estate in the neck or packed in there. I mean, I really respect the head and neck surgeons. The job that tell you is not easy, but basically, there's a lot of real estate in the neck. So you try to cover things up as much as possible so that you don't have one thinner running into the other, right? So in that carotid sheath, the thing that is media is actually the common carotid artery.

The thing that's lateral is the internal jogger living, and then the thing that is posterior to all of this mess is the vigorous nerve, a cranial nerve, 10. Now, you may see divine. Now, why don't you do this crap? Let me explain why you need to know, right? One is clinically, and one is also for your exam, right? So if a person is inserting a central line, right? If you're inserting a central line and let's assume you're doing it blind, probably not the best idea in the world, but again, the surgeon's situations where insertion central line should be done blind, like an atroma situation or emergency situation. But if you're doing a central line blind, that's what you're doing, you're doing it blind, right? The thing is, you usually try to pop it the carotid pulse first, right? Because remember, arteries contain a lot of smoothing also, so they're like pulsatile vessels, and they also contain a lot of elastic fibers, which I'll talk about in a bit, right? So they're pulsatile. So you feel the carotid pulse, and then the next thing you do is later you fill a lateral to the carotid pulse, right? And that's where that's basically where you insert your needle, right? That's where you are throwing the central line, right?

And usually, I mean, you've probably, this is more of a clinical problem, but if people do central lines, you've probably noticed, if you've done any kind of ICU rotation or you've shadowed in a ICU, you notice that central line is usually placed on the right, right? And the reason that that is done is the common carotid arteries, the internal jaw glauvens and whatnot on the right, they sort of run on the own with the vigous nerve, and that's it. But on the left, the thoracic duct is in very close proximity to the common carotid and the internal jaw gala, right? So it probably, you probably don't want to transact the thoracic duct, right? I mean, you can get like a chylothorax, can get a lot of problems doing that. So that's why usually it's usually a lot smarter to attempt to insert a central line on the right, compared to the, compared to the left. Now, another high-youth thing to sort of remember with the yodic arch, right? Is remember that the yodic arch, the left recurrent laryngeal nerve, remember that's one of the branches of the vigous, the left recurrent laryngeal nerve loops around the yodic arch on the left, right? Remember the recurrent laryngeal nerve does not, does not exactly how do I put this? Does not exactly follow the same course on the right of the left, right? Obviously, there are two vigous nerves. There's your right vigous nerve, there's your left vigous nerve. So your right vigous nerve gives rights to your right recurrent laryngeal nerve.

Your recurrent laryngeal nerve on the right actually loops around the right subclavian artery, remember the right subclavian artery is one of the, is one of the branches of the right brichusif alica trunk. And then your left recurrent laryngeal nerve actually loops around the yodic arch, okay? And the thing is the left recurrent laryngeal nerve, it actually has a pretty close approximation to the left atrium, right? So the thing is if a person actually has like dilation of the left atrium from like mitro stenosis, for example, right? Those people actually can have like, they can have like a hoarseness and the reason they have the hoarseness is because they've compressed the recurrent laryngeal nerve on that side, right? So just so that again, keep that at the back of your mind, they've come essentially compressed the left recurrent laryngeal nerve. They can also have dysphysia because again remember that the esophagus, remember the left atrium is actually the most posterior portion of the heart, right? So the esophagus is like smack dab against the, against the left atrium. So if you have left atrium enlargement, that can compress the esophagus and the patient can have dysphysia. Again, kind of like another high-yield thing there is, right? So you may, you may ask yourself, okay, divine, where do people, if you have, what's this whole concept with the TEE, a transesophageal echocardiogram? A TEE basically involves you putting an ultrasound probe down the esophagus.

It gives you the best view of the heart, especially like the left atrium, right? Because again, the esophagus is in very close proximity to the left atrium. That is the primary difference between a TEE, a trans thoracic, right? So trans thoracic, they're putting the ultrasound probe in front of the heart, like literally on the person's chest versus a transesophageal, where you're putting the probe in the esophagus, right? So that's why a TEE is more sensitive than a TEE, right? Because again, the TEE is much closer to the heart, because it's again in the esophagus, which is again smacked up against the left atrium, right? And then don't forget, right? Like in the heart, we have like the Essay node, remember the Essay node has this property of a automaticity, is the primary piece, the speaker of the heart, you find it for the most part in the right atrium, right? It kind of like, basically, the junction of like the SVC and the right atrium, that's where you find the Essay node, the Essay node sort of fires off signals, those signals, and again, I'll talk more about this when we get to the myocardial action potentials, but I mean the peacemaker potentials, you want to be a little more exact, but basically, you fire off signals from the Essay node to the AV node, right? And then the AV node, then basically, it's kind of like a slow down mechanism, right? Because the thing is, if you depolarize the atria, right?

The thing you want to happen first is you want, after the atria depolarized, they squish, they send lots of the ventricles, you kind of want enough time for the blood to get to those ventricles before the ventricles then get depolarized, right? So the AV node sort of helps us slow down mechanism with that to keep signals from immediately traversing BAM, and going straight to the ventricles. And the thing is, before signals even get to the AV node, usually the two atria depolarized first from the Essay node, and then those signals again travel to the AV node, and then they traverse the AV node, go down something called the bundle of his, right? The bundle of his is actually like a kind of a myocardial cell, but the thing is, it doesn't have as much in the way of, it doesn't have as much in the way of saccombs, right? So like it doesn't present as much resistance to the flow of electric current, right? So that thing, so Essay node, then AV node, AV node, bundle of his, and then from the bundle of his, you then have like the right bundle branch and the left bundle branch, and then from the left and right bundle branches, you have things known as the Brachingi fibers that ultimately send signals to the rest of the ventricles, right? So again, kind of like a few high-yield things to know there, right? So you see me talk about like the left and right bundle branches, right?

