DIP Episode 326 - Pediatric Cardiology and Hemodynamic Changes for the USMLE exams

Okay, welcome. My name is Divine. This is episode 326 of the Divine Intervention Podcast. And in this podcast I'm going to be discussing a very important topic. It's just a topic that unfortunately many resources don't cover well. But it's something that shows a very frequent your name being exempt. And when he shows up, good numbers of people get these things wrong. So I'm going to be calling this topic hymodynamic physiology in MBME Pediatric Cardiology Problems. Again, I know it's kind of weird, right? So I'll call it again hymodynamic physiology in Pediatric Cardiology in MBME Pediatric Cardiology Problems. And I'll just leave it at that. You'll get the drift as we go along. And as a quick announcement, if you're taking the USMEL Step 2, I do have a review course coming up next week. First is that's with the MBME Testicking Strategy Scores on Wednesday from 2 to 4 30 p.m. Pacific Standard Time. And then I have the review course that's going to be taking place on Friday Saturday and I mean on Thursday Friday and Saturday next week from the 15th to the 17th. And in that course, we're going to be covering Peds, Surgery, I am, OBGYN, Psych, Neuro, Biosdats, Ethics, Communications, Healthcare Systems, Professionalism. Just again, a very good, broad overview of the material that's routinely tested on the USMEL exams. Okay, so let's just jump right into it. So the thing is because this topic is kind of nebulous and is convoluted, I'm going to try to make it as high as possible.

So how am I going to do that? The way I'm going to do that is I'm going to basically ask myself a bunch of questions, then I'm going to answer them. They're just basically like thought questions. Again, I'll try to explain or simplify the physiology as much as possible. But I promise you, the stuff I'm explaining here is not something you can just mess around with. It's something you do need to understand. It's something that pops up a lot on Indian exams, pops up a lot on practice exams. So definitely something I'm going to find for you. So the first question I'm going to ask myself is why do VS Ds get more symptomatic days to weeks after birth? So why do they get more symptomatic? Why do they get louder these two weeks after birth? Well, the reason here is if you think about it, when a child is in utero, the child is basically not using their lungs. The lungs are basically a bag of fluid. All the oxygen supply for the fetus essentially comes from mom through the placenta. So because the lungs are not getting any oxygen, being a utero is a state of relative hypoxia. That relatively hypoxic state in utero is going to cause pulmonary viso-construction. So if your pulmonary vessels are constricted, then that's going to make the right side of heart pressure is really high. That's why physiologically in utero, you have a right to left shunt. You have multiple right to left shunts.

Just because again the pressure is on the right side of the heart and much greater than the pressures on the left side of the heart. So that's a key important point to know. So in utero, the right side of heart pressure is really high. Well, think about it. The moment the child is born, what is the first thing that happens? First thing that happens is that that child begins to cry. One of the reasons I believe that those kids cry is because by crying their opening of the amount and their bringing oxygen in. When you bring in oxygen, that removal of that in utero hypoxia is going to cause pulmonary viso-dilation. When you get pulmonary viso-dilation, that's going to lower the right side of heart pressures. And the thing is, as the child becomes more and more removed from the time of birth, those pulmonary vasculine pressures go down even more. Again, as the child uses more viso-longs, because you know the lungs will still be wet even after the child is born. But as the child uses those lungs more, uses those lungs more. That's lack of hypoxia, will then cause pulmonary viso-dilation. And when you get that pulmonary viso-dilation, that's going to reduce the right side of heart pressures. So think about it. If you have a VSD, what's going to happen? Well, a VSD, the left ventricle, since it has higher pressures than the right ventricle. Blood is going to be flowing from the left ventricle to the right ventricle.

So because let's say like a normal left ventricle, the pressure is there is like 125 and then a normal right ventricle, the pressure is there like 25. So because the pressure is higher than the left ventricle, things will always flow from the region of high pressure spontaneously to the region of low pressure. So blood is going to flow from the high pressure region, left ventricle to the low pressure region, right ventricle. So if those right ventricular pressures are decreasing even more, so let's say, oh, it's going from 25 at birth to 20 to 15 to 10, right? Then that gradient is getting even bigger, that gradient of flow, because the pressure difference is getting bigger between the left ventricle and the right ventricle. So that's why in general, VSD is the ghetto louder as you go away from the child being born, because again, that increased gradient of flow, there's with more flow, right? So there's going to be more, more sound you're getting, right? And again, that's why those kids can also get more symptomatic, because again, as the pressure gradient gets bigger, there is more flow across the VSD, right? That's going to put more, the left ventricle just have to work harder, right? So classically, those kids, they'll be sweating with feats, sweating with feats is a pretty classic presentation of some kind of cardiac defect on, on in being exempt.

