DIP Episode 464 - Cardiovascular Parameters (for Step 1-3)

Okay, welcome. My name is Devine. This is episode 464 of the Divine Intervention Podcasts. Into this podcast we're going to be discussing cardiovascular parameters, cardiovascular parameters. This is basically going to be a physiology and pathophysiology podcast, but honestly a lot of this stuff is something that in one way or the other caught across step one, step two, see gay and step three. Okay, so we're going to go right into it. So what if you get a question about 35-year-old male or okay, let's make it an older person. Let's see, you have a question about a 67-year-old male. We're told that he comes into the office because for the last four weeks he has been having chest pain that worsens whenever he exercises. And that before he did not have chest pain until after working out for like 30 minutes. But now even with five minutes of activity, he has chest pain. And then you're told that the person has smoked two packs of cigarettes per day for the last 30 years. And in addition to that, he has a history of peripheral arterial disease. And you're told that he symptoms have not responded to a supervised walking program and that he was recently placed on cellostasal. And then you're asked what is the next step in management for this person? So we see this person, let's look at this case. So this person is a vascular path. This person has a history of PED. Then they have not just PED. Now you're having this chest pain.

And I know some of you may be like, oh, divine, angina, angina, angina, angina. Yes, person has angina, angina, angina. What kind of angina does this person have? I'll really hope you're saying, divine, this sounds an awful lot like unstable angina. Because whenever you see a person that has anginous symptoms that are worsening, then you go from the realm of stable angina to unstable angina. What do I mean by that? Notice in the question I said that, oh, this guy would not typically have chest pain until he has worked out for like 30 minutes. But now with five minutes of exercise, his chest starts hurting. So you've seen a worsening of symptoms. Basically, the thing that will upstage you on USML exams from stable angina. And again, I'm the one I'm getting to cardiovascular parameters. But the thing that will upstage you on the USML exams from stable all the way to unstable angina is if with less activity, you're beginning to experience chest pain. Or with the same activity, you're beginning to experience a worsening degree of pain. That will buy you a diagnosis of unstable angina. Now this person, again, I don't, I did not give any indications that this person is kind of like him, what I'm clearly unstable, when they think like that. So what's going to be the next step for this person? Well, the thing that's going to make a lot of sense for this person, the thing that's literally going to make a lot of sense for this person is a stress test.

So now the big question is what kind of stress test do we want to go with? Do we want to do an exercise stress test or do we want to do a pharmacological stress test? Well, for this person, the thing that will probably make the most sense is to do some kind of pharmacological stress test. So what kind of pharmacological stress test could we use? Well, one that we could easily use in this person, we could use something like Duburamine, for example, we can use something like Duburamine. Although there are other things you can use for pharmacological stress test, but for the purposes of our discussion today, since I'm discussing cardiovascular parameters, I'm going to go ahead and discuss Duburamine. And again, really, this cardiovascular parameters, I'm just going to try to integrate many things across different subjects. So, but again, I think it's something I'm going to find to be extremely helpful for your exams. So Duburamine, and again, you may wonder, why are you not doing an exercise stress test? Well, think about it. Those this person have a comorbidity that we make an exercise stress test a little bit difficult. Yeah, this person has peripheral arterial disease. In fact, you see me saying the stem that I generated that weight. This person's symptoms do not seem to be responding well to a supervised walking program. In fact, the person had to be placed on sellosters all.

So, the thing is, the person may not be able to do very well with an exercise stress test, where they have to run or treadmelt just because they have like leg ischemia. So, in those circumstances, I'm going to do something that's more pharmacology based like Duburamine, for example. Okay? So, remember, Duburamine, how does Duburamine work? Duburamine, Duburamine is a beta one agonist. So, because it's a beta one agonist, it's basically going to stimulate your heart. It's going to increase your cardiac output by multiple mechanisms. First, in first, by stimulating those beta one receptors, it's going to increase your heart rate. Remember, your cardiac output is the product of your heart rate and your stroke volume. So, your heart rate is going to go up because you're on Duburamine. And if your heart rate goes up, obviously, your cardiac output will go up. But also, that beta one receptor, it does not just mediate the speed of conduction of your heart, but it also medates the force of contractility of your heart. So, Duburamine is going to increase your contractility. And by increasing your contractility, what else is that going to do? Well, by increasing your contractility, you're going to increase stroke volume. Remember, stroke volume is basically the amount of blood that you eject from the heart with each beat. So, if your contractium morphosfully with each beat, then the amount of blood that you're going to eject with each bit is going to be increasing.

