okay so we're going to continue our talk and we're going to dive into pressure volume loops or the pressure volume relationship so we're going to start by looking at this loop here where you have left ventricular pressure on the y-axis and left ventricular volume on the x-axis you have four different points you have point a point b point c and point d um around here um and this basically is going or this loop let's say represents two components this side of the loop represents diastole while this side of the pressure volume loop represents systole so what is going on here so if we start at point a right here this is where um we are going to start the period of filling um ventricular filling this is what we would call your end systolic volume this is the volume of blood in the left ventricle at the end of systole so this volume is going to um is is is uh is going to be the lowest volume in the left ventricle and the amount of pressure is going to be pretty low around 2 to three millimeters of mercury and so from our previous lecture on the cardiac cycle we know that we can have this period of filling um three phases rapid inflow diastasis and the atrial systole at the end of that we are going to initiate systole ventricular systole now and so the ventricles are going to start contracting this point here this point here is your end diastolic volume or e d v so here you had end systolic volume and at point b you have end diastolic volume which is the amount of ventricular filling basically how much blood is in the ventricle right before we start contraction right before systole the amount of pressure generated in the ventricle before systole is going to be somewhere between five and seven millimeters of mercury now the ventricles are going to start to contract the mitral valve closes remember this is where you would get the s1 heart sound but blood is not going to be ejected right away the ventricle needs to build up pressure and that's what you see here this is that right significant quick rise in pressure with no change in volume all the way until your pressure exceeds about 80 millimeters of mercury or whatever the diastolic blood pressure is going to be after that happens we go into the ejection phase of systole and blood is going to rush out note now that we're going in the opposite direction we're going backwards on the x-axis because now we're ejecting blood which means that left ventricular volume is going to decrease okay left ventricular volume is going to decrease um blood is rushing out until the pressure in the ventricle starts dropping again causing the aortic valve to close which will generate the s2 heart sound or the dub sound and then that's going to be followed by the period of isovolumetric relaxation until we hit we go all the way down and the mitral valve opens again and the loop starts all over the volume at esv or the end systolic volume is going to be around 50 ml while the end diastolic volume is going to be around 120 ml so note here that point a represents and systolic volume but also point b d represents and systolic volume and the same can be said between point b and point c but that is not going to matter the term end diastolic volume is important as well as end systolic volume because they're they actually play an important role in um in cardiac function and so the lower the end systolic volume is that means that the greater the stroke volume right because you this is basically stroke volume right here um the more the wider the stroke volume is the more blood is being ejected the greater the stroke volume the greater the cardiac output because we know that cardiac output is stroke volume times heart rate so when stroke volume increases that means your cardiac output increases and if your stroke volume increases your end systolic volume is going to decrease interestingly when your end diastolic volume is higher this is also going to lead to an increase in cardiac output and an increase in stroke volume and we'll talk about that in just a few more slides i don't want you to forget the frank starling mechanism or the length tension relationship and just like we had this length tension relationship in skeletal muscle we also have it in cardiac muscle and it's very very important it looks a little bit different but it is still there none nonetheless and the concept of that optimal length of the sarcomere is going to be important excessive stretch um is is is not great but also excessive shortening as you see here is not going to be helpful don't forget that this is at the level of the sarcomere um if we start plotting and studying the um the relationship between volume and pressure in in the heart under two different scenarios the first scenario is in studying this relationship in a relaxed heart and the second scenario is studying this relationship in a contracted heart so if we study the relationship between myocardial fiber length or end diastolic volume because the greater the end diastolic volume is the greater the stretch on the heart which also means the greater the fiber length so if we have a relaxed heart and we fill it with blood and we then measure the amount of pressure we can you know get a data point we'll fill it with more blood and we would measure the pressure we get another data point and another and another and we start generating this curve but now if we contract the heart and while it's filled with blood and we contract it and we measure the amount of pressure it's going to look so much different right this is what that relationship would look like we would collect multiple data points and so we would have a relationship in systole that is very different from the relationship in diastole you can see in diastole that the curve is much flat much more flat than in systole i'm telling you that it's just a lot more compliant at the end you know towards greater increases in fiber length we start seeing an increase in slope that you see right here but the first part is more or less you know look at the slope here and compare that with the slope here so very very very different the heart behaves very differently in systole than it does in diastole and so this is you know that diastolic curve and this is that systolic curve physiologically though we will be functioning the pressure volume loop is going to be functioning somewhere around here and you see the different phases so this was point a point b point c point d remember this was your diastole and this was your systole okay look don't forget the force velocity relationship and just like we had the length tension relationship which is important this cur this figure also kind of discusses that and so the the figure in in black or that i'm going to highlight here in blue this is how the force velocity relationship would look like at a shorter length or a less preload less preload means a less end diastolic volume because that and the style of end diastolic volume determines how much stretch you're going to have in the ventricle while let's highlight the other one the red one here let's highlight it in purple right this is what the force velocity relationship would look like and a long initial length or a greater preload which also means a greater end diastolic volume and so if we start looking at different points here if we fixate a velocity of shortening so we look here this dashed line and it's fixed between the two curves what you notice is that at a greater preload the amount of tension exerted is higher so we know that by looking at this point you pull it down this is the low generated the same velocity you pull it down this is the load generated so you can tell that at a greater preload and a constant velocity the amount of tension developed is going to be higher in the stretched muscle versus the shortened muscle but also if we fixate at any given