that I think we are ready for the first lecture. As you can imagine, basic as it is, is on hemodynamics. So when you think about it, the heart is the most efficient pump in the world. So you could run a marathon or you could have a really busy day or night on call and you're exhausted and you go to bed and you pass out, but your heart is still working, okay? So it never stops.
It starts in utero. and it doesn't stop until you're dead. So, yes, this is a watering can, but when I see a picture of a heart like this, I think of this is just a watering can. So you have the mitral valve here coming down to the watering can apex, then it goes out to the watering can spout, which is the LVOT, and the aortic valve.
So it's got to be more complicated. than this or else you wouldn't be able to do 70 beats per minute 60 times an hour 24 hours a day 365 days a year for 75 years which turns out to be like 3 billion so when you did your anatomic dissections yesterday I hope you notice that the myocardial fibers run in various directions and this was known for Leonardo da Vinci time that when they dissected the heart they saw that the myocardial fibers are arranged so that just like when you're twisting water wringing a towel to get out the water that's how the heart actually twists so that you have this that you have this clockwise rotation in the base and a counterclockwise rotation at the apex So that is how the heart normally contracts. And that's how you're able to get 70 beats per minute, 60 times an hour, 24 hours a day, 365 days a year for 75 years, and not even know it many times.
So the role of the mitral valve annulus, the annulus is a dynamic structure. It's always moving everything in your heart. heart is always moving and when the mitral valve is when the mitral valve is open blood rushes in and the the annulus expands as well to get all that blood in and then when you when the mitral valve closes and the ventricle starts contracting, the annulus starts coming in. And the aortomycroton is where the spout is.
On the other side, it's the LVOT. That expands. during systole.
So basically that is to say that in the recent years we know more about what happens inside the heart not just structurally so that there's been many different ways now that we can look at actual blood flow into the heart and so this is a CMR derived image of what the red blood bloods, the path that the red blood cells take when they come into the heart. And they don't just like come in like a watering can. They make certain patterns so that you can see blood flowing into the left atrium goes from the right pulmonary vein, it goes straight down to the mitral valve.
Here's the mitral valve here and the blood from the left pulmonary vein comes toward the right pulmonary vein and it makes this circle, this vortex, okay, so that if you think about it, you don't want the red cells to be touching the sides of the chamber. It makes a vortex, okay, and then it goes down so that this can be seen graphically so that blood comes in from here is the right pulmonary vein, this is the left pulmonary vein, the arrows kind of show. the direction of flow. So it makes a vortex and then goes in atrial, when the atria empties, boom, this is the velocity.
So that's high velocity right here, the velocity scale. So basically this happens in the ventricle as well. So what happens when blood flows into the ventricle is that As you learned yesterday from Dr. Laurie's mitral valve dissection, blood goes directly to the LV apex.
And then some of it goes around this way. This is a posterior mitral valve. and that's the anterior leaflet.
So blood actually goes this way, pushing the posterior mitral leaflet closed in this direction. So this is a small vortex, this is a larger vortex. pushing the anterior leaflet closed.
So when that happens, once that mitral valve's closed, it approximates. It's like a keystone of a Roman arch. So it's pushed together by the forces of blood.
And then once it's closed, this vortex takes over this vortex. And then when systole happens, it rushes out the aorta. So this is actually a color flow Doppler with vector flow mapping that shows the arrows show the direction of blood flow and the length of the arrow shows the velocity of the blood flow and you can see these vortices forming and early diocese so the time in red up here is a time before the r-wave the r-wave is very important as you learned yesterday so you learned it whoever did the um the um balloon pump lecture, the balloon pump demonstration, and also with Dr. Laurie's demonstration, the R wave is the start of isovolemic contraction. Okay, so that's the time before isovolemic contraction.
And you can see the blood flow rushes in, heads to the apex. Some of it goes this way. Some of it goes this way.
And then these arrows show the direction of blood flow. And then once the micro valve... closes right up here so the micro valve is open, post your anterior leaflet, post your anterior leaflet, close.
And then blood rushes out the aorta after the aortic valve opens, but that's the direction of flow. And here you can see normal LV inflow pattern with, this is TTE imaging so it's going to be upside down, but you can see the direction of blood flow into from the left atrium, so from the left atrium to the left ventricle. circling around is the major vortex and out the aorta.
Now this shows what happens basically after diastole. So you have this, this is also vector flow mapping with TTE. You can see how these vortices, this major vortex vortex forms and then comes right out the pathway is out the LVOT and the LVOT is the only part of the left ventricle that actually expands during systole okay so that's about you know when you see that watering can and that doesn't move, it's like this.
But actually it expands, that's the whole thing with the interaction between the mitral annulus and the aorto-mitral curtain. The LVOT expands and that's a very important part of systole. So you can see how the myocardial fibers and the twisting motion helps the formation of these vortices.
There's a reason to it. There have been many other. modalities to image this kind of flow inside the ventricles, but they all confirm the same thing, that you get vortex formation, and that's how you get this efficiency of the heart that you don't even know that it's beating, but it's actually working for you.
So everything starts with the most basic thing, and that's the EKG. And as we know in life, timing is everything. So you know what happens at the R wave is isovolemic contraction. So I gave you some handouts for your take-home enjoyment of the relationship between pulmonary air declusion pressures and central venous pressures. This is on every single board, and I'm sure you remember, that there is the cardiac cycles.
You can start it anywhere you want, but I like to start it with the Y descent because that's... That is going to be your ventricular passive ventricular filling so you can fill out the blanks That I gave you there on a chart. So what I put there is What happens in the atria what happens in the ventricles and if the valves are open or closed?