So, Duburamine is going to raise your stroke volume. So, basically, it's giving you a two for one special. You're increasing the heart rate, increasing the stroke volume. And so, just we know, the cardiac output is heart rate times stroke volume. It would make sense that a cardiac output should be rising when a person is placed on Duburamine. Okay? Now, one other thing our friends at the USNL is going to do to you is they can even give you arrow questions with Duburamine. They can literally give you arrow questions with Duburamine. They can try to see if you can decipher some other parameters that may change with Duburamine. So, you may see, and they give you heart rate, obviously, heart rate is going up, which makes sense. Then they give you stroke volume, which again should go up. Again, that makes sense. Because again, it increases the force of contractility. They can give you cardiac output. Well, again, that should go up, which makes sense, right? Because heart rate and stroke volume is cardiac output. If your heart rate is going up and your stroke volume is going up and your cardiac output should go up. Another one you can also throw in there on exams is systolic blood pressure. Well, how will your systolic blood pressure respond when you give Duburamine? Well, remember, systolic blood pressure, the primary determinant for USNL purposes of your systolic blood pressure is going to be a cardiac output. This is actually something that's very high-autonomous.

Because many people kind of struggle with what exactly systolic blood pressure means. To be honest with you, you can meet your life a whole lot easier by just thinking of it as being directly related to your cardiac output. Whatever happens to your cardiac output in general should happen to your systolic blood pressure. So, because, honestly, the way I think of systolic blood pressure is, I think of it as like that pressure, that max pressure of blood when it just gets into the other. That's actually if you want to look at things at almost like the molecular level, that is really what systolic blood pressure means. It's like the highest pressure of blood that initially makes it to the other from the left ventricle. I mean, literally there's a reason why it's called systolic blood pressure, systolic blood pressure. Because the left ventricle gets blood out of the heart insistently. And as the left ventricle is contracting, it's generating force. So, the blood that's coming out of it is coming out with great force, greater force, greater force, greater force. Because it's squeezing itself down. So, that max pressure of blood that is initially making it to the left ventricle into the other. That pressure is what determines your systolic blood pressure. That pressure is what determines your systolic blood pressure.

So, the beauty of me in the sense that it's raising your cardiac output, then you can easily say that, oh wait, the beauty of me is also going to be raising my systolic blood pressure. It's going to be raising my systolic blood pressure. So, if the beauty of me raises your systolic blood pressure, then what should happen to your pulse pressure when you take the beauty of me? Well, remember, pulse pressure is the difference between your systolic and your mastolic blood pressure. So, if we know that the beauty of me is raising your systolic blood pressure, then it will stand to a reason that it should be widening your pulse pressure. Because if your SBP minus your DPP is pulse pressure and you're raising your SBP, then your pulse pressure should overall increase. Now, another way they can also do an arrow question. I don't know why I'm even going in this arrow direction, but I guess it's a reasonable thing to do. Again, this is supposed to be a physiology podcast. So, again, I want to get you as many points as possible. Again, many people, I know one thing that annoys some people with some of my podcasts is like, get divine. You go from these tangents, go from these tangents. But to be honest, with you, going off on these tangents, on these tangents, is part of what adds to the richness of this podcast. Because the thing is, yes, it'll be great if I just give linear lectures, linear lectures, linear lectures.

But the thing is, that's not very realistic from the context of the USML Es. Because the USML Es, they don't test things in linear fashion. They test things in integrated fashion. So, being able to see the same concept in multiple dimensions, it may be uncomfortable when you're learning things that way. For honestly, that is actually the best way to learn for the USML Es. I know many people don't like it, but honestly, there are certain things that may temporarily be an inconvenience, but long term is actually the best for you. So, I'm going to continue off on this Dubitamina tangent. So, I'm just trying to provide some reasoning. So, people don't think that, man, the van just does this for the sake of it. No, I don't just do it for the sake of it. It's very targeted to help you with exam prep. But basically, they can also give you a bunch of labs to see how you can determine what will happen with Dubitamina. They can give you like potassium and you're like, wait, how can they give me an arrow question in relation to Dubitamina through importasio? Well, again, that's the nature of the USMLE exams. So, let's look at the link between Dubitamina and Potasio. Well, what exactly does Dubitamina do? Well, remember Dubitamina, it's a beta one agonist. And remember, beta one receptors are not found only in the heart. Many people think of it as, oh, wow, we only find this only in the heart. No, that is not true. Dubitamina right? Axo-bidowon receptors.

