DIP Episode 465 - Cardiovascular Parameters 2 (Venous Return and Preload)

Welcome, my name is Divine. This is episode 465 of the Divine Intervention Podcast. And to this podcast we're going to be continuing as discussion of cardiovascular parameters. And again, this podcast applies not just to step one, but also to step three. This is literally for step one or the only step three. If you missed out on the last episode, I would encourage you to take a look at it. We pretty much talked about cardiac output, stroke volumes, systolic and gastrointestolic blood pressures. Today, one thing I think I really want to focus on is preload. I want to focus on preload and venus return. Those concepts are very important. And there are just many different ways that the USM Ls can take those things on exams. So I don't want you to be in a situation where you don't get your answers right. Because again, you're kind of out of the loop on those. So the simplest way to think of preload is basically how much blood is in the left ventricle after it hurts felt. How much blood is left in the left ventricle after it has felt? So basically, what are we talking about here? What is the term we used to refer to filling of the left ventricle? We love to use the term diasteli. So at the end of the systolic feeling, what exactly happens to the amount of blood in the left ventricle? That's literally what preload means. That's literally what preload means. How much is in the left ventricle after the left ventricle has filled with blood?

So a very good approximation for preload is going to be your end diastolic volume, your EDV. Again, look at the name. We'll just memorize it. End diastolic volume. So the volume that is at the end, so the volume of blood in the left ventricle at the end of diasteli. That's literally what your preload means. And the thing is that volume and that pressure, they're kind of related. In general, that volume and pressure, they're kind of related. Now, what is one big determinant of your end diastolic volume? Well, a big determinant is your venous return. Again, what is venous return? It basically, literally what the word says is exactly what it means. It means how much blood returns to your heart through the veins. Because remember, it's the veins that bring blood back to the heart. It's the veins that bring blood back to the heart. So your venous return, right? How much blood comes in through veins back to the heart? That's a very big determinant of preload. Because if more blood is coming back to your heart, your preload, your end diastolic volume is going to be bigger. But if less blood is coming back, your preload, aka your end diastolic volume is going to be smaller. So what are some of the factors that can affect this stuff on an example? So again, I'm going to try to use quite a number of scenarios to address these points. Well, one of the very simple ones is just basically changes in position. Changes in position.

Are you in a stand-in position or are you in a supine position? Obviously as you can think about this logically, when you're in a stand-in position, then blood under the action of gravity is going to pull more in your lower extremities. Because blood is pulling more in your extremities, then it's not going to be coming back towards the heart. But if you imagine when you go from that stand-in position to a supine position, then you notice that, oh, more blood is coming back to the person's heart. Because basically, you're almost going in an anti-gravity format. So you're literally moving blood from your lower extremities back to your heart. You're moving it away from your extremities back to your heart. So when you go from the stand-in to the supine position, that actually increases venous return. And if you increase venous return, you're going to increase preload. Again, what's so nice with you love to test this stuff on exams? A very simple way to love to test this stuff on exams is in the context of valvular disorders. The thing is, many valvular disorders in general, when more blood comes back to the heart, then more blood is going to flow across those bad valves. And if more blood is flowing across those bad valves, the intensity of those murmurs are going to increase. Like, take, for example, a person that has a urinary stenosis. If a person has a urinary stenosis and they go from a standing to a supine position, their venous return is going to increase.

Since their venous return is increasing, the preload, the end-astolic volume for the left ventricle is going to increase. And since there is more blood at the end of the dastard in the left ventricle, there's going to be more blood to inject insistently. As that more blood is being injected, that more blood is flowing through the dietic valve. Because there is more flow across that stenotic valve, you're going to have an increased murmur intensity. You're going to have an increased murmur intensity. There are situations, though, where that root does not apply. The classic examples here are in mitrovov prolapse and in hookum, hypertrophic cardio, myopathic. When people have mitrovov prolapse, when you actually increase preload, when you actually put more blood in the left ventricle, it temporarily, it transiently fixes the prolapse. When that prolapse is fixed, then you're basically fixing the vavillable problem. Again, like I said, with more preload, the vavillable problem transiently goes away. When that vavillable problem goes away, then you're going to have a less intense murmur. Now, for hookum, many of us know the pathophase as asymmetric septal hypertrophy. That asymmetric hypertrophy of the interventricular septum causes an outflow obstruction from the left ventricle. It almost like creates a barricade for blood to leave the left ventricle.

