Cardiovascular | Cardiac Output

our ninja nerds in this video we're going to talk about cardiac output so how do we define cardiac output cardiac output is basically your heart rate multiplied by your stroke volume so let's go ahead and dig into that a little bit more because we're going to go and talk about this in a pretty good detail so first off we're going to say that cardiac output we're going to kind of denote that a CO ok cardiac output CO is equal to your heart rate razón is HR multiplied by your stroke volume okay so what do we know so far we know that the cardiac output is equal to the heart rate multiplied by the stroke volume let's go ahead and dig into this little equation tiny bit more and kind of get a little bit more of an idea of what cardiac output is well first off we need to look at heart rate what's the units for heart rate the units for heart rate is actually going to be in beats per minute so it's in beats per minute whereas stroke volume is the total volume of blood that the actual ventricles are ejecting for every one beat okay so heart rate is the amount of beats that are occurring per minute stroke volume is the total volume of blood and milliliters that is being pumped out of the ventricles with one beat so if you look at it the actual beats cancels out what are you left with here milliliters per minute now let's even get into this a little bit more so we know that cardiac output is a total volume of blood that's being pumped out of the heart within one minute how much is that what's the normal amount well it takes an average heart rate in the average stroke volume so then we have to say okay cardiac output is equal to the heart rate what's the normal heart rate what's somewhere in between 60 to 80 beats per minute right on average let's take in between let's say 70 beats per minute okay and let's multiply that by the stroke volume on average stroke volume happies to be around 70 milliliters and we'll see how in a second so let's say that's about 70 MLS alright per beat when we multiply these two 70 times 70 is about what 4900 right let's round that up let's just round it up to about five thousand what five thousand milliliters per minute so it's approximately about 5,000 MLS per minute which if we just kind of like change that to a little easier number five liters per minute so what do we know so far cardiac output is equal to the heart rate times the stroke volume it's actual units is the total volume of blood that can pump out in milliliters per minute that volume is generally on around five liters per minute but you know that we can increase that significantly during certain situations like an exercise or we can decrease it certain significantly due to parasympathetic innervation or other different types of things that we're going to talk about in this video okay so now we got a good idea of what cardiac output is for right now let's go ahead now and decipher heart rate and decipher stroke line so over here on the left side we are going to primarily talk over here about heart rate so this this side over here is going to be primarily focused on heart rate what we need to do is is we need to talk about what things influence heart rate and again what's the units for heart rate it's right around beats per minute and we said it was an average we said that there was an average heart rate that average heart rate was somewhere around 60 to 80 beats per minute right within that range right we can even bring it up a little bit more we can actually say that normal heart rate is in between 60 to 100 and time you go greater than 100 then it actually is considered to be tachycardia but for right now I want to talk about this one the reason why is who sets this 60 to 80 beats per minute who sets that that is the job of the SA node so if you guys remember the SA node is the one who is setting what's called your sinus rhythm so he's the one that setting the sinus rhythm he's the one that's generating those what he is the one that's generating those intrinsic abilities the action potentials that can be sent out throughout the heart so he is the one that's generating this nice rhythm he's generating the sinus rhythm which is right on 60 to 80 beats per minute now here's something we have to think about we know that the heart has the ability to intrinsically depolarize generated action potentials and send it out to the myocardium to trigger the myocardium to contract and that's right around 60 to 80 beats per minute but how can we increase that how can we fluctuate that heart rate well one way that we can do that is we can actually cause the production of sympathetic nervous system neurotransmitters well one way is the sympathetic nervous system you know the sympathetic nervous system is basically the one that is releasing certain chemicals what are those chemicals and it's releasing remember it's releasing norepinephrine so norepinephrine was one of the big ones they're acting on the beta-1 adrenergic receptors what was another one another one was epinephrine remember epinephrine epinephrine was actually released by the adrenal medulla and this also was influencing the heart rate by acting on the beta-1 adrenergic receptors we already went through that mechanism and extrinsic innervation of the heart so what kind of action would did we say it had if I draw here a positive what does that mean it means it's a positive effect er of the heart rate meaning that it can increase the heart rate that's called chrono tropic action so really what is heathen he's a positive chrono tropic agent so your sympathetic nervous system is a positive chrono trophic Asian it can increase