everyone it's good to see you again after your first exam and your lectures with Dr Rali I'm back to teach you about lungs Now I want to tell you that next week when we meet on Thursday I will send out a team's invite we will have the lecture but I would like again for you to send any questions that you might have from the reading prior to the lecture We'll get started here So today we're going to cover the lungs So this is chapter 11 This is going to cover the structure of the lungs which includes the anatomy basically It's going to cover the function of the lungs What do lungs do Breathing and beyond And then also common diseases basic ones The book just covers a few and they talk about a couple genetic diseases restrictive airway diseases chronic obstructive pulmonary diseases and some vascular considerations such as pulmonary embolism um edema pulmonary hypertension Has some uh pediatric pages So you might want to just look at those in general as well as adult or geriatric changes over time the structural changes and the functional changes It's very crazy but um that decreases starting at age 25 So all of us who are over 25 have already had a decrease in our lung function Same with kidneys by the way Pneumonia infections aspiration type things happen more with geriatrics And then we will talk about some different focuses both for NPS and for PAS with regard to the lungs because they're different for each For example a nurse practitioner would be more interested in asthma as far as treating it and COPD as far as how the mechanisms work and how to make the patient more comfortable and again treatment where the CRNA is going to need to know more about that from the anesthesia standpoint So we will hopefully cover both bases either through this lecture or through our talk um after in the reverse classroom setting Why do we need the lungs That should be obvious We need it to breathe But then we need to ask the follow-up question of what do the what does breathing do for us So the book goes over several factors and these are the most of them um it maintains homeostasis and so this is going to be involved in temperature regulation and also in hydration status items like that acid base balance you're going to think about the CO2 so we have to get rid of CO2 and in get in oxygen and so we have to do that also throughout the body and so that gas exchange for oxidative metabolism is important so the take up of the oxygen in the lungs the getting rid of the CO2 at that level and then the blood cells carrying that to other parts of the body to then pick up CO2 outside of the lung and bring it back So that is the basic gas exchange for oxidative metabolism immune function The lungs have protective me mechanisms for their cells and we're going to talk about some disorders which disrupt that and they also have um you know blood cell functioning You have to get the oxygen onto blood cells and the way the lungs work can affect what type of blood cells we have as well as where that goes And then we also need lungs to communicate And so if I didn't have air rushing over my linex it wouldn't vibrate and I wouldn't be able to talk to you right now So the lungs for have many functions u throughout the body and they will also have impact on other systems say like the kidney or other um structures So just a summary of how this lecture is going to go We're going to talk about the anatomy so you have a better understanding of how the lungs are structured so that we can know how different disease functions can affect the structure of the lung and how that will affect the body in general We'll also talk about muscularkeeletal aspects the inspiration and the expiration And you do need to know this terminology It's very important for your review The physiology we alluded to earlier um but we're going to talk about that a little bit more The nervous system the automaticity of breathing we don't have to think think about it However we can override it and decide to take a deeper breath or not And also that would be in the motor cortex as opposed to the medulla The lyic system can also affect that's the emotional center So when you get anxious it can affect how you breathe Common measures of lung function will be covered as well This is very important and there will be a differentiation between nurse practitioners and again uh CRNAs in that regard CRNAs are going to see pulmonary function and how it relates to anesthesia obviously and you will see that uh throughout cases and um before you um end up putting someone under you might u review those and additionally nurse practitioners would want to know again how COPD and asthma treatment and the response affects those pulmonary function tests We're going to talk about surfactant what it is and what its role is in the body And then we're going to talk about specific lung diseases as well as briefly discuss some mechanical treatments for um these Again in this class we don't test on pharmacologic therapy necessarily but we do like to know how it relates to the basics of the lung Regarding the respiratory structures there's the upper respiratory the lower respiratory and then we could even go to the al alvolar uh cellular level for the lung So the upper respiratory tract there is some argument regarding ownership of the upper airway structures when we're talking about specialists So who treats or who do who do these belong to So there may be some discussion about ENT being in control of the uh upper airway and pulmonology being in control of the lower airway and that linex uh is sometimes in question of who owns it Um but upper respiratory tract would according to the book includes the fernex and the linex There's this dead space and by dead space it just means that there's no oxygen exchange in general going on in this area The upper airway is very prone to infections and allergic reactions It's very common Now as far as the lower respiratory tract it would include the trachea the bronchia the I'm sorry the bronchi the bronchioles the alvolar ducts um the avioli and these are also prone to infections allergic reactions um alterations in mechanical properties and gas exchange because this is where air is transmitted Now you'll notice according to the diagram which I like this diagram in the book that the upper part of the bronchia the bronchial tubes have cartilage and all throughout the inner lining of that are celia and these celia are constantly moving They're little hairike projections and they move secretions constantly up So it's kind of like an elevator Um and we uh we need that function to clear and you will know later in some other slides disorders that um make that not happen in the lower airway So as far as branching of the lungs they are considered generations So the trachea is considered generation zero and then on down it's uh increasing numbers And so again there's really no major air exchange uh from generation zero to a uh generation 16 And then starting at branches um 17 and on then you do have air exchange because that's where your um avoli are Um the avoli we'll go down to that level Now they do have two types of cellular cells in the avoli These will be type one cells These are flat and they do support gas exchange And then you have type two alvolola um which are progenitor cells and these produce your surfactant That surfactant is necessary to keep them open create a surface tension and we'll talk about that a little bit more Before we go into how we breathe I want to talk about the structures of the lungs And it's important that