So, the thing is, when you actually put more blood in the heart, when you increase preload, when you increase endastolic volume, that actually removes that barricade, it removes that obstruction. So, it allows blood to flow normally for a season, for a period of time. That's actually going to decrease the intensity of the murmur. But in general, for most other murmurs, when you put more blood in the heart, you're going to have more blood flowing through those nasty valves. That's ultimately going to cause an increase in murmur intensity. Again, to summarize, that road was not obtained with mitrovolv prolapse, and with hypertrophic cardiomyopathy. Because basically, by increasing preload, increasing endastolic volume, increasing venus return, you're transiently fixing those problems. I didn't see permanently, but transiently, transiently, transiently, transiently. So, that's actually going to be very, very helpful. Now, think about it. What exactly happens to preload when you're exercising? But when you're exercising, if you think about it, let's say you're working on a treadmill. Literally, you're contracting your skeletal muscles in your extremities. As you contract, because remember, your blood vessels run through your muscles. As you're contracting those muscles, what exactly do you think is going to happen? Well, the thing that's going to happen is that you're literally, as those skeletal muscles are contracting, you're going to be squishing your veins.

As you squish your veins, you're basically ejecting blood from them. And veins, where do they eject blood into? They eject blood into the heart. So, if you squeeze on your veins, blood is not tolerated, blood is no longer tolerated and hanging out there. So, that blood has to be ejected and it's going to go all the way back to your heart. Okay? That's why with exercise, your preload increases. That's why with exercise, your preload increases, your preload increases. Now, what if they give you a question about a person that has varicose veins? What actually happens to the preload of people that have varicose veins? Well, the preload of the venous return of people that has varicose veins should be diminished, should be diminished. Because if you think about it, people that have varicose veins, they have incompetent valves. Because remember, veins have valves. Those valves prevent the backflow of blood. They prevent the backflow of blood. They prevent the backflow of blood. But if you have incompetent valves, then that blood in your veins will flow back. If it's flowing back, it's obviously flowing away from the heart. So, those people are going to have decreased venous return. That's why one of the treatments of varicose veins, one of the treatments of venous stasis, is we tell people, oh, please, go ahead and elevate your leg. Because by elevating your leg, you're basically putting yourself in a supine position and you're increasing venous return.

You're increasing venous return. And in doing that, you're going to be increasing preload and your end-astolic volume. And in other words, they can also test this preload business. They can easily give you a question about a person that has an MI. They have chest pain. You give them nitrates for their chest pain. They have STL of Hitchhills, blah, blah, blah, blah. The CDR chest is hurting. You give them nitrates. And then they completely collapse from a cardiovascular perspective. Well, basically, what has happened in that situation is that the person likely has an RCE infart. In fact, if you see a person that has a right coronary artery, you see a person that has an MI before I jump into specifics. You see a person that has an MI and you give them nitrates and then they collapse from a cardiovascular perspective. You want to think about a person that has an RCE infart. That can be a very beautiful way, our friends at the USME Ls, test an RCE infart. Worseening of a person's vitality with administration of a nitrate. Because remember, when you have an RCE infart, you're going to have STL evations. In LITS 2, LITS 3, and EVF. In 2, 3, and EVF. When you have problems in LITS 2, 3, and EVF, your RCE is going to get infarted. If you're infart, then your right heart is basically hanged by a thread. Your right heart is basically hanged by a thread. That's why many times, many, many times, in these people, we try to avoid nitrates in them.

