but now we have to see what things can affect this now let's start there let's say that you're actually going to be let's say we come over here to the blood first let's start with these chemo receptors because these are usually the harder ones to do we'll start with the central then we'll do the peripheral let's start off first and let's say that you have high partial pressure of CO2 within the blood okay you have a high partial pressure of CO2 in the blood so what does that mean that you have more CO2 in the blood if there is excessively large amounts of CO2 in the blood what does that mean okay well you know let's say right here this is specifically the let's say that this is actually the cerebral spinal fluid okay so this is a cerebral spinal fluid this is where your neurons are this is where the central chemo receptors are so if I were to actually draw this here let's say right over here is my C Central chemo receptors Central chemo receptors and I want to stimulate them well I have to cross between the blood and the Brain barrier so in order for me to do that I have to bring the CO2 in because you know protons can't get in right because you guys know that protons don't have the ability to get in because they're charged so CO2 will actually come into the ceros spinal fluid it'll cross the bloodb brain barrier so again what is this structure here called this right here this is actually the blood brain barrier when CO2 crosses the bloodb brain barrier and goes into the cerebros spinal fluid it actually will combine with water when it combines with water it'll actually fuse with the actual water to form carbonic acid h2co3 when h2co3 which is carbonic acid is formed it's very unstable and what it'll do is it'll actually disassociate into two different chemicals one of the chemicals is actually going to be protons and the the other one is going to be bicarbonate why am I telling you this because whenever there is an increas in the amount of CO2 that increases the amount of CO2 here that increases the amount of carbonic acid and that increases the amount of protons if there's more protons that's actually going to stimulate the central chemo receptors then what are the central chemo receptors going to do the central chemo receptors are going to respond to that stimulus and then they're going to s signal so now let's pretend that this Central chemo receptor is this one here what it's going to do is it's going to stimulate the actual let's do this in a bright color let's do this in a pink color here this Central chemo receptors are going to stimulate the drg okay they're going to stimulate the drg you know what else the central chemo receptors are going to do they can also stimulate the pneumotoxic center and then that can send signals down to the drg we'll show that very small here it also can affect the pneumotoxic Center and then the pneumotoxic center can send these signals down to the drg also as well as to the vrg we're going to specifically stick here with the drg in this case but I can't send signals to the vrg right so if this Ino receptors are stimulated due to these high protons what does this mean whenever you have high protons what does that mean for the pH it means the pH is decreasing so you have a decrease in the pH when these are stimulated the drg send down inspiratory signals but guess what else the drg will do the drg is so kind he'll tell some of the inspiratory neurons within the vrg right so come over here and it'll tell some of the inspiratory neurons within the vrg and they'll say hey vrg send some inspiratory signals down and that's what the actual vrg will do so it'll also spend send inspiratory signals down if both of these guys are sending inspiratory signals down what's going to happen to the actual frequency of the impulse is moving along the actual intercostal nerve okay well the are going to increase even more if these increase even more what does that mean for the actual frenic nerve and the intercostal nerve that means that these are going to stimulate the diaphragm and the ex intercostal even more heavily what's that going to do that's going to so again what should I say here I should say the frequency of action potentials so what happens to the frequency here so the frequency is actually going to increase so the frequency of the action potentials is going to increase and so that that's the the case it's going to cause more frequent contractions of the diaphragm and the external intercostals if they contract more frequently what is that going to do that's going to increase ventilation so what is that called whenever you're doing this the overall result of these two effects here is to hyper ventilate right to increase the actual ventilation process okay now when I say hyperventilation I obviously need to be careful because it depends upon what the actual initial stimulus is because it could be hyperventilation or it could be hyperia we don't know exactly why the CO2 levels are rising so I'm not even going to put hyperventilation I'm just going to specifically say there's an increase in the ventilation so let me just put that there's an increase in the actual I'll put this