Well, many times when these kids that have VS Ds that are becoming symptomatic have symptoms, most times, those kids will be acyanotic. So you look at their O2 sets on in-beaming exams, and you'll still be in the mind, right? Because the thing is, if you have a VSD, it's an acyanotic defect, well, at least until the person develops eyes and fingers, which we'll talk about later in this podcast. Okay, so again, I've answered my first question, right? So again, VS Ds, they get more symptomatic days to weeks after birth, because the right ventricular pressure has progressively decreased as you go away from being born, right? And they'll be more flow through those VS Ds because of the increased pressure gradient, right? And again, they're going to get louder because of more flow. Now, my second question here is, why is there a diastolic rumble at the apex in a VSD? Because many people know that, oh, a VSD shows up as a hollow systolic murmur at the left floor external border, right? And then you learn that, oh, there's also an EPICU diastolic rumble at the apex. Well, if you think about this, when a person has a VSD, again, blood is going to flow from the left ventricle to the right ventricle. As if it flows from the left ventricle to the right ventricle, that means the right ventricle is getting its preload from two sources. It's getting its preload first from the right e-trim, but it's also getting its preload from the left ventricle.

So because it's getting more preload by the Frank Stalin mechanism, the cardiac output of the right ventricle will be higher than normal. It's just literally getting blood, before you usually get blood from only one source right e-trim, but now it's getting from right e-trim, left ventricle, right? So because it's getting from both, the preload is high. So the amount of blood in the right ventricle is high. So according to the Frank Stalin principle, if you put more blood in the right thing in a chamber of the heart, it will eject more blood. Because they're putting more blood in the right ventricle, more blood is going to be ejected into the pulmonary arteries. And that more blood is going to go to the pulmonary capillaries, and that more blood is going to go to the pulmonary veins, and that more blood is going to go to the left e-trim. And that more blood is going to flow through the mitrovove into the left ventricle. So because you have an increased amount of blood flow through the mitrovove, that's going to show up as a flow murmur on oscutation. That's why those people have a made diastolic rumble, because the left ventricle is filling with that increased blood from the left e-trim across the mitrovove. That's why here that made that stoic rumble at the apex, right? So again, what are some other ways to contest this information I just described?

When a person has a VSD, the right ventricular endastolic volume is going to go up, because again, you're just getting preload from two sources, from the right e-trim and from the left ventricle. And also every chamber that is distilled to that distilled to the right ventricle is also going to get like increased preload, right? So like for example, when a person has a VSD again, because of that increased blood flow from right ventricle to pulmonary arteries, to pulmonary capillaries, to pulmonary veins, right? The left e-trim is going to be getting more preload. The left e-trim is going to, its volume is going to get better, right? So the left e-trim endastolic volume, left e-trim preload is going to be better, right? In fact, the left e-trim pressures are going to be bigger. So that's something that's particularly high-youtu-no for purposes of the USMLA exams. Okay, now my third question here is, when you fix a VSD, what happens to cardiac hemodynamics, right? So this is something I'm going to talk about in the context of just with a recourse to the second question I just answered. So think about it, right? If you fix a VSD, so let's look at what happens after you fix a VSD. When you fix a VSD, you're literally closing off those pressures that exist between the left ventricle and the right ventricle. So the thing is, when you turn off those, when you turn off that connection, what's going to happen?

Well, the thing that's going to happen is your left ventricle, since it's no longer like leaking blood, your left ventricle pressures will go up. That's very important to know. Because again, the left ventricle before was leaking bloods to the other, but also, you know, which is what should happen normally. But at the same time, it was also leaking blood to your right ventricle. So if it's not leaking that blood, the pressures in it's the left ventricle line that's not able to go up, right? So the LVEDPO will go up, right? So the left ventricle pressures will go up. Now, your right ventricle before the VSD was fixed, it was getting preloaded from the right atrium and from the left ventricle. But now, it's not anymore. It's only getting preloaded from the place it's supposed to get preloaded from, the right atrium. So since it's getting only from the right atrium, the thing that's going to happen is that the right ventricle pressures will actually go down. The right ventricle pressures will actually go down. So again, think about what I just discussed in question number two. If the right ventricle pressures are going down, then that means those things that are distal, right? That are getting flow from the right ventricle, direct flow from the right ventricle, the pressures in them will go down as well, right? So like your pulmonary atrial pressures will go down. Your pulmonary capillary pressures will go down.

