Cardiovascular | Cardiac Output

all right engine 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 as Co okay cardiac output Co is equal to your heart rate we're going to denote that as 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 a 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 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 let's take the average heart rate in the average stroke volume so then we'd have to say Okay cardiac output is equal to the heart rate what's the normal heart rate well it's somewhere in between 60 to 80 beats per minute right on average so let's take in between let's say 70 beats per minute minute okay and let's multiply that by the stroke volume on average stroke volume happens to be around 70 milliliters and we'll see how in a second so let's say that's about 70 MLS All Right per

beat when we multiply these two 70 * 70 is about what 4,900 right let's round that up let's just round that up to about 5,000 what 5,000 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 5 L per minute so what do we know so far cardiac output is equal to the heart rate times the stroke volume it's its actual units is the total volume of blood that can pump out in milliliters per minute that volume is generally around five

lers per minute but you know that we can increase that significantly During certain situations like an exercise or we can decrease this certain significantly due to parasympathetic ination 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 card output is for right now let's go ahead now and decipher heart rate and decipher stroke volume 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 the normal heart rate is in between 60 to 100 anytime you go greater than 100

then it actually is considered to be Tac cardia 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's setting the sinus rhythm he's the one that's generating those what he's 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 around 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 generate Action potentials and send it out to The myocardium to trigger The myocardium to contract and that's right around 60 to 80 BS 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 this sympathetic nervous system is basically the one that is releasing certain chemicals what are those chemicals that it's releasing remember it's releasing norepinephrine so norepinephrine was one of the big ones there acting on the beta 1 agenic 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 aeric receptors we already went through that mechanism and extrinsic inovation of the heart so what kind

of action do we say it had if I draw here a positive what does that mean it means it's a positive effector of the heart rate meaning that it can increase the heart rate that's called chronotropic action so really what is he then he's a positive chronotropic agent so your sympathetic nervous system is a positive chronotropic agent it can increase the heart rate that's one thing but then let's take the flip side let's say that I want to decrease the heart rate if I want to decrease the heart rate 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 onto those muscarinic type two receptors if you remember which was causing the potassium to leave the cell causing the cell to hyperpolarize it was also inhibiting the production of cyclic am and basically causing the cell to slow down the rate of action potentials so this is a negative chronotropic agent so so far we know that the sympathetic nervous system is a positive chronotropic agent the

acetylcholine which is a part of the parasympathetic nervous system is a negative chronotropic agent 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 negative chronotropic is the parasympathetic nervous system via the acetoin so this is the aceto choline and then the sympathetic nervous system was with the presence of epinephrine and nor epinephrine so nor epinephrine 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 show this guy like this look right there this guy is called thyroid hormone so T3 and T4 these also are a very powerful Reg 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 hormones so what's another positive regulator of this we're going to say thyroid hormones so T3 and T4 this is a good one you know what else T3 and T4 can

actually do they can increase your basil metabolic rate when you increase your basil 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 due to T3 and T4 or 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 you're increasing 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 chronotropic agent of the heart now let's talk about something else what about ions ions are very critical here what 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 let's 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 hyper calcemia 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 potential sent out to the heart muscle so that's one thing so really we could 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 chronotropic agent 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 chronotropic agent okay so so far we have calcium being an effect there what else potassium potassium

has 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 they 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 the cell 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 it's

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 its it's not going to move down its 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 hyperemia is very very very dangerous okay so 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 the person to go into cardiac arrest and the same thing though um uh other other things that actually get affected is the low potassium low potassium allows for the potassium to leave more quickly and so again pottassium 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 said that if we have have low calcium levels low calcium levels is going to be an inhibitor now there's something else that's kind of interesting let's say 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 just a little small aorta here and you know coming off the aorta you have what's called that brachio spalc trunk which splits into the common corate which goes into the subclavian and then this common cored here right which splits into the internal corate artery and the external cored artery right there at that bifurcation point we have these specialized cells right here what were these cells here called they were called the chemo receptors they were Cho 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 the central nervous system and when they take it to the central nervous system what does 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 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's the ponds here's the medulla and here's the spinal cord real quick right right here what will happen is these chemo receptors will take 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 exelator center as a result what will the cardiac exelator center do it'll send out these impulses to what it'll send out the impulses to the heart and what will it try to do to the heart