the heart rate that's one thing but let's take the flip side let's say that I want to decrease the heart rate if I want to decrease the heart how do I do that well then I can actually target this with acetylcholine remember acetylcholine is a part of the parasympathetic nervous system so if it's a part of the parasympathetic nervous system this is releasing acetylcholine on to those muscarinic type 2 receptors if you remember which was causing the potassium ions to leave the cell causing the cell to hyperpolarize it was also him inhibiting the production of cyclic GMP and basically causing the cell to slow down the rate of action potentials so this is a negative crew know tropic agent so so far we know that the sympathetic nervous system is a positive Crona tropic agent the acetylcholine which is a part of the parasympathetic nervous system is negative current replication what else so so far what do we have here let's write these down here we have a positive one a positive stimulator is the sympathetic nervous system a negative regulator or a negative chrono tropic is the parasympathetic nervous system via the acetylcholine so this is the acetylcholine and then the sympathetic nervous system was with the presence of epinephrine and norepinephrine so norepinephrine and epinephrine sweet what else hormones hormones also have a very positive effect too you know there's a special hormone who also can come here and actually increase the heart rate too let's actually share this guy like this look right there this guy is called thyroid hormone so t3 and t4 these also are a very powerful regulator very very powerful regulator of the heart rate and they can increase the heart rate okay they can increase the heart rate okay so so far we have hormone so what's another positive regulator of this we're going to say thyroid hormones are t3 and t4 this is a good one you know what else t3 and t4 can actually do they can increase your basal metabolic rate when you increase your basal metabolic rate what does that do what's the what is one of the byproducts of metabolism heat as you start generating a lot of heat what does that do it amps up your metabolic rate so you're actually breaking down substances a lot faster as you start breaking down substances a lot faster you generate more energy you generate more heat so it speeds up the metabolic rate that's another thing about t3 and t4 whenever you have an increase in the internal body temperature whether it be to the t3 and t4 whether it be due to exercise because you know during exercise you generate a lot of heat that amps up your metabolic rate so one of the other things that we can say that actually is going to affect the heart rate here is we can also say it could be body temp okay we can say the body temperature is a huge regulator okay generally if you want to stimulate it you want to have an increase in the body temperature if you want to slow down the heart rate okay so whenever your increase in the body temperature this is increasing the metabolic rate okay so again whenever you increase the body temperature this is going to stimulate and increase the metabolic rate increase the speed of the actual heart rate so again what we say here if you increase the body temperature this is another positive cronut replication of the heart now let's talk about something else we're not ions ions are very critical here well what kind of ions are really important in this area you know there's a calcium calcium is super important calcium is a very important regulator you know whenever you have calcium levels there's two situations I'd say that you have high calcium levels and let's take that the opposite of this and let's say low calcium levels so calcium is a very important regulator of the heart rate if you have high calcium levels this tends to speed up the heart rate there is conflicting evidence on this but for the most part most literature supports that it's going to be hypercalcemia drives an increase in the heart rate because more calcium is coming into the cell triggering the increase in the actual depolarization and the action potentials sent out to the heart muscle so that's one thing so really we can actually let's separate these let's say that this one here is actually the high calcium so high calcium would do what it would act as a positive chronotype engagement but let's take the actual opposite and let's say that we have low calcium levels low calcium means that less calcium is coming in from the extracellular fluid this is going to be a negative Crono tropic agent okay so so far we have calcium being in effect there what else potassium potassium as another has another influence on the heart rate so if we have potassium let's say that our blood is really high in potassium what do you call when they have high potassium levels in the blood be called hyperkalemia what happens is imagine here for a second I draw a cell let's say I draw a small cell here and I just want you to understand something just about to sell our cells are basically filled with a ton of potassium and if you have a blood vessel circulating nearby here let's say here's a blood vessel and circulating nearby and the potassium levels are higher out here in the extracellular fluid and lower here in the cell what's going to happen it's not going to move against it's not going to move down as concentration gradient it's going to have to move against it that means less potassium will leave the cell why is this so bad because this can actually cause the heart to go into cardiac arrest so hyperkalemia is very very very dangerous okay that's one of the really really important regulators