DIP Episode 542 - Floridly HY Cardiac Signs 2 (Step 1-3, Worksheet Included)

Welcome, my name is Divine, this is episode 542 of the Divine Intervention Podcasts. And to this podcast, I'm going to be continuing our series on the Florida High Yield Cardiac Science. So this is going to be part two of that series. So let's just get right into it. So again, if you missed the first part, listen to episode 540. My premises are pretty high-yield podcasts for step one, step two, and step three. And I really hope to do a cardiology study group of some sort very soon. For people that are really struggling with cardiology, it's something I've been thinking about for a while. So if you're interested, you can shoot me an email. I'll give you some more information. So let's jump into it. So if you remember from the last thing we met, we talked about Kusma and Sai, we talked about Paul Suspira and Doxas, we talked about the coronary steel principle, we talked about many different things. So now we're going to continue the conversation. And the thing I want to focus on today is the following. So first things first, let me ask you all this. When a person goes from a standing position to a supine position, what do you think happens to the murmur of the Eardic stenosis? Well, I hope you're saying that the murmur increases in intensity. Well, why is that? The reasoning behind that is when you go from a standing position to a supine position, your preload increases. So let's talk about what preload is and mix some integration.

So that's the next big concept I want to talk about in cardio. That's the concept of preload. Preload is pretty much how much blood comes back to your heart, simple as that. How much blood comes back to your heart. And think about it, that blood that is coming back to your heart is obviously going to be filling up your ventricles. And ventricular feeling we call that dastily. So preload is a very close surrogate for the ventricular in-dastolic volume. And the thing is I found it to be very useful to understand, for example, purposes, the things that affect preload. What are the things that affect preload? Well, it's going to be things like, for example, the position in of your body. If you go from a standing position, blood is in under gravity pulling your legs to a supine position, then you're going horizontal. Blood will no longer pull in your legs. Because remember, the veins are capacitance vessels. So blood will no longer pull in your legs. Instead, that blood is actually going to come right back to your heart. That's going to increase your preload. You're literally sending the blood from those capacitance vessels your legs back to your heart. That's going to increase your preload. And when you're feeling the left ventricle more, then there's going to be more blood living the left ventricle through the order. So the rest of the body flowing across a diseased diodic valve. So the membrane density is going to get louder. Okay, so what else can affect preload?

Well, another thing that can affect preload is if you exercise. Think about if you exercise, you're literally, you know, running or whatever. That can squish the blood vessels in your legs. That can literally squish the blood vessels in your legs. When you squish the blood vessels in your extremities, again, remember, veins are capacitance vessels. That's a concept that many resources don't seem to talk about. But it's actually pretty high up to know for you exams. Vines are capacitance vessels. So the thing that's going to happen is, as you squeeze those veins in your legs, you're going to literally take the blood that is coming out of them and it's going to go right back towards the heart. That's going to raise your preload. Another thing that can raise your preload is just get fluids. Literally get fluids. So if you put more fluids in your body, like you get a normal ceiling infusion, you're literally putting more fluids in your blood vessels, right? You're having more that's going to be coming back to the heart. That's going to raise your preload. That's literally going to raise your preload. Another thing that raises your preload is if you inspire, right? When you inspire, you take a deep breath, you're literally pushing your diaphragm down. When you push your diaphragm down, what happens to the volume of your thorax? When the volume of the thorax is going to increase.

And if you remember boils and all from general chemistry in college, as your intra-thoracic volume goes up, intra-thoracic pressure is going to plummet. It's going to go down. Since your intra-thoracic pressure is plummeted, it's going to make it easy for things to want to come into the heart. So like blood, for example, because everything in the thorax then becomes a low pressure system, including your heart. So when you inspire, that's going to increase preload. That's going to definitely increase preload. Especially for the right side of the heart. One thing that's actually kind of useful to know is that when you expire, that increases preload for the left side of the heart, for the left side, left side. Because whenever you expire, you're going to literally squeeze your opponent's veins. Remember, I said that veins are capacitance vessels. But in this case, that compression of the lungs in expiration is squeezing the pulmonary veins. So the blood in those pulmonary veins will be ejected to the left side of the heart. Believe it or not, this is actually why many left-sided heart murmurs get louder on expiration, on expiration. Because if you were following along from the previous podcast, they pursued 540, where we talked about the Florida Hyalcardiac Science Part 1, I said that when you inspire, more blood comes to the right side of your heart.