Because nitrates are very powerful, Vinodiliters. Nitrates are very, very powerful, Vinodiliters. When you dilute your veins, you're basically increasing their capacitance. You're increasing the ability to hang onto blood instead of giving it up. And if they don't give up that blood, then the heart is not going to receive it. And if the heart does not receive it, you're going to have a crushed, a venous return, a crushed preload, a crushed endastole volume. You can go into like big time cardiogenic shock as a result of that. So people that have RCE infartions, they are very, very, very preload dependent. They are very, very, very preload dependent. So for those people, it's actually extremely important. When you're training their MI, do not give them nitrates. For their chest pain, you can give them something like morphine. Don't give them nitrates. And many times when people have an RCE infart, it is not necessarily a bad idea to give them like a small amount of fluids, just to help them with preload. In fact, to be honest with you, this goes to the next point of what affects preload. One of the big things that affects preload is the volume of blood in your body. So if for example, a person has a lot of hemorrhagic, let's say a person has like hemorrhage or bleeding or something like that. They've lost a lot of blood. When you lose a lot of blood, you've lost blood volume. If you've lost blood volume, then you've lost a lot of stuff that should come back to your heart.

You've lost a lot of blood that should come back to your heart. So decrease blood volume. See for example, because you're taking a diuretic or because you're bleeding, or because you've been sweating, because you're like in a very warm, humid environment or whatever. Can kill your blood volume. If you kill your blood volume, you'll kill your venous return. If you kill your venous return, you're going to kill your preload. That's why many times when people have hypoglymetics shock, typically the smart thing to do for those people is to go ahead and give them fluids. By giving them fluids, you can restore their blood volume or restore their venous return. If you restore their venous return, you can pretty much restore preload and end their stolly volume and their cardiac output. Another thing that also affects venous return is actually your intra-thoracic pressure. Your intra-thoracic pressure. So how can they test this on exams? They can easily test this in the context of a person that has a pneumothorax, for example. For example, a person that has a pneumothorax, for example. So if for example, a person has a pneumothorax, especially like a tension pneumothorax, well guess what? A lot of air is going to be building up within your thoracic cavity. That air that is building up within your thoracic cavity is going to literally compress your SVC, compress your IVC, compress your heart.

Literally by compressing those structures, even if blood is trying to get into the heart, it will not be able to get into the heart. If that blood cannot get into the heart, your preload is basically your venous return is decreasing. If your venous return decreases, then your preload, your end-astory volume, your cardiac output, all those things are going to go down. In fact, many people memorize that, oh, your venous return increases with inspiration. Well, why do you think your venous return increases with inspiration? Because think about it when you inspire, when you inspire, when you inspire, your diaphragm is pulled downwards. When your diaphragm is pulled downwards, the size of your thorax is increasing. The volume of your thorax is increasing. If you think about that, as the volume of your thorax increases, according to boils low, probably remember this from general chemistry in college, according to boils low, as your volume increases, your pressure is going to decrease. Volume and pressure are typically inversely related. So as your intracurusic volume goes up, your intracurusic pressure is going to go down. As your intracurusic pressure goes down, your heart becomes a lower pressure system that is more willing to receive that blood. That's why many times, right? Many times when people inspire, when people inspire, you notice that, wow, your venous return increases. It is for that precise reason.

Because the heart is becoming a lower pressure system, because the intracurusic pressure has gone down. So it has going to invite more blood laterally back to the heart. It's going to invite more blood laterally back to the heart. In fact, that's why on inspiration, your juggler veins are supposed to collapse. Your juggler veins are supposed to collapse, because your heart has become such a low pressure system that is willing to take blood from every vein. So your juggler veins, which are an example of a vein, they should collapse because the blood in them is leaving to the lower pressure system of the heart. In fact, if you see a person where they inspire, they take a deep breath, and their juggler veins expand, that tells you that there is something wrong with those people's hearts. For example, that's something wrong, could be constructive pericarditis. If you have concentrated pericarditis, you're going to have the stomach dysfunction of the heart. So the heart cannot expand in tandem with the thoracic cavity to bring in blood. So since the heart cannot expand to receive that blood, you notice that when you're taking a deep breath, all that venous return is supposed to drop into the heart it doesn't. So it's almost like there's a stalemate in the juggler veins. Since that's stalemate because the heart is not willing to receive that blood, those juggler veins are going to descend. That's actually something known as Kusmoz sign.