here is that high potassium levels can significantly negatively inhibit the heart rate it is one of the more important ones because it's going to affect the heart from being able to send action potentials and cause a person to go into cardiac arrest and the same thing though other other things that actually get affected is the low potassium low potassium loss of the potassium to leave more quickly and so again potassium ions can actually cause arrhythmias okay so any change in these ions can have negative negative effects um they even say you know what else is really weird here so what else do we have here let's actually put over here just in general we said that if we have high potassium levels high potassium levels are going to be a negative inhibitor they're going to be an inhibitor right and if we have high calcium levels high calcium levels are going to be a stimulator we've said that if we have low calcium levels low calcium levels is going to be an inhibitor now this something else is kind of interesting let's stay here I draw quickly the another component which is going to be right here let's say that I have here the aorta so here's it just a little small order here and you know coming off the aorta you have what's called the brachiocephalic trunk which splits into the common carotid which goes into the subclavian and then this common carotid here right which splits into the internal carotid artery and the external carotid artery right there at that bifurcation point we have these specialized cells right here what were these cells here called they were called the chemoreceptors they were chemo receptors there were some there and there were also some here whenever our partial pressure of oxygen is really low or the partial pressure of co2 in the blood is really high or our pH is really low it stimulates these chemo receptors and what do these chemo receptors do they carry this information to a central nervous system and when they take it to the central nervous system what is the central nervous system do it integrates that information right within the medulla and tries to increase your respiration rate but you know what else can do let's say here I have a small little cross-section here of the brain just a small little one here and I draw here like this here's my midbrain here the pond here's the medulla and here's the spinal cord real quick right right here what will happen is these chemo receptors will take the information into the medulla and in the medulla we have that nucleus of tractus solitarius right what will happen is he can stimulate the cardiac accelerator as a result over the cardiac accelerator do it'll send out these impulses to what it'll send out the impulses to the heart and what would try to do to the heart it'll try to result in an increase in the heart rate because going to have sympathetic effect okay so once you guys to realize what is another a factor of this any type of situation which there's hypoxia there's an increase in the partial pressure of co2 there's a decrease in the pH they can activate the chemoreceptors and try in an attempt to increase the heart rate but again it's not a significant of effect as it is on respiration okay because really the more powerful effect that you need to realize as it goes to the respiratory centers and these respiratory centers go to your actual lungs and then try to do what increase the actual respiration rate and the depth just so we're clear this is the more potent effect all right but there is a minor effect here for the heart rate so what can we say them we can say stimulation of these chemo receptors these peripheral chemoreceptors due to some type of situation where there is a decrease in the oxygen increase in the co2 decrease in the pH these things can try to increase the heart rate so again we said stimulation of peripheral chemoreceptors will act as due to what what are the stimuli here low partial pressure of oxygen increased partial pressure of co2 and a decrease in the pH these aren't going to get stimulated here and they do what to the heart rate they stimulate guards so stimulation to the peripheral chemoreceptors due to these things stimulate an increase in the heart rate okay all right sweet deal so we covered that now I want to talk about something else what about just general things what about me being like generally like I said that a child what about a child's heart rate in comparison my heart rate so you know fetus the fetuses have an extremely extremely fast heart rate their heart is pumping like no other so when you talk about age age is also another factor so let's compare here and we were to compare let's say that we have like a fetus or an infant so fetus you know / infant they have super super high heart rates okay so they can go from like 120 or 140 beats per minute okay that's like the fetus they let's take like adults again adults should range adults should range anywhere from 60 to about a hundred beats per minute that's a good range for it now let's even get into this a little bit more adults obviously there's two different types of sexes right hopefully there's going to be males and females so if we tilt look here and we spread split this out let's say that we look here at males and we look here at females what's the difference here do you know that females actually have a faster heart rate so females heart rate ranges because we said it's between sixty to a hundred well really if we take the intrinsic ability it's really eighty anytime you go above 100 is tachycardia so males they have a kind of a slower heartbeat theirs is right around 64 to 72 beats per minute and again this