Your pulmonary venous pressures will go down and your left atrial pressures will go down as well. That's very important to know. Because again, what is the source of preload for the left atrium? It's the right ventricle. So if the right ventricle pressures are going down, then the left atrial pressures will go down as well. But again, don't complete the fact that the left atrial pressure is going down, mean that the left ventricle pressures will go down. No, the left ventricle is no longer leaking blood into two compartments. It's not just leaking blood into the, into the, in order. That's all it's doing, right? So the left ventricle pressures will go up because that VSD has been fixed. So again, in summary, when a VSD is fixed, the left ventricle pressures go up. The right ventricle pressures go down and the left atrial pressures go down as well. I've explained the pathophysiology behind that. Now, question number four, how does transposition of the grid vessels present on an MDM exam? How does transposition of the grid vessels present on an MDM exam? And what do you do about it? So let's talk about this. So the thing is, when a pressing has transposition of the grid vessels, remember, the normal situation that's supposed to happen is that your left ventricle is supposed to drain into your order. And then your right ventricle is supposed to drain into your pulmonary order. That's what's supposed to happen.

But if a pressing has transposition of the grid vessels, usually that happens because there's like some mess up with your eorticopulmonary septum. Then your right ventricle is going to be draining into your order. And your left ventricle is going to be draining into your pulmonary order. As you can see, that's not a good thing. Well, let me explain why. Think about it. If your right ventricle is draining into your order, that means the oxygenated blood, you know, going into your right ventricle, going into the right ventricle, and then draining into the order. And the order is the blood supply for the rest of the body. So that blood you're sending to the rest of the body is the oxygenated blood. And then that blood is going to come right back to the right ventricle. Go through the tricospin half into the right ventricle, going to the order again. So notice you're literally recirculating the oxygenated blood. On the flip side for the left side of the heart, blood is going left, the eutrum left ventricle, where the left ventricle is draining into the pulmonary order. So that blood flowing from the left ventricle into the pulmonary order, right, so go through the pulmonary capillaries, go into the pulmonary veins, and then come right back to the left ventricle. So guess what? On the left side of the heart, you're literally recirculating oxygenated blood. Obviously, that's not going to be consistent with life.

But the thing is, many times, those kids are able to survive in utero because there are many connections between the right side of the circulation and the left side of the circulation. So what are those connections? Well, the key one that you probably want to keep in mind for your test is the doctor's arteriosus, right? Is the doctor's arteriosus. That doctor's arteriosus is the connection between the pulmonary artery and the presynzioid. And because in utero, you know, the pulmonary artery has higher pressures for reasons I've described in the first question. Then blood is going to flow from pulmonary artery to the presynzioid, right? So oxygenated blood literally in those pulmonary arteries, right, that are coming from the left ventricle, and the presynzioid has a transposition of the great vessels, who flow from the pulmonary artery into the utero. And in that oxygenated blood can go from the utero to the rest of the body. So the child can oxygenate in utero, no problem, right? And also, you know, maybe the first few hours of the first, because it's not like the moment the child is born within seconds, the doctor's closes. No, that is not what happens, right? So many times those kids when they are born, for the first few hours, in fact, sometimes up to the first few days of birth, those kids are doing perfectly fine, because that doctor is still open, right?

So blood is still flowing, like they're still mixing of blood across that open doctor's arteriosus between the pulmonary artery and the yorta, right? But the thing is, if the doctor's then starts doing what he's supposed to do, as he starts closing, then that communication between the right side of the circulation and the left side of the circulation will be gone. And once it's gone, then that child is probably going to die pretty soon, right? Many times when you give those kids oxygen, they will not respond appropriately to it. Let's say you give the child oxygen, and you notice that, wow, this child's PO2 went from like, I don't know, like 60 to 61. Or the ACO2 went from like 50% to 51%. That is not a big, basically that child is not responding, right? And those kids are going to die, right? So that's how transposition of the grid vessels, as a concept, presents on endemic exams, right? And they will try to trick you many times into doing like an endotrykyl, an intubation, or all those things, but those are not the right things to do for those people. The right things you want to do for those people on endemic exams, your first step always on an endemic exam, is to give those kids a Prosteglandin E1 analog. I'll say that again, a Prosteglandin E1 analog, like a Prostegl, because by giving an Prostegl, a Prostegl is a potent visual die letter to Prosteglandin analog.