Kusmoz sign on the USMLE is basically the extension of your juggler veins with inspiration. That's something that's pretty classic, pretty prototypical of constructive pericarditis, pretty prototypical of constructive pericarditis. And again, also think about it if a person has like SVC syndrome because they have like some kind of lung cancer or some kind of lymphoma. Those things are basically compressing the SVC. If you compress the SVC again, your venous return is going to go down. Your venous return is going to go down. Again, that's kind of important to keep in mind, for example. And actually, if you actually think about this some more, when you inspire, I said your venous return increases. The venous return, right? Because remember, when blood is coming back into the heart, the first place it goes through is the right heart. The thing is because that right heart has increased venous return, because that right heart is handling more blood, a bigger blood volume. It actually needs a little more wiggle room to expand. Has that right ventricle? Because it's dealing with that extra blood that came in because of inspiration. And as it expands, one place that it expands into, actually it expands into two places. One place it expands into into your pericardium. Another place it expands into is through your interventricular septum into your left ventricle.

So it's almost like the right ventricle in a sense, because of that extra blood in it, flexes its blood a little bit, flexes itself, its cavity size, its walls a little bit, into the left ventricle. So basically, by flexing its muscle, literally into the left ventricle a bit, through the interventricular septum, the amount of space inside the left ventricle goes down. So since the amount of space inside the left ventricle goes down, the left ventricle actually cannot then in that transient period, handle extra blood. In fact, it's going to only be able to handle less blood. That's why your blood pressure physiologically decreases with inspiration. Because remember, the thing that sends blood to the rest of your body is your left ventricle. But the thing that receives blood from the rest of your body is your right ventricle. If you inspire your venous return increases, that's going to make your right ventricle expand. It's going to expand a bit into your pericardium, it's also going to expand a bit into your left ventricle. So because your left ventricle has some of its space taken away from it, by the expansion of that right ventricle, let's probably be able to make it sweet into the left ventricle from the left eater. So your caracouple will decrease, your systolic blood pressure will decrease.

That's why, again, you're going to have a transient decrease in blood pressure with inspiration, because your left ventricle is able to admit less blood, because it's being compressed a little bit by the expanding right ventricle. But typically your systolic blood pressure, that effect is minor. Your systolic blood pressure should not go down by anything up to 10 millimeters of mercury, it should be usually like 10 millimeters of mercury or less in those circumstances. But if, for example, a person has like cardiac tamponad, where there's a lot of fluid in the pericardium, remember I said that when more blood comes into the right ventricle, the way the right ventricle deals with that extra blood is it expands into the pericardium, but it also expands through the interventricular septum into the left ventricle. But if you have a pericardial of fusion, you have cardiac tamponad, where your pericardium has been taken over by fluid, you've basically taken away one option of expansion for the right ventricle. The thing that's then going to happen is that, oh, your right ventricle, then the only option it has to expand, is through that interventricular septum into the left ventricle. So the thing that's going to happen is, is going to bulge really, really big into the left ventricle, through the interventricular septum. So that's going to lower the size of the interventricular septum. I mean, the size of the left ventricle, even more than is normal.

