Acute Respiratory Failure

foreign what's up Ninja nerds in this video today we're going to be talking about acute respiratory failure that includes two types that we'll discuss here the first one we'll describe is type 1 also known as acute hypoxemic respiratory failure then after that we'll talk about type 2 also known as acute hypercapnic respiratory failure then we'll go over some of the clinical features that points maybe to the etiologies and pathophys that we're going to discuss we'll talk about the diagnosis and then we'll end off on the basic principles of treatment we won't count down the rabbit hole of each individual treatment all right let's get started when we talk about acute hypoxia respiratory failure our type 1 respiratory failure we have to have a basic definition so hypoxemia is whenever there's low levels of oxygen within the blood all right and it's due to a lung problem we obviously call that a hypoxemic hypoxia now in these patients what's the actual level of hypoxia or their O2 saturation that we're concerned with it actually tells us hey there could be some acute hypoxemic respiratory failure the first thing you want to look at is their pulse ox their spo2 usually these numbers are arbitrary but for the most part we say less than 90 percent is somewhat concerning for a patient especially if they're on like room air okay it's even worse if they're oxygen saturation is lower right less than 90 or even lower and they're on high like some type of oxygen supplementation that's also a concerning sign the other thing is if you did an ABG you take and you stick into the big red you pull off some blood and you send it off to the lab and they test for the amount of oxygen that's in the arterial blood the partial pressure of oxygen in the arterial blood we look for that to be somewhere less than 60 millimeters of mercury these this these numbers can vary from source to Source but this seems to be kind of an a pretty much standard number across most literature so look for these two particular things you walk into the room you see a pulse ox less than 90 percent or you have an ABG that comes back and you see less than 60 millimeters of mercury that is a concerning sign for acute hypoxemic respiratory failure the first thing you should be thinking about as a clinician and for the boards if they present this is what is the likely etiology and I think the ways that we can break this up is relatively straightforward so the first thing that I want you to think of okay is the problem that the amount of oxygen they're actually getting is low very very low maybe even lower than room air for some particular reason room air is about 21 fraction of inspired oxygen let's say that they're at very high altitudes for some reason very very high altitudes if you're at very very high altitudes Alta toots this could potentially Rob precipitate a situation where there's very low levels of inspired oxygen so at high altitudes what sometimes we actually can potentially see this high altitude levels can really cause less fio2 to be delivered to the alveoli now how does that actually work obviously you take a breath in the oxygen with inside of the atmosphere is going to be sucked down into the bronchial system go to the alveoli and if there's less amount of oxygen that means less will to be diffused into the actual capillary blood that means that the pao2 or the spo2 will drop as a result of less inspired oxygen the fraction of inspired oxygen that we're actually taking in that's one type of thought process the second thing if it's not due to a decreased fio2 all right then it could be due to hypoventilation the patient's not taking in adequate amounts of tidal volumes they're not taking in enough air if they're not taking in enough air they're not taking in as much oxygen they're not putting as much oxygen into the blood and that will drop their oxygen levels within the blood what could be the reasons for patients having hypoventilation and when we talk about ventilation there's important concept here when we talk about ventilation there's actually a formula that I really do want you guys to remember here we're going to write it right here but for ventilation what we call minute ventilation it's actually equal to the title volume multiplied by the respiratory rate so minute ventilation right is basically determines the amount of air that we're actually ventilating is dependent upon these two factors tidal volume and respiratory rate if a patient is not taking in adequate title volumes that'll lower their ventilation if they're actually breathing at a very slow rate that'll lower their ventilation so we have to think about things that would actually cause the patient to not be able to breathe so they won't breathe and if they're not breathing they're breathing at a very slow rate or they can't breathe they're not taking an adequate amounts of tidal volumes in those situations you want to be able to assess those problems so let's break it up into two potential theories of why the patient has hypoventilation one of those theories is that they won't breathe and so you have to think about what actually controls breathing if you guys remember our central nervous system we have these respiratory centers that are basically responsible for our breathing particularly within the brain stem the ponds medulla area if a patient for whatever reason has some type of damage or disease process that injured these neurons will you be able to send action potentials down these particular neurons