DIP Episode 540 - Floridly HY Cardiac Signs (Step 1-3)

Welcome, my name is Divine. This is episode 540 of the Divine Intervention Podcasts. To this podcast, I'm going to be addressing a topic that I call the Florida High Yield Cardiac Signs for the USML Es. The Florida High Yield Cardiac Signs for the USML Es. This podcast is going to easily be one of my seminal podcasts. In other words, there's something that's going to be like super, super high yield and it's going to be something that's going to help any person taking any USMLE exam from step one out of the way to step three. The thing is, many people don't really understand these things and then they notice that they keep getting in trouble on tests because you know, you may think that, oh, this is only relevant for step one, but on step two, step three, these days, those exams are pretty heavy on the basic sciences. What they love to do is they will use these things as filler within questions, but it will guide you towards a certain direction in the answer. So if the understanding is not there, unfortunately, you're going to massively struggle with, especially cardio-based questions. And this is one of the things that they love to use to make integrations with many of the disciplines. So let's just kind of go through these things one by one. Again, I will try to make it short and sweet. If I can finish everything here, we'll talk about it some other time.

So what if they give you a question about a patient and they tell you that this patient, whenever they take a deep breath, they're a neck veins, they're a neck veins get more permanent with inspiration. What should you be thinking about? Well, this person probably has constructive perioditis. And the presentation that this person has is something called Kusmo sign. So again, the goal in this podcast is not just to discuss these signs, but to actually explain pathophys. So what's the pathophysiology here? Well, the thing is, let's ask ourselves, what in the world happens during inspiration? When you inspire, you literally push your diaphragm down. When your diaphragm is pushed down, what do you think happens to your intra-thoracic volume? It's going to go up. It's going to go up. And if you know anything about boils along from college, as volume goes up, pressure comes down. So the intra-thoracic volume is going to go up. So that's going to bring down the intra-thoracic pressures. So because your intra-thoracic pressures are lower, it's going to be easy for literally everything to fall into the heart. Because everything in the thorax then assumes a low pressure, including the heart. So blood is willing to flow into the heart. So think about it. On the normal circumstances, what should happen to your joggerlovings with inspiration? What the thing that should happen is that your joggerlovings are supposed to collapse.

They're supposed to do what collapse because the blood in them is flowing into the heart. So that means they are being emptied of blood. They're literally being emptied of blood. So normally your joggerlovings are supposed to collapse with inspiration. They're not supposed to become more prominent with inspiration. When you see that, you're thinking of Cosmos sign. And typically, we're going to find out in people that have constructive pericorditis. So what's the pathophage there? Basically, when you have constructive pericorditis, the person's heart is encased in calcium. So because the heart is encased in calcium, it's almost like you're putting cement around the concrete around the person's heart. It's not going to be able to expand to accept extra blood. Because when you enter thoracic pressure lowers, it's almost like your heart like, oh, let me get a little bit to accept that blood. But it's not able to do that. So those people, when you inspire, because remembering inspiration increases your preload, right? It brings more blood back to the heart. It brings more blood back to the heart. Because again, remember, flow will always happen whenever you have a pressure differential. So if you inspire, your thorax is a low pressure system. So blood is more willing to flow back towards the thorax. So your preload is going to increase. But you're trying to bring blood back into the heart when the heart is not willing to accept that blood.

So it's almost like your joggerlovings, blood is coming back through them and it's supposed to fall into the heart. But that heart is not able to expand to accept that blood. So your joggerlovings, they're going to be holding onto blood that should fall out of them. So they're going to get bigger with inspiration. That's literally Cosmol sign. And don't get nearer on that. They're many causes of Cosmol sign. Absolutely. But again, on the USMHL Is, when they say Cosmol sign, you're going to be picking the answer that says constrictive paracoditis. I'm going to move right along. All right. Now, next thing I want to ask you, what do you think happens to, what if they give you a question about a person that has, the classic JVD, Mothwood Heart Sounds, High Blood Pressure? I mean, low blood pressure. When you see this, I would hope you're saying, this person probably has cardiac tamponauts. So what is the thing we see in cardiac tamponautory inspiration? I know many of you have memorized that, it's bolstice paradoxes. Well, why? Let's explain this. So again, it all goes back to this understanding of what happens with inspiration. So let's look at the normal situation. Again, many of these things are going to build on each other. So you need to make sure you understood what I discussed in point one. To understand the point I'm discussing right now. So when you inspire again, like I said, your intra-thoracic volume goes up. So your intra-thoracic pressure goes down.