So we'll keep that doctor open, so that you can actually supply, you can still have one mixing of blood between the right side of the circulation and the left side of the circulation, once you can take the child for cardiac surgery. The thing is intubation does not really help those kids, because actually my given more oxygen, if I'm not mistaken, you'd potentially speed up the closure of the doctor's arteriosus, and that can worsen the child's problem, right? So you need to give that our Prostegl first, before you do pretty much any other thing. That's very high, you'll understand. Again, I think given more oxygen actually causes speeds of closure of the doctor's, I mean, not be 100% on that, but that physiologically makes sense to me, and I'll probably talk about that in some future podcast. So is there some other case scenario in the mission, an endemic exam, where given our Prostegl is a good thing, with especially with Pete's cardio, actually I will say another good situation to do this is with a child that has very severe, or a correctition of the order. The thing is when a child has severe, correctition of the order, the order basically is not able to send blood to the rest of the body, right? I'll say that again, the order is not able to send blood to the rest of the body, so the remaining body regions get super hypoxic, right? And they are not getting any nutrients, right?

So given our Prostegl as a first step is actually really helpful there, because by giving our Prostegl again, a Prostegl in E1 analog, you're going to open up the presence of Dr. Sateriosus. That's going to cause more communication between the, between the pulmonary artery and the aorta, right? So blood can pretty much bypass that obstruction in the aorta, because remember normally blood will flow through the aorta's the rest of the body, right? But if the doctor sees open, right? If the doctor sees open, right? Then blood is going to flow from the pulmonary artery through the doctor's ateriosis into the aorta and bypass that partition. That's something that can help until you can take the child to surgery and go ahead and fix the problem. So basically the systemic blood flow is literally coming from the pulmonary artery. What that pulmonary artery is the thing that the shun that gets it to the aorta is that Dr. Sateriosus, so blood will flow from pulmonary artery to Dr. Sateriosus to the aorta. So again, that's very important, very high yield to, to no one understand. And then the next thing I want to talk about here, my next question here is, what is the pathophysiology behind, so this is question number five, what is the pathophysiology behind ismanger syndrome? Well, the pathophysiology behind ismanger syndrome is when you have a large VSD and you don't fix it, right?

When you have a large VSD and you don't fix it, the thing is, again, if you keep getting all this excess blood flow to the right ventricle, over time that excess blood flow through the right ventricle is going to flow through again pulmonary artery, sponular capillary sponular veins. Those things, the right side of the heart is not built to handle those kinds of pressures. So over time, the person will get pulmonary arterial hypertension, and when they get pulmonary arterial hypertension, that your right ventricular pressures will progressively increase. If it progressively increases, at some point, it can increase to the point where it exceeds the 11 circular pressures. If it exceeds 11 circular pressures, then what was previously like less EMVSD where it was like a left to right a cyanotic shunt, would then become a right to left cyanotic shunt. And when that happens, then the child will become hypoxic. Many times, those people have decreased pulmonary vascular markings, because now they has reduced blood flow through the pulmonary arteries. Remember, pulmonary vascular markings are a surrogate for blood flow through the pulmonary arteries, right? They are surrogate for blood flow. So if you have increased pulmonary vascular markings, it means there's a lot of blood flow through pulmonary arteries. If you have decreased pulmonary vascular markings, that means there's very much reduced blood flow through pulmonary arteries.

Now question number six for me is, what causes pulmonary hypertension in utero? Again, I've pretty much talked about this. This is almost like a physiologic pulmonary hypertension. But remember in utero, the thing that happens is that you're not using your lungs, your lungs are literally filled with fluid. So the body senses that are some kind of relative hypoxia. And whenever there is hypoxia, that's going to cause pulmonary vascular constriction. And if you constrict those vessels, that's going to raise the pressures in them. That's going to raise the right-sided heart pressures. Now question seven, then says, what are some consequences of this pulmonary hypertension, not receding at birth? Because again, as I explained from question one, when the child is born and takes in that first gust of air, that's going to cause pulmonary visodilation. But if for some reason that pulmonary visodilation doesn't happen, then the right-sided heart pressures in that child will remain persistently elevated. And if it remains persistently elevated, the many of those shons that existed in utero will stay. Those things that are supposed to close will not close. And if they don't close, you will keep having blood flowing from the right side of the heart to the left side of the heart. Because again, it is a very critical concept to understand. Is that decrease in pulmonary vascular pressures that comes with that newborn ticketing oxygen?