And if you lower the size of the left ventricle even more than is normal, even less blood will come into it. And if less blood comes into it, then less blood is going to be sent out to the rest of the body. So your cardiac output is going to be markedly diminished, and that's actually going to decrease your systolic blood pressure or not. It's going to decrease it by more than 10 millimeters of mercury. Just like an exaggeration of what should normally happen. Because again, just more spiced than is normal, has been taken away from the left ventricle by that expanding right ventricle. So if you may understand what I'm describing as post-aspiradoxes, that's actually the pathophase behind post-aspiradoxes. That's actually the pathophase behind post-aspiradoxes. And one thing that many people often worry about is, oh, divine. Post-aspiradoxes is it only in cardiac tamponat? No. Post-aspiradoxes you can actually find it in situations where you have an increase in chaperacic pressure. Like for example, a person that is going through an asthma exacerbation can also have box-aspiradoxes. Well, why does that happen? The reason that happens is because when you have an asthma exacerbation, your earways closed. It's not working well. So you're not able to eject much air from the thoracic cavity. So all that air will begin to bombard your heart. All that air will begin to squeeze on your heart. So guess what?

When you get, when you inspire, and you get more blood into the right ventricle, the heart cannot really expand well. So the right ventricle is going to be again, be boxing through that interventricular septum into the left ventricle. That will decrease the cavity size of the left ventricle. That will decrease the amount of blood that can feel that left ventricle. And if you decrease the amount of blood that can feel that left ventricle, there's going to be less, there's going to be ejected with the heart beat. So that's going to crush your cardiac output. It can bring down your system blood pressure by more than 10 with that inspiration. That's also spirodoxis. But classicly on the USMELY exams, pulsos spirodoxis is tested, is tested in the context, is tested in the context of cardiac tampon, or repressing having a period of cardio effusion. Again, you can already see all the different integrations that can be made with venous return. I think the last one I'm going to maybe talk about here is this concept of a person having an EV fistula, right on EV malformation. Remember we can see EV fistulas in people that, you know, I've had like catheter replaced in them for like dialysis, or people that have ulcerative labor on due syndrome, people that have a hereditary hemorrhagic telogenject Asia, right? An EV malformation, because maybe before I describe an EV malformation, let me describe the normal situation in the body.

The normal situation in the body is that your arteries are connected to the capillaries, your capillaries are connected to veins. That's how blood is supposed to flow. So, you have an EV malformation, an EV fistula, an EV malformation is a direct connection from an artery to a vein, from an artery to a vein. So guess what? It's almost like you've taken the capillary out of the equation. So, I just kind of think of it this way as, man, blood, not the body, but the body. So, I think that's the first thing that I'm going to do, is to get the blood out of the body. So, I'm going to do the same thing. I'm going to do the same thing. I'm going to do the same thing. I'm going to do the same thing. I'm going to do the same thing. I'm going to do the same thing. I'm going to do the same thing. I'm going to do the same thing. I'm going to do the same thing. I'm going to do the same thing. I'm going to do the same thing. I'm going to do the same thing. I'm going to do the same thing. I'm going to do the same thing. I'm going to do the same thing. I'm going to do the same thing. I'm going to do the same thing. I'm going to do the same thing. I'm going to do the same thing. I'm going to do the same thing. I'm going to do the same thing. I'm going to do the same thing. I'm going to do the same thing. I'm going to do the same thing. I'm going to do the same thing. I'm going to do the same thing. I'm going to do the same thing. I'm going to do the same thing. I'm going to do the same thing.

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I'm going to do the same thing. I'm going to do the same thing. I'm going to do the same thing. I'm going to do the same thing. I'm going to do the same thing. I'm going to do the same thing. I'm going to do the same thing. I'm going to do the same thing. When you increase preload, that will increase cardiac output. That's the French style relationship. That cardiac output increases. That can be a one contributor to high output heart failure. Because your heart is always operating an elevated cardiac output. Because the speed with which blood returns to the heart has increased in that person that has an EV fistula. Has increased in that person that has an EV fistula. Okay. Now the last thing I want to say, I've kind of talked about it already. What it may not be something that's immediately obvious to people. But again, if you think about it, if you think about it, if a person is doing the valve solver maneuver, right? In the valve solver maneuver, something that many people struggle with. Many people memorize that the valve solver maneuver kills preload. Well, how exactly does that happen? Well, when you're doing the valve solver maneuver, don't do it because you could pass out. You're basically blowing air against the closed glottis. You literally close your mouth and keep blowing air. Well, as you're blowing that air, that air has nowhere to go. So it's going to build up your thoracic cavity. That's going to raise your intrathoracic pressures.