So your heart, especially the right side of the heart, becomes a low pressure system. It literally becomes what? A low pressure system. Because it becomes a low pressure system, more blood is willing to come to the right side of the heart. And if more blood comes into the right side of the heart, you know, more blood will flow into the right e-traum and the more blood will flow through the tricospit valve into the right ventricle. So your right ventricle is like, whoa, I have way more blood. I have way more blood than I normally have. Because inspiration has happened because preload has increased. So what does your right ventricle do? Your right ventricle is like, okay, to deal with this extra volume that I have, I'm going to de-stend a little bit. I'm going to bulge out a little bit. And it bulges out into two spots for purposes of the USMELES. It bulges out into the pericardium and it bulges out into the left ventricle. It's going to bulge a little bit through the interventricular septum into the left ventricle. So if you bulge a little bit through the interventricular septum into the left ventricle, you're literally reducing the size, the cavity size, the lumen size of the left ventricle. Because you're reducing the lumen size of the left ventricle, less blood is going to enter into the left ventricle. And if less blood enters into the left ventricle, then the cardiac output from your left ventricle is going to be diminished.

So that's going to lower your systolic blood pressure a little bit. Remember, systolic blood pressure and cardiac output are directly related. So the person's systolic blood pressure is going to drop a little bit. Okay? But typically when it drops, it drops by no more than single digits. If you see a person's systolic blood pressure dropping by more than single digits, so it's dropping by more than 10, for example, millimeters of mercury and inspiration, then there's something weird going on, like pulses, paradoxes. All right? Like pulses, paradoxes, like pulses, paradoxes. So again, I just described no more physiology. Again, just to recap, you inspire, you increase preload. So you're bringing more blood into the right side of the heart. More blood feels the right ventricle. So your right ventricle is like, oh, I'm going to expand a little bit. And it has two spots to expand into it. It expands a little bit into the pericardium and expands a little bit into the left ventricle through the interventricular septum. So that decreases the feeling of the left ventricle, that decreases the output from the left ventricle. So that's going to decrease your systolic blood pressure. But again, it's usually going to be by something less than 10, for example. So and think about it, if your systolic blood pressure goes down a bit, again, let's just look at things very logically.

If your systolic blood pressure goes down a little bit, what will happen to pulses, arterial pulses in your body? Those arterial pulses are supposed to get a little weaker. Because, you know, let's say your systolic normal is like, normal is 120, but because of that decrease, it goes down to like, 111, 111. That small decrease in arterial pressure is going to manifest on a physical exam finding as a person having slightly weaker pressures, slightly weaker pressures. Who that thought as we explain pulses per adoxys? So pulses per adoxys, as you've seen from the JVD, Mofford Heart Sounds, Blue Blood pressure that I gave at the beginning, we typically are going to find it in cardiac tamponat. So what happens in cardiac tamponat? Well, cardiac tamponat, your pericardium is pretty much filled with a ton of fluid. So now, a new tenant, a new renter has occupied your pericardium. Remember, your pericardium is one of those places that your right ventricle says, hey, more blood has come into the right side of the heart. Let me make some room for myself, we said it bulges into two places. One, the pericardium, two, the left ventricle through the interventricular septum. So if you have cardiac tamponat and your ventricle is literally your pericardium, sorry, is filled with fluid and you inspire, you're taking a deep breath. Well, as you taking that deep breath, you're literally bringing more blood back to the right side of the heart, more blood back to the right ventricle.

