hello and welcome to the review of chapter 20 from Gaytan and the halls medical physiology textbook which covers cardiac output and venous return essentially just going over how blood moves around the body if you are feeling generous please feel free to like the video and subscribe it will really help out the channel and if your on neither of the textbook there is a link in the description so it starts off with some pretty basic definitions talking about what cardiac output is which is just the quantity of blood pumped into the aorta each minute by the heart so the quantity of blood out of the heart each minute and venous return must equal cardiac output so the amount of blood returning back to the heart should equal the amount of blood leaving the heart so you can determine the cardiac output of the heart by knowing what the venous return is and the cardiac output can vary widely depending on several factors such as that basically for body metabolism so if you have a higher body metabolism that means you have a greater local tissue blood flow which means your venous return is going to be higher and a higher target output whether someone's exercising so obviously if you're exercising you need a greater tonic output because you need more blood flow to your muscles your person's age so your cardiac output as you can see on this figure 21 your headache output increases up to a certain maximum at around 10 years of age and then it slowly reduces over time so the older you are typically the smaller your cardiac output becomes and then your size of your body so the bigger you are obviously the larger your cardiac output will be and remember one of the main factors contributing to cardiac or others your frank-starling law of your heart so the more blood that returns to your heart the greater stretch of your muscles the greater the contraction and the greater the cardiac output so that's the frank-starling law so if you have more venous return you're going to have greater cardiac output essentially and not only is this frank-starling law helping to increase contraction if you have a greater venous return you have some other factors here too such as if the sinus node stretches which is located within the right if that stretches then that will increase the heart rate automatically so the sinus nose will increase it's all the meta City but then we also have the Bainbridge reflex which is just saying that once the red atrium itself was stretched there is a nervous reflex which tells that cybers node to increase its heart rate so not only are we going to have an increased contraction due to the frank-starling law we're going to also have an increased heart rate as well now we've already talked about how the cardiac output is the sum of all local blood flow regulation so local blood flow determines what al qaida output is going to be so if we were greater local blood flow greater metabolism around the body then we're going to have a greater cardiac output and then that also relates to what we see here in Figure 24 and this is really talking about as we talked about in the last chapter how cardiac output is equal to arterial pressure divided by total peripheral resistance so if you have a reduction in total peripheral resistance you will have an increase in your cardiac output whereas if you have a increase in total proof for a resistance you have a reduction in your cardiac output and that's shown in this figure 24 here which we've already gone over last chapter but as you can see these disease states which have a lowered total peripheral resistance you have an increase in cardiac output and so in example here is hyperthyroidism where metabolism around the body increases your local tissue blood flows to all of your different tissues increases and your total peripheral resistance decreases because of the phaser dilation around the body and then that results in an increased cardiac output one of the factors that they don't touch on here is the kidneys role and their kidney as we talked about in the last chapter increases your blood volume so then you can accommodate this increased cardiac output and that's all to maintain normal arterial pressure now if you have an increased total peripheral resistance than your cardiac output reduces and once again that's all just trying to maintain normal arterial pressure now a cardiac output can be depicted in this little diagram here where we have a normal cardiac output curve showing that with a increasing right atrial pressure initially we do have an increased cardiac output which then plateaus at a certain right atrial pressure and if our right atrial pressure reduces below certain point we have a cessation of cardiac output because all of the major vessels collapse so we don't have any return to the heart they were to do talk about very briefly coming up here as well but as you can see if you have a hyper affective heart your cardiac output will increase relative to a right atrial pressure whereas if you have a hypo effective heart then your cardiac output cannot reach the same levels despite an increase in right atrial pressure and the factors that can create this hyper affective heart of increasing your cardiac output include nervous stimulation so sympathetic innovation to the heart which increases your heart rate and half contraction and then also hypertrophy of the heart muscle making that heart muscle bigger which occurs with increased workload so that's more of a chronic change so sympathetic change is more of an acute adaption whereas hypertrophy is more of a chronic adaption our things that can cause a hypo affective heart include increased arterial pressure and that's because the heart now has an increased pressure to public giimpse so it has a harder job of pushing that blood out of the heart we have inhibition of nervous excitation of the heart so inhibition of sympathetic