That ultimately will lower the right-sided heart pressures. And if that happens, the shons begin to close. But if the child keeps having that pulmonary hypertension, then those right-sided heart pressures will remain elevated. So blood will just keep flowing from the right side of the heart to the left side of the heart. And obviously, in those circumstances, there will be some kind of cyanotic shons. Okay. Now, question 8 says, how can cardiocatheterization show that you are dealing with a VSD? How can cardiocatheterization show that you're dealing with a VSD? This is again a time-honored thing that our friends at the MBM love to test on the exam. So it was one thing when you keep out the back of your mind there. The key thing I want you to keep out the back of your mind here is you're doing a cardiocatheterization. You can literally mention measure like oxygen saturation in the blood in the heart. So, normally, blood that is coming to the right-editrum is supposed to be the oxygen-inthial blood. Blood blood goes from right-editrum to right ventricle. It's supposed to remain the oxygen-inthial blood. So the O2-sats, because I mean, it has not gone to the lungs yet. So the O2-sats of blood in the right ventricle that came from the right-editrum should either be about the same as the O2-sats as the right-editrum blood.

Or you should have a slightly decreased O2-sat because obviously, the higher cardiocelts, the endocardial cells, and extracting some level of oxygen from that blood. So it's always abnormal when the O2-sats of the P little AO2, the partial pressure of oxygen in blood, rises as you go from right-editrum to right ventricle. If that happens, then that means some blood is getting into the right side of the heart from an oxygenated blood source. Many times that will be like through a VSD. If you notice that, wow, a person's right-editrum O2-sats is like 80%. And then you notice that when it gets to the right ventricle becomes 95%, that is completely abnormal. That tells you that that person likely has some kind of VSD that's bringing some oxygenated blood from the left ventricle to the right ventricle. And as he brings that blood and the right ventricle to the O2-sats, well, we'll go up. So that's again one of these unique situations that they love to throw on exams. And then question, my here is, what causes left and right axis deviations on an EEG? Well, the big thing I just want you to keep in mind again, there are many causes of these deviations, but the one that's particularly relevant to know for you exams is hypertrophil of those ventricles. So whenever a person has right ventricle hypertrophy, they're going to have right axis deviation on an in-be-me exam. If a person has left ventricle hypertrophy, they're going to have left axis deviation on an in-be-me exam.

Again, the reasoning behind that is, the reasoning behind that is if you have hypertrophy of those cells, right, then you have more electrical activity around those cells. So we kind of mess up like the axis of depolarization of the ventricles. So that's why again, you have those deviations on an EEG. Okay, now question number 10 is, how does the knee chest position helping individuals with tetralogy of the low to oxygenate better? Well, the thing is, if you think about it, when you're going in the knee chest position, you actually are completely in tetralogy of the low. The reason that those kids get cyanotic, right, is because their right-sided heart pressures are greater than their left-sided heart pressures, right, because remember in tetralogy of the low, you're going to have for monics stenosis. So because the pressures on the right side of the heart are greater than the pressures on the left side of the heart, right, because you're going to have for monics stenosis. So because the pressures on the right side of the heart are greater than the pressures on the left side of the heart, that VSD that exists as one of the findings in tetralogy of the low will be associated with blood flowing from the right ventricle to the left ventricle, right? Obviously, if you have a right to left shunt, that is going to be a cyanotic shunt, right? So a cyanotic shunt. So if it's a cyanotic shunt, that's obviously going to be bad, right? That's going to be bad.

So if that's bad, right, that those kids will then have hypoxia, right? So the thing is, if we could somehow make that right to left shunt, left to right shunt, then those kids will oxygenate well. Enter knee chest position, right? So how does that knee chest position help? Well, it helps in a few ways. The first thing you're doing is that, if I probably the most important thing, so this very high you to know, the most important thing you're doing, is that you're going to have a right hand. is that you're literally, remember your femoral arteries are around your, around your thigh, right? So the thing is, if you do the knee chest position, you're literally going to be squishing on the person's femoral arteries. The femoral arteries are a relatively substantial artery in the human body. By squishing on those arteries, when you literally squishing on an artery, what's going to happen? Your systemic vascular resistance is going to go up. If your systemic vascular resistance goes up, what's going to happen to your left side head heart pressures? It's going to get higher, right? Because it gets harder and harder for blood to leave the left ventricle. So the thing that will happen is when you squish on those femurals, that those increased pressures are going to be transmitted upwards to the other. So that's going to make the afterlude that the left ventricle is experiencing higher. So that's going to make the left ventricle heart pressures go up.