load and a given afterload in this example and we look here so we fixate the load here so we have a data point here and also another data point here you see that the stretch muscle will contract at a higher velocity compared to the shorter muscle again telling you the importance of the preload and diastolic volume the amount of stretch that is going to happen or be present in the left ventricle so the greater the amount of blood that we fill the greater the contractility or the greater the amount of blood that your heart can get out and so there's that positive direct relationship between end diastolic volume and ventricular filling and cardiac output so what determines cardiac output and so we always know and we should not forget cardiac output equals stroke volume multiplied by heart rate and this is what you have here so you have heart rate and you have stroke volume what determines stroke volume is going to be the amount of end diastolic volume we have and and systolic volume so filling pressure the higher the feeling pressure the higher the end diastolic volume and that is going to favor stroke volume filling time is also important as well as ventricular compliance and we will talk about compliance in future lectures when you're thinking about filling time if your heart rate increases too much right the amount of time available to fill the ventricle is reduced that can actually have a negative effect because if your filling time is insufficient you will not be able to fill the ventricle to an adequate degree in order to ensure good end diastolic volume and good preload and that can have a negative effect when we're looking at end systolic volume things that can affect that is heart rate because heart rate and filling time go hand in hand and so if your heart rate increases too much that affects your filling time that can also affect your end systolic volume the amount of preload the greater the preload that you have the less end systolic volume because again preload and end diastolic volume right the greater they are the greater the cardiac output the greater stroke volume and the greater your stroke volume the less blood is going to remain in the heart after contraction that is end systolic volume what about afterload well the greater the afterload you have which is that pressure that the heart has to work against you know you think about the heart as someone trying to push a door and there's another person on the other side and the stronger that other person is the harder it is for you to open the door and so that is afterload so the greater the afterload the higher the end systolic volume is going to be because your stroke volume will be less and finally contractility the greater the contractility the less and systolic volume is going to be so these are all factors that can affect stroke volume uh make sure you think about them and you understand how each one of them will affect either end diastolic or end systolic volume looking at heart rate we have regulating factors that are within the heart and some are outside extrinsic regulating factors these are like the autonomic nervous system um or humoral factors like certain kind of circulating hormones you know like the circulating catecholamines epinephrine for example um we talked about intrinsic regulation we talked about these when we were talking about how we can control or how the autonomic nervous system will control um heart rate by controlling the sa node and the av node controlling the threshold potential resting membrane potential and the rate of depolarization um okay so let's look at the pressure volume loops and look at different scenarios and how that's going to affect the pressure volume loop so in your purple is your control state and in the red is the post state so this is purple is what it would normally look like so what if we have an increase in contractility note here that under both scenarios end diastolic volume did not change it's the same right and diastolic volume did not change the pressure at which the aortic valve is going to open because here the aortic valve opens also did not change but what changed is rather than stopping here right this was your end systolic volume under the first condition rather than stopping here now we're stopping right here so actually the contraction and goes much further back and you can see by stretching and measuring this distance you can see that there is an increase in stroke volume so when we have an increasing car in cardiac contractility we have no necessarily no change has to happen in end diastolic volume but the heart is just contracting harder stretching that pv loop to the left right this is all extra stretching the pv loop to the left reducing end systolic volume and increasing stroke volume therefore increasing cardiac output what if we have a change in preload right so contractility itself is not really changed much but what we're changing here is end diastolic volume and so you can see that this is end diastolic volume under the first control condition and this is end diastolic volume in the experimental condition you can see that there's that stretch we're stretching the heart a little bit more what's the result the result is that your stroke volume increases so this is stroke volume in the experimental condition this is stroke volume in the control condition so this increase in stroke volume is driven by the increase in preload or that stretch that's happening within the muscle you can tell that there's no real change in contractility by looking at the espvr relationship which is known as or which stands for the end systolic pressure volume relationship which is a measure of contractility and you see here that this slope just did not change compare this to what you see here here you see that the slope actually changed from one state to the next it became more the slope became much more steep um in the experimental condition so you don't have to worry much about the espvr relationship really as long as you can interpret what happens with the pressure volume loop under these different scenarios that will be sufficient um and if you're just interested in more cardiac physiology then you can kind of look up the espvr and what it means and read about it a little bit more what about if there is a change in afterload well again afterload is that the pressure that the heart is working against um and then you can see here that end diastolic volume remains constant but what changed here this is the pressure that normally would be sufficient to open up the aortic valve now under the experimental condition that pressure is higher right so normally you would open at 80. let's say now you're opening at 90 millimeters of mercury right because this patient has high blood pressure for example as a result of that increase in afterload if the total amount of work is just remaining constant what you're going to see is a decrease in stroke volume this is stroke volume in the experimental condition and then you can compare that with stroke volume in the control condition now we have a decrease in stroke volume and actually we have an increase in end systolic volume compare this to the end systolic volume happening here um this would happen when there is an increase in total peripheral resistance that leads to that increase in afterload just making it harder to open up the aortic valve and get blood out of the ventricle so he kind of stretches as you see here stretches the pressure volume loop upwards making it thinner telling you there's a decrease in stroke volume due to an increase in afterload here's a question that i have for you so feel free to pause your video read the question take a shot at it and make sure to post your answer on the discussion board and discuss with your classmates all right and that's all for me thank you