So if you have problems with like the left bundle branch or the right bundle branch, that's where the bundle branch blocks come from. Again, I'll talk about those when I talk about arrhythmias. And then if a person has like an issue, right? That the level of like the, the issue at like at the level of like the bundle of his or they have issues like with the Brachingi fibers, those things can cause various serious hard blocks, right? More like the Mobites 2 hard blocks. Remember, there, there is such a thing as a first degree hard block, there's such a thing as a second degree hard block, there's such a thing as a third degree hard block, okay? But the thing is the second degree hard block has two types, right? There's Mobites 1 and Mobites 2. Basically Mobites 2 hard blocks are lower, are things that are arise when you have issues at the level of the bundle of his and the Brachingi fibers. Remember, the Brachingi fibers are conduit for electrical conductivity between the bundle branches and the, and the ventricles. And then the thing is remember, I say that the AV node, right? It's kind of like the only conduit that lets signals flow from the SA node, bam, bam, to the ventricles. The thing is if you create another conduit, right? So like the bundle of, like in Wolf Parkinson white, right? Where you have like this a bundle of Kent and blood flows and signals flow directly from the entrance to the ventricles. You can see how that can cause a problem, right?

Because that slow down mechanism of the AV node is no longer there, right? So the ventricles may not have filled up appropriately before the ventricles are depolarized and are contract. So you can see that if the ventricles have no field appropriately, right? You're essentially having like some kind of a, that's the like dysfunction. It's like, almost like a functional, that's the like dysfunction. So you do not send, you don't have enough of a cardiac output because not much went into the ventricles in the first place. So you can see why a person may be symptomatic if they have a Wolf Parkinson white syndrome. That's kind of like the pathophysiology behind that. And then some other things that kind of want to talk about, right? So remember that if you're looking at this on a histological basis, right? So we have basically like the inner layer of the heart is lined by endocardium, right? So we have endocardium. And the thing is that endocardium, right? Like lines the walls of the each other, lines the walls of the ventricles, lines the walls of the, lines the walls of the, what is it called? Of the valves of the heart, right? So that's why endocarditis, right? It's an information of the endocardium, right? It usually presents as like, volume of problems, right? And then after the endocardium, we actually have something called the myocardium, right? Have the myocardium. After the myocardium, we then have the epicardium, right?

The thing is the epicardium, like has basically has a second name. And a second name for the epicardium is the visceral pericardium, right? Because remember the, the heart has a pouch that surrounds it, right? The pericardium, right? But the thing is we have like the parietal pericardium and visceral pericardium. The visceral pericardium is the thing that literally encases the heart itself. And another name for the visceral pericardium is the epicardium, right? Now the parietal pericardium is the thing that's more on the outside, right? And there's like pericardium fluid that's kind of like between that and the visceral pericardium. And again, remember there's usually just a little amount of fluid, right? Between the pericardial liars. And the reason you have that little amount of fluid, right? It's because it kind of helps you prevent friction, right? Between like the two parts of the, between like the visceral pericardium and the parietal pericardium. We kind of make sense, right? Because remember the heart is constantly moving, right? Whenever you have two moving parts, you want to try to reduce friction between those things, right? Because if there is friction between those things, right? Who knows? Maybe you could also quote the frictioner up on exam in a patient that has a pericarditis, right? And I mean, if obviously if too much fluid builds up in that pericardial cavity, the person can have like a pericardial effusion or they can have like cardiac tamponate, right?

So again, I know like, yeah, I'm talking about cardiac anatomy, but notice I'm trying to integrate it with multiple other things that you could see tested on an exam. So, um, so I guess let's sort of see a few more things about the anatomy of the heart rate. So remember, right, we have like the wall that separates the right each other and the left each other and then we have the wall that separates the right ventricle and the left ventricle. And I will potentially see some more things about this when I talk about like cardiac embryology. That's a different podcast. That certainly is not something I want to cover here. So I don't give you guys a headache because that's like another complex bit of information there. So, um, the left side of the heart in general has much higher pressures than the right side, right? So whenever a person has like a like a hole in the heart, right? So if they have a hole between the right each from left each term, like an ASD, right? Blood will flow from the left each term to the right each term, right? If a person has a VSD, blood will flow from the left ventricle to right ventricle, right? And although over time, if you keep having blood flowing to the right side of the heart, the right side of the heart cannot be with all those pressures for a long, long enough period of time.

So that chronically increased blood flow to the right side of the heart will ultimately like increase like pulmonary at your resistance, present in your pulmonary hypertension. And then at some point, the pressures on the right side of the heart may exceed the pressures on the left side of the heart, right? And then instead of having like a left to right shunt, basically, you then have a right to left shunt, right? That's what's known as isomangra physiology, right? And there's no physiology, it's pathology, it's pathologic, right? Although a right to left shunt is, is physiologic when you're in utero, but it becomes pathologic when you have that after you're born, right? So that's kind of like a bath in that can happen there. And remember, ASD, ASD, ASD, don't forget that we're down syndrome, right? That's the big, big, big association. You want to remember for your exams because again, when I talk about cardiac embryology, I will make some mention of all the stuff known as like the endocardial cushions and all that crap, but those endocardial cushions, they actually derived from neurocrest. And the thing is in Down syndrome, they tend to have a lot of problems with like neurocrest cell migration. So they may have issues with like the endocardial cushions. So they may have like AS Ds. In fact, patients with Down syndrome tend to have more of a primum ASD. A primum ASD is kind of rare, but if you see it, it's usually found in a patient that has a Down syndrome, right?