And in addition to finding them in the heart, we can also find them in the kidneys. Dubitamina receptors, beta one receptors, we can find them on the juxtaglomeral cells of the kidneys. So, they literally have beta one receptors on them. So, if Dubitamina stimulates those beta one receptors on the surfaces of the of the of the GG cells, then the thing that's going to happen is you're going to make more raining because remember, those juxtaglomeral cells make a ton of raining. Well, guess what? If you make a ton of raining, what's going to happen to other things? Well, as your raining goes up, raining is going to convert angiotensin, gen-to-entantin, one angiotensin, one is going to convert, it's going to be converted by ace in the pulmonary capillaries to angiotensin-2. And then that angiotensin-2 is going to cause you to release more of a duster from the zonaglomerulosa of the adrenal cortex. And if you release more of a duster, well, what is one of the big jobs of our duster? It's to make you, basically, you reneed out potassium, to inscribe potassium through your kidneys. So, if that happens, you're going to have hypochyline. So, if a person is on Dubitamina, we should expect a hypochyline, the potassium should go down in that person. Okay, potassium should go down in that person. So, again, we've been talking about Dubitamina from the perspective of, well, it increases your carter capillaries, it increases your heart rate, your stroke volume.

But what are some other things that can cause your carter capillaries to increase? Again, this podcast is about cardiovascular parameters. So, again, let's make some more integrations. Well, there's this drug known as Milrinon. This is called Milrinon. Milrinon is the phosphodiesterase inhibitor. It's a phosphodiesterase inhibitor. That's actually a pretty, pretty, pretty good, pretty, pretty just a phenomenal positive ionotrop, pretty phenomenal positive ionotrop. So, you may wonder, define how those are phosphodiesterase inhibitor help with carter capillaries. Well, let me explain. Here's the thing that you need to get down in your mind. The thing is, phosphodiesterase, the job of phosphodiesterase is to convert cyclic AMP to AMP. Okay? It's to convert cyclic AMP to AMP. Now, if you're a phosphodiesterase inhibitor, you're obviously going to be raising your levels of cyclic AMP because you're no longer breaking it down, right? Because you've basically shut down the enzyme that brings down cyclic AMP. So, now we then need to ask ourselves, what does cyclic AMP do in the heart? Well, the thing that cyclic AMP actually does in the heart is that it stimulates cardiac contraction. Ciclic AMP stimulates cardiac contraction. Well, how does that happen? The way that happens is that cyclic AMP is going to stimulate protein kinase A. And protein kinase A, as we know, is a phosphorylator. Whenever you see kinase in the name of anything, it means that that thing phosphorylates stuff.

Now, when that thing phosphorylates stuff, when it phosphorylates stuff, you're going to promote cardiac contraction. But again, let's go a little deeper, a little deeper than that. The thing is your cardiac muscle has dihydroperidine and ryanodine receptors, right? And the thing is, the big thing to know about those two receptors is when they're phosphorylated, it basically makes more calcium available in the intracellular environment of the heart. It basically makes more calcium available in the intracellular environment of the heart. So if you have activation of protein kinase A, because cyclic AMP is elevated, that protein kinase A is going to phosphorylate and activate your dihydroperidine and your ryanodine receptors. And when those two things are phosphorylated and activated, more calcium is going to come. And if calcium comes in, it's going to bite to troponing. And calcium bound to troponing gets troponing out of the way so that actinamaiosink and get married. And when actinamaiosink get married, you're going to have more cardiac contractility, okay? So that's how meridone literally helps in getting a person to have an increased cardiac output. That's how it works as a positive I know trop. Again, really, I will say probably the big focus of this podcast on cardiovascular parameters. I just think like cardiac output, heart rate, stroke volume and things of that sort. So meridone, again, just to summarize, inhibits phosphodistories, raises your levels of cyclic AMP.

By raising your cyclic AMP levels, it's going to activate protein kinase A. Protein kinase A is going to phosphorylate and activate your dihydroperidine and your ryanodine receptors. And if that happens, if that happens, if that happens, then you're going to have more calcium available intracellularly so that actinamaiosink can interact and you have better calcium, you have better cardiac contractility. So in that setting, your cardiac output is going to be going up because you have more contractility. And remember, if you have more contractility, you're going to have an increased stroke volume. And if you really think about it, since meridone is increasing your stroke volume, what is meridone exactly doing to your end systolic volume? I really hope you're saying, oh, divine, meridone is bringing down my end systolic volume. Again, why does that begin? It makes sense because if you remember, your stroke volume is the difference between your end systolic volume and your end systolic volume. Your end systolic volume is the amount of blood that is in the heart. After the left atron has completely filled the left ventricle. Your end systolic volume is the amount of blood that is left in the heart. After the left ventricle has contracted and injected blood. So if your stroke volume has increased because you have more contractility, then your end systolic volume should be going down. So meridone should bring down your end systolic volume. So bring down your end systolic volume.

