so what I want to do with this video is start talking about cardiac output so cardiac output is a measurement that's calculated often clinically because it gives us information about how the heart is actually functioning so I'm going to give you just kind of a definition of what cardiac output is and then we'll go into how it's actually calculated and then the last thing that we'll do with this particular video is talk a little bit about some things that can affect cardiac output to cause it to increase or cause it to decrease so here's a working definition of what cardiac output is it's the amount of blood pumped by the left ventricle in one minute so another way of thinking about this is It's the amount of blood that's being pushed into the systemic circuit in a minute's time or it's the amount of blood that's going out to the tissues of the body to provide those tissues with oxygen and nutrients in a minute's time here's a formula for calculating cardiac output so cardiac output which you'll often just see abbreviated as Co is equal to the heart rate which is the number of times that the heart beats in a minute times what's known as the stroke volume so stroke volume basically is the amount of blood that is pushed into the circuit with each contraction of the heart so the amount of blood that's moving basically from the left ventricle up into the aorta with each contraction is what is referred to as the stroke volume so what I want to do now that we've kind of defined what cardiac output is and we've come up with the formula for how calculate how you actually calculate cardiac output what I want to do is talk about some things based mathematically on this formula that can cause cardiac output to change so that can either cause increases in cardiac output or that can cause decreases in cardiac output so if you remember back to our formula for cardiac output cardiac output is equal to the heart rate times the stroke volume so effectively anything that changes the heart rate anything that changes the stroke volume is going to cause a change in the overall cardiac output if you think about heart rate this is really quite simple if the heart's rate increases so if it's beating more times in a minute because you're exercising or whatever you're going to see a corresponding increase in cardiac output if your heart rate slows down because you're not stressed you're relaxing you're asleep you're going to see a decrease in cardiac output and that makes sense because under stress or exercising can conditions when heart rate is higher your tissues need a higher volume of blood you need a higher cardiac output to be able to sustain the tissues in the organs of your body when you're under relaxed resting condition s we don't need cardiac output to be so high because the demand of the tissues for oxygen and for nutrients is not as high under those situations so those are heart rate's effects and they're pretty direct and I think a little bit more easy to understand we've talked about what stroke volume is basically that it's the amount of blood that gets pushed from the left ventricle into the systemic circuit with each contraction of the heart so anything that affects stroke volume is also going to be affecting cardiac output we've actually got a formula for calculating stroke volume so I want to talk about this formula a little bit because we're going to be using it as we continue on with this video so stroke volume is equal to what's known as the edv so edv is the end diastolic volume it's the volume of blood in the left ventricle at the end of diastole or at the end of the relaxation of the heart remember that it's during the relaxation that the heart is filling with blood so our edv or our end diastolic volume is going to be the volume of blood that's in the left ventricle at the end of filling this is going to be the highest volume of blood so stroke volume is equal to this edv minus what's known as ESB so if you look down here we've got our definition of ESB This is the End systolic volume systole is the time when the heart is Contracting so systole is the time when blood is being pushed from the left ventricle out of the left ventricle into the aorta so the volume of blood at the end of systole at the end of contraction in the left ventricle is our end systolic volume if you look at these pictures down here this kind of represents it a little bit more visually sometimes these collaborate sessions mess up my PowerPoint so we have an minus sign that's missing from here that I'm going to go ahead and draw in but our stroke volume is equal to in diastolic volume so that's the volume of blood in the left ventricle at the end of filling basically when the left ventricle is full minus the in systolic volume which is the volume of blood that's in The ventricle in the left ventricle specifically at the end of contraction and if you look down here you'll notice there's a little bit of blood that's still sitting down there in the left ventricle at the end of systole all of the rest of the blood that was here has been pushed up into the aorta so it's been pushed into the systemic circuit and that's our stroke volume so basically what we started with minus what we end up with is our stroke volume it's going to be the volume of blood that got pushed into the aorta or got pushed into the systemic circuit so because stroke volume is equal to the e DV minus the ESV anything that affects edv or ESV is going to affect the stroke volume and because it affects the stroke volume it's going to affect the cardiac output so I've got a list of three things on this slide that affect edv or in some cases ESV and because of that affects stroke volume and therefore affect the cardiac output so what I want to do with this slide is talk about what these three things are kind of Define them for you look at whether they're affecting ESV or EDB and then with the last slide we'll talk a little bit about how