And then if a person has a VSD, it's usually like a member of the VSD. But again, I'll talk about this, all this, all this stuff, when I talk about cardiac embryology, right? And again, obviously, I remember that VS Ds are present as like this holocystolic murmur at the left sternal border, right? And then an ASD will cause like the white fixed split of the S2 heart cell. Again, I'm going to talk about the pathophys behind all this stuff because the thing is, many people think that step one is a memorization exam. It's not just a little bit right now. It's not. You don't need to memorize all the stuff. Don't get me wrong. But the thing is, most times when you read questions, you notice that they're not necessarily texting. Do you remember this factoid? They're usually testing to understand this factoid because the thing is they may not test the direct factoid you've memorized, but they will test it in a context where you are not necessarily girded in the factoid, but you are taking the understanding of that factoid you've memorized to apply to that like unfamiliar scenario that closely parallels what you've learned and then use it to solve the question. So again, just as you're studying for a step one, I always tell people the corner stone of any successful study and whether you're a resident or an intern or a med student or a college student doesn't matter.

The first thing you need to do is you need to understand first and then after that, make repeated passes so you're committed to to memory. So I guess since we've sort of talked about the heart, right? So let's talk, kind of talk about the conduits that take blood, away from the heart, right? So like the arteries, right? So the thing is there are many different types of arteries, right? So there's like the muscular arteries, there's the elastic arteries, right? And those two kinds of arteries you kind of want to understand like some salient differences between those things. The thing is the muscular arteries, right? Those arteries, right? So, okay, let me just say a few general things about arteries first, right? So arteries, they have like an intima medial and an ventisha, right? The intima is lined by like simple scrimus epithelium and then the media usually contains smooth muscle and elastic fibers, right? And then the adventisha, I kind of think of it as like surrounding connective tissue, okay? So there's the intima, there's the media and there's the adventisha, okay? So again, some people call it tunica intima, tunica media, tunica, ventisha, okay? And again, intima simple scrimus epithelium, again, that's how you know for step one. Media contains smooth muscle with varying amounts of elastic fibers, right?

And then the adventisha is kind of like connective tissue, it kind of like has like a support structure, it contains like nerves, sometimes it contains viso-visorum, sometimes it contains some other like supportive elements, okay? So now that you have that general understanding, right? So let's sort of talk about the two types of arteries, right? So we have the muscular arteries, the muscular arteries, I sort of think of them as like medium-sized arteries, right? So they are kind of like small arteries, so arteries like your radial artery or your artery that supplies the the spleen, right? So like your splinic artery, right? Those are examples of muscular arteries. The thing is muscular arteries, they contain like the, they contain the tunica intima, they contain the tunica media, they contain the tunica adventisha, but the thing is for the most part in their tunica adventisha, they generally do not have, they generally do not have viso-visorum, so viso-visorum are basically like blood vessels that specifically supply the supply the tunica adventisha, right? Because the thing is if you have a very big artery, right? Like the elastic arteries, for example, and I'll talk about that shortly, the elastic arteries are your big, big, big bad arteries like your yoder, right?

It is an example of an elastic artery, your branch, like your major branches of the yoder, like your SMA, for example, that supplies like your jejunum, your ilium, your ascending colon, and your proximal to thirds of your transverse colon, right? Those are large arteries, right? Those are elastic arteries, those arteries, they are very big, so all parts of the wall of those arteries, right? It doesn't make sense for them to depend on oxygen, diffusing from the lumen of the artery and giving them enough nutrition. That's not very practical. So for those big arteries, they tend to have a crap ton of viso-visorum, okay? The viso-visorum, they are like blood vessels that are literally just for the arteries themselves to help them like, sort of get nutrients and get oxygen on board. Now, but smaller arteries, either don't have viso-visorum or they have very diminished amounts of viso-visorum. So those are, again, higher things you want to keep at the back of your mind for tests. Now, the thing is, in fact, with this whole viso-visorum business, right? Okay, let me talk about the arteries. Again, sorry, I'm sort of jumping all over the place. Again, largely giving this from memory, so I'm kind of, but I again have ideas of what I want to talk about. But the thing is the elastic arteries, right? So the thing that makes them elastic arteries are the fact that they contain a lot of like elastic fibers in the immediate, right?

So remember, I said that most arteries, elastic arteries, the kinds of arteries. And I said that arteries you differentiate them basically by how big they are, that's one. And also by how much elastic fiber, how much they have in the well, the elastic fibers in the immediate, right? So your elastic arteries, they contain a ton of elastic fibers in their media, right? In the Atunica media, so like the middle part of the arterial wall. And remember that these elastic fibers come from things like Fibrillin, right? So if I imagine they give you a question about a person that is like six foot tall and then presents with like severe chest pain, relating to the back, I really hope on the those circumstances, you think about morphine, right? You're thinking about morphine syndrome. In morphine syndrome, remember it's a chromosome 15 issue. It's like autosomodominant inheritance. You have problems with Fibrillin. When you have problems with Fibrillin, right? You're not going to make great elastic fibers, right? So because those people don't make great elastic fibers, they're very so like because the thing is elasticity, right? Means the ability to snap back to your original dimensions after you've been distended. The problem is if you have issues with elastic fibers, you will not have the ability to snap back to your original dimensions after you've been distended. You may get distended. Remember the other is a big elastic artery.