nervous impulsive obviously decrease your effectiveness of your art methodological factors so if you haven't have arrhythmia if you have coronary artery blockages so you don't have blood supply to your heart anymore valvular heart disease congenital heart disease myocarditis which is just inflammation of the heart muscle and cardiac hypoxia so anything that's making that heart muscle not being able to do its job really is the the main key there that will cause an a hypo effective heart and in this little diagram here is just talking about how the nervous system is very important for being able to maintain normal arterial pressure and how they did this was giving this stroke dinitrogen all which causes massive fight that vasodilation around the body which obviously would increase our cardiac output but as you can see without nervous control we can't increase our cardiac output and our arterial pressure just plummets because our we have massive vasodilation which results in reduced peripheral resistance and then our arterial pressure is going to plummet because of that but if we do have nervous control our arterial pressure stays the same because we're able to increase our cardiac output so that's how important our nervous system is and it does that all through increased heart rate increase contractility and then also constricting our veins increasing our venous return and so helping with that frank-starling law to help contraction of the heart again now there are the conditions that can decrease our peripheral resistance we've already talked about these but arteriovenous fistulas or shunts so that's a almost can be thought of like a Popoff valve between your arteries and your veins so that greatly decreases your total peripheral resistance so that would once again increase your fingers returning cardiac output because you suddenly have increased blood flow straight into your venous system hyperthyroidism increasing your metabolism around your body decreasing your peripheral resistance increasing your venous return which increases your cardiac output and then also anemia which just reduces the viscosity of the blood so then you actually have an increased return to your heart but not only that you have a diminished delivery of oxygen causing local vasodilation so so vaso dilating all your local tissues resulting in local increased blood flow and if you have a low cardiac output due to decreased pumping effectiveness of your heart so if your heart's not working well as a muscle or if you have a decreased venous return so your decreased cardiac output from cardiac factors include this coronary blood vessel blockage so if your your heart's not that you're receiving a blood flow not receiving its nutrients and it's obviously not going to pump as well severe valvular disease so if you have a leaky valve and it's not pumping that blood out of the heart something's going backwards okay either this inflammation of the heart just making it work less effectively cardiac tamponade which means that is fluid or something within the pericardial space reducing its effectiveness it's actually filled with blood and in cardiac metabolic derangements so anything that's just basically telling the heart to not work as well as a muscle and they're all results in cardiac shock which means that we don't have enough blood flow around the body and all that goes into shock state now reasons for a decreased cardiac output due to decreased venous return and include a decrease the blood volume so if we don't have enough blood we're obviously not gonna be able to pump that around the body venous dilation so that will allow all the blood to just pull within the venous system and it won't return back to the heart obviously obstruction of large veins and that can occur due to large variety effectors such as just anything pressing against the veins but in there dominoe cavity or a tumor or maybe a thrombus increased tissue mass or decreased skeletal mess so with aging as part of the reason why cardiac output reduces because you actually get less mass to your body you know mainly through your muscles degrading and then also decreased metabolic rate of the tissues so hypothyroidism that can all result in a decrease venous return reducing your cardiac output now it also briefly talks about how intrapleural pressure plays a role in our cardiac output in a just our cardiac output curve and the main key point here is that if you have an increase an intraoral pressure and you will shift your curve to the right but if you have a decrease in intramural pressure your shift your curve to the left which means if you have a shift to the right that means you need an increased right atrial pressure in order to increase your cardiac output whereas if you have a reduction in you're unsure thorough pressure then at a lower right atrial pressure you will have a higher cardiac output so intrapleural pressure just shifts this curve to the left or the right so then here figure 29 it is a little bit confusing because it combines two factors here so a hyper affective heart which is causing that increase in the cardiac output curve and then also increased intrapleural pressure which is to the right where is this other one down the bottom here is a hypo affective heart which has shifted this cardiac output curve down and reduced intrapleural pressure which is shifted it to the left now venous return is another factor that we obviously have to talk about and there's a different graph altogether which we have to look at and it's three factors which affects the venous return to the heart so we have the right atrial pressure the degree of filling of the systemic circulation so I mean systemic filling pressure and then our resistance to blood flow between the peripheral vessels and the right atrium it's a really the best way to think about this is that if you have your