Again, that's one that's pretty, pretty high up to, to know, right? And remember, if, for example, a person gets like dejuoxing, again, we always wonder, oh, dejuoxing is a positive vinyl drop. How does dejuoxing do that? Well, we know that dejuoxing works by inhibiting the sodium potassium eti-p-spomp. When you inhibiting the sodium potassium eti-p-spomp, certain things are going to happen because normally that pump takes three sodiums out of the cell and brings two potassiums into the cell. But if you shot down that pump, then sodiums will not be taken out of the cell. So the intracellular amount of sodium in your cardiac myocytes is going to go up. Now, when the intracellular amount of sodium in your cardiac myocytes goes up, that keeps more calcium inside the myocytes. That keeps more calcium inside the cardiac myocytes. Well, how does that happen? Well, if you think about it, sodium, there's a mechanism in your heart for getting calcium out of the myocardial cell, okay? The thing that actually does that is something known as the sodium calcium exchanger. It's basically like a counter-transporter that, ooh, sodium will flow down is gradient into the cell. A sodium is flowing down is gradient into the cell because remember, sodium is primarily an extracellular ion. A sodium is flowing down is gradient into the cell. Calcium is going to be pumped out in the reverse direction. Calcium is going to be pumped out in the reverse direction.

It's going to be pumped out in the reverse direction. So if calcium is being pumped out in the reverse direction, then calcium is getting out of the cardiac myocytes. That's obviously not going to be helping with contractility. But if you give a drug like de-jocsin that inhibits the sodium potassium ATP is pumped, right? The sodium is no longer coming out of the cardiac myocytes. So a lot of sodium is beginning to concentrate inside the cardiac myocytes. As more and more sodium concentrates inside the cardiac myocytes, then that gradients that usually allow sodium to rush into the cell and for calcium to be pumped out is no longer there. Because remember, gradients happen because they are concentration differences. If you are raising the intracellular amount of sodium, then you are killing that gradient for sodium flowing to the cell. If there is no incentive for sodium to flow into the cell, then the sodium calcium exchange will not work and you will not be able to get calcium out of the cell. So guess what? More calcium is going to stay within that cardiac myocytes. And if more calcium stays within that cardiac myocytes, it's going to bind to troponing, get it out of the way so that acting amizing can get married. You're going to have an increasing cardiac contractility. Okay?

So again, a drug like the joxin, as I hope you know, because it increases contractility, it should increase your cardiac output, it should increase your stroke volume, and it should also decrease your insistolic volume. It should also decrease your insistolic volume. Now, what if you work out? What if you exercise? What happens when you exercise? When if you think about it, when you exercise, you're going to be in a very sympathetic state. I mean, you're very apt when you exercise. So, you're like in a big, big, big time sympathetic state. So typically, when you exercise, what in the world happens to your cardiac output? Well, guess what? Since you're in a sympathetic state, you have a lot of cardiac colomines running all over the place. Your nerve in effring is like going through the roof. Well, what does that nerve in effring do? Well, that nerve in effring, what is going to do is that it's going to stimulate the beta one receptors on your heart. And if you stimulate those beta one receptors on your heart, you're going to increase your heart rate, so your heart rate is going to go up with exercise. You're going to increase your stroke volume, because you're going to have more contractivity because of the stimulation of those beta one receptors. Okay? So, guess what? When you exercise, your systolic blood pressure should go up, because again, your cardiac output is going up. Your heart rate is going up. Your stroke volume is going up.

So your cardiac output is going up, because again, cardiac output is heart rate times stroke volume. And as I've drawn this relationship already, as your cardiac output goes up, then it will make sense that your systolic blood pressure should go up as well. Make sense. The systolic blood pressure should go up as well. But again, let's keep integrating some things here. So what actually happens to your systolic blood pressure during exercise? Because I want to draw like a very nice pulse pressure relationship for exercise. Because one of these weird things that you miss you on, something you're like, well, what's going on? This doesn't make any sense. Well, let me make it make sense for you. So what in the world happens to your pulse pressure with exercise? We've already defended why your systolic blood pressure should go up. But let me tell you this. I'm going to argue with you right now that your systolic blood pressure actually goes down when you exercise. You're like, huh? But divine. I mean, a sympathetic state. How in the world is my systolic blood pressure going down? Well, guess what? Let me explain. The thing is, when you exercise, your muscles are using ATP. Well, as your muscles use of ATP, they're going to make ADP. They're going to make AMP, right? As your muscles use of ATP, they're going to make ADP. And then that ADP is going to be converted to AMP. Now, what high yield thing to know about these derivatives of ATP?