we recognize the anatomy both internally which we talked about on the previous slide and externally which is what we're going to talk about on this slide and be familiar I want you to be very familiar with structure of the lungs and how we breathe That's very important for testing purposes You will want to know these specific portions And so we're going to go from the lung tissue outward Um and this diagram shows it very well So you have the internal lung Um here the lung itself is very sensitive tissue responds to environmental changes and cues If we have a lot of smoke in the air or low oxygen in the air there's too much carbon dioxide it's going to change based on those And it's also driven by internal physiologic needs We need more oxygen We need less oxygen at the time So this this tissue will adjust and adapt The first layer um then outside the lung is the visceral plura Visceral means organ So anytime we talk about visceral we're talking about an organ In this situation we're talking about the lung is the organ The visceral plura it covers the the lung itself So it's the inner layer of this two-layer membrane And then you have the plural space And so you will see that here on the diagram And then you will have the outer layer which is the parietal plura And so the par this is again all fluid and it's meant to reduce friction when we breathe in and out It allows the lungs to expand very nicely while still keeping it um protected So when there's too much fluid or inflammation in this area and say you get some swelling and fluid it will cause friction there And so when you breathe it will actually maybe rub against each other And so that's where you know people have pury and so you can hear that or oscultate it and know that that's what's going on And so in addition to the structures of breathing we have the interccoal muscles which again have cartilage that allow us to expand It's kind of like cheating on these exams I think because you can actually take a breath and see what's going on Your diaphragm which is below your lung basis is the muscle that's needed The frenic nerve is what's involved in uh neurologic control of breathing And then um we know that negative pressure keeps the lungs in close contact with that chest wall and diaphragm So the pressures in the lungs are important to being able to put air into the lungs and out of the lungs So now that we've reviewed the structure of the lungs and how this can function let's review the understanding of how we breathe which is really the most most basic of healthcare concepts First thing you learn when you're doing CPR is look listen and feel And so that's all about breathing Um it's something we take completely for granted basic you know basically Um box one here basically tells you that the lung and chest wall the intercostal muscles and the diaphragm they work as a unit We talked about those structures and showed you on the previous slide And they draw air in through the nose and mouth and down a series of greatly branching narrow airways which we showed you have different generations and where the oxidative um processes start in the lungs with the alvei The elastic recoil of the lungs chest wall and diaphragm store energy and then release it allowing normal expiration So box one really talks about inspiration Box two um explains our expiration and then the pressures and volumes change during inspiration and expiration depending on the compliance of the lungs So we don't want too much compliance and we don't want too little compliance um of the lungs and chest wall So when we talk about compliance it's really stretchability So we'll talk about in COPD how we have too much compliance it's over compliant It's it kind of blows up and doesn't have a lot of strength So a lot of um resources or different um examples will talk about a a sock like when you've gotten your sock and it wears out or a rubber band that's overstretched That's over compliant or too much compliance And then too little compliance would be a stiff lung tissue scarring You think about things that restrict the lung like fibrosis and then resistance is the other portion of how pressures and volume changes occur with inspiration expiration So if you have airway resistance such as in asthma you can't get air in it makes it very difficult to breathe So those two major things compliance and airway resistance are important when we talk about diseases of the lung And then finally the thin walls of the avoli are the interface between the lung air and the pulmonary capillary beds And this surface um is very specialized and it allows for gas exchange primarily O2 and CO2 And the movement of oxygen and carbon dio carbon dioxide occurs by diffusion between the air in the air sack or alvoli and the blood which is the capillary bit A lot of people don't you know think about that concept of you know there's no blood in the lung It's just the airsack and then the capillary lines that airsack each single one of them And I would want you to go back and review simple diffusion And simple diffusion is in your book on page 79 It talks about how carbon dioxide and oxygen occur um which go down a gradient Um it doesn't create any um energy to do that It just happens by simple diffusion So go back to page 79 and read about simple diffusion here because we like to build upon principles that we have covered already Now that we have talked about the structures of the lungs we are able to talk about how we breathe Inspiration So inspiration step one the diaphragm will contract and that happens because of frenic nerve innervation at C3 to C5 The diaphragm then will move down and flatten compressing the abdominal cavity out of the way for the breath The interccoal muscles particularly the external intercostal muscles will contract and these are actually contracting because of motor neurons from the thoracic spine rather than the same area where the diaphragm comes from which is very interesting The ribs will then elevate move out of the way It will increase the chest volume that's there So the circumference will increase and the volume area will increase And this then creates an opening for air to come in or rush into the lungs And so that is a negative pressure then So there's negative pressure in the lungs on inspiration And that's compared to your atmospheric pressure in the room that you're in So that pressure drop uh the negative pressure within the lungs airway uh opens and then it can then the air can flow in The expiration then is just the opposite So the reverse occurs the diaphragm and external uh intercostal muscles will relax and then that will decrease the volume in the lungs creating a positive pressure forcing the air then out The previous slide discussed how we can see actually the muscles work on inspiration and expiration And you can kind of cheat you know you can take a deep breath in and see how your chest and your ribs and your abdomen and you can imagine your diaphragm in there all work and what happens on expiration So for your test you can almost have a physical cheating mechanism there But for the pressures we want to talk about lung pressures This is also an important concept for you to know for your exam We're going to talk about this in relationship to the transpulmonary pressure and how that is in inspiration So transpulmonary pressure should be positive to begin with and then you know as you breathe things change and the equilibrium becomes different and this all relates to both the the the pressures inside the lung and then the alvolar