[Music] so moving on to respirations now let me turn off this other one okay so first things first what is the main thing we are worried about when it comes to the respiratory system the primary homeostatic variable is our O2 are we getting enough oxygen in the system system that's the role of the lungs we can exhale CO2 but the main job is keeping that pa2 uh stable the rate of o2 uptake in the lungs and CO2 excretion must match the rates of O sorry still getting used to all the sensitivities here O2 use and CO2 production so whatever you create or use we have to match whatever we Supply and get rid of main components lungs chest wall and our pulmonary blood vessels we have chemo receptors and their job is to sense what the concentrations of our oxygen and CO2 are so we have to talk about ventilation gas flow diffusion of gases and perfusion blood flow it's great that our lungs can oxygenate and they can get air in but if there's no blood in that area all that O2 is just wasted because it's not getting into the blood there's no perfusion so we're talking about perfusion is dealing with blood always understand that when it comes to lungs and any any real real part of the body perfusion is blood perfusing that tissue our blood gas interface obviously we have a very very large surface area due to all these Alvi they all have small capillaries that surround each Alvi so we have plenty of surface area for all the gas exchange to occur uh ventilation we're going to talk about ventilation so ventilation when it comes to the lungs we call it ve which means minute ventilation it's a flow how much air we're just talking about air when it comes to ventilation how much air are we able to move in and out every minute so the units are lers per minute what also do we learn about in the cardiovascular section that is also reported in liters per minute cardiac output what is the formula for cardiac output heart rate so you have a rate of something and we have a volume of something with ventilation it's the same thing we have tital volume which is just the amount of air you breathe in and out every beat or every breath how much air are you moving multiplied by your respiration rate I'll put R respiration rate how many times a minute do you breathe multiply them together and that tells you your minute ventilation how much air can you move in and out of your lungs each minute just like cardiac output how much blood can your heart pump each minute okay um also all these membranes the blood gas interface less than one micrometer thick and it has four elements so this is the order that oxygen for example has to go through to get into the blood thin layer of surface liquid what's that called what's the little liquid in the alviz surfactant we have surfactant our Alvar lining then we have a very thin layer of interstitial fluid and then finally we have our pulmonary capillaries when you get to start learning about diseases we're talking about diffusion time remember diffusion has to be across a distance the thicker the distance of diffusion the slower it's going to be people have like chronic bronchitis all this mucus is lining everything you're increasing the diffusion distance and they have problems with breathing O2 so again anything that increases any one of these things is going to increase diffusion time and cause a problem with O2 Del to the tissues or getting into the blood okay so all gas occurs via diffusion it's gas exchange they go right through O2 concentration is higher in the lungs than in the blood so therefore O2 will go into the blood and that's the way we want it to go CO2 concentration is higher in the blood because we're producing CO2 as a byproduct of our metabolism and that excess CO2 diffuses into the Alvi and then we exhale it out so that's O2 and CO2 so we have some laws we have to follow when it comes to gas gas behaves differently than blood does because blood is a fluid air is not it's a gas so it can be compressed without changes in volume and pressure so boils law and again you're not going to require I'm on your your exam I'm going to say like what's foil's law but to understand these makes sense why we have the concentrations we do in our body so the first thing has to do with boils law this is just air flow into the lungs with inspiration so the pressure of the gas is inversely proportional to the volume so when it comes to air increase volume decrease in pressure so think about it we have to get air from the outside environment into your lungs if the pressure built up whenever you took a breath in you never be able to get more air in because the diffusion gradient is favoring to go out so by breathing in big volume of air in the pressure keeps dropping allowing more air to get into your lungs if it was the opposite like it is with blood if I increase the volume I'm increase the pressure I can't get any air in because the pressure gradients are off so with Bo's law tells us we can breathe in deep and our inspiration remember intrathoracic pressure drops because of the volume of air in our lungs pressure drops allows air to go in so that's all boils law is telling us so it behaves differently so when you increase the volume of air the pressure inside the lung tissue itself goes down now lung volume is first increased when in inspiratory muscles expand so it's soon you to take that first little bit of a breath you can feel a little bit of resistance but after that you can breathe in really easy but that first little bit you have to overcome your those uh little intercostal muscles your inspiratory muscles so you have to get obviously air in and then your pressure drops and the rest of it goes in so air so breathing is passive we can control our breathing through voluntary muscle but for the most part you're all listening to me you're not thinking about breathing you're just breathing on its own and all it is when you breathe in Air goes in because of pressure and then exhalation is just passive with your normal chest recoil our chest expands but it wants to snap back so expiration at rest is passive and we'll get through what happens later on with exercise so that's Boo's law Dalton's law just states that each gas that's in the air right now has a pressure associated with it so if you basically add up all the gases in the air we have CO2 O2 nitrogen is a lot of whatever else is out there they all have a percentage what's the percentage of air that's oxygen about 21% of the air is oxygen how much is CO2 it's like 3% and there's a lot of nitrogen in there and whatnot but that means that whatever pressure is 21% what's a normal barometric pressure like one bar what's the millimeters of mercury that we look at 760 is a normal atmospheric pressure that's one bar so 760 * 20% 21% that tells you how much pressure that oxygen is exerting in the air then Henry's law just states that whatever gas is dissolved in liquid is proportional to its