increase in the respiration rate and the depth right because now let's think about this for a second if you have a lot of CO2 so let's come over to this corner part of the diagram let's come over here and let's say that you have in the blood high amounts of CO2 if you have this increase in respiration rate and respiration depth so I increase the ventilation process in other words because that's all I'm saying when I say increase respiration respiration depth I'm just basically saying increase my Alvar ventilation that's all I'm saying really alv ventilation so now I'm going to have more air coming in and I'm going to try to cause more air to go out if I increase that ventilation process what does that mean there's going to Bean more gas exchange more CO2 is going to be coming into the alviola and then what leaving out into the atmosphere I'm G to try to breathe off more CO2 then what's gonna happen more oxygen is actually going to funnel into the blood and then what's that going to do if I exhale a lot of CO2 what's going to happen to the CO2 levels in the blood it's going to go down as the CO2 levels go down what happens let's find out let's go back over to this diagram if the CO2 levels decrease oh okay well if the CO2 levels and let's just say this is appropriate decree let's not say it's decreasing significantly like really really bad let's say it's coming back down to normal so it's going to decrease the CO2 okay that's cool it's going to decrease the amount of carbonic acid it's going to decrease the protons and if it does this and brings it back to normal doesn't that take the stimulus away from the central chemo receptors yes and if that's the case then the drg will not be ascending impulses down as well as the VG and the respiration will start to slow down a little bit right and come back to normal so that's the whole purpose so whenever the CO2 levels are high it's going to increase the respiration rate and the respiration depth what happens if our CO2 levels are significantly low so now let's represent this with a different color to show that we're not talking about normal situations let's say that we're talking about very very low what was that call whenever you have really high partial pressure of CO2 this is called hyper capnia now we're going to talk about what happens whenever you have a low partial pressure of CO2 low paral IAL pressure of CO2 is referred to as hypo Capia okay so now let's take the opposite effect let's show this one let's do it in Black since we already wrote that in Black if there's a decrease in the CO2 that means there'll be a decrease in this CO2 if there's a decrease in that that means there's a decrease formation of carbonic acid which means that there's a significant decrease in protons if the protons are so low they're not going to be provided signals to the central chemo receptors if the actual Central chemo receptors are not going to be as frequently stimulated so let's actually put inhibited in this case even though we know they're not inhibited we just know that they're not going to be receiving a lot of stimulus if they're not receiving a lot of stimulus due to these low proton levels are they going to stimulate the drg no so we can think about them not stimulating their drg so let's think about this for a second and we'll write it the opposite way we'll say it's inhibiting the drg okay but again just remember that there's very little signals going to the Dr then we can also say that there's very little signals going to the pneumotaxic center right so very little signals going to the pneumotaxic center and this will also affect the drg and it won't be sending as much impulses to the drg if this is not sending a lot of impulses to the drg then the drg will send very little impulses to the vrg this should you should be getting the point already now then now if the oh my goodness if the vrg and the drgn inhibited then what's going to happen that means that the impulses that are actually going to be being sent down to the actual frenic nerve this is going to decrease these impulses are going to decrease if these impulses are decreasing then what's going to happen the frequency is going to decrease if the frequency decreases what's going to happen to the rate at which these muscles are Contracting well it's going to be a slower rate of contraction right so in other words when the diaphragm contracts and when the external intercostals contract it's not going to be happening at a very high rate so what's going to happen to the respiration rate and the respiration depth that will decrease and if the respiration rate and the respiration uh depth decrease what's going to happen let's come back over here okay well if there's really really low CO2 levels okay and we let's let's get rid of this right here for a second really really low CO2 levels and we're decreasing ing the actual respiration rate and the respiration depth so in other words we're hypoventilating let's say that we're hypoventilating and our ventilation is decreasing that means it's going to be very slow very very shallow breathing whereas before when it was a high CO2 we were actually there was an increase