pressure and also this the pressure in that plural space because we want that pressure in the plural space to not be the same as the atmosphere um it has to be um different So if it is the same as atmosphere or zero your lung is going to collapse So we need that pressure within the lung to be positive so our lungs don't fall down on themselves So transpulmonary pressure is positive and when it's positive the lungs will expand transpulmonary pressure negative then the lung is going to collapse As you breathe in the interplural pressures become negative At the same time the alvolar pressures decrease but still remain less negative than the plural uh pressures So just remember at the beginning inspiration transpulmonary pressure during the inspiration is positive Um the equation is transpulmonary pressure is equal to alvolar pressure minus plural pressure And so if you keep that in mind you can do the math and put different numbers in there and know that you have to keep your lung expanded So inspiration increases lung volume because of the diaphragm's descent and the chest walls expansion And that way you can keep those pressures correct to keep the lung open There's a really good picture on page 406 of your book and it talks about the pressures during relaxation and contraction of those um intercostals And um you can read there in the book what it it says on page 406 Again you want to keep that in mind as an important concept for your exam So we've talked about the lungs expanding and you can almost cheat again and know exactly what's going on when you breathe And we've talked about um the mechanisms of how that works with pressures in the lungs And now we're down to the gas exchange level And so what we're doing is we're exchanging oxygen and carbon dioxide in the lungs And so oxygen and carbon dioxide are soluble gases in aquous or liquid solutions and and they move across the lipid billayer Um in this case at the alvolar level and the movement occurs by simple diffusion Again page 79 of your book go back and read simple diffusion This is going just down the gradient It does not require any energy And um this helps exchange the two gases across that membrane So oxygen then is carried by hemoglobin So on your blood cell hemoglobin each hemoglobin molecule actually has four binding sites for oxygen And when all are occupied when all four of those sites are occupied we we say that the um hemoglobin is 100% saturated with oxygen So oxygen is carried by the hemoglobin and every hemoglobin molecule with that four binding sites 100% occupation when all of those binding sites are saturated Now there's going to be a lot of times when that's not the case and we still can function at that And it's important to understand as in the book on page 422 the book uses numbers like 40 millime of mercury and 100 millime of mercury as it relates to hemoglobin saturation And for example it states that 40 millimeters of mercury when we're talking about saturation is about 75% of your oxygen molecules uh saturated And how much of the oxygen is on that he hemoglobin molecule he hemoglobin molecule as a percentage um of how much it could carry And so a normal say if we're talking about SP O2 you guys see that all the time um which is saturated peripheral oxygenation and so that's we just take a pulseox and that's should be about 95 to 100% uh saturation well depending on age and some other characteristics So we will look at that on the next page Um now partial pressures of dissolved oxygen surrounding hemoglobin actually determines the percentage of oxygen bound to the hemoglobin molecule And then the nonlinear characteristics of this binding are shown by the oxygen hemoglobin association or dissociation curve And again that is on page 423 of your book So be familiar with um both that figure on page 423 and also it talks about a lot of things that influence um the oxygen hemoglobin dissociation curve For example the blood pH Uh we talked about uh respiratory acidosis or alkalossis It can affect the blood pH and it would uh determine how much um the pH would determine how much oxygen can be uh on or off uh the molecule There's also a thing called uh 2 three uh DPG which affects the affinity for binding Um you know iron also affects the affinity for binding um temperature For example when you exercise it would increase your temperature And when you um have hypothermia it would uh decrease your temperature And some of these factors which we can look at that curve can determine you know how much oxygen your tissues need And so we will discuss that oxygen curve next Looking at this curve we have to consider again where we are in relationship to the um gases that we're talking about Uh for your exam you will see questions related to this And be sure you are focused on the space you're being asked about For example is the question asking about the oxygen and CO2 in the lung tissue the aviolar sacks or is it talking about the oxygen and uh carbon dioxide in the capillary bed So make sure you know think of what you're being asked So as you can see that there's three different areas We're talking about blood entering the avular capillary the avular air and then blood arriving at the tissues And so blood entering the avular capillary as it comes in you know into again we don't have direct um access of blood into the lung otherwise we would be breathing blood But this capillary bed runs along the avioli And so when it comes in it has a PO2 pressure of about 40 mm of mercury And we equivalate that to about 75% oxygenation of the hemoglobin on the red blood cell And so as it comes down and comes then in contact the aviolar air the air inside of the air sack in your lung has a p to a pressure of 100 mm of mercury So that's clearly higher than the 40 mg in the uh capillary bed And so that allows for simple diffusion um from 100% or of 100 millimeters of mercury to 40 mill of mercury to try to equivalate that And then as the blood supply continues you know we hope that that reaches um 100 millm of mercury in the blood vessel by the end of of its contact with the avoli As that's happening CO2 is being released from the blood supply back into the avular sack So that then you know through the actions of breathing you breathe out carbon dioxide That's how we get it from our bodies production and then get rid of it So there's this indirect correlation It's not you know exact that you exchange the exact amount of O2 for CO2 um but CO2 is then um at the point of in uh exiting higher and then when when blood arrives at the tissues it will equivalate with the uh tissue P2 and have the same type of transmission there and so oxygen leaves binding sites on hemoglobin and enters the tissue and then the hemoglobin saturation falls then after it's delivered it's oxygen that's needed by the tissue and then comes back uh to get replenished So again I just want to go over this slide Blood entering the avular capillary the average is P2 of about 40 millime 40 millm of mercury with the average hemoglobin of about 75% The aviolar air at that point is a P2 of 100 millm of mercury and then avolar air quickly equilibrates with the blood plasma and brings the blood pH to the same level And then hemoglobin at that point we hope is about 100% saturated with oxygen and then blood arriving at the tissues equivalates uh or equil equilibrates with the tissue P2 oxygen leaves the binding sites and enters the tissue and then hemoglobin saturation falls again be able to discuss circulation of oxygen in the blood tissues we have to talk about