These things where you've locked off a bunch of phosphates from ATP. Those things are very powerful visual dilators. They're very powerful visual dilators. So because those things are powerful visual dilators, they're literally going to decrease your systemic vascular resistance. And that makes sense because you're trying to get more blood to your muscle. You're literally trying to get more blood to your muscle so you can keep working out so you can keep exercising. So because your systemic vascular resistance is going down, your systolic blood pressure actually goes down. Okay? So let me introduce you to a new concept as well. The primary determinant on USMLE exams of your systolic blood pressure is going to be your systemic vascular resistance, which we also called a total peripheral resistance. Okay? The primary determinant of your systolic blood pressure is going to be your systemic vascular resistance. As your SVR or your TPR goes down, your systolic blood pressure is going to go down. Okay? As your SVR, as your TPR goes down, your DPP is going to go down. Again, if you make these relationships in your mind, it's going to make your life very, very simple on many of these USMLE exams. Okay? So exercise raises your systolic blood pressure, brings down your systolic blood pressure. So it's going to widen your pulse pressure. It's going to widen your pulse pressure. It's going to widen your pulse pressure. Right? Because again, your pulse pressure is SVP minus DPP.

As your SVP goes up and your DPP goes down, the spread between them is going to widen. The spread between them is going to widen. The spread between them is going to widen. And if you really think about this, right? This is why if you notice when a person has just worked out, if you press on your carotid or you check any pulse in your body, do you notice that your pulse is very strong? It's very robust. Why is that pulse very strong and very robust? It's very strong and it's very robust because your pulse pressure has literally gone up. I'm telling you this, your pulse pressure has literally gone up because you have such a high systolic blood pressure and such a low-dastolic blood pressure that the spread between them is big. So it's almost like that spread. That big gradient is manifested as a very strong pulse. Whenever your pulse pressure is wide, you're going to have strong pulses. Something may put you don't think about, but honestly, let's get back to the sort of like euric regurg. Euric regurg is one of those classic cardiovascular classic vascular problems where a person has a white pulse pressure. Well, many of you have probably heard that, oh, when a person has euric regurg, they have like head, head, bobbin, they have the quinky pulse, they have this, they have that, yada, yada, yada. And you may wonder, divide what causes all those things. Well, let me tell you this. Let me break it to you right now, breaking news. Guess what?

It's because they have a white pulse pressure. It's the white pulse pressure. Those really strong robust pulses that causes those people, right? It's the very, very strong robust pulses that causes those people that causes those people to have that causes those people to have those crazy phenomena like the head, bobbin and all those things. It's because the pulse pressure is wide. So I guess the question, I know some of you may be like, ah, divide, come on, please, explain why the pulse pressure gets wider in your decrease. Okay, I'm not going to leave you hanging. Let's talk about it. So in your euric regurg, your sister, I'm going to argue with you first, but your sisterly blood pressure goes up. So why does it go up? Again, I said the primary determinant of your sisterly blood pressure is your cardiac output. Okay. So that means in people that have euric regurg, your cardiac output generally has to be high. Why is that? Okay, well, think about it. Normally, the left ventric, remember, maybe let me start off here. The one of the big determinants of your cardiac output is your preload. How much blood did you put in the left ventricle? If you put more blood in the left ventricle at baseline, that's literally the Frank-Stahlian relationship. You put more blood in the left ventricle at baseline. If you put more preload there, then you're going to have a greater cardiac output. You put more in, you're going to get more out of it. Simple as that. Okay.

So now the next question I want to ask you is, where does the left ventricle typically in a normal human being, where does the left ventricle typically get its preload from? Well, it gets its preload from the left atrium. The left atrium is the blood supplier for the left ventricle. But now think about this. If a person has euric regurg, where does the left ventricle get its preload from? Hmm. The left ventricle is going to be getting some preload from the left atrium, but that's not the only place it's now getting preload from. It's also going to be getting some preload from the atrium. So since preload is coming from the atrium and preload is coming from the left atrium, overall, you have an increase in preload for the left ventricle. And if you increase preload for the left ventricle, according to the Frank Stalin relationship, you're going to increase the cardiac output for the left ventricle. And if the cardiac output for the left ventricle goes up, guess what? Your systolic blood pressure is going to go up. So defended one half of the equation I'll wait when people have euric regurg, yeah, SbP is going to go up. Okay. So now I'm going to argue with you again that people that have euric regurg are going to have a decrease in the at the stolic blood pressure. They're going to have a decrease in the at the stolic blood pressure. They're going to have a decrease in the at the stolic blood pressure. So why is that that stolic blood pressure decreased?