It constantly pulsates, pulsates, pulsates because it's receiving blood from the left ventricle. The left ventricle operates on the very, very high pressures, right? So if a person has morphine syndrome, they have like weak elastic fibers and then they're boom, pulsating, pulsating, pulsating, pulsating, they're either you can kind of imagine that the other will not always snap back to its original dimensions with with each distension. So over time, those people actually have like distension, distension, distension, distension of your other, right? And that's why aortic, like aortic regurgitation is fairly common in morphines, right? And the reason is common in morphines is again because they have like massive dilution of their aortic root, right? So if they have dilution of the aortic root, of course they are going to have like aortic regurgutri because you're basically pulling the aortic cossips apart, right? So again, that's a high-o thing to understand. And remember that again, patients with morphines, again, this kind of explains why they had high risk for aortic dissection because again, the media is not as strong as it should be. And please, please, please, I'll just go ahead and see this. I'm going to repeat this so many times. I've probably repeated it many, many times in many different podcasts that I have given.

But don't forget that the boss phrase pathophysiology, you want to remember, for aortic dissection on the end, it is something called cystic medionic roses, or cystic medial regeneration. The boss phrase pathophysiology, you want to remember for a micro valve prolapse, okay? For a micro valve prolapse is mix some of those degeneration, right? And then the boss phrase pathophysiology, you want to remember for aortic stenosis is calcification of the valve, okay? It's calcification of the valve that causes those problems, right? And then another classic series of NVME questions, right, is that what's like the biggest risk factor for micro stenosis? The biggest risk factor is rheumatic fever, right? And then you can ask you, what is the biggest risk factor for a fib? The biggest risk factor for a fib is micro stenosis, right? And then you can ask you, what is the biggest risk factor for a myocardial infarction? The biggest risk factor for an MI is guess what? Smoking. Smoking is the biggest risk factor for myocardial infarctions and for triple age, right? So, abdominal eortic aneurysms. And again, I'll get to that in a bit. And then the biggest risk factor for strokes and the eortic dissection is hypertension, okay? Again, I promise you all these words I just said, I'll be shocked if you don't see at least one or 12 of these things tested on any USMEL exam you take in some way, shape or form.

Okay, so again, I've sort of talked about the elastic arteries and how they have a ton of elastic fibers in the immediate, right? The most good arteries, they really do not have much in the well, the elastic fibers in the immediate, right? And remember, I kind of like the way things flow, right? So, you have blood flow from your arteries and then they go to your arterios and then they go to your capillaries and then they go to your venus and then those go to veins and then those veins return back to the heart, right? So, the thing is you kind of want to remember is some specific properties of these vessels, right? So, your arterios, your resistance vessels, they are the biggest point of resistance in your arterial system, right? So, I mean, your blood vessel system, so it kind of makes sense that those things have a ton of smooth muscle. In fact, in general, you tend to find more smooth muscle in your arterios compared to your venus, for example. In general, arteries just have more smooth muscle than veins. Venus do have smooth muscle, they're very limited, right? So, it should make sense that you should find a lot of like alpha one receptors on your arteries because again, if you activate those alpha one receptors, we drugs like phenol effring or effedraine, right? Those will clamp down on those vessels, right? Those will increase resistance, that will increase systemic vascular resistance.

And remember that whenever systemic vascular resistance increases, your systolic blood pressure goes up, right? So, if your SVR is going up and that's the only thing that's been varied, right? That means your pulse pressure should get smaller, right? And again, if your systemic vascular resistance is increasing, your afterload is going up and if your afterload is going up, your heart won't be able to send enough blood out, right? So, that means your cardiac output is going down. Again, all these like physiologic parameters, I'll talk about those in a different podcast, okay? But again, I'm just trying to give you a preview of common attractions, if you may. And then your venuals, your venuals are, in fact, the venuals that come right after your capillary, right? So, they're called like post-capillary venuals. They're kind of high up to know for certain reasons, right? So, the first thing is, those venuals actually do not have much in the way of, they don't have much in the way of smooth muscle, if any, right? Most post-capillary venus actually don't have smooth muscle like at all, right? It's literally like most of them just have like an epithelial layer and then you have like some parasites, some parasites, they're kind of like cells that constitute like something called like a baisolamina. They sort of surround those like that single layer of epithelial cells. So, those things are very susceptible to high pressures, right?

And you may say divine, so what, these post-capillary venus are so thin, they're so thin because you kind of need them, you kind of need things to be able to go through those walls, right? So, like your immune system cells, right? So, what is it called? Your, like when you have like an acute inflammatory response, right? Where you have like your neutrophils, extravacetane and all that stuff with all those proteins like macron, LFA1 and all that crap. How do you think you're able to go through those walls? They would go through those post-capillary venual walls because those walls are thin, okay? Again, that's actually something that's high up to now, right? Most times your immune system cells extravacetane to the interstitial surrounding your blood vessels by doing what? By going across the walls of post-capillary venuals. In fact, when I get to the immunology podcast, the comprehensive immunology reviews that I'll make in the future, hopefully, you'll learn about how you can target like antigens and like your dendritic cells and whatnot to lymph nodes and stuff like that. And you target those things through these things called HE-G Vs, like your high endothelial venuals. It so happens that those high endothelial venuals actually are specialized type of post-capillary venual, right? So, again, that's kind of like a nice immunology integration there.