in the respiration rate in the respiration depth now there's going to be a decrease so it's going to be very slow and shallow breathing that means that very little CO2 is actually going to be moving across acoss this actual respiratory membrane if very little CO2 is moving across this membrane what happens to the CO2 that's going to be exhaled the CO2 that's going to be exhaled is actually going to be a lot lower so what does that mean then so if there's actually this consistently low uh output of CO2 that means that some of this CO2 in the blood is going to start slowly building up because we're not getting rid of a lot of it so we're not ridding it out of the blood and putting it into the alvioli and then exhaling it very little of it is actually being exhaled so it's actually being retained in the blood due to this slow shallow breathing if that's the case then what's going to happen let's come back over here if that happens then then what will happen to the CO2 levels in the blood eventually right it'll slowly start Rising if it slowly starts Rising this will go up as this goes up this will go up and as that goes up this will go up and then what will happen this will no longer be inhibited and it'll start being stimulated right to allow for normal respirations to begin again and then if he's stimulated then this guy will be stimulated and you're going to get the point here this is stimulated and then this would be stimulated and then this guy would send stimulation and then the frequency would go back to normal and then we'd have normal respiration rate and normal respiration depth assuming that we're doing this normally right but again the whole concept is that what is this whole these whole inspiratory inspiratory Center trying to do they're trying to control the pH in response to the changing fluctuating CO2 levels because you know the partial pressure of CO2 is the most powerful respiratory stimulant unless oxygen levels drop below 60 and then it becomes the most powerful okay so understanding that is critical okay so that's that for the central chemo receptors okay now what we're going to do is we're going to hop over here and we're going to see how the peripheral chemo receptors are playing a role in this very similar um but they're responding to pH in a different way okay so those were the Central chemo receptors you see these little blue dudes here they're right around well first off Let's do let's look at our anatomy here real quick so this right here is actually going to be the left atrium this is the left ventricle then coming up out of here is actually going to be your aorta then off of the order you have your first artery here you know have your brachio calic artery so I'll put here ba then off of the brachio calic artery it splits it goes into the right subclavian artery and then it goes into the common corroded artery and this would be the right one this is the left common cored artery and then this is the left subclavian artery and then again it'll go down to the descending aorta then the right comic car artery will come up here and split well at that splitting point when it goes into let's say that this is the external cored artery internal cored artery internal cored artery this one will be right this one will be right this would be left and this would be the left external cored artery that point where they're bifurcating there's these specialized chemo receptors and they're in these actual body formation right so these peripheral chemo receptors are right here they're located right here on this point here what is this point right here called this point here is actually called the corroded bodies okay and that's where some of the peripheral chemo receptors are the other ones are going to be right here in the aorta this is actually called the aortic bodies so these are called the aortic bodies now these are again your aortic bodies and your cortic bodies are actually a component of what's called your peripheral chemo receptors okay now the peripheral chemo receptors are special because they respond to three different stimuli let me write those stimula down they can respond to partial pressure of CO2 so they can respond to a partial pressure of CO2 they can respond to the partial pressure of oxygen and they can respond to the pH but we're going to go into a little bit more detail on this okay so now the peripheral chemo receptors are special because we said that they can respond to CO2 changes they can respond to oxygen changes and they can respond to pH out of all of these the most significant one that we need to remember out of all of these is going to be the partial pressure of oxygen so whenever the partial pressure of oxygen drops below 60 mm of mercury it is the most powerful respiratory stimulus out of all of the other certain types of chemicals it's greater than the CO2 stimulus and greater than the pH stimulus now generally oxygen is usually normal right in certain situations the partial pressure of ox is usually normal so we're assuming that it's greater than 60 and so CO2 is the most powerful stimulus and then pH is also contributing to this now CO2 was affecting the