hemoglobin and So a hemoglobin molecule is composed really of these three units uh an alpha subunit a beta subunit which are required to compact together their proteins that make up this molecule and then an iron containing hem group and this this allows for sites for oxygen binding and there are four oxygen binding sites As we explore things and discuss next week we will talk about why hemoglobin has to bind loosely or be reversible So think about that as you're reading your material and why that's important Again on page 422 um you can see that hemoglobin is usually related in terms of saturation So 25% 50% 75% or 100% 0% would be bad right Um for our concerns you in the uh peripheral tissues 75% oxygen saturation is the average of the Venus or the systemic blood supply and 100% for arterial blood And we're going to talk about in a minute the difference uh in the lung because it's the only place where an artery um carries unoxygenated blood and a vein carries oxygenated blood Um so we will talk about that one minute A lot of times we're um looking at the unhealthy lung in this chapter because this is pathophysiology But I want you to consider the the healthy lung and um know and be very familiar with healthy lung um profusion dusion So this is a very good picture It's in your book on page 425 It has a lot of uh talk verbiage uh about figure 1127 I would think you need to be uh familiar with that process Talks about the healthy lung So again um you can see that as the blood supply comes into the lung um and it goes by these two healthy aviolar sacks the the partial um the pressure of oxygen is about 40% as it comes in and the part uh pressure of carbon dioxide is about uh 46 uh millimeters of mercury I think I said percent but these are pressures millimeters of mercury and inside the havar sack Again the pressure of oxygen is 100 and the pressure of carbon dioxide is 40 And so that allows for dusion And so the blood supply picks up the oxygen and the blood supply lets go of the carbon dioxide and it goes into the alveular sacks And so then that's how you expire or get rid of your carbon dioxide So the goal of breathing is the oxygen comes in to the lungs and it creates a higher pressure diffuses out into the blood supply and then that blood supply um going from the aviolar capillary beds to the right atrium that is full of oxygen and low in carbon dioxide So again should have a high oxygen content um high oxygen pressure and a low carbon dioxide pressure So again remember where you are in the body when we're talking about things So final blood composition traveling to the left atrium is equal to the avular blood gases This makes me want to cover the blood supply actually of the lungs being a little bit original in this is the only place that artery carries deoxxygenated blood and the only place that the pulmonary vein carries fully oxygenated blood So we're talking about the tissue It's a whole different story because again those um those are um arteries going away from the heart should carry oxygenated blood and low in CO2 But those that are coming back to the heart um those tissues in the circulation are going to you know have gotten rid of their oxygen and be have picked up oxygen from the periphery and bringing it back to be exchanged and breathed out So goes from circulation to the right heart Then the pulmonary artery will um go to the lungs because it's de and it's deoxxygenated at that point It picks up O2 in the lung capillaries exits the lung via the pulmonary vein which dumps into the left heart and that's full of oxygenated blood and then uh goes out to the circulation How does breathing work Well it is under neural control um it is a rhythmic pattern We have discovered or scientists discovered for us really as recently as 2016 We didn't know this before that time that there's actually a spot in the medularary uh center Um it's called the prebotzinger complex And so this is in your brain stem but we know that these particular locations loi um are actually what controls our automatic breathing And so this area will receive messages um about the lung volumes about the blood pH and the O2 and the CO2 very similar to how we would see maybe thyroid um given it's given messages and it sends out neural responses in relationship to what it knows and it it controls your regular breathing how much you need to breathe And so obviously this must uh have some play in um like obstructive sleep apnea or some other um neurocontrolled breathing disorders And so we need we need this bot pre-botzinger complex It is in red so it's probably important Um so when you when you see um recent data it will tell us that this is how we breathe And obviously uh this can be temporarily overridden You can take conscious control of your breathing which I think is totally fascinating and that's in the primary motor complex of the brain and the frontal lobe and it controls the movement of the diaphragm and intercostal muscles we talked about earlier And then also the lyic system again the motions that center brain can also influence breathing Talked about gas exchange We talked about metabolic processes and now we're going to talk about that immune function of the lung So the the lung has goblet cells which secrete mucus that forms a thin lining over the surface of the the lung tissue or the epithelium of that uh lung surface and the celiated epithelial cells line the airway So they got little hairike projections I think of them like anemone Um and celia have a constant beating motion and it's always going up So it will push anything in the lung up and out So you can expectate that uh mucus or fluid whatever it is And so mucus there needs to be more fluid and it that depends on the secretion of chloride by the epithelial cells And so that um chloride then exerts osmotic pull on water so pulls water in there to dilute it Um and so that water mixes with the mucus and that causes it to be more dilute and then easier for those beating psyia that are pushing it up to get it out And so that's why you know if you're dehydrated it affects this Um and so the water supply in our bodies are affected um and it affects our immune response So be sure to drink plenty of water stay hydrated Um and that allows your lungs to also uh create homeostasis and immune protection in your lungs And the mechanism of that fluoride transport and cystic fibrosis is altered And so that would be a disease that can affect the immune protection of the lung And uh celic cystic fibrosis is a autotoal autotoal recessive trait And so just to review what we talked about in the previous genetics chapter I always like to try to review just a little bit if we have a chance to do that And so um just to relate back to that genetics module If you have an affected father and a um unaffected mother think about what that would be and we can talk about um how that would be in that punet square Or if you had a carrier mother and a carrier father uh in that case you would have uh 50% of your children being carriers 25% affected 25% unaffected So um just do those in your head um or on a piece of paper again just to review autotoal recessive traits We have one other autotosomal uh recessive genetic disorder that we will talk about which is alpha 1 anotrippen deficiency a little bit later on So um this slide does contain a third one which your book does not contain It's primary siliary disanesia where basically the celia just don't move So in cystic fibrosis it's more a concern with that thick and viscous like molasses like um secretions