And you know we can do that later and you can show me. So what happens in the atria is the opposite of what happens in the ventricle and I think that's how people get confused sometimes. So you just have to know that the pulmonary artery occlusion and the central venous pressures reflect what's happening in the atria. not in the ventricle. Okay and any positive rise is pressure is going up and anything negative means pressure going down and you can fill that out later.
So the descents can only mean two things one of two things relaxation and emptying the waves can only mean one of two things contraction and filling so you got a 50-50 shot and what you fill it out if it's right or wrong so tissue Doppler velocity so we can measure this on echo putting up your your cursor right on the either the mitral or tricuspid annulus you can see this is annular movement like we were talking before annular movement is very important so you can document isovolemic contraction time, that's the R wave, how long that is, to the point that the ventricle ejects. Then you have isovolemic relaxation time, which is the first phase of diastole. Then the ventricular filling, fast filling, and then diastasis, and then atrial contraction. So you can see this happens in both the right and left ventricle. You can time this up with the EKG.
And you can see just from annular motion what the timing of what the events occur in the heart. Now pulmonary venous flow patterns, you have blood always flowing, blood is always flowing. And it's like a weird concept to understand that it's like always flowing into the atria. It never stops flowing. Okay, the only time blood does not flow into the atrium from the pulmonary vein or the IVC, SVC is when the atrium contracts and the pressure in the atrium is the atrium is just too high so it goes backwards.
So that's the only physiologic time you're going to get reversible flow into the pulmonary veins. And you can put your cursor in the pulmonary vein and you can see this flow. Same thing with the mitral inflow pattern.
So you have this, when the pressure in the left atrium gets to be higher than the pressure in the left ventricle, bam, the mitral valve opens, you get a fast rush of blood into the left ventricle. And then at some point the pressure in the left atrium and the pressure in the left ventricle left ventricle equalize, so you get diastasis. It's like one chamber. And then the A wave on the EKG stimulates the atria to contract.
Boom, you get that second rush of flow, and that's the A wave on the mitral inflow pattern. The aortic inflow pattern, this is normal LVOT inflow. God is good. It's one meter per second. Very easy.
How do we get that? So, echo is different from, you know, getting gradients from the cath lab. In the cath lab, you stick a transducer in there and you measure it. That's what you do.
But for us, we actually have to... use the frequency shift of red blood cells to calculate a velocity. And the caveat with that is that there's a cosine theta so that your transducer has to be within 20 degrees of your red blood cell direction.
So this could be off a little bit if you're not parallel to the direction of flow. However, we measure the velocity, and we use that to get pressure. So that we use the simplified Bernoulli equation. The change in pressure between the upstream and downstream is 4 times V max squared. So what's the normal velocity of blood through the heart?
We all said that blood is always moving, moving, moving. So you can see that the velocity of flow on the left side of the heart is a little bit faster than the blood flow velocities on the right side of the heart and Standard is one meter per second. So what if the blood flow velocity in the aorta was four meters per second?
What would be the pressure gradient between the LVOT and? the aorta 64, right? So it would be, the pressure would be 4 times 4 squared, 64. Okay? So that means that you have flow acceleration.
That means there's aortic stenosis and the ventricle is squeezing well. It's just like when you have a hose, garden hose, and you put your finger over the nozzle or the open hose and it accelerates. Okay? So that's flow acceleration. That's what happens.
So putting all that together, it all starts with the EKG. You have the R wave is isovolemic contraction. So you know that. You can look at the mitral inflow velocities, pulmonary veins, and hepatic vein inflow, and tissue doppler. So that's like the basics of echo, but it's also the basics of hemodynamics.
So you have to know all this. And this is a... Something from Dr. Lay at the University of Minnesota. What they did was they used electrophysiology and MRI to divide diastole into 2,700 time steps. So this is a computational grid of what happens with blood flow coming into the ventricle, creating these rings.
And there's an E-ring and an A-ring. And everything that we have now in science confirms. The importance of the vortex, and you'll see that in many, many, many lectures probably today, that the vortical formation is very, very important to the efficiency of the heart.
So basically, in conclusion, the efficiency of the heart to provide maximal forward stroke volume depends on optimal timing, diastolic formation of vortices, and contraction in all chambers, atria and ventricle. So abnormalities in any of these factors will decrease the efficiency of the heart. So if you can think of something, what's an abnormality that concerns timing and arrhythmia? If you, I guarantee you, if your normal heart rate is 70 and all of a sudden you go into SVT at 180, you'll know it.
You'll know it and you'll feel that short of breath in one heartbeat. Okay, so that's going to affect it. Diastolic formation of vortices, what's going to happen to change that?
Okay, mitral stenosis. The blood flow is going to be messed up when it comes into the left ventricle. Or hypertrophic cardiomyopathy, the ventricular shape in diastole is going to affect it. It's going to move that blood in a weird direction.
How about contraction, regional wall motion abnormalities? That's going to affect the flow, the efficiency of the heart. So all these things. you know, affect the efficiency of the heart, and that's because the heart is the most efficient pump. And the body, our body likes homeostasis, okay?
So our pH is about the same range. our temperature is maintained in the same range, our electrolytes are in the same range. Our bodies can adjust to things given time, like aortic stenosis.
Takes a long time for someone to have a problem with aortic stenosis. And arrhythmia, bam, that happens fast, you're going to notice it right away. So this is a segue into my very good friend, Dr. Jamie Ramsey's presentation, Physiology of Cardiopulmonary Bypass, because that's something that happens in one heartbeat too, and the body doesn't like that. Thank you so much. Thank you.