central chemo receptors 70% of it is affecting the central chemo receptors 30% of it is only really affecting the peripheral chemo receptors but again oxygen is the most powerful stimulus and here's another thing for the pH the pH is not due to the changes in CO2 it's due to the changes in metabol I acids so like what like Ketone bodies you know these are produced whenever you have prolong starvation or in type 1 diabetes metis that's not properly controlled or lactic acid or other different types of metabolic acids we can keep going right the whole point is metabolic acids are the main influence of this arterial pH not the fluctuations in CO2 okay so again peripheral chemo receptors they're responding to the partial pressure of CO2 about 30% of that actual CO2 is going to be you know specifically stimulating the chemo receptors right and then uh if the partial pressure of oxygen is below 60 millimeters of mercury becomes the most powerful respiratory stimulus and the last thing is that these actual peripheral receptors are specifically responding to changes in PH due to metabolic acids like lactic acid Ketone bodies and stuff like that okay okay so now let's see the mechanism of how this is working so let's see the mechanism of how this is working so here I'm actually zooming in on the actual Kate body or the the actual aortic body now in these Kate bodies aortic bodies you have two types of cells this is actually called the type one cell or the type two cell now they Tech technically they call the type two cell they call it um it's like the susten cells not the susten acular cells in the testy so don't get that confused so suac cells CU it's basically supporting cell and this type one cell is actually called your glomus cells okay anyway in the glomus cells they actually consist of these packages these vesicles of neurotransmitter specifically that of dopamine so that's consisting of these actual dopamine containing vesicles now the whole purpose of this is is we either want to cause the release of dopamine or we actually don't want to release the dopamine so let's see how we actually do this now in this actual glomus cell you have specialized potassium iium channels so you have these specialized potassium channels now these potassium channels have three different stimuli okay so see here's our potassium ion we're going to determine whether the pottassium ion is going out or in generally this potassium channel is sensitive to oxygen protons so oxygen and protons now let's say that your oxygen levels are decreasing they decrease below what they decrease below 60 millim Mercury they become the main respiratory stimulus what are they going to do when oxygen levels are low hypoxia it inhibits these actual channels it inhibits these channels now let's say that the actual proton levels are going up what does that mean when the proton levels go up that means that the actual pH is going down right in that situation that is also inhibiting these actual potassium channels closing the pottassium channel and the last one you know if CO2 is rising CO2 will come into the cell and combine with water when it combines with the water what will it do it'll CO2 and water will fuse together in the presence of an enzyme right called Carbonic anhydrates that also that enzyme would have been over there with the central chemo receptor area what it's doing is it's fusing them together and forming carbonic acid and then carbonic acid is disassociating into protons and bicarb those protons are stimul I'm sorry inhibiting this potassium channel so these protons here are coming from metabolic acids but these protons here are coming from the CO2 right so whenever the how does the CO2 actually inhibit this channel it's directly through these actual protons so CO2 will come in get converted into carbonic acid break down into protons and bicarb and the protons w't hit these potassium channels but these protons these single protons are actually coming from metal abolic acids like lactic acid and Ketone bodies like aceto acetate and B hydroxy berate things like that and whenever the oxygen levels are less than 60 millim of mercury that will also inhibit this channel if these channels are inhibited can potassium leave the cell no so potassium can't leave the cell if the potassium levels accumulate in the cell what happens to the actual inside of the cell the inside of the cell becomes more positive if the inside of the cell starts becoming more electropos positive it leads to an activation of these specialized calcium channels and when these calcium channels open they are the ones who are going to make the difference look at these suckers here so look here's the calcium channel and we'll put another calcium channel over here these calcium channels are stimulated due to these potassium ions increasing and increas in the actual membrane potential when the calcium ions rush into these these actual glomac cells they trigger these actual vesicles to fuse and when the vesicles start fusing with this actual glomma cell membrane what happens well you're about to find out here we go look at this it fuses and what starts getting released the actual