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Current time:0:00Total duration:12:41

Video transcript

we talk a lot about pressure and I thought it would be kind of a neat exercise to go through what exactly is the point behind pressure why does it matter so much what the end diastolic pressure is and that's what that IDI means and to do that I think one of the best ways is to say well you know what happens if we change it what what would be the results of changing the pressure at the end of diastole so the first change that you would see is you remember there's that equation around preload equaling we know pressure at the end of diastole times radius at the end of diastole and of course then if pressure goes up then preload would go up and we know that wall thickness times two is in the denominator so the first thing I would say is well if you say pressure goes up or if that's our assumption then we have to assume that preload would go up as well so that's the next thing well you might say okay well let's take it a step further so what that preload goes up how does that change anything well again I think it's helpful to kind of think about what preload is and then some things will become very very obvious right away so if we look at a cut section of the left ventricle this is my left ventricle and I've kind of sliced through it and you know you've got pressure kind of hanging out in here this is our end diastolic pressure the same thing we started with right pressure at the end of diastole and if you increase that pressure then you know you're going to cause some changes around the walls right you're going to have wall stress and we know that wall stress at the end of deaths that we call preload so basically these yellow arrows represent preload and in fact I might even point out to you that if I actually zoomed in there would be a little red cell like little squarish and that little red guy a little red cell let's draw him over here he's actually gonna start feeling he's going to literally start feeling the effects of stretch so he's hanging out nice and happy and all of a sudden this little fella is going to get stretched he's going to start looking like this and I don't think he would be upset I think he would look just as happy but he might look like that it all stretched out his eyes stretched away from his smile so this is what our cell will begin to look like if we continue to stretch and the reason is is because you're literally yanking on the two sides right so that's what what becomes of this process this causes these cells to almost look like little pancakes and I say pancakes just because I enjoy pancakes so much but just remember that the cells flatten out and they stretch out and that's a direct consequence of the increased preload so this causes increase I'm just going to write stretching stretching so in fact maybe I should even say stretching of heart cells just so we don't forget exactly what we're talking about so stretching of heart cells and you can literally imagine it right you can imagine these little cells getting stretched out and you can also imagine if you think for a moment of all of the contents of the cells getting stretched out so stretching actually stretches out not just the cell itself but everything inside the cell and a few interesting things begin to happen when all the proteins inside of a cell gets stretched out so there are two important things that happen with stretching and now we're getting into kind of the meat and potatoes of increased pressure what it causes so stretching itself is going to happen I think that part you know you can kind of Reason through that and kind of assume that you know that makes sense and one thing that it causes is what we call the frank-starling mechanism so you know obviously named after two folks named Frank and Starling and the frank-starling mechanism will actually get into some details about this separately but the frank-starling mechanism is put simply it's going to be something like this I'm going to draw out another myosin and actin so remember myosins got these fantastic little myosin heads always looking to work right they're always looking to bind actin and they're on both sides and so I'm going to just draw it here so here in purple is just my myosin bit and I'm going to actually cut and taste this and show you what it could look like on the side so I'm going to draw kind of two versions and we're going to start seeing how the frank-starling mechanism very quickly how it makes sense so we've got this actin kind of sitting here and it's on both sides right so it's going to be on both sides in this first kind of drawing I've drawn things very crowded right there's a lot of crowding happening there and so you basically get these areas where for example let's draw here these two myosin heads and these two myosin heads are literally being blocked by this actin so that for example this these two myosin heads are being blocked by that actin and these two are being blocked by that actin because they would both like to be on their other side right they would like to be on this binding to that actin and this set would like to bind to that actin so you've got actin crowding out other actin right which sounds kind of funny because you think well so what akhom the myosin doesn't just simply bind the actin that's closest to it right that seems like an obvious solution but in fact actin has a polarity right so it can only really bind in one direction so when things actually get crowded that becomes a major problem because now myosin literally can't get to the actin with the correct polarity as you see in the first diagram so what happens at the frank-starling