So the right ventricle in usual fashion is saying, hey, okay, let me bulge into the pericardium and through the interventricular septum. But the pericardium is like, ah, there is another tenant here. So it can bulge in there. So all of its bulge is going to be just for the left ventricle through that interventricular septum. So because all of its bulge is going to that left ventricle through the interventricular septum, you're going to have a bigger decrease in the lumen size, in the cavity size of the left ventricle. So you're going to have even less left ventricular feeling. If you have even less left ventricular feeling, what do you think is going to happen to your cardiac output? It's going to drop even more. So your systolic blood pressure is going to drop even more. It's going to drop what? Even more. So it's going to drop by more than 10 millimeters of mercury. That's what Paul Susperer-Adoxis is. It's a drop in systolic blood pressures by more than 10 millimeters of mercury with inspiration. And again, it's not something you have to memorize. It makes absolute pathophysiological sense. Literally, makes absolute pathophysiological sense. And let me ask you this. If a person has a pulse, let's say like they have cardiac tamponat. Well, I mean, when you have cardiac tamponat, you're already hypotensive. So your pulse is already weak and thready. Let me ask you this.

Those weak and thready pulses, what do you think is going to happen to them when you inspire in the setting of cardiac tamponat? If the person's blood pressure is sufficiently low, those weak and thready pulses will get even weaker. Sometimes, they may even absolutely disappear. They may literally disappear. So if they give you a question on the USML Es and they tell you that, oh, this person, you know, they describe a classic cardiac tamponat and they say that, wow, this person's a pulses. This person has weak thready pulses that disappear with inspiration. Do you know what they're telling you? They're pretty much telling you pulses paradoxes. In fact, that is the time-honored way our friends at the MVM is love to test pulses paradoxes without giving you systolic blood pressures. Because when they give you systolic blood pressures, a person that does it on the stand pathophys can do basic math. And we're like, whoa, okay, look at the blood pressure before inspiration. It was this value. Look at the blood pressure, systolic blood pressure after inspiration. It's gone down by more than 10. Yay, pulses paradoxes. So sometimes they don't let you have that. Yay, pulses paradoxes moment. And what they're doing steady is to say, oh, this person has weak thready pulses that just disappear with inspiration. When you see that, that's a beautiful target on the USML Es for what? For pulses, paradoxes for pulses, paradoxes. All right. So that's the second concept I wanted to describe.

Now, next concept I want to describe, that's going to be concept number three. What if they give you a question about a person that, you know, for every reason, they cannot exercise and they need a stress test. So whatever is in, they can exercise. And you know, for whatever reason, you don't see dubulum as an answer. Because, you know, if a person cannot exercise in the setting of a stress test, the next thing you think about is, hey, let's use dubulum. It's a bit of an agonist. It will chemical stress test. Stress out the heart, make it contract, see how the heart responds. But let's say you don't see dubulum in as an answer. And what are you going to do on your test? Well, I hope you're going to say, wait, I'm going to do the adenosine, you know, the stress test where we use adenosine, we can use like a diperidomal, for example. And many people have always wondered like, why in the world, well, I'd be able to use something like diperidomal, for example, for a stress test, it makes almost no sense. But man, if you understand cardio physiology, it makes perfect sense. I'm kind of giggling, giving this podcast, I love this stuff. Whenever something's physiology based is like, yep, I love it. So think about it. Obviously, you're going to be doing a stress test. Now, let's kind of break this down. You're obviously going to be doing a stress test in a person that has coronary artery disease. So this person, obviously, probably has some kind of atherosclerotic coronary vessel.

Now, we need to understand, what does the body do to a coronary vessel that is atherosclerotic? Literally, what does the body do? The body says that, wow, this atherosclerotic vessel, there's all these cholesterol, plaques, and whatnot that's taking up some of the lumen of this coronary artery. So you know what, let's try to dilute this thing as much as possible. So let me tell you this, whenever a person has an atherosclerotic coronary vessel, the body responds by diluting that vessel maximally. It dilutes it as much as possible just to create some space within that atherosclerotic vessel for blood to go through. So at baseline, an atherosclerotic coronary vessel is maximally dilated. I'm going to say that again, at baseline, an atherosclerotic coronary vessel is already maximally dilated. Literally, it's already what? Maximally dilated. So because it's maximally dilated, if you expose it to a viso-dialiter, it cannot dilute any further. I'm going to say that again, if you're already maximally dilated, if you're exposed to a viso-dialiter, you will not be able to dilute any further. Literally, you will not be able to dilute any further. All right, now hold that thought. But if you're a coronary vessel that does not have atherosclerosis, so it doesn't have you know, much atherosclerosis, you probably will not be maximally viso-dialitered.