Another interesting integration, I'm not saying this because the intresting, I mean, obviously, the interesting, I mean, you can tell from the one I'm talking about, there's a Kalan. Basically, I'll just tell you this. I love tutoring, I love teaching, teaching the best is the most amazing job in the world. I don't know why we don't have more teachers, but that's a different story for another day. But so that's again, kind of like a high-ealth thing to know. And then another reason you want to remember these post-capillary venuals is that they tend to be dialyfed by ACE inhibitors, right? So, the thing is, remember I said that capillaries, right? Remember, arterios feed capillaries. And then from capillaries, so a capillary is fed by an arterial, and a capillary is drained by a venual, right? So, a capillary is drained by an arterial, a capillary is, sorry, a capillary is fed by an arterial, a capillary is drained by a venual, right? The thing is your calcium channel blockers to be more specific, your dihydroperidine, calcium channel blockers, like verapamil, and no, not verapamilodotiasum, like amlodopin, phylodepine, like cardepin and whatnot. The primary mechanism of action is that the dilute pre-capillary arterios, okay? The dilute pre-capillary arterios. So, think about it, if you dilute pre-capillary arterios, right? You can already begin to imagine that you'll be sending more blood to the capillaries themselves, right?

Because again, they're pre-capillary, they're before the capillary arterios. So, you send more blood to the capillaries, and the thing is when you send more blood to those capillaries, right? The hydrostatic pressures in those capillaries begin to increase, right? Remember, those, remember your whole business with these are stallion forces, right? So, there's like four stallion forces you always want to think about in capillaries. So, there's the hydrostatic pressures that exist within the capillaries themselves, right? If those hydrostatic pressures in those capillaries increase, that will send more blood across the capillary wall, right? That will promote extravacition of fluid. And then there's hydrostatic pressures that you find in the interstitial that surrounds the capillary wall, right? If you have increased hydrostatic pressures in those in the interstitial, that tends to push more blood into the capillaries, right? So, that disfavorers extravacition of fluid, right? And then the other two pressures, right? So, you can have oncotic pressures inside the capillaries, right? So, oncotic pressures inside the capillaries, those oncotic pressures, I sort of think of them as like osmotic pressures, and like every osmotic pressure, osmotic pressure draws water towards itself, right? So, whenever you have high oncotic pressures inside capillary beds, that does not favor or disfavorers extravacition of fluid, right? And if you kind of think about that, right?

So, for example, if a person has a nephrodite syndrome, whether you're peeing out protein in the ureth, right? They become hypo-abuminemic because the albumin constitutes the primary protein that you find within your blood strain. It's the primary contributor to your oncotic pressure. So, if a person has like nephrodite syndrome where they are peeing out protein in the ureth, or they have liver disease where they are not making up, you mean in the first place, or they have many trace disease on occasional limb disease, they call many trace disease of protein-losing gastropathy, where they are literally like getting rid of protein through the agi-tracts. Those people become hypo-abuminemic, right? Or if a person even has like a quashir core where they have a deficiency of protein, right? If you're not taking protein, you're not going to be, if you're not taking protein, you're not going to be making out your men, right? So, whenever you have long-coated pressures because you're a hypo-abuminemic, your oncotic pressures go down. If your oncotic pressures go down, right? You're not going to be able to retain enough fluid inside capillaries. If you don't retain enough fluid inside capillaries, that will favor extravacition of fluid, right? So, that's why people that have nephrodite syndrome or liver disease or many trace disease or quashir core, they tend to have like a dima, right? Of their extremities, right? And even people that have quashir core, right?

Then you see those kids that have like big bellies, that big belly is actually from a dima. It's actually not from like, is like many people say like, oh, why do they have those big bellies that you see in the classic images? They usually have those big bellies literally, it's from a dima because the hypo-abuminemic, right? So, they have low oncotic pressures. Now, and then the fourth high-starling force, right, is like the oncotic pressure that exists in the interstitial that surrounds again, the capillary walls. If you have high oncotic pressures in interstitial that surrounds the capillary walls, again, that will draw water towards itself, that will favor extravacition of fluid, okay? So, again, kind of to summarize the things that favor extravacition of fluid are high hydrostatic pressures within inside the capillary or high oncotic pressures in the interstitial that surrounds the capillary, right? So, if for example, a person has ARDS, right? And they have like immune cells and all that stuff kind of like leaking to their to the interstitial of their lungs, that attracts fluid, right? And that causes like pulmonary dima. If a person has inflammation, right? So, remember, like color, rumor, no, not rumor, color, tumor, rubra and dollar, right? So, the tumor, right, is like swelling, right? The reason people get swelling when they have inflammation is again, there's an increase in vasculopromability from things like histamine and bradykinein.

So, your immune system cells and like cell like soup that runs in your blood vessel sort of leaks into the interstitial and that sort of attracts fluid with that, right? And again, that causes a lot of trouble, right? That causes the dima because you attract fluid. So, kind of back to my original story, where I was talking about like your my dihydroperidine calcium channel blockers. So, the dilate pre-capillary arterial, right? So, those things, if the dilate those pre-capillary arterials, you get more blood flowing to your capillaries, right? So, the hydrostatic pressures, your capillaries go up and that promotes the extravacition of fluid from your capillaries. And when you have extravacition of fluid from your capillaries, you get peripheral edema. That is the mechanism behind the peripheral edema that is associated with taking a dihydroperidina calcium channel blocker. So, it should make sense then that if you want to treat that peripheral edema associated with taking a dihydroperidine calcium channel blocker, you would want to potentially dilate the post-capillary venuums, right? The post-capillary venuums, right? Because when you dilate those post-capillary venuums, guess what happens? You decrease the hydrostatic pressures within those capillaries and when you decrease those hydrostatic pressures within the capillaries, that disfavoris or does not encourage extravacition of fluid.

