Frank-Starling mechanism (video) | Khan Academy
Medical definition of Starling's law of the heart: a statement in physiology: the called also Frank-Starling law, Frank-Starling law of the heart, Starling's law. Therefore, at a given LVEDP, shifting the Frank-Starling curve up and to the left will by the length-tension and force-velocity relationships for cardiac muscle. The Frank-Starling Law states that the stroke volume of the left ventricle will increase as the left ventricular volume increases due to the myocyte stretch causing.
Decreasing afterload and increasing inotropy shifts the curve up and to the left. At a given state of ventricular inotropy and afterload, the ventricle responds to changes in venous return and ventricular filling based on the unique curve for those conditions.
To summarize, changes in venous return cause the ventricle to move up or down along a single Frank-Starling curve; however, the slope of that curve is defined by the existing conditions of afterload and inotropy. Frank-Starling curves show how changes in ventricular preload lead to changes in stroke volume.
This type of graphical representation, however, does not show how changes in venous return affect end-diastolic and end-systolic volumes. In order to do this, it is necessary to describe ventricular function in terms of pressure-volume diagrams.
When venous return is increased, there is increased filling of the ventricle along its passive pressure curve leading to an increase in end-diastolic volume see Figure. If the ventricle now contracts at this increased preload, and the afterload and inotropy are held constant, the ventricle empties to the same end-systolic volume, thereby increasing its stroke volume, which is defined as end-diastolic minus end-systolic volume. The increased stroke volume is displayed as an increase in the width of the pressure-volume loop.
The normal ventricle, therefore, is capable of increasing its stroke volume to match physiological increases in venous return.
This is not, however, the case for ventricles that are in failure. Mechanisms Increased venous return increases the ventricular filling end-diastolic volume and therefore preloadwhich is the initial stretching of the cardiac myocytes prior to contraction. Myocyte stretching increases the sarcomere lengthwhich causes an increase in force generation and enables the heart to eject the additional venous return, thereby increasing stroke volume. This phenomenon can be described in mechanical terms by the length-tension and force-velocity relationships for cardiac muscle.
Increasing preload increases the active tension developed by the muscle fiber and increases the velocity of fiber shortening at a given afterload and inotropic state. One mechanism to explain how preload influences contractile force is that increasing the sarcomere length increases troponin C calcium sensitivity, which increases the rate of cross-bridge attachment and detachment, and the amount of tension developed by the muscle fiber see Excitation-Contraction Coupling.
Other mechanisms are undoubtedly involved. Pressure volume loops Video transcript So a long time ago, there were two gentlemen, one by the name of Frank, and the other, his last name was Starling. So Frank and Starling coming from two different countries. Frank was from Germany, and Starling was from England. Came up with a set of ideas that we still use today.
And not just use, but actually are pretty relevant to how we think about how the heart works. And so these two guys, I just want to give a little shout out to both of them because they were leaders in their field plus years ago. And their ideas are still very, very relevant to how we think about things today. So what they came up with-- and this is kind of the content of the video-- is related to pressure and volume. Let's talk about both pressure on this axis and volume on this axis. And you understand that P and V are "Pressure" and "Volume.
It's going to kind of go up near the end as you start really packing in the fluid. And we call this the "end-diastolic"-- that's where the "ED" comes from-- "pressure-volume relationship. And I could take different points on this curve. I'm just going to kind of choose some points arbitrarily. Let's say 3, 4. Let's choose one up here. And you realize that, as you go up from point 1 through point let's say this is point 1, 2, 3, 4, and 5.
And as you go from point 1 through point 5, your preload is going up. Remember that preload is related to pressure.
And preload is really a sense for-- what is the stress on the walls? And of course, within the walls, you've got these little heart cells.
So what's the stress on these heart cells? We know that as, the stress goes up, the heart cells themselves begin to really stretch out. And so I'm going to just kind of show that to you in this little diagram. Let's say this could be 1. This could be 3. And this could be 5. So this is kind of what's happening with heart cells as you go up, up, up in terms of the preload. So thinking about heart cells stretching out-- and of course, this is before they contract-- what does this mean for contraction?
And this is something that Frank and Starling thought about. And that's what I want to kind of jump into next. So just think about these 5 points-- 1, 2, 3, 4, 5. And we're going to go kind of point by point through them each.
So let's start with point 1. And here in point 1, you've got very little preload. Very, very little preload. And maybe it'll be useful to kind of just draw some myosin. So this will be our myosin. And I'll draw the myosin heads. I'm drawing, let's say, about 20 or so on the bottom and on the top.
This is our myosin molecule in purple.
And I want you to keep an eye on how many myosin heads are actually working, almost as if you're the taskmaster and you've got to make sure that the myosin heads are all working. Make sure you keep an eye on exactly how many are doing what we want them to do, which is contract or pull in the actin.
So let me actually just take a little shortcut here so I don't have to keep redrawing this. I'm going to move this down here, and I'll do it again. And I'll move it even lower. So we have our myosin there. Now, around the myosin-- in fact, let me label it while I still can. This is our myosin. Around our myosin, we have, of course, actin. I'll write it bigger just so you can see it very clearly. We have actin, and actin is we'll do in red.
But because we have a very low preload-- or almost no preload-- I'm going to show you what that means for our molecules. You're going to have something like this where you have everything kind of crowded together. And that's kind of the core issue I want to point out to you. You have lots of crowding problems. And of course, the myosin-- on the ends of here-- this is our Z-Disk.
I'm going to write "Z-Disk. What I'm showing you is kind of a part of the sarcomere. Remember, the sarcomere is kind of the basic unit of contraction, and it usually goes from Z-Disk to Z-Disk. So this is just a part of it because you'd have many, many more actins and myosins stacked up and below it.
But this is just to kind of give you a sense for what we're looking at. And this is, of course, our actin. The question is-- and I guess I should-- sorry. Before the question, let me throw in titin.
CV Physiology | Frank-Starling Mechanism
This little green molecule is titin. So the question is-- how would contraction occur? If you were to look at this scenario and you're kind of an inspector, you're just kind of assessing for problems, would you expect that there would be any problems? Would you expect any problems here? And afterwards, I also want you to think about force. What kind of force do you expect to get out of this sort of arrangement? A lot of force, or a little force? What do you think? Well, immediately, I can see some problems.
I mean, you know that the whole goal is to pull the Z-Disks in closer to each other. That's the whole point. The myosin is going to yank on the actin ropes-- you could think of it as a rope-- and yank the Z-Disks in. And if there's really almost no space here-- see this right here, there's almost no space here. And this myosin is basically almost touching the Z-Disk.The Frank-Starling Law of the Heart Part 1
This guy right here is almost touching the Z-Disk already. Well, then, what do I really expect to happen? There's going to be almost no force because the problem-- and I'm going to write it very clearly-- is that the myosin is crowded. Meaning it's right up against the Z-Disk right from the beginning. And that's a problem. Because that means-- what can you really hope to achieve if you've already gotten the myosin already against the Z-Disk?
There's really no space for you to yank the actin in to bring the Z-Disk in closer. There's no space there.
So I would say that's the biggest problem. And secondly, there's actually another problem here. And that's around actin. Because the actin has polarity, and this is an important issue. These two actin molecules that I've drawn arrows around are fundamentally different because there's a directionality to the way those proteins are laid out. And we call that "polarity. And what that means is that then myosin can't simply reach up and grab the nearest actin.
It has to grab the correct actin. So for example, these four right here-- I'm going to draw a little circle around them in yellow-- these four really want this actin on this side.