partial pressure so whatever you're breathing in the air is what's going to get inside you that's why when you go to high altitude people have problems breathing because the O2 is less in altitude so because it's less in altitude people have problems breathing because there's less oxygen in the air so whatever is in the air is what goes into our bloodstream and they're all related now we have to talk about water vapor okay if you go breathe out hot you get your hand gets wet we have water vapor in our lungs to moisturize the air no matter how cold it is outside by the time the air reaches your Alvi it's up to normal body temperature it's been humidified and heated up as it gets through the lungs no matter how cold it is you feel the burning right in your broncus in those main areas but once it gets to the Alvi those further down it's up to room temperature so the reason why we have to talk about water vapor is because yes we have a certain pressure of oxygen in the air but when we breathe in we're adding in water pressure and water vapor you have to lose something from somewhere else it's like a big pizza pie if you're taking from one you got to lose to the other so when we get to the actual what is in your blood it's a little bit less than the environment because we're adding in water vapor so you'll see the numbers are going to change when we get to the actual blood O2 concentrations because we have to add in water vapor so let's talk about how we breathe okay so getting air in and out of the lungs is all based off of pressure gradients high to low we all go from high to low pressure so when we breathe in the pressure drops getting lower in our lungs so air can get into our lungs breathing will become difficult if the chest wall becomes stiff here's our compliance again we have to breathe in if our chest wall is very stiff you can't expand it's like put your hands around your arms and try and breathe in deep you can't do it it's like wearing a straight jacket it's a restrictive disease resistance is High um resistance when we talk about resistance it's resistance to flow what's in the way compliance is dealing with the elasticity of the lungs okay the lungs have elastic properties as well empyema is a disease that destroys the elastic properties of these lungs and you start losing blood Vol Air volume lung volume because of the empyema so resistance is Dynamic Property happens during flow are we resisting your flow to air making it harder to breathe asthma bronchitis those obstructive diseases and then compliance is um elasticity of the lungs so we have to talk about lung volumes we're going to draw it out so all these are just definitions and we'll talk about these as we draw out our lung volumes on this curve so the first thing we're going to talk talk about is our title volume this is just the air that we breathe In and Out With Every Beat okay so we'll start right here and our title volume okay TV for title volume so that's just you all right now you're breathing in and out nice and relaxed this is your title volume in and then out and then in and then out that's just your normal title volume now I'm going to tell you okay do a normal breath now I want you to breathe in as much as you can all the way in so we're going to breathe we're go all the way up Brea in all the way in so you can't breathe in anymore and then we'll come back down to our normal title volume again okay this segment is called our inspiratory capacity or inspiratory I'll put inspiratory Reserve volum I'm sorry I me to put that instead inspiratory Reserve volume how much air can I breathe in above your normal tital volume how much air do you have in your lungs all the way in it goes all the way up now we're going to say go back to your normal will title breathing change the color now I'm going to tell you to Exhale all the air you can out of your lungs okay so now we're going to breathe out and back up again and this is known as your expiratory reserve volume how much air is left in the lungs or how much air can you get out of your lung lungs for exhalation so this is your expiratory reserve volume then the last thing we're going to have them do is we're going to breathe in all the way in and then all the way back out again so after a title breath we're going to go all the way up in and then all the way back out again and then back to normal title volume this segment the red is called our vital capacity what does vital mean life okay this is the amount of air we can breathe in and out of our lungs at Max Capacity all the way in all the way out this is the total amount of air that we have for exchange we do have a little bit of residual volume left in our lungs and it's called residual volume volume there's just a little bit left that we can't get out and that's called residual volume it's just whatever is left in the lungs so they don't collapse on themselves remember we don't want our lungs to collapse once they collapse it's hard to get them unstuck so by having a little bit of air left in the lungs it keeps those alv propped open enough that surfactant helps keep them open as well so they don't collapse and then you can breathe again so volumes are always one unit by itself so vital Capac uh title volume inspiratory Reserve volume so what we do is start adding them together so we get inspiratory capacity how much can we Inspire which is the title volume plus your inspiratory reserve volume that's our inspiratory capacity how much air can we breathe in total okay we have expiratory capacity title Volume Plus expiratory Reserve volume it's another capacity all the these are on the previous slide they're all the same in that table it's the same thing okay we also have see me right we have TLC not the group total lung capacity and that is I plus e C plus your residual volume gets added in here now okay this gets everything so basically well plus your title volume so basically all three of these things is your vital capacity so TLC vital capacity Plus your residual volume that's pretty much all the lung volumes added up together is your total lung capacity okay includes all the air your vital capacity all the way in all the way back out but remember there's still a little bit of volume of air left in the lung that's your residual volume residual Volume Plus vital capacity equals your total lung capacity so capacities are always two volumes added together the volumes are just the plain volumes by themselves okay there will be one question on your exam explaining what is of residual volume or what's what makes up vital capacity I'll say these are the things that make a v capacity which one's the right one that'll be a type of example of a question based off of this graph any questions about lungs and how we breathe in and out this is just normal breathing I didn't want to hear ever do these pulmonary function tests due to asthma okay so you should know this one this last