So if a viso-dialiter is brought around, for viso-dialiter is brought around, then the thing that's going to happen is you're going to dilate in response to that viso-dialiter because you're reasonably normal ordering. You're reasonably what? Normal ordering. So now if you understand this, you then understand the principle we're going to discuss here shortly. Like why you can use something like dipyridomol, for example, to do a stress test, a chemical stress test. So the thing is dipyridomol is a forceful diesterase inhibitor. So because dipyridomol is a forceful diesterase inhibitor, it can raise your levels of cyclic AMP. And in the smooth muscle that lines are coronary vessels, are coronary arteries, when you have high levels of cyclic AMP, that can cause dilution of those, that's going to cause smooth muscle relaxation, and it's going to cause those coronary vessels to dilate. All right. Now we know that generally the heart has a fixed blood supply. For the most parts, just for purposes of this discussion, assume that it has a fixed blood supply. So let's say that, oh, the heart at each time, if you're trying to spray blood into your coronary vessels, you spray like 100 milliliters of blood. Or let's say 120, I'm just making up this number. Let's see, you spray 120 milliliters of blood.

So let's say like 40 milliliters goes into your RCA, your right coronary artery, 40 milliliters goes into your LED, your left anterior descending, and 40 milliliters goes into your left circumplex. Again, I'm just learning making up these numbers. So the thing is, let's assume you then say, this person that has coronary artery disease, let's inject them with some dipyridomol or some adenosine. Again, these things are very powerful visual dilators. So what are they going to do? They're going to dilate your coronary vessels. And let's see, this person has atherosclerotic disease in the LED. Remember, the LED is the most common region of coronary artery disease, right? Like most people that have MR Is is going to be from the LED. There is a reason it's called the Widowmaker. So basically, I shouldn't say that that's probably a little insensitive. Sorry about that. So the thing that pretty much happens is, let's say the LED is the one that has like heavy atherosclerosis. So we know that weight. The LED is maximally visual dilated. But if you then expose the coronary vessels to a visual dilator, like dipyridomol or adenosine, what do you think is going to happen to the left circumplex and the RCA, the right coronary artery that are relatively normal compared to the LED? Well, because they are relatively normal, they're going to literally respond to that visual dilator. Because they are not maximally dilated at baseline, they're going to respond to that visual dilator.

So what's going to happen? Your left circumplex is going to dilate, your right coronary artery is going to dilate. And when those two arteries dilate, that fixed blood supply that the heart is getting, they're going to get more of that blood. They're literally going to get more of that blood. So instead of getting maybe 40 milliliters, people to get like 50 milliliters each. And think about if the total amount of blood you supply each time is 120 and 50 is going to the RCA and 50 is going to the LCX. How much is going to be left for the LED? It's going to be 20. But I know some of you may be like, put define why won't the LED just get its 40? Well, the thing is the LED will not get its 40 because it cannot dilate anymore. Because it has bad atherosclerosis, it's already maximally dilated at baseline. So when a visual dilator comes on the scene, the other coronary arteries that dilate are literally going to steal some blood from the LED. The blood that is supposed to go to the LED because those other coronary arteries are able, they have the ability to dilate, they're going to receive some of that LED blood. In essence, you've stolen some blood from a coronary artery. You've stolen some blood from the LED. That is what is known as the coronary steel principle. Literally, the coronary steel principle. You're literally stealing some blood from an LED that is maximally dilated at baseline that is unable, that is literally unable to dilate any further.

And typically when we're doing these nuclear medicine stress tests with like Di-Priodomol or Adenosine, what typically are going to do with an echocardiogram. So I know some of you may wonder like, divine, can you please just land those through here? How will an echocardiogram show this problem? Well, think about it. A person that has atherosclerotic disease of the LED, you know, the cardiac tissues that have been supplied by that LED already is key make a little bit because of that decreased fluid baseline because you already have atherosclerosis in your LED. So if you still even more blood from that LED, the regions it supplies will become even more ischemic. Literally, the regions it supplies will become what even more ischemic. And when they become more ischemic, you're going to start seeing wall motion abnormalities. You're going to see what wall motion abnormalities. You may notice that, wow, I see a part of the Lev ventricle that before I started this whole test with Di-Priodomol or Adenosine, this part of the Lev ventricle was at least contracting decently well. But then you notice that its contractivity just goes down precipitously. When you inject this viso-di-liter, that tells you that, oh, this person has some problems with the LED because you can map out that way. This region of the Lev ventricle is probably supplied by the LED. And the thing is, obviously, that's not all that's done.