heart here and you've got your right atrium do you mean systemic filling pressure if this is all your tissues what you need to see this blood back to the right atrium you mean systemic filling pressure is just the pressure yeah right and then your right atrial pressure is here and then your resistance is the flow back so if we just think about normal hemodynamics here our pressure gradient between this portion and this portion determines blood flow so your means systemic filling pressure if this is high that means that there will be a greater return back to your right atrial pressure and then if there's an increased resistance then you're gonna have a reduced blood flow back to your right atrium so remember this pressure gradient between the mean systemic filling pressure and your right atrium and then the resistance as well so if we haven't looked at that on the graph here you can see that our right atrial pressure is depicted on the x axis and our venous return is depicted on the y axis and then the point at which the right atrial pressure and the venous return had zero that is our mean systemic filling pressure because obviously if you do not have a pressure gradient between your systemic first your filling pressure and your right atrial pressure you will not have blood flow so a zero Venus so that's just going back to what we talked about here where if there is zero pressure gradient between these two we will not have blood flow which is zero venous return so if you have an increase that means systemic pressure you will then increase this value up to here because our pressure gradient has now increased to a certain point and now once the right atrial pressure reaches the same as the mean systemic filling pressure then we will then move our entire slope all the way over to the right and that's depicted over here and figure 2012 here we're gonna just jump around a little bit as we explain this but so foul means the filling pressure increases then our right atrial pressure has to increase and all the for venous return to become zero so our entire curve moves to the right whereas if our systemic filling pressure decreases in venous return will be zero at a much lower right atrial pressure so I'll shoot curve shifts to the left and if we go into the different components of the actual slope itself we have a increase in venous return and is our right atrial pressure decreases up until we get around about zero millimeters of mercury from a right atrial pressure then that starts to plateau and this transition zone and then eventually we're going to have a cessation and an increase in venous return so we have this plateau mainly because granted negative pressure we will actually have collapse of our main veins within our thoracic cavity because all that negative pressure is just gonna collapse those veins so we can't actually increase our furnace return anymore with an increased negative pressure so that's why there's a plateau at this point now if we go back to our systemic filling pressure so now we have two factors they're influenced our main circulatory filling pressure one is blood volume and add volume with an increase in blood volume we're gonna have an increase in our main circulatory filling pressure so if we just only look at the red line here a figure twenty eleven then you can see an increase in volume so an increase now x-axis will directly result in an increase in mean filling pressure so the factor alone or increase out means circulatory filling pressure which means that we shift our entire venous return curve to the right and now another factor as well as our sympathetic innovation and sympathetic innovation as we know about causes vasoconstriction of our arteries and baicao constriction of our veins as well so that vasoconstriction is going to increase our pressure within those vessels so with an increase in pressure within those vessels we're going to shift this curve to the left here where a smaller amount of volume will result in an increased pressure so sympathetic stimulation increases our main circulatory filling pressure so moves it over to the right so those are our two factors that can increase our venous return by shifting the entire venous curve to the right is increased blood volume and increases sympathetic stimulation now one other fact that we have to talk about here is resistance to venous return remember resistance is something that's going to stop our blood flow so that's going to reduce our venous return now this can get a little confusing but the best way to think about this is that the venous return is going to blunt our curve so if you increase your resistance you're going to make it lower yeah as shown here to figure 2013 whereas if you reduce your resistance you're going to actually increase your curve it's not going to shift your circulatory filling pressure because that's going to stay the same because this stool that pressure gradient between the systemic filling pressure and your right atrium all it's going to do is reduce your actual blood flow so that's going to alter but the degree of your gradient of your venous return curve you may get confused thinking that sympathetic stimulation which will increase your resistance so you would think that that would reduce your venous return the factor that moves your system at feeling pressure to the right actually has a greater influence in the resistance that it supplies so although you have a shift to the right your slope will still so out but you'll still have an increase in your venous return and that's shown all the way over here at figure 2016 where this green line is sympathetic stimulation and you can see that the filling pressure has been moved over to the right and the curve has been flattened but it's still greater than normal so that's the effect of sympathetic stimulation and how resistance plays a role so if you