down the phrenic nerve down the intercostal nerve to contract those muscles and bring air in no so you'll decrease the patient's electrical activity to their intercostal muscles and into their diaphragm and so because of that any kind of CNS disease process so think about patients who maybe have some type of stroke so they've infarcted this piece of tissue they have a tumor here that's actually compressing onto this area these would be particular things to be thinking about a second reason is that you have something that is really shutting down or sedating or inhibiting and preventing that actual respiratory center from being able to trigger the respiratory drive what could be things that actually would suppress a respiratory drive some degree of sedation or analgesia so maybe it could be opioids and having too much of them overdosing on this or benzodiazepines in these situations here this could be potential reasons because you're having a lot of inhibition or dropping of their respiratory drive so these drugs that you may be giving the patient may be inhibiting suppressing the respiratory drive not sending Action potentials down these intercostal phrenic nerves and then therefore they're not going to be taking in adequate tidal volumes if they don't take inadequate title volumes they're not going to bring enough air into the alveoli they're not going to allow for a good gas exchange done what's another reason the patient could have less ventilation hypoventilation we already know that if we actually suppress the respiratory Center we have less drive to breathe so there may be a drop in the respiratory rate right they not might not be taking in deep breaths they might actually become apnic so that's an important concept what if the patient can't breathe so their respiratory drive is intact but something's wrong with the structures around the actual lungs maybe it's lungs the airway itself maybe it's the pleura maybe it's the chest fall if there's some type of abnormality here but the respiratory drive centers intact the the actual central nervous system is telling the actual structures that are involved in breathing to breathe then we got to think about what's causing them to not be able to so go to the chest wall what kind of things could alter us from being able to properly take in adequate title volumes what if I didn't have a lot of flexibility within my actual thoracic spine what if I had like some type of abnormal curvature and I had scoliosis or kyphosis or I was super obese that's really going to make it hard because when patients are really obese you flatten you actually push their diaphragm up really really high on top of that you have to be able to breathe against this large type of tissue on the chest wall so in those situations it's really hard to bring in adequate title volumes so think about three particular types of things one is if they have some type of chest wall deformity such as Maybe kypho scoliosis or massive obesity then what if there's a big big whop in a fusion that's actually sitting within this pleural cavity and now you have to be able to inhale and try to expand the lungs into this big fluid cavity that's pressing on it that's not gonna allow for you to be able to completely inflate those lungs and so situations where you have big plural disorders such as I think pleural effusions would be more of a important one to be able to remember here okay now the next thing is what if the actual chest wall is intact there's no kyphosoliosis there's no obesity what if there's no pleural disorders but it's the nerves you know how you have to have nerves that actually are going to stimulate these particular muscles now if there's some type of damage to the nerves they're inhibited for some particular reason can they stimulate these muscles to be able to contract no if they don't contract you you're going to be able to allow for the expansion of the chest wall bring air in no will you be able to ventilate properly no so think about disorders of the nerves something uh particularly maybe something like um Guillain-Barre syndrome where they demyelinate the actual pns neurons or some type of cervical spinal cord damage sometimes sometimes that's a really big one to be able to remember so some type of cervical spine damage especially in where it involves the phrenic nerve okay so you have any kind of compression of the cervical spinal cord or damage of that that could be an important one sometimes you may see this in like ALS or polio or botulinum toxins those are kind of rare cause but I would think about these two muscles what if there's actually disease of the muscles where the muscles aren't able to contract properly or they're not getting enough signal to be able to allow for them to contract and actually increase the thoracic cage volume and bring air in in those situations think about maybe myasthenia gravis Minister gravis you know what else these are really rare but dermatomyositis polymyositis maybe even if you really want to muscular dystrophy may be another one to think about these are muscular disorders where the actual muscles themselves are weak or damaged and they're not able to be able to contract properly and generate enough Force to increase the chest cavity volume and bring air in that should make sense so they have a good respiratory drive but they can't breathe properly because they got some type of chest wall deformity or they're obese or because they have some type of pleural disorder if that's not the case think about the