There's some nuclear medicine, Mombu jumbo that they do with flow, like flow things that they can like literally measure and all the stuff. But that's not for the level of a medical student. That's more for the level of a radiology resident doing a nuclear medicine rotation or cardiology resident cardiology fellow. So I'm not going to be talking about those things. I promise you, like that stuff is actually pretty cool. But again, if I start going into those things, I am very going to permanently lose, lose everybody listening to this podcast. So I think, honestly, I'm going to stop right here because this series, I think, is something that's going to be very helpful for a lot of people. So literally, I'm just going to be checking of these boxes as from time to time. I just address these cardiac signs. Again, you may think that the stuff is low yield. On the UCN exam question, we're having this detailed understanding is what will help you thoroughly analyze and process the question and answer it correctly. So I'm going to go ahead and stop here. And if you're interested, if you love the way I teach, you're probably going to be interested in the courses I offer. I have classes for step one, all the way to step three, taking place in the month of July. In fact, the classes start off next week Tuesday. I have a test taking class for step one to three. I have a bio-stats class. I have a social sciences ethics, quality improvement, healthcare systems class.

I have a last minute review for step two, step three, I have a 20-hour step two, step three class. I have a 25-hour step one class. So if you're interested in any of these classes, just shoot me an email through the website. These classes are not lectures. If you're looking for lectures, wrong class. But if you're looking for a class that will use like exam style questions and scenarios to teach you the concepts, show you how they are presented on exams, explain pathways to you, show you how integrations are made across these concepts. Then I think you're really going to enjoy these classes. So again, if you're interested in any of them, just shoot me an email and I can give you some more information. And I have this podcast on Apple, Google and Spotify. And I have a You Tube channel you can check out and also offer to your interests. Step one, two, step three, and come back. One, two, three. And I also help people with e-race applications and personal statements and regulators and things like that. And then finally, I have another website called divineinterventionlifelessons.com. Every week I post about one to two podcasts where from a biblical perspective, address a life lesson. So thank you for joining me today. I will see you in episode 541. God bless you and have a wonderful day and bye for now. Thank you.

Kussmaul's sign (JVD increases with inspiration).

Inspiration lowers intra-thoracic pressure, increasing venous return (preload), but the rigid pericardium prevents the heart from expanding to accept this blood.

Elevated JVD, muffled heart sounds, and hypotension (Beck's Triad).

The right ventricle expands into the pericardium and left ventricle during inspiration, severely restricting LV filling and dropping SBP by >10 mm Hg.

Pulsus paradoxus (a time-honored way to test for tamponade without measuring blood pressure).

The Coronary Steal Phenomenon—normal vessels dilate and steal blood from the maximally dilated, stenosed vessel.

Inspiration $\rightarrow$ Low intra-thoracic pressure $\rightarrow$ Increased venous return (preload) $\rightarrow$ Rigid pericardium cannot accommodate volume $\rightarrow$ JVD increases.

Jugular veins should collapse slightly due to increased blood flow into the heart.

Cardiac Tamponade.

The agent dilates normal, non-stenosed vessels, causing them to receive more blood flow and "steal" supply from the already maximally dilated, stenosed vessel.

Intra-thoracic volume increases $\rightarrow$ Intra-thoracic pressure decreases (becomes a low-pressure system).

Inspiration $\rightarrow$ Low intra-thoracic pressure $\rightarrow$ Increased venous return (preload) $\rightarrow$ Rigid pericardium cannot accommodate volume $\rightarrow$ JVD increases.

Jugular veins should collapse slightly due to increased blood flow into the heart.

Cardiac Tamponade.

The agent dilates normal, non-stenosed vessels, causing them to receive more blood flow and "steal" supply from the already maximally dilated, stenosed vessel.

Intra-thoracic volume increases $\rightarrow$ Intra-thoracic pressure decreases (becomes a low-pressure system).