If you raise the left ventricle heart pressures enough, it can transiently get bigger than the pressures in the right ventricle. And if the left ventricle heart pressures exceed the pressures in the right ventricle, then blood is going to be flowing down that pressure gradient from the left ventricle to the right ventricle. So what was previously a right to left cyanotic shunt? You're now reversing it by causing a left to right, a cyanotic shunt, right? And obviously that's going to improve oxygenation because you're essentially sending oxygenated, you know, you're essentially reversing that shunt and helping the person oxygenate better. So that's why the Nietzsche's position helps people with the trilogy of fallow to oxygenate better. Remember, the trilogy of fallow is made up of pomoanics, stenosis, right ventricle hypertrophy, VSD, and an overriding yoder. And again, I've kind of talked about the pathophys behind that in many different podcasts. Okay, now question 11 says, what happens, how does the size of a VSD impact how loud it is? This one is a pretty easy one, right? Basically, if you have a smaller VSD, it's going to be louder because it's just more turbulence or flow. An easy way to understand this is if, for example, you have a hose, if you turn on the hose and water flows out of it, that's a situation A. But then let's assume you put like your thumb over like a good, like a good cross sectional area of the edge of the hose.

Then less water is going to come up without water is coming out on the turbulent flow. It's going to start producing a sound, right? So the smaller a VSD is, the louder it becomes, right? So that's very high up to no, for example. Now question 12, again, I promise we're getting to the end of this here is I want to talk about the oxygen delivery equation. So what's the oxygen delivery equation? Basically, the oxygen delivery equation is that your oxygen delivery to the body is going to be the product. So it's going to be equal to your cardiac output multiplied by your blood oxygen content. I'll say that again, the oxygen delivery equation talks about how your cardiac output is basically the product of your cardiac output and your blood oxygen content. So why is it important to understand this situation? Well, the key thing I want you to understand here is that if you want to maintain oxygen delivery to the body, whenever the oxygen content of the person's blood goes down, then the cardiac output has to go up as a compensatory measure. Because basically it's almost like your cells are like, oh, before blood only had to come around here like 50 times in a minute. But because oxygen has been depleted in the person's blood, then to get the same amount of oxygen in the body, the same amount of oxygen supply, you may have to make more runs. So you may have to like, shop like 100 times a minute for example.

So that's something that may help you understand the pathophysiology behind high output heart failure in a person that has severe anemia, for example. In fact, that's my next question here. What happens to cardiac output in an individual with severe anemia? Well, for a person who has severe anemia, the oxygen content of the blood is going to go down. Remember that oxygen content equation is 1.36 multiplied by your hemoglobin. Multiplied by your SAO2, so the saturation of oxygen in your hemoglobin plus 0.0031 multiplied by your P little AO2. But basically the key thing I want to emphasize here is when a person has a severe anemia, that hemoglobin part of the equation, which is actually a major part of the equation goes down. If that goes down, then the oxygen content of your blood is going to go down. If the oxygen content of your blood goes down, then your cardiac output has to go up. Because again, remember, if you want to maintain a constant oxygen, remember I said oxygen delivery, it's equal to your cardiac output times your oxygen content of blood. So if your oxygen content of blood has gone down because the hemoglobin has gone down, then your cardiac output has to go up if you want to maintain oxygen delivery to the rest of the body. Again, just very important, higher principles to understand there. Then, the question 14 I want to discuss here is, what's the difference between volume and pressure overload?