increase your resistance you've Bloods your curve if you reduce your resistance you make the curve much higher now if we put these two curves together our cardiac output curve in our venous return curve then we have a point at a which is our equilibrium point and that's just showing that our cardiac output matches our venous return so a right extra pressure is zero now cardiac output venous return is around about 5 liters per minute oh so good 2016 here puts in to effect these two curves our sympathetic stimulation and really that's going over and summarizing everything that we've talked about so if you have a normal patient you have this red line here and this red venous return here a is our point at which which is showing orthotic output RL liters per minute blood flow now if we will increase our sympathetic stimulation we what do we do we increase our cardiac output curve right so that goes all the way up to this green dotted line but not only that we increase our systemic filling pressure because we have caused phaser constriction but then we also blunt the curve because we've increased resistance so then we end up with the point D where cardiac output has increased to 10 liters per minute maintaining our right atrial pressure at zero so it's sympathetic stimulation ultimately increases our cardiac output increases our venous return increases blood flow around the body and then they talk about spinal anesthesia which just blood cells sympathetic response so filling pressure reduces we get a reduction in katic output and you know we are only moving around say 3 liters per minute so blood flow around the body reduces now if we get even more complicated we'll talk about what happens if you create an arteriovenous fistula so if you create that what are you going to do you're instantly going to reduce your resistance dramatically because you're creating a Popoff valve and you're just creating a shot between your other in your vein so since you've dramatically reduced resistance what does that do to our venous return curve initially we don't do anything to assist ohmic filling pressure because we haven't altered anything there what we do is we increase that slope to our venous return so suddenly we've gone from a all the way up to B so we create this mess of venous return and then over time as our blood volume increases and how sympathetic nervous system kind of kicks in our cardiac output is going to increase as our blood volume increases and with an increased blood volume and a sympathetic response then we get a movement to the right as well so our systemic filling pressure increases moving the entire curve to the right our resistance stays low so we still have this increase in slope and our cardiac output increases because of the sympathetic stimulation and also increased blood volume obviously the sympathetic stimulation is the acute response which is shown here and that Browns other clients whereas the increased blood volume is the chronic response which is the green dotted lines and we've touched on those in the previous two chapters which talked about acute and long-term control blood pressure now lastly here we talk about how we can actually measure cardiac output and really the key here is just to memorize these equations now understanding how it works is is definitely important but the equations really just give us the key here now we have two methods the Fick method and the indicated dilution method and the third method is just really understanding that there is a certain amount of oxygen that gets absorbed in the pulmonary circulation and we can determine the cardiac output if we know what the oxygen concentration is before the intensive pulmonary circulation so in the right heart and then what it is after it leaves on the left had or that Tyrael system and if we know what that oxygen content is so the moles of oxygen who liter and we also know how much oxygen is absorbed minutes to mils per minute and we can divide our oxygen absorbed permanent by the lungs by out the difference between the oxygen concentration so oxygen and that arterial system - oxygen and the venous system which in this example is 40 so 200 - 160 then if the oxygen absorbed by the lungs moles per minute which in this example is 200 then 200 divided by 40 equals 5 liters per minute so we have 5 liters of blood moving through the body which is our cardiac output and this is really calculating the rate of oxygen absorption by the lungs and in the clinical situation you can measure this by getting a blood sample from ideally the right atrium or the venous blood and then the arterial blood so then you can get your difference and then you can get your rate of oxygen absorption by the rate of disappearance of oxygen from the respire ear using an ox any oxygen type meter and then the second one is the indicator dilutive method which is shown here in this diagram where you inject a little bit of indicator you take blood throughout time and you can see when the dye appears and starts that disappeared now obviously as it recycles around the heart then it reappears again so we see this plateau here is that sad and go around the heart so you have to kind of correlate this down and see where would have gone if it didn't recycle then you just calculate the area under the curve to see what the cardiac output is and that's by seeing the milligrams have died ejected times 60 you can't to convert seconds into minute divided by the average concentration of diet and each millimeter of blood for the duration of the curve times the duration of the curve and seekin so that's getting the area under the curve so the milligrams of time injected per minute divided by the area under the curve that's how you calculate cardiac output and that summarizes our chapter for today I hope you enjoy that feel free to drop a comment otherwise we'll see in the next chapter