And then we talked about this whole thing about the bulge of the interventricular septum into the left ventricle, which makes it harder for the left ventricle to feel. So preload of the left ventricle actually goes down when you inspire. But when you expire, you're squeezing on your pulmonary veins. When you squeeze on your pulmonary veins, that's actually going to make it, you're literally causing them to eject the blood they have in the vessel lumens to the left side of the heart. That seems like a low yield point until you see it on your exams. I will certainly know that stuff if I were you. So that's another thing that I've experienced preload. Well, what's another thing that I've experienced preload? Another thing that I've experienced preload is having like an AV fistula, right? An atyrovenous fistula. Atyrovenous fistula basically, it's a direct connection between an artery and a vein. It's literally a direct connection between an artery and a vein. And that's really anomalous. That should not happen. That really should not happen. Now, typically, naturally in your body, an artery leads to a capillary, and then a capillary leads to a vein. Or more accurately, an arterial leads to a capillary, and then a capillary leads to a venial, and then a venial becomes a vein. Now, here's the thing. Here's the thing. Here's the thing. That's the normal situation.

And I like to think of the capillary as, you know, obviously that's the part of your blood vessel network where gas exchange happens. So if gas exchange is happening, I like to think of it as like. It kind of slows down the blood on the body a little bit. Slow it down a little bit. Slow it down a little bit. But here's the thing. Here's the problem there. If you lose that capillary, and you have a direct connection between an artery and a vein, that's a fistula, then blood is just zipping from the artery straight to the vein. Literally zipping from the artery straight to the vein. Artery straight to the vein. So it doesn't get that slow down effect you're getting capillary. So it's just going literally right back to the heart. That's going to jack up your preload. That's literally going to raise your preload. So that's pretty high you to know for, for example. Again, there's other things that I've picked preload that I'm sure I am not remembering at this time. But the thing is, these things ones I've mentioned are the ones I will see you definitely need to know for your exams. You really shouldn't be taking your exams without knowing this stuff. All right, so there's that. So now the next thing I'm going to talk about is the concept of afterload. So in this discussion of a fairly high yield cardiac science, I'm going to talk about afterload.

So like for example, what do you think is going to happen to the intensity of the murmur of aortic stenosis if a person gets a drug like phenyl effron? Huh, well, phenyl effron is an awful one agonist. So it's going to constrict your arteries. When it constricts your arteries, it's going to make it hard for blood to live the heart. Right? Whenever you climb down on your arteries, you're making it a lot harder for blood to live the heart. If you make it a lot harder for blood to live the heart, that's not very good. Right? So if blood is not living your heart as effectively, then there's going to be less blood flowing through that stenotic eiotic valve. If there's less flow across a diseased valve, then the murmur is going to get quieter. So whenever you have an increase in afterload, that typically will reduce the intensity of the murmur of eiotic stenosis. So since we're talking about afterload, let's talk about some of the concepts that affect afterload. That affect afterload. Again, like let's make our lives easier. You don't have to think about these things too hard. Afterload basically just means resistance to flow of blood out of the left ventricle. Done. Resistance to flow of blood, let's even get more general. Resistance to flow of blood out of a ventricle. Resistance to flow of blood out of a ventricle. Right? Remember, the left ventricle is not the only ventricle. There's the right ventricle as well.

We know that the right ventricle ejects blood into the pulmonary arteries. For patients pulmonary hypertension for whatever reason, usually it's probably going to be from left heart failure. Remember, the most common cause of right heart failure is left heart failure. For patients who has left heart failure, then blood is going to back up into the person's pulmonary vessels, it's going to cause pulmonary hypertension. That pulmonary hypertension will make it very hard for blood to be ejected from the right ventricle. That's going to be problematic. That's going to raise the afterload for the right ventricle. Or you can have pulmonary hypertension because you have a BMPR2 mutation, which is going to cause that like idiopathic pulmonary hypertension. That's going to basically cause hypertrophy of the smooth muscle of your pulmonary arteries. It's going to make it really hard for your pulmonary arteries for your right ventricle to empty. That's going to make it really hard because over time, because the left side of the heart has greater pressures than the right side. A lot of blood is going to be flowing from the left side of the heart. It's going to be a little bit more difficult to get it out of the way. It's going to be a little bit more difficult to get it out of the way. It's going to be a little bit more difficult to get it out of the way. It's going to be a little bit more difficult to get it out of the way.

It's going to be a little bit more difficult to get it out of the way. It's going to be a little bit more difficult to get it out of the way. It's going to be a little bit more difficult to get it out of the way.