So, it so happens that your ACE inhibitors are very good dilators of your post-capillary venuums, okay? So, ACE inhibitors are the drugs of choice in the treatment of the peripheral edema that is associated with taking a dihydroperidine calcium channel blocker. Now, the thing is, you may see why those that make sense. Remember, ACE inhibitor decreases the synthesis of anzutensin 2. Anzutensin 2 is one of the most powerful viso constructors in the body. So, if you're making less anzutensin 2, you're making less of a powerful viso constructor, so you have net viso dilation, right? And I just said that, so again, that's a higher tidbit to know there. So, notice, I'm talking about like anatomy as it relates to the cardiovascular system, but you see that I'm not, again, I'm just not just giving straight facts, again, because again, if the US Emily was an exam of straight facts, everyone will get a 270. Obviously, that doesn't happen, right? The reason that doesn't happen is situations like this, where again, they want you to be able to integrate concepts amongst the multiple disciplines, right? So, another higher thing to kind of be aware of here. So, I just said earlier, before I went on this rant, that capillaries are fed by arterials, and then capillaries are drained by venus. That is not always true, right? The thing is, you can have certain situations in the body where a capillary is fed by an arterial, and a capillary is drained by an arterial, okay?

That is something known as an arterial portal system, okay? arterial portal system. You generally create portal systems when you need to have some complex regulation going on, right? So, take, for example, the kidneys, right? So, remember that your glomerular capillaries, right? Your glomerulus literally is a capillary system. It is fed by the afrin arterial. It is drained by the effrin arterial. That is an example of an arterial portal system. If you are looking for another situation where you have a capillary that, instead of being fed by an arterial, it is fed by a venial and drained by a venial, think about the portal system that will pre-train the liver, right? So, remember that you have sinusoidal capillaries that are pre-train your liver. Those sinusoidal capillaries are fed by portal veins, and those sinusoidal capillaries are drained by the hepatic vein, right? So, that is an example of a venous portal system. Another place where you have a venous portal system is like in the hypothalamus, okay? So, like they call it like the hypofysil portal system. So, again, these are again all kind of like high-oat integrations. You want to keep in mind for for exams, right? And then I've been making this big fuss about the viso visorum, the viso visorum, the viso visorum, right?

So, I say that the viso visorum is important because again, it kind of supplies blood to elements of the arterial wall, especially like big arteries, like elastic arteries, that are not necessarily able to get oxygen and nutrients by street diffusion from the lumen of the artery, right? So, why is that important? The thing is, if a person has atherosclerosis, right? In the walls of like an artery, right? By having atherosclerosis, think about it, you're essentially increasing the diffusion distance that oxygen and nutrients have to go through to get to other layers of the arterial wall that are kind of like distal to the to the lumen, right? So, if you have atherosclerosis, you get really thankful that you have a viso visorum, right? So, the thing is, think about this. The other, right? So, we have like the other, we have the isending the other, the other carc, descending the other, and then we have the ather that is above the, above the renal arteries, and then we have the ather that is below the renal arteries. So, here's the thing that happens. The thing is, once you get beneath the renal artery, like the other, like the ather beneath the renal artery actually does not have, like the walls of the other beneath the renal artery lacks a viso visor. So, think about it. Who, if a person, right, has atherosclerosis of their infernaly order, right? You can already begin to see that nutrients and oxygen will have a very hard time diffusing across that wall.

And if the nutrients and oxygen have a hard time diffusing across that wall, the more peripheral parts of the wall of the infernaly order gets like super weak dyes, right? And then begins to descend, descend, descend. Right? So, that's why triple A is a very common, right? That's why abdominal leotic aneurysms are very, very, very, very common, right? If you want to take this to an even more logical or conclusion, right? So, if you kind of look at syphilis, right? So, why do syphilis cause like an erotitis? What's the erotitis that happens with syphilis? The truth is, the erotitis that happens with syphilis actually happens because syphilis, so like T-paladam, remember it's a spirocheet, loves to actually causes like an inflammation and destruction of the vis-a-visorum of the vis-a-visorum that you find around the aortic arch and descending aorta, right? So, again, by destroying those vis-a-visorra, you're beginning to create ischemia in those more peripheral walls of the ascending aorta and the aortic arch. So, again, that can cause dilation. That's why aortic regurg and like eotic dissection of things that can happen to people that have syphilis, right? That's that's that really is the pathophysiology behind the erotitis that accompanies syphilis. And I know this has kind of gone on for a long time. I'm gonna round up soon, but again, don't forget your don't forget these high-yield things with your with your arteries.

Again, I promise you this is one of those things where if you just understand, it just makes it a lot easier for you to approach, to approach our exam questions, right? So, I've been saying a lot of things about arteries, right? So, let me just say a few quick things about veins, right? So, veins, right? Again, the send-blood back to the heart, right? Your pulmonary veins send blood back to the left-eatrium, your systemic veins like your SVC-IBC send blood back to the right-eatrium, right? And the thing is, again, your veins kind of like your arteries. They have like the tunica intema, they have the tunica media, they have the tunica adventisha, and your large veins, again, kind of like your SVC-IBC, for example, in their tunica adventisha, they tend to have a lot of, they tend to have a lot of vis-a-visura. Okay, so vis-a, vis-a, this whole construct of vis-a-visura is very, very, very important, okay? Very, very, very important. And again, your, your, the walls of your veins, right? Like the media has smooth muscle, but doesn't have as much smooth muscle as your arteries, right? So, if you have smooth muscle, right, it should make sense that you should be responsive to alpha-1 stimulation that causes viso-construction or beta-2 stimulation, which causes a vis-a-visura dilution, right? So, your arteries and your veins both respond to those two types of receptors. Now, the thing is, with your veins, right? So, because your veins don't have as much smooth muscle, right?