they're affecting edv or ESV and what effect that translates to with cardiac output so the first thing that I have on this list is the preload and I've got my kind of simplified drawing of a heart over here with some arrows drawn into it to represent which what each of these three different things are so the preload is blood that returning to the heart this is the blood that's coming in from the systemic circulation and from the pulmonary circulation into the heart this is going to be based on what's known as venous return so venous return is how quickly that blood is returning and there are situations where we see blood returning to the heart faster for example when you're exercising heart rate increases the faster that blood goes out to the body the faster it's going to come back to the heart and so venous return is increased under an exercising situation if you're resting if you're relaxed we're going to see blood returning to the heart at a slower rate maybe than what you would see under active conditions so venous return can change and venous return is basically what the preload is it's how much blood is returning to the heart if you think about what preload is okay by definition it's blood returning to the heart So the faster the Blood returns to the heart the more blood we're going to have in the left ventricle at the end of diastole the slower the blood returns to the heart the less blood we're going to have in the ventricles at the end of diastole so preload is affecting specifically the edv or the end diastolic volume it's affecting how much blood is in the left ventricle at the end of diastole or at the end of filling contractility is basically how strongly the heart is Contracting so if you look at these arrows over here you'll notice I've got these arrows that are just pointing inward they are meant to represent a squeezing of the heart which is really what contractility is it's how strongly the heart is Contracting if the heart contracts stronger such as under an exercise condition or under a condition of being stressed sometimes you'll start to really feel your heart pound that's when that contractility has increased and if the heart is Contracting with more force it makes sense that it's going to push more blood than it otherwise would out of the body if it's Contracting with less Force because maybe you're in heart failure or maybe it's just you're relaxing you're not stressed then it's not going to push push as much blood out of its Chambers and specifically out of the left ventricle as it otherwise would so what contractility affects is the ESV which you'll remember is the end systolic volume it's the volume of blood in the heart following contraction or in the left ventricle specifically following contraction and if that left ventricle has a high contractility it's going to push more blood out so your ESV is going to be less there's going to be less blood left in The ventricle after that heart contracts with a lot of force if your contractility has decreased maybe because of heart failure or whatever it's not going to be able to squeeze as hard there's going to be more blood sitting in the left ventricle following contraction and that means that that in systolic volume which is that volume left following contraction of blood in the heart is going to increase sure and you're going to see why I teach anatomy and physiology and not art here's my silly representation of a heart because it's the best I can do and actually that heart turned out pretty good I'm pretty proud um here is my representation of the left ventricle and also of the aorta coming up off of the left ventricle and you guys know that sitting in between the left ventricle and the aorta is a valve which is known as the aortic semilunar valve so that's right there afterload is back pressure on the heart and that's my dog afterload is back pressure on the heart so it's pressure that the heart is having to overcome in order to move blood from the left ventricle in the into the aorta one thing that you should know about blood is it always moves from an area of higher pressure to an area of lower pressure so if we want the blood that's in the left ventricle to move up into the aorta we've got to generate a higher pressure here in the left ventricle than the pressure that's in the aorta and if we do that if we generate a higher pressure down in here then we overcome the afterload and that opens up this valve and allows the blood to move from an area where we've generated a higher pressure into an area where there's a lower pressure afterload really starts to have its effects on the heart so this back pressure on the heart that the heart has to overcome to move blood from the left ventricle into the aorta it really starts to have its effect in hypertensive situations and I want to give you an example of why so let's say that a normal healthy blood pressure in the aorta is equal to 120 over 80. I actually don't even know if that's true that's normal for the brachial artery I don't know what it is in the aorta but it's going to be somewhere close to that if that's the case the normal blood pressure in the aorta is equal to 93 so that's our average if you're looking at that and saying hey that's not a straight average you're right it's not the way that we calculate the average blood pressure in a blood vessel is a little bit different and we're going to get into that in the blood pressure exercise but just trust me on this for now what that means basically is if the left ventricle wants to move blood up into the aorta and we've got a normal healthy average blood pressure of 93 through here and the left ventricle is going to have to generate a pressure of 94 to get that blood to move from the left ventricle up into the aorta so again that's under a normal healthy blood pressure situation let's say that somebody has terribly high blood pressure so we're gonna go with a situation where their blood pressure is