Well, the thing is volume overload is something you get many times when you have a regurgitant lesion. Pressure overload is something you get many times when you have a stenotic lesion. I think a very good example to explain this is erotic stenosis versus a scionic regurg. The thing is when a person has erotic stenosis, it's just harder for blood to leave the left ventricle. Because it's harder for blood to leave the left ventricle, the left ventricle is like, I need to get bigger and beefier so I can force this blood out. The way the left ventricle is going to get bigger and beefier is it wants to be essentially become more muscular. The way it becomes more muscular is by adding saccombs in parallel. Because when you add saccombs in parallel, it's almost like you're stacking them on top of each other. Those saccombs are getting more muscular. You can push out that blood. That's an example of concentric hypertrophy. That's an example of concentric hypertrophy. Many times that's going to be as good as an S4 heart sound. Many times, those people end up getting into some kind of a stolic dysfunction. Because yes, the left ventricle is getting bigger and beefier, it's getting more muscular and pump out more blood. But the problem is all that muscle that is in the way is going to reduce the cavity size of the left ventricle. So that's going to make it harder for it to fill with blood. Because this is just not enough space since so much muscle has taken, taken out control.

Now, if a person has a yodic regurg, remember if a person has a yodic regurg, then blood is literally flowing from the yoder back into the left ventricle. The left ventricle, the problem it's facing is not that old. I need to get this blood out of the left ventricle. No, the problem is facing is that, gee, I seem to have all this extra volume that I have to deal with. Because normally, other left ventricle ejects, you know, normal ejection fraction is like 60%. You know, it just only has to deal with that, oh, 40% of the blood that was originally in the end of the asteli. But if a person has a yodic regurg, the left ventricle may have to go from dealing with 40% of the original blood that was there at the end of the asteli. So now having to deal with like 70%, 80%. So your left ventricle is like, hmm, you know what? I need to be combed better at storing this blood. So what does it do? It's going to get bigger. It's going to say, you know what? Because I don't have a pumping problem. So I don't seem to need this muscle so much. Let me just make my cavity size bigger. So how do you make the cavity size bigger? You do that by adding saccomers in series. You do that by adding saccomers in series. So you add them from end to end to end, right? I mean, think about it. It's just kind of like a blood vessel. I think I heard like I was watching a documentary recently. If you take out blood vessels and line them into end, it can struggle for a single human being.

It can struggle the entire globe, like basically the entire world. I think like what, like four times or something ridiculous, right? Or maybe I'm, but it's a really large number. Let's just put it that way, right? So essentially your body is like, your lever entry is like, well, making a business decision. I don't have a pumping problem. I have a storage problem. So the way you fix your storage problem is by just lining your saccomers into end. That's what's called eccentric hypertrophy. As you do that, instead of eccentric hypertrophy, that's going to make your lever entry will cavity size bigger. That's great. You're going to be able to handle those increased volumes. The only problem you're going to then have to face, unfortunately, right? Unfortunately, the problem you're going to have to face is that, because those saccomers are so far apart, it's going to be so hard for the lever entry to contract well. They are so far apart, right? They are so far apart. It's like, let's say you're trying to squish someone. You get a very good squish when your arms are as close together as possible, because it means you're like literally squishing those people down or even. But if your arms are super, super far apart, you can provide much squishing to that person. So the lever entry is not going to be able to squish your blood very well. So those people have systemic dysfunction. They'll have an S3 heart sound.

That's many times ultimately the pathogenesis behind a heart failure would reduce ejection fraction. Okay. And then the final question that I'm going to talk about is why are kids policed by themica birth? Again, this is something we should understand. Just based on what I've discussed already. These are just pretty much all related ideas. But the thing is that birth, again, while the kids were not using their lungs, so again, that's interpreted as a state of relative hypoxia. Whenever your hypoxic, right, you're going to have an increasing epiproduction. So if you have an increase in epiproduction, that's going to ultimately cause you to begin to pump out of tonal red blood cells. And if that happens, you're going to be policed by themica. That's why that's one of those reasons that kids are at high risk of getting a jaundice at birth, right? Because if you think about it, you literally are having to like, oh, man, I have all this hemoglobin and hemacrid, I need to destroy because it's excess when you're born. But also as a newborn, you have like 1% activity of like, you have like 1% activity of UDP glucoronacyl transfer, compared to like a regular adult, right? So it's almost like you don't have the enzyme to help you deal with that bilirubin problem from bringing down red blood cells. But then you also have a ton of red blood cells at baseline. That's obviously going to cause a problem, right? So that's why kids are policed by themica at birth, right?