is our rest we talk about females there's a little bit higher there's can go from about 72 to 80 beats per minute okay so there's a little bit higher than ours lasting I guess it's like the circle of life so therefore the fetus in the infant it's really high for the adults it's kind of low we're going to write it within this age and certain as you start to get a little older as you get a little older and actually can go back up sometimes there's this fluctuate this obviously varies but generally there's can actually increase a little bit as you get older okay so that's kind of the factor of age so we said that with age fetus has a very high heart rate adults we can say they try to keep a heart rate around 60 to 80 beats per minute but and females okay I'm sorry males so right around 64 to 72 females is a little faster 72 to 80 PS per minute okay so we talked about that Wow a lot of things that are affecting the heart rate isn't there significant amount of things now last thing I want to talk about is what is this thing that we talked about with tachycardia and stuff so there's two terms that we need to get straight here what is called Brad Acharya Brad Acharya which is basically defined as whenever the heart rate is less than 60 beats per minute so this is a situation in which the heart rate is less than 60 beats per minute it's a terrible situation right for certain things what could be causes of bradycardic it could be many causes of brennick kardia it could be due to a comparison but that ignorance is though is activated there could be due to other things such as certain drugs certain drugs could even slow it down could be due to another thing you know really weird in endurance rather runners people who run excessively they put their heart through a lot of work it's kind of a good thing in a way but as their actual they're actually exercising they're doing these long endurance act activities the heart that's getting really strong very very strong and so it doesn't require as much high of a heart rate because their stroke volume and their actual cardiac so you know let me explain like this we know that cardiac output is dependent upon heart rate stroke volume because these endurance runners are working so hard okay so these endurance runners people who are doing like marathons and stuff we can split up cardiac output we set in to heart rate times the stroke volume these people their stroke volume is so high why because the myocardium is really strong they're having good preload they're having good contractility so for these people to have good a lot of preload and a lot of contractility that's increasing their stroke volume because of that the heart rate can slow down because the stroke volume is taking over the primary effect of cardiac output so we can bring the heart rate down a little bit okay so to allow the heart dello allow for the heart to have time to rest so again cardiac output we said is depend upon heart rate and stroke volume and endurance activities people who are doing this consistently their heart rate will start to drop really really low because their stroke volume is so high because their myocardial is very strong okay so that's something you might see in people who are bradycardic but then if you take the opposite side of that you take someone who's actually going to be on the opposite scheme so now we see that the person is tachycardic so now that we said that the person has tachycardia in other words they're having a heart rate that is greater than 100 beats per minute and obviously that could be mini cause of this could be sympathetic nervous system activity could be due to high T 3 and T 4 could even be due to certain drugs could even be do it like anxiety so certain types of emotional factors you know every you know if you ever notice someone who's having like certain psychological disorders are very anxious they have a very very very fast heart rate okay okay so that covers that part for heart rate now what I want to talk about is I want to go into the actual stroke flow I'm going to talk about stroke volume loads so let's come over here now let me get all my markers over here let's make this nice and colorful alright now we're going to talk about stroke volume so we said that Shrove volume is basically what do we say we say it was basically the milliliters that is being pumped out of the ventricles per beat well let's actually dig into this a little bit more so there's actually an equation for stroke fully there's actually an equation the equation for stroke volume is you can take the total volume of blood that's coming to the heart and filling the heart so let's say that I have blood coming from the inferior vena cava I have blood coming from the superior vena cava and I have blood coming from the coronary sinus and emptying into the right atrium I have blood coming from the pulmonary veins from the right side and the left side and these are emptying into the actual left atrium and then it's emptying into the ventricles as a result right whenever the atria undergoes systole they push it down but if you remember we talked about this in cardiac cycle about 70 to 80 percent of the blood passively flows down without contractile activity so that the blood is sitting here in the heart just accumulating there right so the Bloods just sitting there in the heart and accumulating that volume blood that is sitting in the heart for the heart even contracts during the relaxation prayer when the heart isn't diastole this is called the end diastolic volume okay on average the EBV is approximately around 120 mill years it could range from out 120 to 140 we're going to