nerves and the muscles maybe some type of neurological disorder or muscular disorder if you've gone through those the next thing to think about is could it be something with the airway something with the actual like lung tissue itself or something with the actual bronchial alveolar system so if that is the case here's what I want you to think about big big thing here if I have a big upper Airway obstruction so let's say for whatever reason there's some type of obstruction of this upper Airway maybe this is a tumor maybe this is a foreign body right maybe this is a big fat mucus plug or you know sometimes in patients who get like a lot of Edema of their their larynx they can have like laryngospasm sometimes that massive obstruction within the airway can prevent air from being able to get down into the alveoli and so because of that that means that less of this air is going to be able to get to this alveoli less oxygen moves into the blood so think about big big upper Airway obstruction what could be big upper Airway obstruction I already kind of told you it could be a foreign body could be a tumor or it could be laryngospasm so I want you to think about these as more of the upper Airway obstructions but what if we get into the lower airway obstructions what if for some particular reason we have a patient who has something called COPD or asthma so think about COPD another one I want you to think about because this is a very weird interesting type of disorder sometimes this may slightly confuse people so here's what I want you to remember and these disorders oftentimes they say oh their problem isn't being able to get air in Zach we I thought from the COPD and obstructive lectures that was getting air out that is true and that's the problem they can't get air out because they can't get air out what happens to these poor patients lungs they can't get air out they're going to be hyperinflated so they have this massive hyperinflation now I dare you to take a deep breath in as deep as you possibly can and then hold it hold it at the peak of when you take that deep breath your lungs are filled to the max try to take a deep breath on top of that imagine how difficult it must be to take a breath on top of a hyper-inflated lung that's what these patients struggle with so whenever they have hyperinflation their lungs are already completely filled so you have this massive increase in total lung capacity and you have to try to breathe beyond that on top of that their diaphragm flat right if it is flat imagine whenever you actually take a breath in what happens to your diaphragm it's supposed to kind of like try to come down it generally becomes flat or it domes downwards to be able to increase the thoracic cavity volume to expand the lungs if it's already flat and you're supposed to be able to take a deep breath in and contract that muscle to try to bring it down even more imagine how difficult that's going to be that's going to require a lot of effort so in these patients think about yes the problem with COPD and Asthma is more getting air out but that is the issue they can't get air out they hyperinflate their lungs and they can't take in deep breaths so they hypoventilate they take in lower volumes because their lungs are already filled and their diaphragm is already flat all right that'll cover these parts so we have a patient comes in low spo2 we get an ABG they have less than 60. we think hypoxemia is it low fio2 are they high altitudes pretty rare cause it's a hypoventilation is there a CNS catastrophe of some reason big sedation drugs like opioids benzodiazepines or some type of stroke or tumor okay that's not it what if they can't breathe chest wall pleura nerves muscles then get into lungs and Airways big upper Airway obstruction or hyperinflation like COPD asthma if that is not the case then you go to the next thought process which is going to be VQ mismatch decrease diffusion capacity or some type of shunt let's talk about those now all right so the next concept that I want you guys to think about and this is oftentimes tends to be the most common cause is a VQ mismatch so there's something wrong between the ventilation of the alveoli so basically how much oxygen gets into the alveoli and then how much perfusion is moving through the pulmonary capillaries there is a mismatch between the two in perfect world you want normal ventilation normal perfusion but sometimes that's not the case with pathology there may be a decrease in ventilation or a decrease in the perfusion so you have to be able to think about those things so what kind of things would cause a decreased ventilation not enough option to be able to get into the alveoli I want you to think about this at three levels one is there's a problem with the Airways delivering oxygen to the alveoli one there's a problem with the alveoli or one there's a problem with the pulmonary vessels and it makes it a lot easier to think about if it's an airwave problem there's got to be some type of bronchospasm or mucous plug that's narrowing the airway it's making it so much smaller that it's really hard it's easy to get oxygen to this alveoli so oxygen is really going well into this one but it's not moving very well into this one so because of that you're getting less oxygen into this alveoli and an increased amount of oxygen into this alveoli so there's a good ventilation to this one and a poor ventilation to this one in this situation here where there's some type of mucus plug so maybe there's a little bit of mucus within