unit we talk about with brief is called forced expiratory volume test or fe1 what we're testing for here is how much of your total lung capacity that you have in your lungs how much of that can you get out of your lungs in one second so it's a forceful inhalation forceful all the way out very very fast and forceful get all that air out as much as you can we want to see how you do in one second how much can you get out graphs look like this you breathe in in and then out and we see in one second how much of that air came out what does that tell us obstructive diseases okay COPD asthma they have obstructions to flow will they be able to get out a lot of air in one second no so those patients were like cop PD fe1 goes down now what is the other type of lung diseases you have obstructive diseases and you have what's the other one restrictive diseases restrictive diseases have no problems with flow their problem is volume they just can't get a lot of volume of air in but they can move it very easily think about having a straight jacket on you try and take a big breath with a straight jacket you can't do it it's a restrictive disease it's restricting the volume but I can still get the flow out fast just give you real world examples of why we know and look at this number so F1 just know how much air can I get out in one second that's all you got to know about fe1 for now and then we just talk about that muscles of ventilation I they are diap Fram is a big one when it comes to inspiration the external intercostal muscles provide create this bucket handle right here so it allows your lungs to expand like this that's why pa when you do that diaph uh thoratic expansion you put your hands on the side of the ribs and they breathe and you see the rib go like this your hands should move like that that's what's going on there expiration is passive at rest but active with exercise you have to be actively exhaling during exercise okay so what happens when you start running for people who don't run very much what do you get you get side splints right little pains in your sides why because those muscles are being used probably for the first time in a very long time because you don't exercise and you start exercising and doing it you start getting pain here because those muscles are fatiguing out because now with exercise expiration is active we actively have to squeeze our abdominals abdominal wall those uh intercostal muscles to Exhale during exercise if you eat ribs it's those little rib meat in between the ribs that's what you're eating those muscles that help you with breathing so when I taught I taught high school and uh we did all the muscles and everything so we brought chicken wings in I told them to like identify like what what are the muscles um so way so your in internal intercostal muscles are right angles to your external obliques and that assists with the exhalation that occurs during exercise Airway Anatomy we have two major zones the conduction Zone just conducts air they're just tubes there's no diffusion happening these are your trachea bronchus M uh the right and left broni and the bronchioles and then finally we get to the respiratory zone and this is where start gas the gas exchange starts to happen okay we have a thing called a lung asinus which is just a functional unit formed by the Termino bronchioles alvary ducts basically that's what it is so an asinus is like one little stock of broccoli with all the alveoli on the end that's an asinus it's a functional unit that's all elasticity so remember we talked about recoil when we breathe in our chest wall expands but the natural properties of our chest wall are to recoil and again that's why breathing is passive at rest with expiration it's just your normal chest wall collapsing on itself um so they're always under elastic tension because they're attached to the thoracic wall so the lungs the outer layer the visceral layer of the the lungs are attached to the chest wall when you get a num thorax and that the lung collapses it pulls away from that chest wall and you lose that suction so you have to do is you have to do a chest tube to pull the air out that got into that lung cavity sometimes I'll put like talcum powder like baby powder on the lung and it helps it attach back to the wall so that's what's going on there again again tension increases during inspiration and then passively recoil and that let's air out and obviously this tensions reduced by elastic recoil during exercise and expiration um and that allows us to get back to our normal setting the law of the plas we talked about um not really um it's all going along with like Bo's law that the pressure is inversely proportional to the radius of the Alvis as the Alvi gets bigger the pressure goes down again we need air to travel goes from high to low pressure we have to create these low pressure environments um all we're saying here is that small alvioli would be at risk of collapse without surfactant so as those alvioli start getting smaller and smaller remember we need to have a little bit of air left in there to keep them open the surfactant helps as well um keeping that surface tension there so that the Alvi won't collapse on themselves we don't want them to collapse here's just another one talk about surfactant um secreted by type 2 alveolar cells hydrophobic proteins so that water loving or water hating water hating so it's going to resist water push it away reduces surface tension between water molecules prevents collapse is the big one and again allows residual volume to remain in the lungs that's the role of surfactant uh just a quick clinical correlation regarding surfactant this respiratory distress syndrome of the newborn called highin membrane disease um usually associated with premature babies when they're born without surfactant because the lungs are the very last thing to develop in babies the entire time they're developing mother provides all the oxygen for them but so they don't need the lungs so the lungs are the last thing to develop so when prees are born they usually give them some steroids to get that surfactant being made so that they're they can breathe and not have any respiratory problems so that's kind of where this is going from don't go crazy okay regulation of breathing how do we regulate our breathing this is a vital processes so of course it's going to happen in the brain stem your medulla aanga heart rate control is there breathing control is there as well so breathing comes from motor neurons from two different areas of the brain why two different areas for breathing what's special about breathing what can we do with it we can control it so we have voluntary and involuntary inputs into our lungs so that you can breathe at night when you're sleeping and you don't need to think about it obviously we have the voluntary breathing motor control from the cerebral CeX remember the cortex is where all the