Well, that means I'm going to essentially try to defend to you that your system infrastructure resistance goes down when you have euric regurg, so SvR goes down. All right. So why does that SvR go down? Well, let's explain. Okay. Now the blood that comes into the yoder, normally the yoder just sends it to the rest of the body. There's only one highway for the blood that is entering to the yoder. It just goes into the vessels, your arteries for the rest of the body. And that's it. That's it. So it's almost like wow, they if you're going from New York to New Jersey, I'm just making up an example. Okay, let me leave a use that. Let's just say you're whatever. Let's say you're going to New Jersey and there's only one road from New York to New Jersey. Every single car going from New York to New Jersey, you're like, wait, you've got to take this one road. But think about the at the stolic regurg. Now the yoder has two roads available to empty blood into. The yoder doesn't have to only empty blood into the rest of the body. The yoder can also empty blood back into the left ventricle. So it's almost like instead of having one road from New York to New Jersey, now you have two roads. Since you have two roads, some cars will take one road and because of traffic reasons, we know New York is like a hotbed of traffic, right? Because of they're like, wait, I mean, this one road has so much traffic, but is this other road that exists? So some blood is going to take that other road.

So what's that going to do to the overall level of traffic? He's going to bring it down. So the traffic in your yoder is going to go down a little bit because you have the early regurg. Because some of that blood is not being offloaded exclusively through the yoder. So if it is going to be offloaded back into the left ventricle. So if that happens, that's going to cause a functional decrease in your systemic vascular resistance. That's going to cause a functional decrease in your systemic vascular resistance, right? So your mom is actually having a visual dilation happening. But you're actually having some blood that should be flowing in the yoder being offloaded back to the left ventricle. So the pressure of blood inside the yoder is not going to be great. So remember, it is not only visual dilation that causes a decrease in systemic vascular resistance, right? Again, this is one of these things. This is why understanding physiology and pathophysiology is really, really helpful. Because many people are like, oh, wait, if you visual dilate your SVR is going to go down. That's true. But that's not the only cause of an SVR decrease. So I'm going to propose to you now another high yield cause of an SVR decrease. Another high yield cause of an SVR decrease or a TPR decrease is when the yoder has multiple options for offloading blood. Normally, the yoder has only one option to offload blood just in the yoder downstream to the rest of the body.

But in a person that has a yodic regurgitation, the yoder has two options. You know, floats blood into the yoder, you know, to the rest of the body. But it also has the ability to offload blood back into your left ventricle. So because it has more options, blood has more pathways, it can take the blood. We don't have to have as much blood congestion. Think of it as like a traffic congestion in the highway of the yoder. You don't need to have all of that. So even if visual dilation has not technically happened, you've actually caused a functional decrease in systemic vascular resistance. You've caused a functional decrease in systemic vascular resistance. So as your SVR has gone down, well, guess what? Your DBP is going to go down. Your DBP is going to go down. And if your DBP goes down, then your pulse pressure is going to get wider because we've already defended how for a yoder creature, your systemic blood pressure goes up. And we've already defended for a yoder creature, so that's not a blood pressure goes down. So as your SVP is going up and as your DBP is going down, your pulse pressure is going to get very wide. Okay. That's why people that have a yoder creature, they tend to have these various robots, robots, robots, pulses. Right. And so people that think in real time with me right now as a making this podcast, you may also begin to say that, oh, divine. Also, I see why patent doctors, arteriosus is also associated with a white pulse pressure.

Well, you can already begin to see that if you have a pda, the yoder also is in that same situation of having two places to a float blood too. The yoder still is able to a float blood to the rest of the body, but in a pda, it can also float blood through that doctor's arteriosus that is patent to the pulmonary arteries. So it has two places to a float blood to. Again, that's going to cause a functional decrease in systemic vassular resistance. And guess what? That's going to decrease your mastoline blood pressure. So again, this is why in a pda, you're going to have a widening of your pulse pressure. You're going to have a widening of your pulse pressure. So it would make sense that the prison that has a pda should also have very strong pulses, just like we see people that have a yodic regurg. Again, anything that is widening your pulse pressure is going to cause you to have a very strong pulse. It's going to cause you to have a much stronger pulse. It's going to cause you to have a much stronger pulse. Okay, you can tell I'm probably getting a little too excited by this stuff. So here's the thing. Let's pause here. I really hope in the future I can have another opportunity to talk about cardiovascular parameters because honestly, there's so many more things I feel like I can talk about with the heart. I mean, there's all this stuff with like venous return, just like a whole big topic in and of its own.