it'll try to result in an increase in the heart rate because it's going to have sympathetic effect okay so I want you guys to realize what is another factor of this any type of situation which there is hypoxia there's an increase in the partial pressure of CO2 there's a decrease in the pH they can activate the chemo receptors and try in an attempt to increase the heart rate but again it's not as significant of effect as it is on respiration okay because really the more powerful effect that you need to realize is 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 then we can say stimulation of these chemo receptors these peripheral chemo receptors due to some type of situation which 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 chemo receptors will act as due to what what are the stimuli here low partial pressure of oxygen increase partial pressure of CO2 and a decrease in the pH these are they get stimulated here and they do what to the heart rate they stimulate allate so stimulation to The pripo receptors 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 a like generally like I's say

that uh a child what about a child's heart rate in comparison to 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 if we were to compare let's say that we have like a fetus or an infant so fetus you know SL infant they have super super super high heart rates okay so they can go from like 120 to 140 beats per minute okay that's like the fetus then

let's take like adults again adults should range adults should range anywhere from 60 to about a 100 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 to 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

cuz we said it's between 60 to 100 well really if we take the intrinsic ability it's really 80 anytime you go above 100 is Tac cardio so males they have a kind of a slower heartbeat theirs is right around 64 to 72 beats per minute and again this is at rest when we talk about females there's a little bit higher theirs can go from about 72 to 80 beats per minute okay so there is a little bit higher than ours last thing so I guess it's like the circle of life so for the fetus and

the infant it's really high for the adults it's kind of low you know write it within this age and certain as you start to get a little older as you get a little older it actually can go back up sometimes this this fluctuates this obviously varies but generally theirs 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 it's right around 64 to 72 females is a little faster 72 to 80 beats 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 tacac cardia and stuff so there's two terms that we need to get straight here one is called brat cardia bradicardia 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 rat cardia there could be many causes of bradicardia could be due to like a parasympathetic nervous system 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 run Runners people who run excessively they put their heart through a lot of work and it's

kind of a good thing in a way but as they're actual they're they're actually exercising and they're doing these long endurance act activities the heart starts 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 it like this we know that cardiac output is dependent upon heart rate and 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 said into 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 they have good a lot of preload and a lot of contractility so 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 to to allow the heart to allow for the heart

to have time to rest so again cardiac output we said is depend upon heart rate and stroke volume in endurance activities people who are doing this consistently their heart rate will start to drop drop really really low because their stroke volume is so high because their myocardium is very strong okay so that's something you might see in people who are bradic cartic 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 say that the person is tacac cardic so now that

we say that the person has tacac cardia in other words they're having a heart rate that is greater than 100 beats per minute and obviously there could be many causes of this could be sympathetic nervous system activity could be due to high high T3 and T4 could even be due to certain drugs could even be due to like anxiety so certain types of emotional factors you you know if you ever notice someone who's having like certain psychological disorders or or 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 the actual stroke volume I want to talk about stroke volume a little bit so let's come over here here now let me get all my markers over here let's make this nice and colorful all right now we're going to talk about stroke volume so we said that stroke volume is basically what do we say we said it was basically the milliliters that is being pumped out of the ventricles per beat but let's actually dig into this a

little bit more so there's actually an equation for stroke volume 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 vava I have blood coming from the superior vena and I have blood coming from the coronary sinus and it's 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 empting into the ventricles as a result right whenever the atrion under goes cyly they push it down but if you remember we talked about this in cardiac cycle about 70 to 80% of the blood passively flows down without contractile activity so let's say that the blood is sitting here in the heart just accumulating there right so the blood's just sitting there in the heart and accumulating that volume of blood that is sitting in the heart before the heart even contracts it's during the relaxation period when the heart is in diast this is called