motor function comes from okay and our involuntary breathing comes from the respiratory control centers in our medulla alagada and the ponds so respiratory control centers are there for our normal day-to-day and voluntary breathing so here is our voluntary coming from the cortex we get input from other receptors because remember if you ever had an anxiety attack and you start breathing heavy that is the input coming from these areas saying we're having an attack are breathing heavy it's induced from those other places to control your breathing and make your breathe heavier we have stretch receptors okay they're going to want to know like uh how big the lungs are being stretched if it gets too much we can reduce our breathing so we don't you know exhaust our inspiratory muscles out and so forth we have irritant receptors okay if you ever cough on water we go down the wrong tube that's your irritant receptors that are being triggered to make you cough to get stuff out we also have our peripheral chemo receptors kateed body aortic Arch they're looking at O2 levels CO2 and H hydrogen the pH of the blood that will tell us a lot of information what's going on with your breathing metabolic requirements when we start seeing changes in your pH we have Central chemo receptors again CO2 and hydrogen and we have receptors in our muscles and our joints when you start exercising the fact that you're moving your muscles and doing things will make your breathing rate go up because we have a greater demand of oxygen because we're exercising we're doing some activity we have to get more oxygen in we need to breathe more to get more air in more oxygen available for a diffusion so these peripheral and cenal chemo receptors are the same ones that we talked about the barrel receptors for the cardiovascular system they follow the same nerve so make sure you know which nerve controls what or senses what when you're studying it's the same one so brain sem receptors motor neurons the major nerve is our frenic nerve C3 to C5 is the frenic nerve and that goes right to our diaphragm and that helps control diaphragmatic muscle um other ones that going to help arrive rise from the thoraco lumbar uh region of the spinal cord to go to the lungs as well obviously we have the blue which is parasympathetic intervation red is your sympathetic we know because of that sympathetic side chain ganglion that's right there and we have our motor which is all the green arising from C3 through C5 to make that frenic nerve ponds obviously is going to influence our medular activity has an appn Center promotes inspiration and a num numot toxic Center which inhibits respiration so sometimes you have um buildup of CO2 we have to get rid of it so we need to induce hyperventilation to get up rid of that CO2 that's our response in the the austic center to get blow off that excess CO2 um if we have too low CO2 through um hyperventilation we try and get that pneumotoxic Center involved to inhibit your breathing to slow your breathing down so just know apneustic if I'm going to stimulate the apneustic center I'm going to stimulate breathing if I stimulate the pneumotaxic center I'm going to inhibit your breathing and then here are the centers we have our pneumotaxic Center attic now what was the apneustic area is that going to stimulate or inhibit breathing stimulate the pneumotaxic center what's that going to do inhibit now remember what we learned about our neurons and the way that neurons get the impulses from the preceding neurons through dendrites acting on that Soma in the cell body remember where the inhibitory ones were right towards the end right before you went to the main part of the neuron where you send the signal look where the inhibitory ones are here it's going to block any stimulatory if you stimulate the pneumotoxic center it's closer up it's going to have an an hibitory effect and stop any ostic stimulation in its tra so again we have the inhibitory one right at the end so we can block any stimulation to provide that negative feedback again here are the chemo receptors okay um they can control breathing based off the feedback from our chemo receptors they're going to monitor pH of the blood and then here's your answer for the one I told you before your cored body cranial nerve 9 the aortic Arch is your Vagas nerve so make sure you understand what type of pressures they're looking for because they have Barrel receptors there they high pressure low pressure when you're doing the cardiac but in the pulmonary they're also monitoring blood uh O2 levels CO2 levels and pH as well so regulation of ventilation we have the cerebral cortex is involved here's our ponds with our apneustic and our pneumotaxic centers they're going to have an influence on the medulla aanga which then will regulate your breathing to a spinal cord through its pns SNS inputs or if it's voluntary breathing still goes to the spinal cord and then obviously through your frenic nerve to get you breathing more so this is a graphical way of just looking at how our breathing is regulated um okay we'll do this and we'll stop for a break so effects of pH and CO2 on ventilation in hypoventilation is that fast breathing or slow breathing slow breathing CO2 levels rise we're going to go up we're not breathing enough hypoventilation because we're not having a lot of breathing we're not having a lot of gas exchange CO2 will start building up in our blood because we're not breathing enough to Exhale it so if CO2 level goes up is CO2 an acid or a base acid so our pH levels start to fall we become more acidic so hypoventilation causes a respiratory acidosis the respiration is causing the acidity by not breathing enough in hyperventilation now we're breathing too much CO2 levels fall because we're breathing a lot a lot of gas exchange CO2 goes off really fast and our CO2 levels drop called hypocapnea and the pH levels rise because we're losing CO2 we're losing the acidity our pH levels will start to rise ventilation is controlled to maintain constant CO2 and a blood pH between 735 and 745 increased CO2 is the primary drive for breathing CO2 is what does it not lack of oxygen so let's take take this step by step first block emotional and voluntary control okay anxiety attacks scared okay these remember these go to your olymic system higher brain centers we look at the scenario we compare it to what we've had experience in the past is this a scary environment yes induce anxiety goes through all these systems we do OT and ponds we increase our breathing and we have an anxiety attack so that's one way we can alter our breathing through uh emotions how does co2 by itself have an issue CO2 is sensed by our medular chemo receptors and the cored and aortic chemo receptors so this one is Central these are your peripheral CO2 is sensed three different areas three areas are sens ing CO2 again CO2 is the main driving force for your breathing