They are not super-contractile, right? So, that's why most of your veins tend to have like valves that essentially like prevent like backflow of blood, so that blood flows in just one direction, right? Your arteries don't necessarily need valves to prevent backflow, right? So, if you kind of think about it, if a person has veins and the valves in their veins don't work so well, right? That's where they can begin to get into trouble with like varicose veins, right? Because they begin to have like pulling of blood in their veins, because your veins actually, this is actually high, you know, your veins are capacitance vessels. So, because they are capacitance vessels, they can actually pull blood for pretty long periods of time, right? So, they have like a very high capacity for blood, right? First of all, your arterios that are more your resistance vessels, right? So, your veins, if a person has varicose veins, their blood just basically, their veins essentially just have like more, they get more compliant because they don't, I guess maybe I shouldn't use that term because that's not very accurate, but they pull more blood in their veins, so they have like low extremity, a D-marie. Remember, those people, classically, on NB Ms, they tend to have ulcers above the medial malionless, right? That's something kind of high-yield, you want to keep in mind, for example. And then, so if your veins don't have enough smooth muscle in their walls, right?

It kind of makes sense that the skeletal muscle that kind of surrounds your veins can clear pretty big rule in how much blood is stored in a vein or how much blood goes away from a vein, right? So, if you kind of think of it this way, right? So, if, for example, a person is like hypotensive, classically in the ICU, they would just like raise the person's legs up because by raising the person's legs up, guess what happens, right? You're essentially contracting their veins with like the skeletal muscle that sort of surrounds them, right? And when you hit those veins hard, that blood flows back to the heart, so you're basically getting more venus return because by getting more of that venus return, you get more of a cardiac output. And the thing is, if, for example, right? So, again, just kind of going with this whole skeletal muscle, eating in contraction of veins are construct. If, for example, you're going to long trip, right? Let's say you're going to long trip and you don't wiggle your legs or you're in a long flight or whatever, guess what happens, right? Blood begins to pull in your veins and when you have stasis of blood, can you remember the she memonic for venus thromboyblosum? So, like stasis, hypercognibility and endothelial damage, right? So, you have stasis of blood, when you have stasis of blood, guess what happens? That increases your risk of forming clot, right? That increases your risk of forming a, forming a DVT, okay?

So, again, those are all higher things you want to keep, you want to keep at the back of your mind, right? For example, and the thing is, this is probably a little low yield, but I remember learning this back in the day when I was studying for step one, there are things like your deep veins and their things like your superficial veins. The thing is your deep veins tend to operate on the higher pressures, your superficial veins tend to operate on the lower pressures, right? So, whenever you have, whenever you have an occlusion of a deep vein, right? That essentially shuns blood to your superficial veins, okay? That shuns blood to your superficial veins and if you shun blood to your superficial veins, right? They are superficial. So, literally, you can see them. That's why you can see like leg swelling and all that stuff. When a person has like a DVT, right? And again, don't forget that if you have a thrombus of your deep vein, that is the thing that can cause a PE. When you have a thrombus of your superficial vein, those things really, if ever, cause P Es. And then the final thing I will say is there is one thing I want to talk about. It's going to skip my mind. Come on, divine. What did you want to talk about? If they give you an NVME question, because this shows up quite commonly and since I'm talking about things, I might as well talk about it. If they give you a question, actually two things. I apologize. Two things.

So they give you an NVME question about a patient that has like pain, like severe leg pain or like arm pain. And then they tell you that they have a palpable cord, like a linear thick palpable cord on one of the extremities. And then they say what's the next step in management? They will try to trick you into giving those people like anti-couagulation. Don't do that. Those people do actually have thrombosis of a vein, but the vein that they've thrombosed is a superficial vein. And again, superficial venous thrombocies do not cause P Es. It's deep venous thrombosis that cause P Es. If a person thrombosis is a superficial vein and then they have inflammation around it, that's something called superficial thrombophilobitis. It's one of those relatively common causes of post-op fever where you're like, this person has given antibiotics, no working. I've wrote out our lectases. I've wrote out wound infection. I've wrote out this. I wrote out that. And they don't seem to be getting better. Think about superficial thrombophilobitis under those circumstances. So those people just give them NSAI Ds, trade inflammation, that's all they need. They do not need anti-couagulation. They do not need Heparin, right? Versus a DVT that is traded with Heparin. And then the last thing I want to say, and then I promise I'll round up again. Many of these lectures, I have like list of topics I'm going to talk about. But as I talk about things, other things begin to pop in my mind that relate.

And then I just try to integrate them in. So, and the thing that popped up in my mind is this concept of an EV Festula, right? So remember, I just said that you have like arteries, arterios, capillaries, then venus, then veins, right? The thing is, capillaries are where like exchange of oxygen and nutrients and all that crap happens. So the thing is, your capillaries kind of like slow down blood a little. I almost think of capillaries as like the AV note of your secretary system. So the thing is when you create an EV Festula, guess what you're taking out of circulation? You're taking those, you're taking that kind of like slow down mechanism that exists between arterios and venus, right? So if you have an EV Festula, you take that out. And when you take that out and blood is flowing directly from like an artery to a vein, that's what's called an EV Festula. The problem is, if you take out that slow down capillary mechanism, then your heart becomes more overworked, right? Because your heart like I sort of think of it as like a fried train that never stops. Blood just keeps flowing at high speed. Aridu vein, Aridu vein, Aridu vein, Aridu vein, Aridu vein. Nothing is slowing down within your capillaries. When that happens, that's a problem, right? Because your heart, I sort of think of it as your heart, sort of depends on blood slowing down in capillaries to sort of take a breather and then recover before it starts pumping again.