dopamine and whenever the dopamine is released what happens dopamine is going to act on these actual nerve terminals what are these nerve terminals here it depends on which body we're talking about let's look and see it's a beautiful mechanism I think that's so cool okay that nerve terminal right there it could be connected with the karate bodies or it could be connected with the aortic bodies if this actual nerve terminal is connected to the Kate bodies it's specifically going to be cranial nerve nine there's a one before the a all right cranial nerve nine glossop farial nerve if it's coming from the aortic bodies it's cranial nerve 10 and that is the Vegas nerve so again if these actual kateed bodies are stimulated due to low oxygen High protons due to metabolic acids or CO2 which indirectly gets converted into protons and inhibits this potassium Channel causes the inside of the cell become more positive activates calcium voltage channels which come in and cause dopamine to be released right now imagine if all of these things were opposite it would be the exact opposite thing so imagine if CO2 levels were actually low if CO2 levels were low if oxygen was normal and if the pH was high so we did everything whenever CO2 was high P2 was low and pH was low right and the opposite if oxygen is high it's going to stimulate these pottassium channels and potassium will go out and will not cause the calcium to come in no dopamine will be be be released holy crap if the actual pH is high that means that the protons are low and they won't be inhibiting the potassium channels and pottassium will be able to leak out if CO2 levels are low it won't be forming as much protons and it won't be inhibiting this channel it'll be stimulating it and allowing for potassium mins to come out and will prevent the cell from releasing dopamine so you can imagine if dopamine is being released what happens to the actual signals the signals will increase so if that happens these signals carried on cranial nerve 10 and cranial nerve 9 will be increased if there's very little or no dopamine release the signals will be not present or very very low signals okay beautiful so now let's take those guys and see what they're doing now let's bring them up over here so we're going to say we'll put them right here let's say here's those right here's the other one and again what is this coming from this one is coming from let's say let's say this one here is cranial nerve 10 which is the Vegas this is cranial nerve n which is glossop faral we know that the cranial nerve nine which is glossop faral responding to the kateed bodies so cute right and then the cranial nerve 10 is responding to the aortic bodies and again if there's low PH due to mean meaning High protons oxygen is below 60 and CO2 is elevated it can actually stimulate these and send action potentials down these suckers here if the pH was opposite if the pH was high the CO2 was low and the oxygen was normal the action potentials would not be being sent here now look what they do they take these signals in to the drg it's amazing if they stimulate the drg what's it going to do the drg is going to stimulate the vrg if the vrg and the drg are stimulated what's going to happen to the impulse is going down down to these descending Pathways it's going to increase if the pathway is going downwards increase what happens to the frequency of the action potentials coming out here to the frenic nerve and the intercostal nerves that's going to increase if that increases what is that going to do then it's going to cause more frequent contractions of the diaphragm and the EXT on costals what's that going to do increase the respiration rate and the respiration depth in other words you're increasing the ventilation if you increase the ventilation process what that what's that going to try to do let's come over here where your CO2 levels are high if you increase the ventilation process you're going to move more CO2 across this membrane if you have more CO2 moving across this membrane and more oxygen across this membrane right so let's say the stimulus was low oxygen it's going to cause increased ventilation to get more oxygen into the blood if the s was low CO2 it's going to stimulate the actual I'm sorry if the stimulus was high CO2 it would actually stimulate this increase ventilation across the membrane which will cause more CO2 to get exhaled so more CO2 would get lost and the CO2 levels in the blood would decrease and the proton concentration would decrease but there's another problem what about the metabolic acids like Ketone bodies you can't exhale Ketone bodies you can exhale what's called acetone which is a breakdown product of them but you can't exhale them and so in situ ation in which you have this uh change in the pH like a decrease in the pH or an increase in the pH but right now we're talking about decrease if the pH is decreasing due to metabolic acids like lactic acid and Ketone bodies you can't breathe these out if this is due to a situation like metabolic acidosis how would you treat this well one way is your actual buffers will come into play your B bicarbonate carbonic acid buffer system