put down 120 fright now okay then if I take the EBV and I subtract it from what's called the ESV so how do we define edv once you actually write this out IDI V is defined as end diastolic volume okay so EBV it's basically defined as the end diastolic volume I like to think about it as basically like the pre pumping volume so it's the volume of blood that's in the heart before your ventricles are going to contract so e DV is basically the end diastolic volume ESV stands for end systolic volume so this is the volume of blood that's remaining in the heart after the ventricles are contracted or undergone systole so let's say after this you take the blood and you eject it up through into the pulmonary trunk and out to the lungs or you eject the blood from the left ventricle up into the aorta and onto the actual peripheral and systemic circulation the blood that's remaining so we said originally let's say it was like 120 now let's say that we just decrease this a little bit now the amount of blood that's sitting in here after that time so less blood now you're right that volume of blood that's remaining after the contraction is called es e this is on average about 50 milliliters it can range from 50 to like kinda like 70 so now what I'm going to do is I'm going to take and subtract this so if I take and subtract this that's my stroke volume my stroke volume is equal to 120 minus 50 at 70 so 70 milliliters okay and then again how much per beat so this is what we can say is equal to the shrill voice now we've got even going to a little bit more depth unfortunately because now we can actually say the stroke volume is divided into three other subcategories so let's say that we take stroke volume and we divide this take stroke volume here and I'm going to take and divide stroke volume into three categories let's actually bring it down here so we have plenty of room here I should bring it down here so go right here show volume is actually broken into three categories one of the categories is called preload this is your stroke volume one is dependent upon preload the other one is dependent upon what's called contractility so contractility and the last one is dependent upon a term called after load after load all right let's go ahead and decipher each one of these things and what effects then how that effects trial going and how that affects cardiac output okay so first off preload how will we define preload preload is basically the degree of stretch of the cardiac muscle so we can really just the simplest way of defining preload is how much the actual myocardium of the heart is stretching when it's getting filled with blood okay that's how we define preload so we can really just say that this is kind of like the stretch of the heart so the stretch of the heart more stretched the more preload there is the less stretch the less preload it is okay well how do we stretch the heart out how do we do that get a lot of volume in there so what's the volume of blood that's accumulating in the heart one the heart is actually in diastole or relaxation edv in diastolic volume the more that I have the more it's going to push on the hard stretch the heart and that's going to increase the preload okay so one of the things I can say right away for this is if ie create increase my in diastolic volume I'm going to increase my prelim when I stretch the walls even more okay well that leads to a next question how in the heck do I increase my end heist I like volume one way that you can do it is to get a lot of venous return what is that you know how we actually have here let's say I make a tiny little heart here real quick tiny little one okay let's say here okay I have let's say I have here this vein here this is my inferior vena cava right inferior vena cava let's say down I have some veins in my legs here I can do veins have valves we talked about this in blood vessel characteristics we said that veins are very low pressure though these are low very low pressures they have a hard time being able to get blood up on their own so one of the ways that we can increase that is you know we have some muscles nearby and we can actually have these muscles we said contract and when they contract they squeeze on the veins and help to pump some of the blood upwards we call that that muscular milking activity right we call the milking activity sounds weird but that's one of them one of the ways that we can increase this venous return is by increasing the muscular milking that's one way another one whenever you're breathing let's imagine I taking some good breath right I'm changing my thoracic cavity volume and I'm changing my abdominal pressure so whenever you're breathing during that breathing process the abdominal cavity pressure actually goes up and that compresses some of the veins in the abdominal cavity when you're breathing your thoracic cavity volume is going to increase so the pressure in there is going to decrease so what did I say abdominal cavity pressure is going to increase thoracic cavity pressure is going to decrease what happens is when kind of think it like this let's say that I actually get rid of no let's say I make another little heart here another little heart here and let's say I kind of do like this right here okay let's say here is actually going to be where my diaphragm is let's say here's the diaphragm the pressure in the abdominal cavity is going to be very high so high abdominal pressure but the thoracic cavity pressure above the diaphragm is going to be low where do things like to move on up of TBB the thoracic cavity pressure so the tcp if this is high things like to go from high pressure to low