And again, that's also why if a child has a sonodic congenital heart defect again, currently hypoxic, that's going to cause an increase in ipo, that's going to make them policed by themica, or cystic fibrosis patients. Patient, they are long-sth don't work well, right? Or COPD patient, if you're long-sth don't work well, you're going to be hypoxic, or if you have sleep apnea. Again, that's going to raise your ipo, right? And that's going to cause you to be policed by themica. So I'm going to go ahead and stop here, pretty much visited all the scenarios that I wanted to talk about. I think again, if you understand these things, because again, I'm sure people that are listening to this podcast understand exactly what I'm saying, where they'll give you a pediatric cardiology problem. They'll give you these physiologic arrows and all that stuff, right? And again, it just causes people a ton of anxiety. So hopefully this podcast really clears up many of these points for you. So I wish all the best. Again, as I do at the end of every podcast, I'd offer one on one tutoring for all the USML exams, step one to step three, pre-clean conventional exams, 30-ish off exams. And then I offer a review course for the USML is step two, see key slash step three exam. It's also applicable to people taking the complex level 23 exams. And then I have this podcast on Apple podcasts on Google podcasts and on Spotify, at least the most recent 150 podcasts.

It's a Word Press for there's no real way I have around that. So if you want all the episodes from episode one, all the way to the present time, go on the website, divininginterventionpodcasts.com. If you actually sign up on, if you actually subscribe to the podcast website, you get an email notification whenever I make a new podcast. And then also on the You Tube channel, diviningintervention, USML podcast and the videos. That's where I post my videos. Although if you want the slides, I'll search there with those videos. You need to go on that those respective episodes on my website. And also, I also work with people on Eras applications. I know we're going through Eras season now. So if that's something you need help with, just shoot me an email, tricky applications, wanting to match into a complex or, you know, very competitive specialty. Again, I've worked with people that have, that are residents in many different residency programs across the country, all the way from higher, higher around top of the line programs to lower-round programs. And then, many people love the life lessons. I put at the end of my podcast. So I actually studied a new podcast. It's called diviningintervention life lessons. The website for that is divininginterventionlifelessens.com. And also I have the podcast on Apple Podcast. Divininginter, you know, it's, it's clear if you check Apple Podcast, diviningintervention life lessons. I do have those. And again, again, it's just Bible-based teaching.

It's just less than 10 minutes, right? And again, I just bought some key life lessons I feel can really help you navigate your way through, through humanity as a successful person. So thank you for listening to me. I wish you all the best. Have a wonderful day. God bless you. Thank you.

Relative hypoxia (due to lack of oxygenated blood flow through the lungs).

Pulmonary vascular resistance decreases post-birth, causing RV pressures to drop. This increases the pressure gradient between the LV and RV, increasing flow across the VSD.

A loud, holosystolic murmur at the left lower sternal border. (Also note an apical diastolic rumble).

The ductus arteriosus.

Volume overload occurs with regurgitant lesions; Pressure overload occurs with stenotic lesions.

Cardiac Output (CO) must increase because the $\text{O}_2$ content is decreased.

Relative hypoxia.

Decreased pulmonary vascular resistance lowers RV pressure, increasing the LV-RV pressure gradient and thus increasing flow across the VSD.

Concentric hypertrophy (the ventricle builds muscle in parallel to overcome high outflow resistance).

Cardiac Output increases, as $\text{DO}_2 = \text{CO} \times \text{CaO}_2$, and the drop in hemoglobin reduces $\text{O}_2$ content ($\text{CaO}_2$).

L $\rightarrow$ R shunts are acyanotic; R $\rightarrow$ L shunts are cyanotic.

Right Axis Deviation (RAD) suggests RV hypertrophy; Left Axis Deviation (LAD) suggests LV hypertrophy.

Administering a Prostaglandin E1 analog to keep the ductus arteriosus open.

Relative hypoxia.

Decreased pulmonary vascular resistance lowers RV pressure, increasing the LV-RV pressure gradient and thus increasing flow across the VSD.

Concentric hypertrophy (the ventricle builds muscle in parallel to overcome high outflow resistance).

Cardiac Output increases, as $\text{DO}_2 = \text{CO} \times \text{CaO}_2$, and the drop in hemoglobin reduces $\text{O}_2$ content ($\text{CaO}_2$).

L $\rightarrow$ R shunts are acyanotic; R $\rightarrow$ L shunts are cyanotic.

Right Axis Deviation (RAD) suggests RV hypertrophy; Left Axis Deviation (LAD) suggests LV hypertrophy.

Administering a Prostaglandin E1 analog to keep the ductus arteriosus open.