in the lungs and then they kind of just wear down the psyia So it makes the cyia hard harder uh to get that out um h those celia move very slowly so it doesn't help uh transport things out of the lungs and so the secretions are thicker They make the psyia really just slower moving and and you can't get it out and so then you get all the germs and particles and debris that should come up easily with that fast beating celia um it just doesn't happen in cystic fibrosis and again it has to do with this um cystic fibrosis transmembrane conductance regulator um that's the gene that is affected as well and so um we have ineffective transport and then we have this denisonin monof phosphate um stimulated ion channel affected so then there's a the chloride doesn't create that osmotic pressure to pull water into the lung and you get disease infections The lungs also have very delicate tissue Um they're very vulnerable and sensitive uh to external components and compounds especially uh particulate matter such as pollutants um you know our air and environment and then inhaled cigarette smoke An example also maybe after 911 we had a lot in the air there was a lot of just particulate matter and we had a lot of lung issues in New York City after that it was significant Um our veterans who are exposed to burn pits uh have considerable uh increased risk for lung damage And so when these extra things are in the air that aren't supposed to be um these compounds then we have protective mechanisms macrofasages and um the one specific to the lung the white blood cell specific to the lung is called a neutrfil protease And so these go in and try to break down that particular matter And then there's also some things called react uh reactive oxygen species that can also react to those substances entering the lungs to try to help us um rid our bodies of those or our lungs of those And so the protective mechanisms would include mucosiliary clearance You have imu imunoglobulin IgA which you have talked about in your um other chapters um alvolar macrofasages that actually um create fagocytosis of the invaders and kill them with the proteasis and those reactive oxygen species and then alpha 1 anotriin proteasis also just called alpha 1 anotriin these are made by the liver and they they block that process from happening and so there's a condition called alpha 1 anotriin deficiency again I'll talk about it a little bit further um and that keeps that from overreacting you know Sometimes when we're overexposed that is a genetic condition but sometimes when we're overexposed to particular uh matter then that's what causes the disease processed you know there's an overreaction so we want these uh immune protections to a certain extent but um there can be an overactive or unchecked immune response and that can cause uh tissue damage uh in the lung Let's switch now to discussing lung volume and capacity Um just as the slide says it is a measurement regarding pulmonary function test These are done sometimes in office involved other names would be maybe a spometry test or includes a spometry test Now um these are you these can be utilized also for the CRNA people here um during anesthesia before anesthesia and it's important to understand that um as it's shown on this slide the volumes don't overlap but capacities can so just look at the the picture it shows you different um reser you know inspiratory reserve volume total title volume expiratory volume residual volume You notice that those are discrete categories However the capacities do overlap Um for example vital capacity inspiratory capacity um in some function of residual capacity are in or can overlap there as opposed to the volumes The residual volume here can't be measured by spometry It's measured by other tests that we're not going to talk about Your book does mention um a couple of them like helium dilution Um but we're not going to talk about that What is important to know is that residual volume is higher when you have poor lung compliance or like that floppy lung with uh COPD So you can notice in the um the graphs here there are se several these are different uh health problems So lung problems the first one is normal The graph shows you that the forced expiratory volume one which is the forced expiratory volume of what you can blow out over one second and most people can blow out most of their air in one second And then the the second part the FVC is forced vital capacity And so that's just you forcibly pushing out the rest of the air And so the first curve the FEV is pretty quick and then you know it flattens out for the FVC In asthma and COPD this may be reduced Asthma as you see in the second graph there it does follow uh not too bad of a curve Most of the air can be forced out immediately um in asthma because the lungs are still compliant for the most part in asthma It's more of a airway restriction So may be reduced because you're having trouble blowing out through an airway Um COPD you can see is blunted a lot further It's that on the second level there So you can see that the FEV1 is much reduced um because there is you know the compliance uh in the lungs is very altered in COPD They're floppy lungs It's like a a sock that you pull on again The stretchiness is gone and so air stays in the lungs Um and so you can see it here And then if you have this asthma COP COPD overlap then you're going to see um even further blunting of it Now the red line indicates once it's been treated with a bronco dilator So bronco dilators open the airways um and they can help improve um FEV1 and how much air you can get in and out of the lung So for a CRNA this is important We use this to manage respiratory status before and during anesthesia It's going to help you assess preop risk know what ventilator settings are used and how to manage that patient post-op You will use these types of testing Now I want to make sure you know that if you have a patient who comes in preop and there's some changes in these and maybe they have a cough or another problem you're not going to just ignore that You're and especially if it's been chronic So you would want to refer that patient for additional testing prior to any anesthesia So these tests can be used to manage patients understand their position and know what to do next We are going to switch from talking about the healthy lung and healthy tissue and testing and now talk about different lung disorders which this class is pathophysiology advanced pathophysiology So this is the pathophysiology of the lung Keep in mind why this might be important from both a CRNA perspective and um an NP perspective The next few slides I have divided into types of lung disorders The first one is lung or chest wall Basically the way that it's shaped or formed it can be affected primarily um by aging So as we age we develop rounding of our spine maybe even um alteration of the trajectory of the spine kyphosis or scoliosis The lung tissues just like every other muscle and joint in our body get stiff Um we decrease the amount of strength our muscles have and so this can affect the way we breathe Arthritis I have patients who have severe rheumatoid arthritis and their lungs just don't expand well Dysphasia I put here because this can create a situation of aspiration So they can't swallow especially upper esophage you know upper throat or feringial dysphasia where you know you could test for this with a swallowing study Those types of dysphas create the chance of aspiration more and that definitely could affect the lung Alvolar changes can