pressure so what it does is it sucks the blood upwards if it sucks the blood upwards it's kind of acting like a nice little vacuum or pump that's called the respiratory pump so the respiratory bump is pump is whenever you're breathing you increase the abdominal cavity pressure decrease the thoracic cavity pressure and suck blood up like a vacuum and that helps to increase the actual respiratory venous return here sorry so this would be the respiratory pump another thing is your sympathetic nervous system they have control over your vino motor tone so your sympathetic nervous system can actually come over here and do what it can act on the smooth muscle in this area by releasing what chemicals Norrell epinephrine and this can actually stimulate the contractility the smooth muscle to cause a small little increases in the contractility to push the blood upwards so we can also say another positive regulator of this is going to be what's called Vino motor tone Vino motor tone or just Vino constriction so we can actually sub classify this as Vino constriction so this is kind of helping to squeeze some of the blood upwards alright one more thing is the filling time that's the other that's important if you don't give the heart enough time to fill with blood that's not going to stretch the heart so giving the heart adequate time to fill with blood what does that mean then you really this is where that heart rate thing can actually be very very devastating if you have an increased heart rate you don't give the heart enough time to fill with blood because you just keep causing it to push and push and push as much blood as it can out it's not relaxing enough so because of that if you increase the heart rate to lunch that can actually decrease the actual filling time and if you decrease the filling time you're going to decrease your actual preload okay and that's that's not good okay one other thing is just related to the stretch what if you actually what if your heart can't stretch very well because of myocardial infarctions so let's say that for whatever reason you've had many myocardial infarctions mi what happens to the heart muscle it gets replaced with fibrous tissue does fibrous tissue stretch very well not really it's not doesn't have a lot of give so because that it's going to affect the preload so that's what we know about preload we know that preload is the stretch of the muscle if there's an increase in the EDB do to increase venous return from muscular milking respiratory pump vino motor tone right or there's a lot of there's enough time to fill the heart so you're going to have to increase the diastole by doing that you're not going to want to have the heart rate too high because the heart it's too high it doesn't have enough time to fill with blood and the last thing is you want the heart to be healthy you don't want it to be not able to stretch so you don't want there to be a lot of fibrous tissue from Mis all right it covers that thing last thing I want to relate with this is a law and laws are important okay well those are important this law here is a really important law let's actually make it a different color this law is related to this it's called Frank starlings law and what Frank starlings law says is that whenever you have an increased stretch on the heart so whenever there's increase stretching of the heart it allows for this link tension relationship more cross-bridges to be active so whenever they're stretching of the heart and there's optimal cross bridge connections that increases the preload if you increase the preload you're going to significantly increase the stroke volume so Frank's darlings all the heart just in basic like terms here says the greater the stretch the greater the force of contraction so how will we say Frank starlings law just to sum it up here greater stretch there's more cross bridges and the more cross bridges with an optimal length is the best greater stretch equals greater contraction that's the relationship between this so greater the stretch the greater the actual force of the contraction all right sweet deal that's that part next thing we have to talk about is contractility contractility is super super crucial this is a really really important one so one of the things about contractility is that we can actually say that contractility is actually dependent upon one of the big things is the sympathetic nervous system so contractility is super super dependent upon the sympathetic nervous system how because if you release the chemicals like epinephrine and norepinephrine what are these guys doing they're acting on those beta-1 adrenergic receptors if they're acting on these beta-1 adrenergic receptors what was their overall effect they were increasing the calcium levels in the cell as you increase the calcium levels in the cell what starts happening to the actual cross bridges they increase this increases the actual contractility so you're going to have more frequent contractions and that increased the stroke volume what else hormones same thing but this is interesting some people kind of get like a little messed up with as well let me get this over here so we don't confuse this way okay so we know that don't know if a nephron acts on the beta-1 adrenergic receptors and basically increase the calcium which increases the contractility okay hormones are an important one what kind of hormones t3 and t4 these guys are crucial but how do they do it this is a real weird one um probably talked about in the thyroid hormone video but what happened to let's say I have a cell here let's say that's a myocardial cell and let's say here's my t3 MIT 4 okay and