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thick grease which one is harder to move along it's the thick grease that's like police academia right there which one is easier to move along is the water is easier to move along because it's not as viscous so whenever your viscosity goes down it's easier to move that blood along the left ventral who can pump that blood easily that's going to reduce your after load but if you have police academia like police academia Vera or you have police academia for any reason let's say you have like some kind of chronic hypoxia like COPD 65 broses that jacks up your ipo or let's say you have like an iposy creding like hepato cellulocarsinoma right now cell carcinoma he might go blastoma which we know is a search that would want you pulling down of each hell what is the more dominant disease right there that's going to make it much harder like your blood is going to be super thick it's going to make it really hard for blood to get out of your heart it's going to make it really really hard for blood to get out of your heart because your life eventually is pumping blood that is so concentrated so thick so viscous that's going to increase your after load that's what you can think about it there's actually another week and think about it mathematically besides this logical sentence reason but if you remember pa cells law pa cells law that's this is an integration right here remember pa cells law in pa cells law we know that viscosity and to do prefer resistance are directly related viscosity and to do prefer resistance are directly related so let me ask you a question if your blood gets more viscous what's happening to your to do prefer resistance is going up it's literally going up it's literally going up if your to do prefer resistance goes up you're going to make it harder for blood to come out of the left ventricle that's raising your after load now contrast that with a person th

at has anemia present that has anemia a present that has anemia present has anemia their blood is not as viscous because they don't have enough enough hemoglobin that's going to decrease the to do prefer resistance if your to do prefer resistance goes down it's going to make it a lot easier for blood to come out of the heart lollithic for blood to come out of the left ventricle that's going to decrease your after load that's going to decrease your after load and that's why people that have anemia can develop high up or heart failure because if you have anemia your blood is less viscous your to do prefer resistance goes down right if it goes down your credit output is going to be really high because your after load has been decreased your after load has been decreased so it's going to be easier for your left ventricle to reject blood that's going to jack up your credit output the thing is you don't want your credit output to always always always be high but if you have chronic anemia your credit output will always always always be high over time your heart is going to get tired of working at that chronic lividic credit output so because of that chronic lividic credit output the heart will feel that's high output heart failure it's heart failure because of a chronic lividic credit output heart failure because of what chronic lividic cardiac output and then if you think about it as well when a person has chronic anemia what happens to the blood oxygen content it's low right the blood oxygen content is low because they don't have enough carriers of oxygen remember hemoglobin is a big time carrier of oxygen in the blood that's tissue hypoxia the tissues are going to be big in the heart for oxygen like crazy they're going to be like heart please please please we need oxygen so your heart is going to be like okay I'm going to send blood around the body more frequently well i

f that happens that's going to be problematic okay if it happens for a season not a big deal fix the anemia not a big deal but if that's happening for months for years over time the heart is going to get tired of that chronic lividic cardiac output that's going to cause high output heart failure what if you do something like the hand grip maneuver because many people wonder like man divine the hand grip maneuver why exactly does they reduce the intensity of the murmur of aortic stenosis simple think about it if you do a hand remember there's some big vessels in your hands right like there's your radial artery that's your honor artery if your grip of pressing hands are real good or like the wrists then you're literally clogging off a ton of blood flow through an artery you're raising the total prefer resistance if you do that what do you think is going to happen to the what do you think is going to happen to the intensity of the murmur of aortic stenosis well it's going to decrease because by compressing those vessels you're increasing after load when you increase after load you're going to make it hard for that for blood to come out of the left ventricle so it's going to be less blood flow across that disease theortic valve right so that's going to reduce the intensity of the murmur or think about it let's make an integration with tetralogy of the low many of you recognize that man when a pressing that has tetralogy of the low goes to the knee chest position it can relieve your sanosis well why do you think that happens think about it if you squat if you squat if you squat what do you think is happening to the space between your belly and your thighs it's decreasing and there is a big vessel that runs there like your femoral artery so you're literally squishing both femoral arteries when you squish both femoral arteries those are big arteries those are very big arteri