the size of the alvoli can actually increase which can affect surface tension and make it more difficult to keep the avoli open and this would be a situation similar to COPD and it can be just from normal aging where that lung becomes floppy and less comp or has a compliance issue structural um injury you know crushes history of multiple fractures of the ribs sternal issues can all contribute to uh the expansion of the lung Some patients have congenital abnormalities and there's several that can occur that flatten the chest or make it more of a barrel chest initially And then there's neurologic disorders We see patients who have paralysis of the hemi diaphragm Um certainly any other uh paralysis high uh within the spinal cord musculardrophe or ALS can also affect chest wall lung wall Second category we want to discuss is chronic obstructive pulmonary diseases and these are primarily categorized into these three different entities There can be crossover of emphyma and chronic bronchitis Eyes is primarily a disease of increased lung compliance And so when we say increased lung compliance we don't mean that it's better We mean that the lung actually again that stretchiness the ability for it to recoil is gone And so we we decrease elastic recoil It's just a worn out rubber band So in that case we cannot push the breath out as easily emphyma occurs a lot in the upper lungs initially where there's exposure and that stimula it will stimulate uh the release of alvolar macrofasages and neutrfils and lymphosytes that will also promote the release of proteasis Proteiases are things that go and uh chew up or dissolve other things in the lungs that are bad Um we need those proteases but then if it gets out of control it will lead to damage which causes the loss of the elastin or the elastic the elasticity of the lung you get structural changes and dilation of that airspace and that leads to air trapping and to decreased gas exchange The O2 and CO2 um doesn't come in and out like it should The max air out is the maximum air out is decreased you will have a reduced force vital capacity and the FEV1 u forced expiratory volume in 1 second like we showed on the previous slide is also decreased Eventually you will actually have structural changes which will result in a barreled chest Um so you will have increased um AP diameter These patients will often you'll see them do purse lip breathing that just helps them keep their um breathing better They they used to be termed pink puffers We don't uh desri describe them that way anymore And with these patients um when they're having more problems or exacerbations of their COPD because this can wax and wayne over time um in the infyma specifically they will have weight loss because the increased work of breathing So fatigue and weight loss are very common The work of breathing just actually wears them out and uses calories So just keep that in mind when you see these patients Chronic bronchitis again um is often associated by the symptom of cough It's a lot in the upper airway there as well And you can get this um change in gas exchange as well with this condition for alpha 1 anotriin deficiency This is a fairly rare disorder and again it is an autotomo recessive disease So um just do different p um putt squares So for example if you have a affected parent or an unaffected parent a carrier parent or two carrier parents just try to figure that out to see if you can remember your previous chapters So this is basically a disease where you it's a deficiency just like it says you don't produce alpha 1 anti antitrium So when you would test for it a lot of times on blood tests we're looking for something that is high or abnormal and this one you're looking for um a level to be low So if you have an alpha 1 anotrippin level and it's low then you would know the patient could have this problem So alpha 1 anotrippin is actually produced by the liver and it is an off switch It is actually an anti-p proteiase So the proteiase in the lung um that fights infection So we know that we need these neutrfil elastases and so when the neutrfil elastace needs to stop our body has an off switch and the off switch is alpha 1 antotripen So it will keep that in check If you do not have alpha 1 antitrien to keep the uh neutrfil elastace in check then it results in damage and so the pro uh it keeps happening So we need it to to turn off the damage that's occurring So it keep it's a basically a balanced mechanism If not then alpha anotriin builds up and you you get in trouble and it can just create this nastiness in the lungs and it will kind of eat away at the lung tissue Now I will also say that alpha 1 anotrippson is produced in the liver and so this is uh something that patients can get um I've diagnosed as a um he you know in hepatology and so we need to be careful if you have somebody who has a I always tell people if you have somebody who has a liver problem and they're having lung problems you better check for alpha 1 anotrippson uh deficiency So next we'll turn our attention to restrictive airway diseases And the two that are mentioned in your book are allergies and asthma Easy to remember They both have A's and we won't talk too much about allergies because you will cover that in other chapters We'll talk a bit about asthma Asthma is a chronic issue often starting in childhood We see it mostly in the school age child is the peak of it It's always the focus um of or I'm sorry the airway is the focus of type one hypersensitivity So asthma is a it's a chronic inflammatory disease of the airway and the features have overlap and so we know that it is this inflammatory process which creates hyper sensitivity of the airway and also then the response is narrowing of the airway squeezing swelling and airway obstruction which leads to your clinical symptoms of wheezing a lot on inspiration more than expiration Um we know that when we're listening to lungs asthmatics have more wheezing on inspiration some on expiration as well Cytoine elevations can occur These include interlucan 4 five and 13 there is an IGG response which later switches to an Ig response and that IG binds to the mass cells So that also creates more swelling Subsequent because the mass cells have histamine Subsequent uh allergic exposures can cause damage to that tissue and um the waxing and waning of these symptoms can you know you have asthma attacks So acute asthma attacks again first mediated by histamine with the mass cells and then late response mediated by infiltration of actual type of white blood cell the eucosinophil and other inflammatory cells Patients who have asthma should avoid aspirin because it can mediate an attack exercise um exposure to cold air or infections You can have exercise induced asthma especially if you can have that if you're exercising and outside in the cold air would be a big trigger definitely when you get an infection or it can promote infections as well Chronic airway changes with you eventually because again I said this was a condition where there's a problem with the squeeze So the smooth muscles get worn out and you can get hypertrophy um or I guess thickening basically they can cause um when it's used over and over the scar tissue that occurs in that smooth muscle causes hypertrophy and damage mucous hypers secretion So the allergic response allergic type response or inflammation makes your um airways make more mucus and then you get a persistent limitation of that expiratory air flow the further in you are management aims to suppress inflammation using uh