Maybe I may actually make a podcast literally just on venous return because again, I feel like many people that we are creating medicine these days, they don't have a very firm grasp on many of these concepts. They just got to memorize their way through things. And then you wonder why they're not very effective one on exams, but also in clinical practice. Again, obviously, these podcasts are not for clinical practice. They're just to teach you and prepare you for tests. But I really want to spend some time on this kind of cardiovascular parameters. So I think I'm going to go ahead and stop here. I mean, literally just talking about cardiac output, heart rate, stroke volume, SBP, DBP, pulse pressure has taken up, what, like more than 30 minutes already. So I'm going to go ahead and pause here. But I really, really hope I can have a more, more, more time in the future to make some more cardiovascular parameter related podcasts. And again, I'm really grateful that today I was able to again, not just give a linear lecture because I could have said, oh, what is this stomach blood pressure? What is that? Stolly blood pressure? What is pulse pressure? No, it's better to use scenarios. When you're scenarios like this, the memories are just much stronger. It's harder to learn. But as you learn it, you notice that, man, okay, I can start making because you can notice just from describing theortic regurg. We then went off on this tangent to a pda. You can see that weight.

It's just a different illustration of the exact same concept of a functional decrease in systemic vascular resistance. And again, I want to encourage you to try to get your learning that way. If you can think in many dimensions like this, I'm telling you, you're going to be in really good shape on the USMD exams. So I'm going to go ahead and pause here. Again, I offer one or one tutoring for step one to step three, preclinical medical exams, 30-ish-off exams. I also have review courses for step one, I have a 25-hour course for that. And then I have a 20-hour review course for step two, step three. I have an MBA Me testing and strategy course, social sciences, ethics, quality improvement, and communications course. That one is a five-hour course. And then I have a biostatistics bootcamp. That's a four-hour course. I'm really like these. The biostat's class, the social sciences class, the testing and strategies class is for step one or the way to step three. And then I also help with ERAS applications and recommendation letters and personal statements and things of that nature. I have these podcasts on the major apps, Apple, Google, Spotify, I have a You Tube channel, Divine Intervention USMD podcasts and videos. That's why I post the videos that I make. And then finally, I also have another website called Divine Intervention Life Lessons.com. Many of you listening to this podcast know my Christian. I have another website, Divine Intervention Life Lessons.com.

And basically, on that website, I, from a biblical perspective, every week I post two podcasts, I discuss a life lesson. I try to, you know, use a biblical perspective, you know, give out a 10 to 20-minute podcast where I address a common life problem that many people face. I actually have almost 200 podcasts on that. And there's actually an Apple podcast associated with that. It's called the Divine Intervention Life Lessons podcast. So just check that out. I think you're going to find it to be really helpful. Now, a quick life lesson I just want to throw in here is the danger of multi-tasking. So to be honest with you, multi-tasking is something that many people do these days and is looked at as a valuable skill. But to be honest with you. And honestly, actually, because, again, let's, let's do some true talk here. Honestly, multi-tasking is something I'd always believed was a good skill to have. But over the course of time, I've studied realizing that multi-tasking is a really horrible thing for many people. What do I mean by that? The reason multi-tasking is generally a bad idea for many people is that multi-tasking is almost like the opposite of being able to focus on one thing. Because people that are multi-tasking, they are not focused on any one thing. They are focused on so many things at once. If your attention is divided across many things, then you're not going to be able to focus truly well on any one thing.

Like, for example, you may be like divine, how is multi-tasking bad? Well, think about it, for example. You see a person, they're studying for an exam. But at the same time as they're studying for the exam, they're checking their email, they're on their phones, they're checking social media, they're chatting with someone, they're doing this, they're doing that, they're doing this, they're doing that. They don't get much from that study time because they are mentally multi-tasking. So, I'll just encourage you, multi-tasking is actually not a good thing. Again, it's something I used to think was good, but it's really not. It's really not. It's really not. It's really not. It's really not. Because the person that is a multi-tasker, we are mind is completely unstable. Their mind is unstable. Their mind is unstable. Even there's this Bible verse that says that a double-minded man is unstable in all his ways. So, a person that is multi-tasking is almost like double-minded. Their mind is not in one thing. Their mind is not in one thing. You should be able to focus on one thing, finish it, and then go to the next thing. I'm telling you that is one of the smartest ways to handle your life. Because you see many people, they go through the day, they seem busy. But they end the day and they wonder, why did I get nothing from ID? One of the common causes of that to be honest with you, especially amongst the younger generation of today, is a lack of focus.