will come into play but it's going to get you know sucked up and used up pretty quick within seconds then you're going to try to do this respiration but it's only going to breathe off CO2 it's not going to take care of the real issue which is these Ketone bodies and lactic acid you're still going to be stuck but it might only last for a little bit of minutes then how would you deal with these actual Ketone bodies and lactic acid your kidneys so your kidneys would be the long-term compensation mechanisms and they would urinate out the actual Ketone bodies and they would urinate out the protein of the lactic acid and they would try to bring more bicarbon to your bloodstream okay so that is the way that your actual body would deal with this so breathing them off isn't going to help you at all that's why whenever you see people have uncontrolled diabetes metis what does their breath smell like smells like acetone because they're trying to breathe off the acid but all they're doing is actually breathing off CO2 and that's why people who have uncontrolled type one diabetes mtis they have what's called cusms breathing which is very very abnormal breathing okay all right so that covers the peripheral chemo receptors and what they're doing right and then again let's apply what happens whenever there was the opposite so this was being stimulated due to what let's actually do this here this was being stimulated we'll put here stimulated by what low partial pressure of oxygen has to be less than 60 millim of mercury it was also being stimulated by high partial pressure of CO2 and it was also being stimulated by low PH but it was due to metabolic acid now let's say the opposite let's say that you want to inhibit this one so now you're trying to do the opposite you want to inhibit these Kate bodies and aortic bodies then you would want to do what do the exact opposite have normal partial pressure of oxygen okay decrease the partial pressure of CO2 and increase the ph and if that happens let's see what that would do so if these are inhibiting the actual corate bodies and aortic bodies the impulses that are coming from the aortic bodies and the corate bodies via the glossop faral nerve cranial nerve 9 or Vegas cranial nerve 10 is going to be decreasing or almost absent so what will that do to the drg it will inhibit the drg if the drg is inhibited what is it going to do it's not going to really send down a lot of action potentials down to the frenic nerve and intercostal nerve it's also not going to stimulate the vrg it might actually slightly inhibit the VG so the impulse is going down to the actual frenic nerve and intercostal nerves are actually going to decrease and then the frequency of the action potential is going to the actual exter costales and the diaphragm is going to decrease which is then going to decrease the ventilation and it's also going to again it'll decrease the respiration rate and the respiration depth which in other words is a decrease in the alveol ventilation holy crap if you decrease the alveolar ventilation in other words what was wrong here your CO2 levels were low if you decrease the actual alular ventilation what does that mean you're having very slow shallow breathing whereas whenever was low PH high CO2 low oxygen you were having very rapid and very very deep breathing to bring in more oxygen exhale more CO2 well now it's very slow and shallow so very very little CO2 is getting exhale and if very little CO2 is getting exhaled and very little oxygen is moving across here what's going to happen Okay well if there's very little CO2 that means I'm not going to Exhale a lot of CO2 so I won't exhale a lot of CO2 so a lot of the CO2 is going to maintain in the bloodstream also if that's the case then what would that do okay well if there was a low partial pressure of CO2 we said that that would decrease the carbonic acid formation decrease the protons and that would also uh decrease the actual action here on these actual corate bodies ortic bodies same thing when there was metabolic alkalosis if there's metabolic alkalosis due to a decrease in the actual uh maybe there's excessive amount of bicarbonate you're actually going to want to slow down the respirations right so if there's a lot of bicarbonate building up causing metabolic alkalosis so that's another thing we we said that it was due to metabolic acids like Ketone bodies and lactic acid but you could also change the pH due to other things like besides these things we could actually say metabolic bases right and if those metabolic bases they would be things like by carbonate so these would be a base so if there's an excessive amounts of him that could cause metabolic alkalosis what actually would do what increase the pH you're not going to want to increase your respiration you're going to want to decrease your actual respiration so to accumulate more CO2 accumulate more carbonic acid and then have that disassociate into more protons right okay so that's the whole goal there so we did peripheral chemo receptors we did Central chemo receptors sweet deal now let's go ahead and talk about some of these actual receptors over here in the lungs