corticosteroids to decrease the inflammation LT antagonists and also that's fluotry antagonist and bronco dilators to try to decrease this reaction from happening It's interesting that in the um literature we we treat this acute reaction but it doesn't prevent the prolonged or uh continued promotion of this or progression of the disease and how it affects the tissues long term So we don't have a good necessarily cure and the the treatment doesn't necessarily knock out um damage from occurring long term A graphical display of a flow volume loop and it's different in COPD or even asthma um during asthma attack So this just shows obstructive airway disease effect on lung volume The graphic display shows here an acute asthma attack in the blue line compared to yellow being the normal line You can see the peak flow is less than half of what it should be and the residual volume and total lung capacity are significantly shifted to the left due to air trapping trapping behind that blocked airway So whether in this case it's COPD or asthma um it's still blocked airway at that moment So the expiratory curve is also scooped out due to premature closure of the airway And this this is a classic sign of obstructive disease again whether it's acute asthma attack or chronic COPD I will also say that a lot of on the pulmonary function tests I didn't mention on the earlier slide that you can have completely normal um FEVs one and FEV um signs even with pulmonary disease So keep that in mind that we don't always pick these up or identify based on uh a test So they can be normal depending on which disease entity you're talking about as well I do have some slides further on that will show that as well This is just a slide of again some generalities You have your chronic obstructive pulmonary diseases which are we discussed emphyma chronic bronchitis and alpha 1 anatriin deficiency They would increase the lung compliance make the lung floppier the FEV1 to FVC cap uh force vital capacity would actually decrease most of these patients would get a barrel chest or increase AP diameter and there's some symptoms that you can review not all inclusive obviously just some generalities interstitial lung disease um this is where you get fibrootic changes hardening of the tissues you get p and pulmonary fibrosis sarcoidosis rheumatoid arthritis lupus scleroderma your autoimmune diseases These are also also involved in those are your numaconosis which are asbestous siliconosis and coal worker lung So if you live in West Virginia you would be significantly uh treating or seeing this again that those would show you a normal FEV1 to FEC The chest on these typically doesn't get bigger it flattens out and then they're going to have a lot of disna cough shortness of breath and then you have the disease primarily of airway resistance Um that would be your asthma The lung compliance can remain normal in asthma Um the FEV actually can be normal or can go down over time The ch the shape of the chest can change over time um as well And then you know they are going to get a lot of dismia and that inspiratory re uh we and again all these can cause fatigue and weight loss you're not oxygenating well um and then the increased work of breathing uh I always I have a lot of patients referred to me for weight loss um and it actually ends up being their lungs that are causing it so they're they're just breathing so hard that they're using a lot of uh calories to to breathe book mentions several lung vascular disorders that can affect breathing in the lung The first is pulmonary embolism This is a medical crisis or emergency These people about 25% of them will die u at the moment of the embis or the the clot releasing We know that co 19 plays a high role in a pulmonary embolism And so these would if you have a patient who lives with that pulmonary emilis you know they go to the ER they're short of breath they do a CT um angiogram and we find this then you know we should be working these people up for uh different clotting disorders um and um the use of anti-coagulation may or may not come into play um but that would be something to work up um separate pulmonary edema in your book is defined defined as the accumulation of fluid in the avioli So we should not have a lot of fluid That should be a air fil space I'm not going to go through a lot of that You can read this in your book But you know there in this section you would notice ours or acute respiratory distress um syndrome and so and also uh COVID would can create uh some pulmonary edema issues as well you'll see in your book All right Pulmonary hypertension is where you have too much pressure in um the main pulmonary artery and this can then cause uh issues with the heart So right-sided heart failure is often associated with high pulmonary tension So I will I will let you again review those in your book and how uh those are associated Obesity is also um an issue with um that can affect the lung but we're not going to talk about that as well but please do uh review that on your own Infectious disease affects the lung We will not cover specifics on infections related to the lung in this chapter testing wise other than there may be some questions related to CO 19 So infectious disease CO 19 pneumonia uh respiratory sensitial virus you will see that a lot in the elderly and in um young people And then influenza and its effect again those are going to affect uh the old and the young We did cover some of this in infectious disease We will not cover it additionally here There is a chapter there is page 437 which talks about pneumonia aspiration pneumonia and how again aging affects the older adult Um we may review a case study on CO 19 Um so keep those in mind as you read through your book There was not a lot on CO 19 in this chapter but we did cover infectious disease and I provided you with a video I would encourage you to watch that video and look at the um the graph that I showed you on the previous um infectious disease lecture uh related to CO 19 and how surfactant is related and how it produces the inflammatory cascade Those are the types of things I would like for you to pay attention to So just to give you just a little bit more about CO 19 effect on the lungs the replication of COVID we talked about again in infectious disease actually occurs at the avular cells um where ACE2 which is angotensin converting enzyme 2 is and this impact affects the production of surfactant and so when we produce uh an issue where we can't make surfactant you know this would decrease that ability to keep that alvear sack open and uh that would collapse that o alvolar sack So how might that affect respiration Um think about that Um and then you know there's also the symptom of increased muc uh mucus production and when we have too much mucus again think about how that might affect both the upper and the lower airway and um as far as thinking about co 19 effect on the lungs Think about the volume and the capacity of the lungs as well as the function of the avular cells And why might incentive spometry which is where you you know breathe in and breathe out with the little device the incentive sperometer And and then what other things might help um improve uh CO 19 What are what are we doing with CO 19 when we see it There's actually been like we talked about that resurgence and they had some problems in Switzerland So I don't think we're ever going to be beyond it We'll also talk here about sleep apnnea So this is a sleep disorder It's a neurologic disorder You will see neurologists taking care