it comes into this cell and it acts on a basically an inter nuclear receptor and when it binds on to this entry nuclear receptor it stimulates these genes and what these genes can do is they can produce a bunch of different types of proteins one of the proteins is it increases the expression of those beta-1 adrenergic receptors so t3 and t4 can act on the myocardial cells by increasing the expression of beta-1 adrenergic receptors so that's a beautiful thing if you have more of these you have more receptors for norepinephrine and epinephrine to bind to if they bind on to this they're going to have a more amplified effect okay so that's one thing another really interesting one is glucagon glucagon also has the ability to do this too so increase in the actual glucagon so glucagon can actually also increase the extra contractility something else here is drugs obviously certain drugs can do this - like digitalis digitalis actually has that effect dopamine has that effect epinephrine has that effect there's so many different drugs here epinephrine I'm not even gonna try to spell that because I always butcher that one I'm going to put a P okay so you guys get it there's a lot of different types of drugs that you could use here you can even use what's called dobutamine and isoprene alene there's a lot of different drugs here atropine but these are trying to increase so I'm going to put here on the side here they're trying to stimulate the increase in contractility their various different mechanism like digitalis is a sodium potassium ATPase inhibitor which increases the calcium levels inside of the cell dopamine he actually works through different weird ways dope dobutamine actual in the beta-1 adrenergic receptors and atropine actually blocks the acetylcholine on the m2 receptors basically it's trying to increase the calcium levels inside of the cell to increase the contractility but at the same time you have to have those that oppose alright so you even have those who can block certain channels you can use beta blockers okay like metoprolol Atena law or Pannalal you can even use calcium channel blockers and these calcium channel blockers you could use like verapamil you can use the Atty as in the FATA pean so calcium channel blockers are also really good ones too okay there's a ton of different things that you could use to try to be able to inhibit the contractility alright sweet so these guys here are inhibitors so beta blockers and even some calcium channel blockers right alright so that covers that part now one other thing though is ions are neurons also have an effect here too so ions it's kind of interesting here we could say same thing here things like calcium if you have increasing calcium levels this is actually a stimulator because there's more calcium that's going to be coming into the cell if there's less calcium hypocalcemia this is an inhibitor of contractility if there's actually high amounts of potassium this is actually an inhibitor of contractility and if there's high amounts of sodium hypernatremia this is actually inhibitor of contractility so certain situations ions can actually have a negative effect here too you know what else has a really negative effect protons and acidosis so when someone has really high amounts of protons during acidosis this is also a very very powerful inhibitor of the actual heart the contractility leads me to another term whenever you're trying to increase the contractility of the heart it's dependent for what's called inotropic action so if something is trying to stimulate the contractility of the heart they're called a positive inotropic agent so for example calcium is a positive either adentro application if it's in high levels epinephrine or epinephrine or positive inotropic agents t3 and t4 and glucagon de positive inotropic agents digitalis dopamine dobutamine a scorpion epinephrine all those guys are positive inotropic agents but things like beta blockers or calcium channel blockers or other different types of drugs those are negative inotropic ages and if you think about like this potassium high amounts of potassium is a negative inotropic asian high amounts of sodium is a negative inotropic agent high amounts of protons like acidosis is a negative inotropic agent okay I think we'd be the dead horse therefore the inotropic agents let's go to the last thing here let's bring afterload over here a little bit okay let's bring us afterload over here a little bit so afterload is kind of a really interesting one because it has a lot of clinical relevance here too because this is one of the common things that people suffer with a lot is a hypertension means that they're going to have a lot of afterload coming up so if we come over to this last one this last one here that shows how do we define after load after load is basically defined as the amount of resistance that must be overcome in order for what in order for the ventricles to eject blood into the actual a order or into the pulmonary trunk so for example here let's say I draw another little mini heart here real quick here so have another little mini heart here and I show it like this let's say here's my actual right ventricle here so here's my right ventricle I'm trying to pump blood out as I'm trying to pump blood out let's say that these this valve here stenotic and I'm at a hard time to be able to push the blood out so there's a stenotic valve it's going to be really really hard to push blood across that stenotic valve that's a lot of resistance that's a lot of resistance that I have to overcome to push the blood out what about if I look at the other side look at I look at the left