the airway or there's bronchospasm so maybe you can see this in situations like a little bit of mucus within the airway or such situations like COPD or asthma you may be able to see these but there's less oxygen getting to these alveoli so at this point here if the perfusion is normal so your Q the perfusion is normal then what's going to happen here you're going to send deoxygenated blood into this out this to this actual pulmonary capillary blood and then oxygenated blood into this pulmonary capillary blood so there's a VQ mismatch at this particular alveolar capillary interface and this could be one particular reason so think about small mucus within these the actual bronchial system or bronchospasm of the bronchial system which is narrowing the Airways and reducing the amount of oxygen getting into the alveoli things like maybe COPD asthma Etc okay the next type of thing that I want you to think about is what if it's at the alveolar level so it's not an airway problem it's an alveolar process so there's something that's filling the alveoli or the alveoli has collapsed so if the alveoli is collapsed this is called atelectasis so there's collapse of the alveoli if it's collapsed it's smaller if it's smaller you're not going to be able to get as much oxygen into that poor little alveoli so therefore there's going to be a mismatch now because here you can have normal perfusion but there's a decrease in the ventilation process so there will be less O2 going into this pulmonary capillary blood that's going to lead to hypoxemia in the same situation there could be some type of material that's actually plugging up or blocking oxygen from being able to get into this alveoli because there's some type of material let's say And depending upon what that material is in the alveol I could determine the underlying etiology but this is blocking the O2 from being able to has to move against fluid or pus or blood or lots of protein and cellular debris across this and get into the pulmonary capillary blood that's definitely going to cause hypoxemia right so what are these things what if it's pus then you think about pneumonia sometimes this can even be ards what if it's some type of fluid well then then you can think about maybe cardiogenic pulmonary edema secondary to CHF sometimes it could even be due to ards what if it's due to blood then it could be situations like diffuse alveolar Hemorrhage and there's a lot of other miscellaneous types of situations but they're not super high yield where you can get lots of lipids like lipoid pneumonia you can get calcium like pulsing pulmonary calcinosis a lot of these different types of things Cancers and yada yada but I don't want you to focus on that I want you to focus on the most common ones so in this situation where you get a VQ mismatch is because of the alveolic collapsing or the alveoli is filled with some type of material whether it be pus blood or some type of fluid okay think about those particular things the last one is that there is nothing wrong with the alveoli these alveolar are perfectly ventilated there's no mucus there's no alveolar atelectasis there's no alveolar filling process so oxygen is going well into these alveoli they're ventilating perfectly but there is a clot and one of these pulmonary vessels and so the blood flow to be able to pick up the oxygen is the problem and so you never get this gas exchange process because not enough blood or no blood is coming to this actual alveolar capillary interface and so even though you have good ventilation the perfusion is what is decreased and so again if I have a clot right here I'm not going to be able to allow for this ventilation process and so blood is just going to completely bypass this area not get oxygenated and because of that the blood that will leave this will still have low levels of oxygen because it's never going to be able to pick up the oxygen from the alveoli because there's a clot blocking the gas exchange process in this situation where you have a thrombus or the pulmonary vessels think about a PE okay all right so VQ mismatch here's the way I want you to think about it there's some type of small mucus or bronchospasm that's probably going to be the least likely one or there's atelectasis of the alveoli there's an alveolar filling process with pneumonia ards pulmonary edema or diffuse alveolar Hemorrhage that's going to be probably one of the most common ones and then the last one is that there's some type of PE that's blocking the perfusion to the alveoli to pick up the oxygen that's another really common one don't forget these this one can be kind of a last one that you could think about in situations such as maybe COPD or asthma and then some of the actual Broncho pneumonia so sometimes you can see this in Bronco pneumonia okay the next one this one's a very very uh relatively rare I wouldn't even really kind of think about this one but for the consistency of being all engulfing approach here we should think about decreased diffusion capacity as well so generally this has nothing to do with the alveoli this has nothing to do with the perfusion this has nothing to do with the um the actual bronchial system or the airway system it's the interstitial space that is the problem and there's a thickness of the respiratory membrane or there's a decreased surface area of the respiratory membrane and that tends to be the problem if there's this big thickness because there's a lot of fibrosis so what if a patient has a massive interstitial lung disease