so by having a lot of sensors for it makes sense it helps us out then it's going to have whatever effect it needs to do O2 and pH are just sens by your cored and aortic chemo receptors so that's where the difference comes in O2 and pH are just peripheral affect your aeren Sensory neurons going into the brain and then has its effect Downstream somatic motor neurons for expiration your inter intern costal and your abdominal muscles that's how we expire those are the two muscles involved for that if we're going to deal with inspiration diaphragm your external intercostals and then your um scaling cloid muscles those are your accessory muscles to breathing if you see a patient and they're in a really bad asthma attack and you see them breathing like crazy and you can see all their SC sticking out the scaly muscle sticking out of their neck that means they're really trying to get air into their lungs they're using all their muscles to really get the air in because they have such obstruction they have to generate a lot of force to get the air in they have to breathe in really hard the problem is they're GNA fatigue out fast they can't keep that inspiration going for a while when they can't hold it anymore they can't breathe as much anymore CO2 starts to build up they hypercapnic and they start causing other problems from there that's why CO2 is so bad so again understand that with regards to um O2 CO2 pH and where they are sensed okay so here's effect of pco2 on ventilation again with hypoventilation we're not breathing very much arterial pco2 is very high normal ventilation we're right around 40 and then with hyperventilation we're blowing off all the CO2 CO2 drops down to there so you can see how these changes in CO2 occur just by changing your breathing patterns chemo receptor control now we're dealing with our CO2 here okay so we have a decreased ventilation as the stimulus we're not breathing enough we have an increased arterial pco2 CO2 are to build up in our system because we're not breathing enough that's going to cause your blood pH to drop that's being sensed by your peripheral chemo receptors remember pH and O2 are only peripheral CO2 is Central and peripheral and these Sensory neurons go to the your respiratory Center in your medulla amata obviously to increase your ventilation the plasma CO2 also by itself can get to the brain causing decreased pH of the intral fluid within the brain activating your central chemo receptors in your medulla ablang again we need to increase our respirations to drop our CO2 so these are the responses that our body takes in response to decreased ventilation okay remember CO2 is the main drive for breathing the effect of oxygen on ventilation O2 levels will indirectly affect ventilation by making sensitivity to CO2 greater so if your O2 levels start to drop the O2 dropping makes your receptors to carbon dioxide more sensitive so it has a greater response so the O2 drops just makes CED bodies more sensitive to carbon dioxide it's also called the hypoxic drive the cored bodies will respond directly to low O2 dissolved in the plasma below 70 so below 70 is you get to that hypoxic drive you knock out your O2 your CO2 becomes more sensitive to receptors increasing your breathing and then here's just a summary slide of what happen so we'll take a break come back at 130 talk about blood flow okay let's get started so we' talked about how air gets into our lungs we talked about the effect of CO2 O2 and pH on our lungs what happens let's talk about pulmonary blood flow because obviously blood has to get through the system to be perused so we can get O2 we can deliver CO2 and so forth so because we're dealing with the pulmonary system we're going to be dealing with the right side of the heart now right ventricle pumps to the pulmonary system so any changes that go on with the pulmonary system are going to be reflected in the right ventrical the mean pulmonary so again make sure you really read the words because they're going to start combining similar topics and make sure you understand that we're talking about pulmonary artery pressure so your map for the pulmonary system is about 10 and your systolic about 25 and your diastolic is about eight very very very low pressures on the right side of the heart the left atrial pressure is about 5 mm of mercury and again that provides the gradient CU remember for the pulmonary system it's the right ventricle pressure that we generate and it where does it what chamber of the heart does it feed into left atrial that's the gradient to allow blood to flow through the pulmonary system as long as that gradient is still there we're okay blood will flow through the pulmonary system um why it's nice let's continue on though for the systemic circulation left ventricle pressure and where do we have to wind up right atrial and that's the pressure gradient for the systemic circulation okay whatever The ventricle is to the right Atri lower BP in our pulmonary system reduces workload on the right ventricle and reduces risk of excessive intertial fluid formation which will obviously anytime you see excess interstitial fluid formation remember that's one of those layers you have to go through for diffusion and if we're increasing the interstitial fluid formation we'll interfere with our O2 diffusion because we have a thicker layer to get through core ponal is one of the only times you'll see right sided failure by itself the main cause for right-sided heart failure is left-sided heart failure but there are causes sometimes where the right side will fail by itself and it's usually due to specific problems with the lungs itself a clot in the lungs Scleroderma which is vascular disease and COPD these are things that again don't worry it's not going be on your test just reinforcing that things that affect the lungs by themselves have an effect on the right ventricle itself okay we're talking about pulmonary vascular resistance not systemic vascular resistance if I increase systemic vascular resistance that's on the body and the the left side of the heart we're talking about pulmonary vascular resistance what's the resistance through the pulmonary vasculature and how does it have an effect on our breathing so low profusion pressure drives pulmonary flow because pulmonary vascular resistance is low everything flows really easily resistance is shared between arterials capillaries and venules we have Alvar vessels that are influenced by Alvar pressure when we talk about the alveolar pressure it's the pressure inside the Alvis due to air that's in there or may not be in there at that time our extra alveolar pre vessels these are the ones remember we had that picture way before where we had the Alvi and then you had remember we had that all the capillaries were right around the Alvi that's what we're talking about these extra alveolar vessel as the lung expands the radial forces increase and causes