If you, obviously that's not what happens, but I'm just giving you like a nice way to understand it. So if you take those capillaries out of the equation, if you have an AV Festula, that can ultimately cause something called a high-upor heart failure. That's can ultimately cause a high-upor heart failure. And I mean an AV Festula is good for certain reasons, right? Like if a person wants to go on dialysis, right? You create an AV Festula, so you have like more efficient filtration of their blood. Well, guess what? One of the, in fact, the most common cause of death in patients that have that on dialysis is actually it's not one of the most common, it's the most common cause of death in patients that have dialysis is cardiovascular disease. And this potentially explains part of why that may be the case, right? Because again, by creating an AV Festula, you essentially putting those people in a situation where they have high-upor heart failure. Now, on the whole context of high-upor heart failure, right? There are many things that cause high-upor heart failure on NV Me's. One is an AV Festula, right? If a person has an AV Mile formation, again, where they have a direct connection between like arteries and veins, right? So if a person has an AV Mile formation in the brain or in the lungs or in whatever, right? Again, that can also cause a high-upor heart failure. If a person has like bones that are hypervascular, like in pages disease, that can again also cause high-upor heart failure.

Because the thing is, again, when you don't have those capillaries, you essentially have a functional decrease in systemic vascular resistance. So the heart has to always work super, super, super hard. That's the thing that causes the high-upor heart failure. And then the last thing that can cause high-upor heart failure is that a person has like severe anemia. Because think about it, right? If you think about the oxygen delivery equation, I mean, the oxygen content equation. And again, I'll talk about these, this podcast, I'm just focused on anatomy. I'll talk about cardiac physiology and other podcasts. But basically, if a person has low hemoglobin, the oxygen content of their blood goes down, right? So what is like, hmm, you know what, I kind of need this oxygen real bad, right? So the way your heart compensates is by increasing cardiac output to compensate for that decreased oxygen supply to organs, so that you basically have like more goar rounds of blood through your tissues so that you can get a non-voxygen, right? So since the heart is needing to supply greater than normal amounts of blood, that again can cause high-upor heart failure. So the classic MDME equation will be a person that has like a hemoglobin of like 304. And then they tell you that the ejection fraction measured by echocardiography is 70%. Those people have high-upor heart failure. So again, I promise you, this podcast is basically all these cardiology podcasts I'm going to make.

They're like, floridly high-o for the SMN Step 1. You kind of want to understand all these things I've talked about. And again, as I round up, I do offer one on one tutoring for the USM and the Step 1, Step 2 CK, Step 2 CS, and Step 3 exams. And also like the pre-clinical medical exams and the third year, clerkship, a shelf exams. And then if you have a college buddy that's like pre-med basically, I essentially tutor every pre-med subjects, so like physics, general chemistry, organic chemistry, physiology, histology, biochemistry, all that stuff. And then if you're a college student applying to a med school, so like an Amcass application or a med school applying to residency, so like an ERAS application, I do offer one on one advice and consulting for that. I mean, I've been on the admissions committee of a top two med school for a year. So I've sifted through thousands of high-quality applications. And I mean, this past like ERAS cycle, I worked with hundreds of people. And pretty much everyone I worked with matched. And almost like 90-ish percent, actually matched into their first choice. So, um, take that for what you will, but I have a very good track record with these things. So, I hope you've enjoyed this podcast. Have a wonderful rest of your day, and I'll see you in the next podcast. God bless you. Thank you.

Common Carotid Artery (CCA), Internal Jugular Vein (IJV), and Vagus Nerve.

The tricuspid valve (tricospid).

An AV fistula/AV malformation, AVM formation, or severe anemia.

The aortic arch (specifically, it loops in the tracheo-bronchial angle).

TIPS (Tricuspid insufficiency/regurgitation, flushing, and pulmonic stenosis).

Large elastic arteries (e.g., aorta, major branches of the aorta).

Physiologic R $\to$ L shunts occur in utero; pathologic R $\to$ L shunts (Eisenmenger) occur after birth due to pulmonary hypertension.

Atherosclerosis, specifically involving the lack of vis-a-visura in the infrarenal aorta segment.

Arterial portal system (fed by afferent arteriole, drained by efferent arteriole).

They dilate post-capillary venules, thereby decreasing capillary hydrostatic pressure and reducing fluid extravasation.

The SA node is located in the junction of the SVC and right atrium; the AV node is located within the posterior aspect of the right atrium.

Connective tissue, nerves, and sometimes vis-a-visura.

Physiologic R $\to$ L shunts occur in utero; pathologic R $\to$ L shunts (Eisenmenger) occur after birth due to pulmonary hypertension.

Atherosclerosis, specifically involving the lack of vis-a-visura in the infrarenal aorta segment.

Arterial portal system (fed by afferent arteriole, drained by efferent arteriole).

They dilate post-capillary venules, thereby decreasing capillary hydrostatic pressure and reducing fluid extravasation.

The SA node is located in the junction of the SVC and right atrium; the AV node is located within the posterior aspect of the right atrium.

Connective tissue, nerves, and sometimes vis-a-visura.