And what is the one big thing that brings a lack of focus? It's just again the presence of multi-tasking. So, again, I know that it may sound counter-intuitive, some people may think that, ooh, by being a multi-tasker, I'm able to get tasks done quickly. You're not. If you actually really sit down and do an analysis, you're not really getting very much from that multi-tasking bit. So, again, I really encourage you, be focused, be focused. Like you see many people, they have a multi-task with resources. They're like, ooh, they start off, let's see, starting from step one, step two, step three. And they're like, wait, I'm going to focus on this one resource. I'm going to focus on this one resource, on this one resource. Instead of them to just focus on that one thing and be single-minded, be single-minded, be single-minded and focus on that one thing, they keep jumping from one resource to the other. They read already that, ooh, there's this person that used this awesome resource, ooh, and they did well on the exam. So, they add that one into their study plan. And then they read on SDN, ah, there's this other study resource that I saw someone doing. They added to their study plan. And then they hear from their friends, ooh, you know, I took my USM, it's like, I got a 265. And there was this awesome resource I used. And then they added 10.

And then you notice, they're going through their days, they're spending time on like six, seven things, and they're literally getting nothing from it. They're literally getting nothing from it. I'm telling you this, don't discount the power of intense focus. Don't discard the power of intense focus. I'm telling you this, people that focus on one thing and see through, they're more likely to be successful. Based because I'm telling you, the time you spend focusing on something, think of this concept of opportunity cost. Whatever you're spending your time focusing on, it's time taken away from another thing. You could be focusing on. So, that's the thing, right? But if your attention is so divided, you can see anything through, right? Like, for example, you see like some of these would have achieved some very great things in life. They just had this intense focus. They just literally stuck with one thing. And by sticking with that one thing, they just saw it through all the way to the end, right? There's like this Bible verse some people have probably heard of where it says that, you know, enter by the narrow gate for, you know, there's this narrow way that leads to life. And then there's this broad road that leads to destruction. And I almost think of the broad road as like the multi-tasking road. There are so many options available to you. But a narrow path is a path that you're like, wow, I need to just be very single-minded. I need to stay with these very limited options.

But I'm going to focus on it. I'm going to go through with it, right? And then I'm going to get the reward at the end. So, again, I encourage you. Be a person that just focuses. I'm telling you this, that's one of the biggest dangers of social media these days. It has just killed the focus of so many people, so many people, so many people, right? So, and this is something that I, to be honest with you, I'm not going to be speaking to you here as like a perfect person. No, no, no, no, no, no, this is something I'm still working on to this day. I'm still working on it to this day. But I am making some progress. I'm telling you this, learn to focus on things and stop being a multi-tasker. Multi-tasking, it may look like you're helping yourself in the present, but long term you're actually kind of hurting yourself. Well, thank you for listening to my podcast today. I will see you in the next episode. God bless you and have a wonderful weekend. Bye for now. Thank you.

It acts as a $\beta_1$ agonist, increasing both heart rate (chronotropy) and contractility/stroke volume (inotropy).

The presence of peripheral arterial disease makes the physical exertion required for the test unsafe due to potential limb ischemia.

Hypokalemia (low potassium) is expected because $\beta_1$ stimulation on juxtaglomerular cells increases renin release, activating the RAAS system, which promotes potassium excretion.

It inhibits phosphodiesterase, raising cAMP levels. This activates Protein Kinase A (PKA), which phosphorylates and enhances calcium release from the sarcoplasmic reticulum via RyR receptors.

While CO increases, SBP is primarily determined by Systemic Vascular Resistance (SVR). During exercise, metabolic waste products cause massive vasodilation, leading to a decrease in SVR and thus a drop in SBP.

The regurgitant valve provides an additional outflow pathway for blood returning from the aorta into the left ventricle during diastole, effectively bypassing systemic circulation and lowering overall SVR.

Dobutamine.

Milrinone (or other PDE inhibitors).

Wide pulse pressure; functional decrease in SVR.

It inhibits the $\text{Na}^+/\text{K}^+$-AT Pase pump, increasing intracellular sodium ($\text{Na}^+$). This prevents the $\text{Na}/\text{Ca}$ exchanger from pumping calcium out, thus retaining more calcium and increasing contractility.

AMP (Adenosine Monophosphate), derived from ATP breakdown.

In AR, the left ventricle receives additional preload not only from the left atrium but also from the systemic circulation via the regurgitant aortic valve.

Dobutamine.

Milrinone (or other PDE inhibitors).

Wide pulse pressure; functional decrease in SVR.

It inhibits the $\text{Na}^+/\text{K}^+$-AT Pase pump, increasing intracellular sodium ($\text{Na}^+$). This prevents the $\text{Na}/\text{Ca}$ exchanger from pumping calcium out, thus retaining more calcium and increasing contractility.

AMP (Adenosine Monophosphate), derived from ATP breakdown.

In AR, the left ventricle receives additional preload not only from the left atrium but also from the systemic circulation via the regurgitant aortic valve.