mechanism is that when you stretch out your heart cell you're also stretching out as I said all the proteins within and now you've got a lot of happy-happy myosin heads these guys are happy right these guys are happy and these guys are happy as well so basically what you see is that by stretching things out you can actually get more myosins back on the job and so that's kind of the key with the frank-starling mechanism is that you have more myosin more myosin heads at work myosin heads at work so this is a key point and there's some nuance is to it I've kind of simplified the Frank strongly mechanism there are some important nuances we'll get into as I said later but this is one of the key elements of it and the other stretching related mechanism is called an inotropic mechanism inotropic and usually when you think of inotropic you're probably thinking that it has something to do with calcium and you're right I know tropic does have to do with calcium and what it means is that basically let me actually give a little bit more space if we were to zoom in now remember we have our actin and myosin you know how valuable it is to have the two binding to each other if you have something like this where your actin is there and let's say you've got a myosin here hoping to bind to it this is our myosin then what you see is that the actin is guarded you remember it's guarded by what it's guarded by tropomyosin right that's the protein that's kind of acting like a chaperone right making sure that the two the myosin actin don't interact so this is our tropomyosin again you can think of it as a chaperone right just protecting that actin and the thing that's going to help us move the tropomyosin out of the way the thing that's going to help us move it out of the way is none other than our friend troponin so this is our troponin and troponin is going to scooch the tropomyosin away and troponin comes in three protein bits and we call them troponin see troponin I drew ponen T and it's the troponin C that I'm going to focus on for right now so the troponin C let's say is looking like this right this is our troponin C and remember it's going to potentially bind to calcium in fact it will bind to calcium this is my calcium right so this is my troponin C and my calcium when things are stretched out so when things get stretchy I'm going to say stretched well the proteins feel that and the troponin C is going to look stretched it's going to look like like that this is my troponin C right all stretched out and troponin C the stretched out version literally behaves slightly different than the troponin C when it's not stretched out so troponin C when it's not stretched out is thinking to itself well yeah maybe I can find calcium maybe not you know I'm not particularly plus teether way so it's thinking ah maybe I don't want to bind calcium maybe I do but the troponin C that's stretched out is saying yes please let's bind so it's screaming to bind with calcium so that's a big change isn't it because if troponin C wants to bind calcium and that's exactly what happens when things get stretched out is that troponin C kind of changes its its shape and now it really wants to bind calcium if that happens then all of a sudden the troponin C is going to be more effective at getting tropomyosin out of the way and myosin can now bind actin so let's recap these two mechanisms they have a lot to do with each other right so when things stretch out the frank-starling mechanism allows more myosin heads to get to work and the inotropic mechanism basically is kind of a change in the way that troponin C's shape is and that change in shape makes it want to bind calcium very eagerly so let's put it together you've got more myosin heads at work that's what Frank Starling taught us and as far as the inotropic mechanism you may not have more calcium but what calcium in do have is going to have a bigger effect right because the troponin C really wants to bind to it so calcium has a bigger effect so if you think about them you've got more myosin now and the calcium is obviously going to help the myosin bind to actin more easily so putting it all together you're going to basically get more myosin burning up ATP and turning it into mechanical force right or mechanical energy so the the end result of all this is that you have a larger mechanical force larger I'll say left ventricular force of contraction so this is kind of the end of the day what you're going to get and as you get that larger force of contraction I could go even further and say well what what is that force well it's pushing against blood and that's pushing out on a certain area and force over areas pressure so a larger force of contraction really translates into what you're saying is a larger left ventricular pressure larger left ventricular pressure and this just to be very very clear is going to be drawing systole so we started talking about diastole right the question was well you know what the heck is the point of you know knowing about preload and end diastolic pressure and the point is now very very clear right because if you can have a higher preload set up the stretching of heart cells that's going to cause two mechanisms to start changing the way that molecules within those heart cells are working right the actin and myosin is actually going to be able to bind more easily to each other and also the calcium has a bigger effect kind of freeing up the actin and at the end of the day you get this larger left ventricular pressure during systole so really diastolic preload or what happens at the end of diastole which we call preload is going to have a huge effect on the left ventricular pressure during systole