awful it's 160 over 120 in that particular case the average blood pressure through here is 133 and what that means is our afterload has increased so there's much more back pressure on the left ventricle effectively in this situation what the left ventricle is going to have to do is generate 134 in pressure so that we have a higher pressure in The ventricle a pressure that's higher than what's up here in the aorta and that's going to in this high blood pressure or after tension situation allow us to move the blood from the left ventricle into the aorta basically what this means is the higher the blood pressure becomes the more back pressure the more afterload there is on the heart that means that the more the afterload increases the more that back pressure increase says the more we're going to see the heart having to generate a higher Force each time it contracts to move blood from the left ventricle into the aorta so that's why hypertension why high blood pressure even if it's just a little bit elevated is not good for the heart every time blood pressure goes up the heart has to generate more force with each contraction due to that afterload or due to the back pressure so here's the last slide that I want to talk about where we start looking at um uh how preload is affecting cardiac output how contractility is affecting cardiac output and how afterload is doing the same so I mentioned and here again is that little diagram the preload is the rate basically at which blood is returning to the heart so if preload increases maybe because you're exercising or whatever that's going to set up a situation where the edv is going to increase because blood is returning to the heart faster so the heart's going to fill faster edv increases and when our edv increases if you look down here at this formula if this number increases assuming everything else Remains the Same that's going to cause an increase in stroke volume and if you look at our formula for calculating cardiac output if stroke volume increases we're going to get an increase in cardiac output as well conversely if preload has decreased because blood is returning to the heart slower for whatever reason maybe you're sleeping maybe you're calm and peaceful if blood is returning to the heart slower then the heart is going to fill with blood slower than it normally would so in that case we're going to see a decrease in EDB if edv decreases assuming everything else Remains the Same we're going to see a decrease in stroke volume and that's going to lead to a decrease in cardiac output contractility you'll remember is the strength with which the heart is Contracting so that's going to affect our ESB if the heart is really Contracting with a lot of force maybe you're exercising maybe you're stressed your heart is pounding whatever when it's Contracting with a lot of force it's going to push more blood out of the ventricles than it otherwise would and in that case that means there's going to be less blood left in the ventricles at the end of systole if there's less blood left in the ventricles at the end of systole stroke volume increases because if that blood isn't in the ventricles that means it's gotten pushed out to the systemic circuit so stroke volume has increased and when stroke volume increases we get an increase in cardiac output if we have a situation where the heart's not beating with as much force so we've got decreased contractility then we have a situation where the heart's not squeezing as hard if it's not squeezing as hard more blood is going to stay in the left ventricle at the end of contraction and in that particular scenario because more blood staying in the left ventricle we're going to have an increase in ESV or an increase in the amount of blood in the left ventricle at the end of systole if ESB increases that means less blood is going into the systemic circuit so our stroke volume decreases when our stroke volume decreases you guys know cardiac output is going to decrease as well after load we've talked about so again that's that back pressure that we have on the heart that's represented by my little simplified drawing down there win after load increases there's more back pressure on the heart that means it's harder the heart has to generate a higher force in order to move blood from the left ventricle into the systemic circuit if that's the case if it's harder for it to move blood we're going to see more blood remaining in the heart at the end of systole and that's going to increase our in systolic volume when we increase the in systolic volume that's going to cause our stroke volume to decrease because in this case more blood staying in the heart less is actually making its way into the aorta the stroke volume decreases now we're going to have a corresponding decrease in cardiac output so remember after load increases with hypertension with more back pressure on the heart and you can see one of the effects of increased afterload of hypertension is that we get an overall decrease in cardiac output so the heart's working harder but the amount of blood that's actually getting to the tissues of the body to give up oxygen and nutrients to those tissues has actually decreased if you have high blood pressure and you're on a blood pressure medication or you don't have high blood pressure you've got normal healthy blood pressure then the afterload that back pressure on the heart is decreased and if there's not as much pressure resisting the movement of blood from the left ventricle into the aorta what we're going to see is that blood is going to move easier from that left ventricle into the aorta and that means there's going to be less blood left over in that ventricle at the end of contraction so if we have less blood left over because more of it was pumped to the tissues of the body we're going to see stroke volume increasing and when stroke volume increases we're going to see an increase in cardiac output as well