es you're going to increase total prefer resistance so if you increase total prefer resistance it's going to be your your jacket on the after load as you jack up that after load you're going to make it very very hard for blood to come out of the left ventricle so if it's hard for blood to come out of the left ventricle then the left ventricle is going to start seeking other routes for blood to flow through like what like the VSD that exists like the VSD that exists in tetralogy of the low so you're going to start having blood flowing from left ventricle preferentially to the right ventricle instead of right ventricle to left ventricle because remember in tetralogy of the low one of the findings is pomeonic stenosis right and because of that pomeonic stenosis blood is flowing from the right ventricle to left ventricle and then going to the rest of the body which is not good because the blood in the right ventricle has no good enough oxygen if it so that's that's why it's a sanotic congenital heart defect but if you're going in that niche esposition squish the femoral arteries increase after load increase total prefer resistance make it harder for the left ventricle to eject that blood then the left ventricle is going to start moving blood preferentially because remember again flow happens across a pressure gradient if by increasing that after load by going to the niche esposition you increase the pressure within the left ventricle because it's harder for blood to come out of it then blood is going to flow preferentially from left ventricle to right ventricle across that VSD that we see remember that's one of the findings in tetralogy of the low and if blood is flowing from left to right ventricle then that's going to relieve the sanosis because the blood in the left ventricle has been oxygenated in the lungs so can you just see like man do you see all these integration

s they can make an example that's why understanding really matters I'm telling you this cardio I love cardio number one but cardio is also one of these subjects that men are friends at the mbm is they can go to town on the questions they write like literally just in talking about just literally two concepts preload and after load look at all the integrations that could be made look at the diverse array of processes this could be applied to like I'm sure I'm not even scratching the surface of the main integrations that could be made so I think I'm going to go ahead and stop here because this is something I want you to internalize so hopefully in the future we'll have some more opportunities to talk about some of these are 30 higher cardiac signs so as I am this podcast again I do offer 101 to run for all the USMLE exams all the complex exams actually have a pretty good track record with people have worked with 101 they've done really well on their tests like people that have been like struggling they get a period of it's for weeks for months I work with them and they do well I also offer review courses if you're taking step one have a 25 hour step one class studying next week monday it's a 25 hour class it's for those tickets that want to come next one or if you're taking step two step three or complex two or three and you have a poor basic science foundation that class is perfect for you because again if you love the way I teach basically you get an idea of how I'm going to teach and the class is not a bunch of lectures no no no no it's a bunch of scenarios and then I use those scenarios to make like tons and tons and tons of integrations and then also for review classes for step two and step three a 20 hour class last minute review a test taking class a biostat class a social science class I have a podcast where I talk about all those things so you can check those ou

t have those at the towards the end of this month and then I also help with your applications personal statements mock interviews and things like that and I have this podcast on Apple Google and Spotify and I have a You Tube channel you can check out and then I have another website called divininginterventionlifelessons.com every week I post like a podcast or two where from the little group perspective I address a life lesson there's actually an Apple podcast associated with that called the divining intervention life lessons podcast so thank you for listening to me today again I really hope you find this podcast with beneficial again this stuff is pretty high I'll see you in episode 543 have a wonderful weekend God bless you and bye for now thank you

A measure of how much blood has returned to the heart (venous return) and serves as a close surrogate for ventricular end-diastolic volume.

It increases preload because gravity no longer pulls blood into the lower extremities, allowing that blood to return directly to the heart.

Inspiration (deep breath) decreases intra-thoracic pressure, making it easier for blood to enter the low-pressure system of the heart.

Pulmonary vein compression during exhalation forces blood into the left side of the heart, increasing preload (a high-yield point).

Afterload increases because the elevated hematocrit raises blood viscosity, making it harder for the ventricle to pump.

It significantly increases preload by bypassing the capillary bed's natural slow-down effect on blood flow.

Squatting increases total peripheral resistance (afterload), increasing left ventricular pressure, which forces a shunt from the high-pressure LV to the low-pressure RV across the VSD.

1) Moving from standing to supine; 2) Fluid infusion/volume expansion; 3) Exercise (squeezing capacitance vessels).

It decreases the murmur intensity because it increases afterload, making it harder for blood to flow through the stenotic valve.

Anemia decreases viscosity, which lowers total peripheral resistance and thus decreases afterload.

Inspiration increases right-sided preload; Expiration increases left-sided preload (due to pulmonary vein compression).

Capacitance vessels. They hold large volumes of blood, meaning positional changes or external compression can significantly alter venous return/preload.

Squatting increases total peripheral resistance (afterload), increasing left ventricular pressure, which forces a shunt from the high-pressure LV to the low-pressure RV across the VSD.

1) Moving from standing to supine; 2) Fluid infusion/volume expansion; 3) Exercise (squeezing capacitance vessels).

It decreases the murmur intensity because it increases afterload, making it harder for blood to flow through the stenotic valve.

Anemia decreases viscosity, which lowers total peripheral resistance and thus decreases afterload.

Inspiration increases right-sided preload; Expiration increases left-sided preload (due to pulmonary vein compression).

Capacitance vessels. They hold large volumes of blood, meaning positional changes or external compression can significantly alter venous return/preload.