these extra Alvar vessels to open which reduces resistance so remember as the lungs expand the radial forces that push out and it just pops these vessels open allowing for capillary blood flow if we have capillary blood flow and we have ventilation in the alv we're going to have gas exchange you have to have both things there ventilation and perfusion those of you who worked in the hospital if you did anything with nuclear stuff have you ever seen what's called a VQ scan V is what ventilation what's the Q profusion cardiac output we do a Mis see if there's a mismatch there to see if there's a clot in your lungs if you have PE pulmonary embolism means there's we have a mismatch somewhere you don't have to know it again just putting s information if you've heard it before now you know why what it means where's the rest of the stuff me just close this re open it okay so look at this graph pulmonary vascular resistance pulmonary circulation is forced to accommodate large increases in blood flow when cardiac output increases EXT exercise we need more blood going into the lungs so that we can profuse it and get more oxygen into the system so as cardiac output increases pulmonary vascular resistance decreases why is that important what's going to happen to flow if the resistance decreases increases why is increasing flow of blood very important for exercise we need more oxygen in the system we got to breathe heavier yeah we can breathe heavier but if we don't increase the amount of blood going into the lungs it's not going to matter they have to be the same so we have this match of ventilation with perfusion so we can get our blood oxygenated so here's our pulmonary vascular resistance here's arterial blood pressure during exercise because pulmonary vascular resistance occurs because of distension of the pulmonary capillaries and recruitment of capillaries so those extra Alvar capillaries that surround each alvioli the diameter is going to increase if the diameter increases of a capillary what happens to the volume that can get through it increases we have more the other thing we do too is recruitment of pulmonary capillaries right now we are all at rest we're all upright most of your blood is pooling in the lower in the base of your lungs so the 2/3 The Zone one and or the numbers but the top two zones of your lungs right now have the ability to be perused but you don't need it because you're not exercising there's no demand for oxygen so they just stay ventilated you breathe in and out you can hear on the lungs but they're not being profused we don't need it when we need it blood pre blood pressure starts going up we're exercising we need more oxygen going through we need to breathe deeper and heavier as we start doing that Blood starts to fill up all those remaining parts of the lungs now we have a reservoir of o2 waiting there when we need it we recruit more capillaries incorporate more parts of our lungs they're all being perused they're all getting oxygenated therefore our tissues will get oxygenated as as well this is talking about lung volumes and Pulmonary vascular resistance at low lung volumes like a restrictive disease restrictive disease will compress your extra alveolar vessels leading to an increased resistance so low volumes restrictive lung diseases these are your lung volumes these are the low side we get compression of the vessels when you compress them the radius decreases right if the radius decreases what happens to the resistance increases so at low lung volumes all those extra Alvar vessels all collapse they don't stay open remember the opposite we learned before when the alvioli increase and they get big what happens those extra alveolar vessels they get big as well but now there's low lug volumes those alveoli get very small they start to collapse when they collapse the extra Alvar vessels collapse as well if you're losing surface area resistance goes up now at very high volumes like empyema your pulmonary capillaries get stretched when you stretch something what happens through the width of that object it decreases we have very high lung volumes now so all the alvioli are not they're normal popped open now they're bigger when they get really big all those little capillaries that travel around them they get stretched they get stretched resistance goes up and that's why up here we have these two sides of the story we to operate right there that's a great normal lung volumes we're right in that sweet spot of pulmonary vascular resistance when you start adding in pathology and different problems you get changes in pulmonary vascular resistance on the low side and the high side so when you're studying this understand why at low lung volumes does PVR go up and why at high lung volumes does PVR go up as well pulmonary vascular resistance not anything else so smoking destroys the alveolar membrane and your corresponding capillaries with smoking so we're going to decrease pulmonary capillary cross-sectional area because we're losing capillaries and they get an increase in pulmonary vascular pressure that's why smoking is so bad so it destroys your lung tissue causing less capillaries less capillaries there less cross-sectional area resistance goes up Regional differences in perfusion like I said before blood flow is greater at the base of the lungs than at the Apex again due to gravity blood just going to sit in the base of your lungs nothing wrong with that and because of that we get three lung zones that are created within this gradient so here are the lung zones Zone Zone one in blue let me change my color to Blue so we're all the same Zone one is over here Zone one if you look is at the Apex it's one two three so three is the base one's the Apex in zone one arterial and Venus pressures are both less than the Alvar pressure so here big a is arterial big V is V Venus pressure the little a is Alvar pressure alveolar pressure is right in the middle of these two remember we're at the Apex now we get compression of pulmonary capillaries no perfusion so in this case in zone one you can see here we're clamped off alveolar pressure isn't greater enough so Zone one it's ventilated but no profusion it's called alveolar Dead Space ventilated but not profused zone two in zone two is the green is the middle of our lungs Alvar pressure is between AR and Venus pressure you can see here little a is greater than arterial and Venus this is the middle of our lung vessels are partially constricted blood flow is limited in zone two zone three is at the base zone three increase High hydrostatic pressure of blood why why does hydrostatic pressure go up in in the base zone three that's where all the blood is more blood volume more hydroid pressure it goes up in this case arterial and Venus pressure both exceed the alveolar pressure and therefore they'll be open and they'll be ventilated and profused you can see that in the picture the vessels are wide