if you have a big old interstitial lung disease that thickens the actual respiratory membrane it's harder for oxygen to be able to move over into this actual capillary system or what if there's a big waterlogged fluid log interstitial type of Edema that's actually locking up all this area and blocking the diffusion of oxygen into here in situations like severe pulmonary edema that's affecting the interstitial fluid that could be another reason or you have a decreased surface area and emphysema all of those things are decreasing the diffusion across the respiratory membrane all right that's enough said about that one the last one that I really want you guys to think about as well is a shunt so this one tends to be the worst so a shunt is basically when you can think about in two ways one is that blood actually never goes to the lungs and never is involved in gas exchange whatsoever so there's no gas exchange process that's occurring because we're bypassing the lungs or bypassing a huge portion of the lungs so that's the way I want you to think about it either we're completely bypassing the lungs or we're bypassing a huge portion of the alveoli and just having blood pass right by it let me explain why in a situation where you're not even going through the lungs it's because you have an intracardiac shunt so if you have an intracardiac shunt what you're looking to see here is that blood is going from the right side of the heart deoxygenated into the oxygenated system you're pushing low oxygenated blood into the oxygenated system and so now you're going to mix the blood that's going to definitely drop the actual oxygen concentration within the blood and cause hypoxemia so think about maybe ASDS vsds pdas all of these things that are acting particularly they'd have to have eisenmingers and if you remember from our congenital heart disease they have to have some degree of right to left shunt so usually in the early life they usually are left to right but if they have eisenminger syndrome they may develop a right to left shunt so think about those particular types of situations other one is a really interesting one where maybe the pulmonary vessels so you have your pulmonary arteries and they're supposed to go to these alveoli and they form these different capillaries but sometimes due to a congenital malformation the capillary network doesn't even involve gas exchange because there's such a big like nitus where there's this abnormal capillary kind of connection between the arteries and the veins and so no gas exchange occurs at multiple areas of the lungs and so because that you kind of just think about this connection where you go from an artery to a vein without even having any gas exchange this is called a pulmonary AVM relatively rare but something to think about when we talk about how to diagnose these later all right so think about shunt intra cardiac shunt ASD vsd PDA some right to left shunt or a pulmonary AVM here's the other thing remember I told you that VQ mismatch was one of the really big problems so here's what I want you to remember the VQ mismatch if it becomes really severe can actually develop into a shunt let me explain what I mean remember a shunt is where there is a massive there's either no blood moving through the lungs so there's no gas exchange that's occurring at the lungs or there is very little gas exchange that is occurring at the lungs almost none here's the way I want you to think about this let's say for whatever reason a patient has a huge mucus plug for some reason they have a huge mucus plug of this entire bright bronchus no air is going to go into multiple alveoli in this entire lung this entire lung will collapse right they'll develop massive severe atelectasis and severe atelectasis now all of these alveoli and the entire right lung will have no oxygen going to it if no oxygen is going to these alveoli what do you expect to happen in this situation are you going to be able to deliver any oxygenated blood into these alveoli no and so because of that you're not going to be able to deliver any oxygen from all of these alveoli into the actual pulmonary capillary blood there's going to be almost no O2 that'll get into this actual pulmonary capillary blood because they're going to be completely blocked no air getting into these alveoli and that is the problem oftentimes what happens in these situations when these alveoli aren't getting a good enough ventilation you know what happens to the pulmonary capillaries it's really interesting concept imagine here I have an alveoli okay and then here I have another alveoli and imagine here is the actual pulmonary blood if in this situation here this alveoli is well ventilated then I'd have good blood flow to that actual alveoli but in situations where maybe this alveoli is very very poorly ventilated it's filled up with plaster there's no air in it I will not want blood flow to go to this area and so what often happens is that these pulmonary vessels undergo intense vasoconstriction and because they undergo this intense vasoconstrictive response they completely bypass no blood will go to this alveoli and you'll try to shunt it to other areas where maybe other alveoli tend to be well ventilated but guess what this entire lung is not well ventilated so you're going to have a massive shunt here where even if you try to shunt blood into other areas which may be slightly more ventilated it's still not going to be good so think about that if a patient has a massive hypoxemia not responsive to oxygen