the enddiastolic volume okay on average the edv is approximately around 120 milliliters it could range from about 120 to 140 we're going to put down 120 for right now okay then if I take the edv and I subtract it from What's called the ESV so how do we Define edv we should actually write this out edv is defined as end diastolic volume okay so edv is 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 the heart

before your ventricles are going to contract so edv is basically the IND diastolic volume ESV stands for and systolic volume so this is the volume of blood that's remaining in the heart after the ventricles have contracted or undergone cyly so let's say that 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 out into 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 there's less blood now here right that volume of blood that's remaining after the contraction is called the ESV this is on average about 50 Millers it can range from 50 to like kind of 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 120us 50 that's 70 so

70 milliliters okay and then again how much per beat so this is what we can say is equal to the stroke volume now we got to even go into a little bit more depth unfortunately because now we can actually say that stroke volume is divided into three other subcategories so let's say that we take stroke volume and we we divide this take stroke volume here and I'm going to take and divide stroke volume into three categories let actually bring it down here so we have plenty of room here actually bring it down here so right

here stroke volume is actually broken into three categories one of the categories is called preload okay so this is 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 afterload all right let's go ahead and decipher each one of these things and what affects them and how that affects stroke volume how that affects cardiac output okay so first off preload how would 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 defined 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 stretch 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 when the heart is actually in diaso or relaxation edv in diastolic volume the more of that I have the more it's going to push on the heart and 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 I in increase my IND diastolic volume I'm going to increase my prelo I'm going to stretch the walls even more okay well that leads to a next question how in the heck do I increase my antolic volume one way that you

can do it is to get a lot of Venus return what is that you know how uh 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 right V CA let's say down I have some veins in my legs here okay you know veins have valves we talked about this in blood vessel characteristics we said the veins are very low pressure though veins are very low pressure 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 it the milking activity sounds weird but that's one of them one of the ways that we can increase this Venus return is by increasing the muscular milking that's one way another

one whenever you're breathing let's imagine I taking some good breaths 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 within the abdomin 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 you can kind of think of 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 it 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 why I put TBB the thoracic cavity pressure so put TCP if this is

high things like to go from high pressure to low pressure so what it does 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 um Venus return here sorry so this would be the respiratory pump another thing is your sympathetic nervous system they have control

over your Venom 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 neuro epine and this can actually stimulate the contractility of the smooth muscle to cause 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 venomotor tone Venom motor tone or just venoc constriction so we could actually subclassify this as Veno constriction so this is kind of helping to squeeze

some of the blood upwards all right one more thing is the filling time that's another thing 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 too much 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 Mis what happens to the heart muscle it gets replaced with fiber tissue

does fibrous tissue stretch very well not really it's not it's not doesn't have a lot of give so because of 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 edv due to increased venous return from muscular milking respiratory pump Venom 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 diast by doing that you're not going to want to have the heart rate

too high because if the heart rate'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 that kind of covers that thing last thing I want to relate with this is a a law and laws are important okay laws 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 starling's law and what Frank starling's law says is that whenever you have an increased stretch on the heart so whenever there's increased stretching of the heart it allows for this length tension relationship more cross Bridges to be active so whenever there's stretching of the heart and there's optimal crossbridge connections that increases the preload if you increase the preload you're going to significantly increase the stroke volume so Frank starling's law of 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 starling's law just to sum it up here greater stretch there's more cross Bridges and the more cross Bridges within the 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 neuro epinephrine what if 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 increases the stroke volume what else hormones same thing but this is interesting some people kind of get like a little messed up with this one let me get this over here so we don't confuse this one here okay so we know that the norepinephrine acts on the beta 1 adrenergic receptors and basically increases 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 we probably talked about

in the thyroid hormone video but what happens here let's say I have a cell here let's say that's a myocardial cell and let's say here's my T3 and my T4 okay and it comes into this cell and it acts on uh basically an intranuclear receptor and when it binds onto this intranuclear 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 agenic receptors so T3 and T4 can act on the myocardial