ventricle this is more common with an left ventricle let's say that I draw here is tiny little heart here and here's my aorta and there's the aortic valve there where that stenotic or what if I have by some terrible situation here I have some type of plaque there some type of cornerian theorist chlorotic plaque or whatever it might be that's including the blood flow and area that's another negative thing that's also going to increase the amount of persistence I'm gonna have to overcome what if I have you know how when your vessels they come down here they go to capillary beds and then these they branch out here and we've said that one of the most important guides for resistance here is your arterioles because your arterioles have that smooth muscle that responds like epinephrine and norepinephrine so whenever these guys these different types of vasoconstrictors here I'm going to put here for positive for the Basel constrictors they're going to act on that smooth muscle and cause the smooth muscle to contract as the smooth muscle contracts what happens to his blood flow its impeded from moving through there and so what can happen is this pressure can actually move this way backwards so because you're constricting this the pressure is backing up behind it as this pressure is backing up behind it then look what happens to the pressure within the aorta it increases if the pressure in the aorta increases that's going to be a harder harder for me to be able to push blood out let me explain it another way let's say here's my already valve there's my mitral valve let's say that I have the pressure in this area so here's the pressure in my ventricles right the pressure in the ventricles is normally you want it to be about 120 millimeters of mercury that's what you want it to be generally the diastolic blood pressure is around 80 millimeters of mercury if I increase this pressure let's that increase it to like 100 I increase it to a hundred millimeters of mercury before it was a difference of 120 to 80 but now I'm going from 120 to 100 that's a 20 millimeter mercury difference so going from 120 millimeter mercury to 80 gave me a 40 millimeter mercury difference when I go from 120 to a hundred that only gives me a 20 millimeter mercury difference that means I'm going to have to move from high pressure to kind of like a little bit higher pressure than normal if I move from this it's a little bit lower so more Bloods going to go out so if I increase that pressure that's increasing the after that I'm increasing the amount of resistance that I have to overcome to push blood from this ventricle into that vessel there and again what things could change that one is plaques that could be one one is whenever the aortic valves are kind of stenotic and sclerotic another thing is because of that vascular resistance so now you remember we have the capillary beds right here and they branch out here it's like your arterioles we said right we said that they control that smooth muscle contraction so if these guys are actually contracting they're increasing the systemic vascular resistance that's backing that pressure up the pressure starts backing up and guess what it does it's one of the things that also can contribute to this change for me going from 80 to 100 for example in this situation so again one of the things could be some valve stenosis another one could be plaque buildup another one could be hypertension do this high systemic vascular resistance there's a lot of things that can contribute to this but the whole point here that I really need you guys to understand is is that as compared to these two whenever there is an increase in after load there's a decrease in the stroke volume whereas when there's an increase in the preload there's an increase in the short volume whenever there's an increase in the contractility there is an increase in stroke volume this is the only one that's inversely proportional after load so again what things could actually inhibit the after load causing a lot of problems one is a or two valve dysfunctions primarily that it like stenosis or sclerosis or it's hard to open up the valve or another negative in fluid flow and another negative influence is going to be some type of plaque buildup so maybe some type of plaque or occlusion so an occlusion of a blood vessel or could be due to hypertension so high blood pressure okay due to the high systemic vascular resistance okay so that's the idea here one other thing I want to mention because I forgot to mention it real quick is with respect to the sorry there's just weird reflex this reflex here is called the atrial bainbridge reflex it's one of the other regulators here of the heart rate it actually can stimulate the heart so it's actually kind of a positive effect on the heart rate there's an increase in the venous return that means it's going to cause an increase in the stretch increasing the stretch is going to stimulate the cardiac Excel to enter which is going to go to the SA node and that's going to increase the heart rate okay so that's that little tidbit on the atria being big reflux ninja turns recovered so much information in this video on cardiac output I really hope that you guys liked it I really hope it made sense I truly do if it did help if it did make sense if you guys liked it please put some comments on the comment section subscribe hit that like button maybe even share the video if you can alright as nerds as always until next time

Channel: Ninja Nerd

Views: 994,867

Keywords: cardiovascular, cardiac output, frank starling's law

Id: 0O3FfHPE9PU

Length: 44min 59sec (2699 seconds)

Published: Thu Aug 03 2017