think about a big big mucus plug that's causing massive shunting because multiple pulmonary vessels are vasoconstricting trying to send blood elsewhere okay this is the very persistent concept to remember with shunting and very severe poorly ventilated alveoli is that whenever they're poorly ventilated you'll have what's called pulmonary vasoconstriction to take blood away from this pulmonary vessel going to this alveoli and instead that blood that you could be wasting going to that one send it to this well perfused and well ventilated alveoli so increase the actual blood flow to the well ventilated alveolis decrease the blood flow to the poorly ventilated alveoli that's kind of the concept of shunting all right that's one thing now go back to all the other Concepts if it's not severe atelectasis then it has to be something that's filling up the actual alveoli so now the alveoli is filled with a massive amount of fluid what is this called severe pulmonary edema so if a patient has severe pulmonary edema that's going to fill up multiple alveoli multiple alveoli won't participate in the ventilation process and they're not going to be able to give oxygen to the actual blood so multiple pulmonary capillaries will basically constrict and take blood away from those alveoli and try to send it to another well-ventilated alveoli okay but massive pulmonary edema will be one or you're filling them with a massive amount of pus so there's a massive amount of pus that's actually filling Within These actual alveoli so this could be serious pneumonia so a very socked in pneumonia very severe socked in pneumonia and the last one that I want you guys to think about is if it's not due to a lot of pulmonary edema it's not too atelectasis it's not due to a lot of a really socked up type of pneumonia what are the other kind of things that it could actually be considered to be ards and so ards is kind of when you have a mixture of fluid and proteins and a lot of like white cells and even a lot of infection that can actually sock up in this entire lung area so this could be thinking about ards as well so you can have VQ mismatchers that cause shunt when they just get more severe so atelectasis pulmonary edema pneumonia ards these would have to be very severe to cause a shunt but that is another possibility so remember shunts are basically whenever there's almost no blood going to the actual lung no gas exchange process is occurring within the lung because you're bypassing it unless there's an intra cardiac sign or pulmonary AVM or very little gas exchanges occurring at the lungs very very little due to severe VQ mismatch such as severe pneumonia severe adelectas a severe pulmonary edema or severe ards okay that covers the pathophys I think that this now takes us from acute hypoxia respiratory failure into acute hypercapnic which guess what it should be super easy now because we've already covered a part of it I'll see you there all right my friends now type 2 respiratory feather also known as acute hypercapnic respiratory failure guess what one of the pieces that was a cause of hypoxemia is the primary cause for hypercapnia and acute hypercaptnic respiratory failure so let's test your knowledge and then understand why this happens the primary cause for acute hypercapnic respiratory failure is hypoventilation do you guys are remember that remember what I told you was the formula for ventilation particularly many ventilation many ventilation was really equal to your title volume multiplied by your respiratory rate so if a patient has a drop in their respiratory rate or a drop in their title volume that will cause a drop in there minute ventilation and then if their minute ventilation is decreasing their paco2 will increase let's explain why a basic concept remember when we were talking about oxygen moving from the alveoli into the blood over in the acute hypoxemia so if there's decreased ventilation there's decreased movement of oxygen to the alveoli decreased movement of oxygen into the blood in the same way decrease ventilation leads to decreased CO2 moving from the pulmonary capillary blood to the alveoli and from the alveoli out into the atmosphere so if there is less ventilation that means air coming in and out don't forget that that means less CO2 is leaving and exhaled out that means CO2 will start to build what happens if you guys remember from that equation that CO2 plus water yields something called carbonic acid and then that disassociates in two protons and into bicarb as we increase the CO2 what does that do with at least principle shift it to the right we make more protons what does protons do to your pH they drop the pH so in these patients I'm going to see an increased amount of CO2 within their blood and a decreased pH of their blood so oftentimes we can't pick this up off a monitor sometimes if the patient is intubated or ventilated or we can stick a monitor down we can check what's called in Tidal CO2 but the proper way is to send off a vbg or an ABG and get the amount of actual CO2 that's in their blood preferably abgs and if we get a paco2 the partial pressure of arterial CO2 it has to be at least greater than and again this is a well kind of like standardized number greater than 50. millimeters of mercury now on top of that we also look to see because usually in these situations where there's acute hypercaptic respiratory failure is acute so sometimes if you build up CO2 you should see a drop in PH over time if it's chronic and the patient has time to compensate what