of patients with sleep apnnea as well as pulmonologists Um it is increasing and the reason we're having more problem with it is because we have more obesity It is reversible airway obstruction that occurs while sleeping especially when people are lying on their back And sleep study test numbers of apneic and hypo uh hypo hypopniac episodes per hour um are documented during tests And um then these patients who stop breathing which was what that means for a minute um or less we can determine on that sleep study how long that they stop breathing they actually wake up So they or partially aroused So that disturbs their sleep and that causes them to be very tired So often first test and someone who comes in complaining of fatigue they will do this sleep study Um other studies that you can do are just like oxygenation um O2 sats during sleep uh also is something they will check and untreated sleep apnnea does have a high cardiac risk profile um because it can cause um the sympathetic stimulation when as a rebound and so that drop and then sympathetic um stimulation causes issues over time and then um it's managed primarily with continuous positive pressure um airway continuous positive airway pressure or CPAP We do also have new treatments There's one called Inspire which is implanted it's implanted like uh just above the clavicle and it's designed to raise the tongue or keep the tongue from falling uh back during sleep And so people have good good luck with that And they especially good for patients who can't wear the CPAP mask We have said the word surfactant over and over in this lecture but we really never stopped to discuss what it is And so this discussion begins on page 412 in your book And surfactant is you know this nice fluid that lines the avoli uh it's a major factor to uh lung compliance that we talked about keeping that lung elastic and keeping that aviolar open So it is an aquous fluid Now the fluid itself has a high surface tension but we need this um as this phospholipid protein solution to spread out over the aviolar surface and as we do that the surfactant actually reduces surface tension and that makes inspiration easier So um it is a phospholipid protein secreted by type 2 alvolar epithelial cells it spreads or um releases and then goes along the aviular cell structure It does have a high surface tension if you'll notice on page four page 412 but it makes the avular inflation easier by reducing the avular surface tension and reduces avular collapse So and I know that people say avular or aer So um it just depends I think on our region Um so nice surfactant layer it helps um reduce the the issues of keeping that lung expanded where it would not happen without that So that's that's what I want you to know about surfactant You will notice again it is a red letter uh concept This is just a general chart again shows you that some of the pulmonary function test um even with a disease can be normal you will it shows your normal pump pulmonary function test results what you see in COPD asthma muscle weakness and then your interstitial lung diseases Um they're all just kind of uh factored out here So you will uh be able to look at a pulmonary function test and decide um what they have I'm not necessarily testing specifically on that but maybe just um whether something's high low normal or can it be normal Again we we kind of talked about force expiratory maneuvers and we talked about asthma and COPD earlier and its effect on pulmonary function tests So force expiratory maneuvers are just components of pulmonary function tests where you um are just asking the the patient to take a maximal inspiration and then attempt to blow that air out as fast and hard as possible And so this is going to require that they engage their muscles of respiration uh specifically expiration And so those internal muscles or internal intercostals again during this um would pull the ribs down and in Again you can kind of cheat when you're doing this The abdominal muscles uh force the abdominal content against the diaphrag diaphragm and decrease the length of the thorax And then force expiration creates this positive plural pressure when you push the air out And the success of this maneuver is limited then by the compression of the small airways Okay So when we meet on Thursday we can do a general review of the content I would appreciate your um questions ahead of time We will um have some um specific questions we'll ask and here are some examples Which of the following is not an imunologic function of the lung So keep these in mind and ask yourself these questions as you're reading your material Um true or false asthmatics always have abnormal lung functions or pulmonary function uh test findings True or false And then um asthmatics can have a normal FEV1 Is this true or false You know if you if you have a patient with asthma would insp or or not And then why Um or why not And then what disease would incentive spometry be helpful for if it's not helpful in asthma And then not to be tested over but um there is a significant issue with um could there be a significant in issue with beta blockers for asthmatics or not and what would be the problem So um I will ask that question when we meet and you guys can um have the answer for me And then another is where in the body are most are blood gases most equal to that in the avular vessel Um just thinking of where um aso when we talked about the P2 and the PC2 where would it be most equal to the aviolar vessel and then key takeaways should be know the anatomy know the function of the lungs understand the processes of breathing the muscles used the volume change what is s a surfactant how does it work Understanding the gas exchange where it's carried where it occurs what pressures are needed what they mean Um know two areas of the brain that affect the breathing Um know whether it's sympathetic or not sympathetic or can it be both Understand what the goblet cells do celia function what happens when they don't properly function Um understand the values For example what is total vital capacity What is the purpose of pulmonary function tests and sporometry when we're using it What we do when we have people who have abnormal uh findings or symptoms um understanding the discussed lung disorders in generalities um and the ones I specifically stated So um we will meet then on Thursday Your test is not until June This content will cover 15 questions um of your test So um and then the remainder of the test will be uh Dr Rali's content um that you will have prior to uh the the test in June So that's all we got for I did uh include this um just a couple resources for you The first is a book called Breathe by James Nester And you may need to uh do this prior to your test and studying Um it is a very interesting book about um how breathing can affect your sympathetic and parasympathetic functioning Um breathing through your nose as opposed to breathing through your mouth Um it was a very interesting um concept and so this is just like an overview of this book breathe by James Netor So u again just something interesting for you to look into and be sure that you are taking deep breaths um as you go through this course And then there is a pulmonary function uh test explained um a couple resources there and it's just this graph that I thought was um very nicely done and concise and you can just look at it and see u how different um processes affect the pulmonary function tests at a glance So I will speak with you guys again on Thursday and um have a great week