open the capillaries are wide open allows for profusion of the blood therefore we have ventilation we have diffusion of oxygen and so forth so just know for this one at zone three at rest zone three is the base everything is open we're being profused in the Apex because of gravity there's no profusion in the Apex but they are still being ventilated but there's no profusion therefore no gas exchange occurs in the Apes when you exercise all these systems open up the whole lung gets profused and you will have profusion and ventilation in all parts of your lungs when they start to exercise so let talk about gas exchange so in the very beginning we talked about partial pressures of oxygen at zero feet which is right about where we are we talked about atmospheric pressure is 760 we know that 21% of the air is oxygen so if you divide 21% of 760 you get 159 and then that's in the air and then finally when it gets into the lungs we have you know 105 and then finally 100 why do we have this drop what is going on that we have this drop drop an O2 from the air into the lungs water vapor we're adding in moisturize we're adding air water into the air we're moisturizing and humidifying the air so it can get into your lungs for a better exchange when you go very high um so Mount Everest 30,000 ft 19 is your partial pressure of oxygen that's why they wear gas tanks when they go up there's some people that refuse they want to do it no tanks and they don't have any Air Supply they just go up on their own but again you can see how by going in altitude if ever even gone to like Denver you may have problems breathing for the first few hours when you're there we'll go through that what happens with adaptation to altitude in a little bit as well so we measure O2 dissolved in the blood plasma when you do your pulse ox it does not measure oxygen bound to hemoglobin in the red blood cells we are just looking at free dissolved plasma of o2 and when the lungs are functioning properly there's only a 5 millimeter mercury drop and again at about 100 hemoglobin is completely filled with O2 as long as that P2 is at 100 you'll have sufficient loading of o2 into all the hemoglobin they'll be all satisfied in the blood remember we have to be set up in a way that allows for diffusion from high to low so in this is the lungs breathing into the air we have 105 units of o2 and 40 of CO2 this is in the capillaries in the lungs they get dissolved in by the time it gets to the pulmonary vein we're at 140 this travels around goes to Our arteries and now we're in the tissues at the tissue level we have unloading of oxygen going into the cells and we have CO2 being dumped into the blood it's a waste product we have to get rid of it so we are adding CO2 and we're reducing O2 because we're extracting it so when you look on the syic veins po2 drops down to 40 we've taken 60% of the oxygen out of the blood when it comes back to the uh right side of the heart it's down to 40 we're adding CO2 so CO2 goes up to 46 because all cell respiration produce CO2 it's going to build up obviously on the Venus side which takes all the waste products CO2 Rises so that when we finally get back to the lungs we have the appropriate setup where we have P2 at 40 pco2 at 46 so we have the right setup for diffusion so that CO2 will leave the blood go into the lungs CU only 40 in the lungs it's 46 in the blood so CO2 will def fuse into the lungs so we can exhale it out O2 is only 40 coming back to the lungs it's 100 in the Alvi so O2 gets dumped into the blood because the diffusion gradient favors that direction that's pretty much it on pressures of gas long as you understand that there has to be a diffusion gradient going those directions understand we have to get rid of CO2 so CO2 has to diffuse into the lungs we need O2 we have to get it into the bloodstream so how do we get all this transport to occur hemoglobin is the molecule that does it they're in the red blood cells majority of all the oxygen that we breathe in that gets diffused into the blood majority of it gets bound to hemoglobin each hemoglobin can carry four molecules of o2 obviously we have millions of hemoglobin per red blood cell so therefore each red blood cell can carry millions of o2 molecules to the body wherever it's got to go oxyhemoglobin saturation so percent of oxy hemoglobin what is been oxidized because it's bound to the hemoglobin versus your total hemoglobin this is your pulsox how well the lungs have oxygenated the blood a normal O2 set 9 7% okay so 97% of our hemoglobin should be saturated with oxygen um and you get your pulseox for that okay hemoglobin concentration obviously if you have anemia you have below normal hemoglobin levels polycythemia higher than normal arthop poan is the one we learned about that in the blood when O2 levels drop in the blood we're not breathing get enough oxygen we can't peruse it our lungs well diffusion is altered somehow we're anemic we're not getting enough oxygen kidneys will sense it and they'll kick out urethal potin goes to your bone to start making more red blood cells so we have more carrying capacity for oxygen O2 levels go back to normal because we made all these cells EPO production slows down because we're not anemic anymore so that's what EPO does with the we have to load oxygen we have to get rid of it so when we talk about loading of oxygen loading always occurs in the lungs unloading is in the tissues so we're going to learn how do we get oxygen and how do we unload it into the tissues and what kind of things will favor that to happen so here's an oxyhemoglobin dissociation curve we have on the Y AIS percent oxygen saturation of hemoglobin so we know 97% is normal and on the bottom we have our po2 and millim of mercury so in our systemic arteries it's about 100 and 100 we're close to it so we're about 100% saturated at 97% and we're good systemic veins remember they're at 40 millimeters of mercury in the systemic veins as they're coming back to the lungs back to the heart that's at 40 so we're still at like 78% 79 whatever 80% saturated with hemoglobin or oxygen saturated with hemoglobin so again like I was saying only 22% of our oxygen is unloaded in the tissues we still have 78% oxygen floating around in your blood that's what I talked about yesterday with CPR you don't have to breathe anymore there's enough oxygen in the blood to last you the time while you're doing compressions it's more getting the heart beating to provide oxygen to your tissues than getting oxygen in you have oxygen still you still have 78% of it okay we're not losing all 100% of our oxygen in the blood every time we breathe we still have a lot left so what happens with different types of problems so pH on oxygen Affinity what is the what is Affinity what does that mean binding if I have a high affinity for something I like it I want to be close to it that's Affinity so pH will change the affinity for hemoglobin