would happen they would actually start trying to reabsorb bicarb excrete protons and they would compensate metabolically but acutely they might not have enough time so we would expect a pH to drop less than 7.35 so we would expect to see some type of respiratory acidosis in this patient that's a very common particular finding now what would cause CO2 to build up go through everything we talked about just a recap hypoventilation doo doo CNS not triggering your actual respiratory Center triggering the actual process of breathing so you won't breathe CNS diseases CNS depression due to opioids benzodiazepines any kind of thing that can actually suppress the respiratory drive or you can't breathe you got the drive but there's something wrong with your chest while you're pleura kyphosoliosis obesity or pleural effusions there's something wrong with the nerves like uh maybe particularly Guillain-Barre syndrome cervical spinal cord damage ALS polio botulin toxin or muscles so this could be myasthenia gravis at the neuromuscular Junction dermatomyositis polymyositis muscular dystrophy Etc and if it's not that it's some type of upper Airway obstruction that's blocking the CO2 from being able to get pushed out such as a big upper air obstruction like a tumor a foreign body or some type of laryngospasm and if it's not that it's due to hyperinflation disorders where they can't take a deep breath in but they're also guess what air trapping they're not getting air out because their bronchials are collapsing or they have such bronchospasm and in those situations like COPD and Asthma they trap air and they trap CO2 these would be the things that I need you to think about for acute hypercapnic respiratory failure now we talk about the features they're generalized okay not everybody is going to have the same exact features classically if a patient has hypoxemia their reflexive reaction is to breathe faster so they become to kipnic tachycardic they may have some degree of changes within their mental status as well as people build up CO2 they may usually because they're having a decreased tidal volume and a decreased respiratory rate they may have very shallow breasts they may actually become apnic they may have some degree of CNS depression or somnolence or altered mental status so again very generalized but ways that can help you to key you up to the actual etiology or the pathophysiology just a few of these is if a patient has a fever cough maybe they actually have a pneumonia that's triggering this process and the pneumonia is a socked up area of alveolar filling and that's causing a VQ mismatch or it's an upper Airway obstruction that's causing hypoventilation so look for Strider in the upper Airways look for wheezing during expiration in the lower Airways potentially the other thing is crackle so if their lungs are filled up and filled up with lots of fluids and whenever they take a deep breath in it sounds like velcro is being ripped apart that could be fluid within the actual bronchial Airways and that's something like ards or lots of pulmonary edema if they have Associated muscle weakness of other extremities besides their diaphragm intercostals their eye muscles their upper extremity muscles thinks about those actual like this not muscular disorders such as mycena gravis such as Guillain-Barre syndrome such as muscular dystrophy dermatomyositis polymyositis Etc and if there's some degree of altered mental status neurode deficits they're very difficult to arouse a decreasing level of Consciousness they have sonorous respirations they're not opening their eyes or falling commands there's a decreased level of mental set it's a declining GCS status think about some degree of CNS depression is there a neurological catastrophe like a stroke a tumor a bleed or are they not actually taking drugs is there an opioid overdoses this is a benzodiazepine overdose is this some type of drug overdose think about those particular things that might lead you down to what's the actual cause and how to treat them so now that we've done that we come to the next challenging part how to diagnose these two all right so now we move on to the diagnostic approach of these respiratory failures so you get type 1 type 2 acute hypoxemic or acute hypercaptic now when we think about these I I hate saying it but it is actually a relatively important thing to consider especially for your clinical vignettes is that you want to get an ABG on these patients and the reason why is on the clinical vignettes they're actually going to have you kind of determine which phenotype of hypoxemia is this is this a low delivered fio2 such as high altitude is this a hypoventilatory cause because in those situations they have a normal aa gradient and I'll explain what the heck that means in a second or is it the other phenotypes which is this an increased aa gradient due to a VQ mismatch a shunt or very very uncommon a low diffusion capacity in those situations we have to kind of then talk about what the heck is the AAA grading because it's something you may see on your exam now I doubt that they're going to require you to do any calculations but to at least have an understanding of what the heck aa gradient means I'm going to give you a kind of a quick brief overview of it the AAA gradient is really kind of looking particularly at the alveolar partial pressure of oxygen and subtracting it from the arterial partial pressure of oxygen and that tells us the difference between the two right it really tells us for example if I bring