cells by increasing the expression of beta 1 aeric 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 actual contractility something else here is drugs obviously certain drugs can do this too 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 going to try to spell that because I always butcher that one I'm going to put Epi okay so you guys get it there's a lot of different types of drugs that you could use here you could even use what's called dobutamine and isoprenaline 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 contraction through various different mechanisms like

digitalis is a sodium potassium ATP inhibitor which increases the calcium levels inside of the cell dopamine he actually works through different weird ways dop dobutamine act on the beta 1 adrenergic receptors and atropine actually blocks 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 right so you even have those who can block certain channels you can use beta blockers okay like m coal law aeno law propenol La you can even use calcium

channel blockers and these calcium channel blockers you could use like Verapamil you can use deltm neopine 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 all right sweet so these guys here are Inhibitors so beta blockers and even some calcium channel blockers right all right so that covers that part now one other thing though is ions ions 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 hypernet treia this is actually an 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 pro

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 upon 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 inotropic agent if it's in high levels epinephrine or epinephrine are positive inotropic agents T3 and T4 and glucagon is a positive inotropic agents digitalis dopamine dobutamine atropine 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 agents and if you think about like this potassium high amounts of potassium is a negative inotropic agent high amounts of sodium is a negative inotropic agent high amounts of protons like acidosis is a negative inotropic agent okay I think we beat the dead horse there for the inotropic agents let's go to the last thing here let's bring afterload over here a little bit okay let's bring this 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 uh hypertension which 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 is afterload how do we Define afterload afterload 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 aorta or into the pulmonary trunk so for

example here let's say I draw another little mini heart here real quick here see I have another little mini heart here and I show it like this let's say here's my actual uh 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 is stenotic and I'm having a hard time to be able to push the blood out so if there's a stenotic valve that'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 let's say that I look at the left ventricle because this is more common with the left ventricle let's say that I draw here a tiny little heart here and here's my aorta and there's the aortic valve there what if that's thetic or what if I have by some terrible situation here I have some type of plaque there some type of coronary atherosclerotic plaque or whatever it might be that's uding

the blood flow in that area that's another negative thing that's also going to increase the amount of resistance I'm going to 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 said that one of the most important guys for resistance here is your arterials because your arterials have that smooth muscle that respond to like epinephrine and norepinephrine so whenever These Guys these different types of Vaso constrictors here I'm going to put here for positive for

the Vaso 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 this blood flow it's 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 ortic valve there's my mitro 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 millimet 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 say I increase it to like 100 I increase it to 100 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 millim Mercury difference so going from 120 millim Mercury to 80 gave me a 40 millim Mercury difference when I go from 120 to 100 that only gives me a 20 millimet 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 blood's going to go out so if I increase that pressure that's increasing the afterload 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 how we have the capillary beds right here and they Branch out here into like the arterials 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 that PR pressure starts backing up and guess what it does it's one of the things that also can contri contribute to this change from it 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 buildups another one could be hypertension due to 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's an increase in afterload there's a decrease in the stroke volume whereas Whenever there there's an increase in the preload there's an increase in the stroke volume whenever there's an increase in the contractility there's an increase in stroke volume this is the only one that's inversely proportional as afterload so again what things could actually inhibit the afterload causing a lot of problems one is aortic valve dysfunctions primarily that of like stenosis or sclerosis where it's hard to open up the valve or another negative influ influ in another negative influence is going to be some type

of plaque buildup so maybe some type of plaque or occlusion so an occlusion of the 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 this heart rate there's this weird reflex this reflex here is called called the atrial Bane Bridge reflex it's one of the other Regulators here of the heart rate it actually can stimulate the heart rate so it's actually

kind of a positive effect on the heart rate there's an increase in the Venus return that means it's going to cause an increase in the stretch increase in the stretch is going to stimulate the cardiac accelator center 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 atrial Bane bid reflex ninja n we covered 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 down in the comment section subscribe hit that like button maybe even share the video if you can all right Engineers as always until next time