for oxygen if the affinity for O2 decreases less binding to it with a low PH it shifts it to the right down and to the right if the affinity for O2 increases like at higher phes it shifts to the left up here so you can hold on to more O2 during periods when our blood is alkaline when our blood is acidic we don't hold on to O2 as much we can get rid of it faster and this is just called the bore effect when this happens this is the effect of pH on a for hemoglobin so you can see here when Affinity is normal we are O2 counts about 19.8 but look at how much O2 is unloaded at the tissues five when you have a decrease Affinity pH goes down we unload more oxygen 6.6 Mill so just know where the just know the values go up yes what is the yis on this one oh um just that hemoglobin dissociation curve like percent oxygen that's it's in different ranges this is one so you can be draw it as 100 50 and we know that you know there's that 80% okay temperature as your temperature the affinity for O2 is decreased at increased temperatures it's going to shift it to the right what's an example of when your body is going to heat up naturally and normally in a normal physiologic process exercise right when you start exercising your body gets hot you start sweating get overheated when you're exercising the temperature goes up it promotes unloading of o2 to your tissues does that make sense we're exercising we need more demand of oxygen in our tissues when their temperature goes up it favors unloading of oxygen to the tissues where they need it the blood doesn't need oxygen the tissues do so when you increase the temperature you favor unloading of o2 so it can go to the tissues where it's needed for demand affinity for O2 is increased with decreased temperatures as you get colder and colder and colder your hemoglobin is going to stick and bind to that hemoglobin tighter um when your temperatures are colder so that's that's temperature on the effect and we'll skip that one um let's see where we are at here okay we'll finish this part and we're done okay you have the real one is this everything I already talked about on that part carbon dioxide transport carbon dioxide is in three forms and how it can get around in our bloodstream 5% will be dissolved in plasma remember it's a it's a gas that can dissolve in uh the liquid so go right in 5% will be bound to hemoglobin it's called carbino hemoglobin the majority of it 90% will get converted into B carb through the use of chloride and we'll talk about that in a minute so 90% the CO2 gets converted to bicarb and we'll see what happens as we go through the body what that bicarb does so we use this thing called the chloride shift one bicarb ion it's formed in the red blood cell it diffuses into the plasma so there is our bicarb right there in green it comes out but a chloride ion will come in as an exchanger they're both negative chloride is negative bicarb is negative as well hc3 minus they're both Negative they just help each other out on the way out so we have our CO2 goes into the blood plasma some of it will stay in the blood but remember some of it will also bind to hemoglobin that's that second type 5% will stay there 5% stay there but the majority of the CO2 will combine with water to form carbonic acid this carbonic acid also undergoes a bidirectional uh event with enzymes to give you bicarb plus an hydrogen and this bicarb here is what diffuses out in that chloride shift so this where is this happening in the tissue or in the lungs this is happening in the tissue so the chloride shift occurs at the tissues okay chloride shift occurs in the tissues when we get to the lungs the opposite happens and it's called the reverse chloride shift to get it back to CO2 so you can exhale it we'll talk about that in a second these double arrows are under the influence of an enzyme called Carbonic and hydrates Carbonic and hydrates it's an enzyme it allows the conversion of this to happen so CO2 with H2O makes carbonic acid the carbonic acid then dissociates to make bicarb and a hydrogen ion that hydrogen ion in the red blood cells attracts the chloride to want to come into the cell H is positive chloride is negative they're going to attract so it helps bring that chloride into this into the cell so this is at the tissues now we're at the lungs okay we have to get rid of it okay so this is the bore effect talking about binding the hydrogen to the hemoglobin which is made in this process right here or back out again helps carry more carbon dioxide and this is what happens here's the reverse okay here we are here's the reverse chloride shift we have to get that bicarb back to carbon dioxide we can't exhale bicarb so we repeat the process we do it the opposite way now so the chloride shift the bicarb in the lungs will go into the lung or into the red blood cell chloride will leave the red blood cell let me erase that chloride leaves the red blood cell it's called the reverse chloride shift and everything happens in reverse so we get bicarb coming in it's going to bind with the hydrogen again causing Carbonic uh h23 carbonic acid to form then under goes again with Carbonic and hydrates to make CO2 and water the CO2 you just exhale so chloride shift is in the [Music] tissues the reverse chloride shift happens in the lungs so you can get rid of CO2 yesc it's always in the RBC that's only where it is so this whole reaction occurs within the red blood cell that's where Carbonic and hydrates is located in the red blood cell so if you understand the formula up here the long way to write it I'll just do the whole thing again so it's all one line you can do one way is CO2 plus H2O where does this equation occur tissue or the lungs then in the lungs we have to do the reverse chloride shift so we get H CO3 minus plus the hydrogen carbonic acid and that's in the lungs just the same formula front and backs one's in the tissue one's in the lungs we have to get rid of CO2 we can't let CO2 float in our blood for by itself what's going to happen well if we leave if we remember only 5% is actually dissolved in the plasma if more was dissolved in the plasma what happens to our pH it's going to drop we have a lot of CO2 floating around so we have to get rid of the CO2 we can't just let it be there so by putting it into the red blood cell converting it into bicarb we're able to reduce the acidity of the blood so we don't go we don't get acidic all the time chloride shift in the tissues reverse chloride shift in the lungs so we can exhale the CO2 and get rid of it so reverse chloride shift at the AL at the Alvis Carbonic and hydrates C the enzyme converts carbonic acid back into CO2 and water and we exhale the CO2 and that's how we can move Chlor uh the Chlor shift occurs due to CO2 um regulation and we'll do acid base tomorrow any questions see me otherwise I'll see you guys tomorrow work on if you have any question with the exam Master let me know