When you raise your intrathoracic pressures, you're going to be compressing your SVC, compressing your IVC, right? So it's going to make it very hard for blood to get into the heart. That's why you see many cardiac murmurs. They get softer with the valve solver maneuver. Because the valve solver maneuver is a venous return reducing maneuver. That air that's building up into thoracic cavity is compressing your SVC and your IVC. And it's making it even more difficult for blood to get into the heart. So I think I'm going to go ahead and stop here. Again, if you love the way I integrate things, then you may be interested in some of the reviews. I actually offer review costs for step one. And that's a 25-hour class. And then a 20-hour class for step two and step three. I also offer a bio-statistic class that's four hours. It's for step one to three. A test-taking strategy course. That's for step one to three. A five-hour social sciences quality improvement, you know, ethics and communication class. That's also for step one to three. So if you're interested in any of these classes, just shoot me an email. I actually have a bunch taking place in the month of July. Shoot me an email. I'll give you some more information on those. And then I also offer one or one tutoring for all the USMID exams. And I have these podcasts on the major apps, Apple, Google and Spotify. And then I have a You Tube channel called Divine Intervention, USMID podcasts and videos.

That's where I post the videos that I make. And then finally, I have another website called Divine Intervention Lifelessens.com. You know, every now and then with these my, you know, podcast site, put life lessons at the end. But many people said, oh, man, Divine, I really love your life lessons. I made a separate website. We're from a Biblical perspective, many of you know, I'm a Christian. From a Biblical perspective, I discuss two life lessons every week. I usually upload two podcasts. In fact, we have, I believe, 193 podcasts right now. So just go to Divine Intervention Lifelessens.com. You'll actually see those podcasts from a Biblical perspective, usually in a 10 to 20-minute podcast address a life lesson. There's actually an Apple podcast associated with that. It's called the Divine Intervention Life Lessens Podcast. And then finally, I also help with Eras Applications, Personal Steep Ments, Recommendation Letters, Editing Eras Applications, Mocking Reviews, I do all those things. So if you're interested in any of those, just shoot me an email and I'll be happy to give you some more information. But again, I'm really glad that we were able to talk about this preload of a thing. Again, it's just one of these things you want to make sure you deeply understand for your, for your exams. Okay, so until the next podcast until episode 466, have a wonderful weekend. God bless you and I'll bye for now. Thank you.

It is the amount of blood in the left ventricle at the end of diastole (End-Diastolic Volume, EDV).

Moving from standing to supine increases venous return because gravity no longer pools blood in the lower extremities.

Pneumothorax or Valsalva maneuver (both compress SVC/IVC).

Nitrates are venodilators, which drastically reduce venous return and preload, leading to shock. These patients are preload-dependent.

Kussmaul's sign (JVP does not decrease or increases with inspiration).

The expanding right ventricle pushes into the left ventricle through the septum, reducing the LV cavity size and thus decreasing cardiac output.

Venous return (the amount of blood returning to the heart via the veins).

Varicose veins (backflow prevents effective return).

Mitral valve prolapse (MVP) and Hypertrophic Cardiomyopathy (HOCM).

Decreased intrathoracic pressure (Boyle's Law), making the heart a lower-pressure system that accepts more blood.

Increased preload and high output failure due to bypassing the capillary bed.

Fluid administration (to restore lost blood volume/venous return).

Venous return (the amount of blood returning to the heart via the veins).

Varicose veins (backflow prevents effective return).

Mitral valve prolapse (MVP) and Hypertrophic Cardiomyopathy (HOCM).

Decreased intrathoracic pressure (Boyle's Law), making the heart a lower-pressure system that accepts more blood.

Increased preload and high output failure due to bypassing the capillary bed.

Fluid administration (to restore lost blood volume/venous return).