O2 into this alveoli ventilate this alveoli right and I have a very particular pressure there in that alveoli the pao2 and then from here I look at how much of this actual oxygen moved into the actual pulmonary arterial blood and then therefore went into the systemic circulation what I'm going to measure here is how much of that oxygen actually got into the systemic circulation so if for example most of the O2 that I'm moving from this actual alveoli into the blood is about the same if our for example there's a good exchange process that's occurring there's a good exchange process occurring that is between the alveoli and the actual capillary blood meaning there's no impaired gas exchange what kind of diseases have impaired gas exchange VQ mismatch shunting and some type of diffusion capacity problem which ones do not have impaired gas exchanges a problem with the patient either not bringing enough O2 in or not bringing enough volume of air into their actual lungs those would be situations so the normal aa gradient right so that's the basic concept now how do we actually determine this if you were to do this and we'll do a case example on one of these when we talk about our cases but the partial pressure of oxygen in the alveoli is calculated off of this equation so it's fio2 which if we're taking room air that's 21 The Inspired pressure which is usually the atmospheric so 760 millimeters of mercury the pressure of water which is usually 47 millimeters of mercury and then what we do is we subtract the from the arterial partial pressure of CO2 over the the respiratory quotient which is 0.8 now it's like Zach I can't remember all these don't worry oftentimes if the patient is breathing room air we simplify this whole left side of the equation by making it 150 that's just what you'll get 21 760 47 you do all that you get my 150. then all what we need is to really look at the ABG and from the ABG I can get my partial pressure of arterial CO2 and put that over this constant of 0.8 for the respiratory quotient and then I can get my pao2 then all I need to do is get there partial pressure of artillery oxygen from the ABG and subtract it and what that gives me is that gives me that patient's a a gradient but then you know what you actually have to do is you have to compare that a a gradient at that moment of time of what would be an estimated normal a gradient for that patient so for example if the patient had a normal aa gradient we would expect that the AA for this one let's just say for one example it was normal so we have normal then we have increased let's say that this was 120 for that a gradient and when you calculate it for this patient it happens to be 120. well then these are pretty close to equal so that's a normal a gradient but let's say for whatever reason that the patient's a gradient when you do this was 120 and what you calculated actually let's make it even like higher let's make it extremely higher let's make it like 340. and once you actually calculate for this patient is 120. then you're looking at a huge difference the AAA gradient for that did you actually calculated off of this is massively higher than what it should be that's an increased aa gradient and really what we're looking at to really kind of differentiate these without getting too complicated with the equation is if you have a normal aa gradient you can kind of just look at the patient's paco2 if the patient's paco2 is really high what does that mean that means that they have a hypercapnic respiratory failure or acute hypoxemic due to hypoventilation they're not ventilating and if they're not ventilating due to a decreased tidal volume or a decrease respiratory rate they're building up CO2 so high paco2 tells me the etiology it is hypoventilation so think about that that's why sometimes you don't even really need to do this equation if you get the patient's ABG and from an ABG you get pao2 paco2 you get pH and you also get bicarb from this I can kind of have an idea if their paco2 is super super high and their pH is low then I have an idea that it's actually again what more likely it's hypoventilation but again the AAA grading will also give me some type of help especially if there's Associated hypoxemia so if the patient also has a low pao2 and a high paco2 I can likely tell that their cause is due to hypoventilation because I can calculate their AAA gradient and if their paaco2 is also super elevated it's hypoventilation now here's where it's a little complicated what if the patient has a normal paco2 their AA grading is normal this is why it's super rare so you don't always use this but normal a gradient normal paco2 in a low pao2 well now they're not hyperventilating they're hypoxemic for some reason but the problem has nothing to do with gas exchange because the normal gradient means that there's no impairment in gas exchange what was the other cause low fio2 so it's a relatively con you know uncommon situation but think about it in case it comes up on the exam low fio2 so again when there's a normal a gradient there is good gas exchange this is important concept here when there is an increase a a gradient what you calculate off of their pao2 and their pa uh their pa Little P little ao2 what you calculate in comparison to their actual estimated if it is much much higher that's an increase a gradient that tells me that there is impaired gas exchange and what that will help me to determine is to figure out my differential and my differential for impaired gas exchange increase a a gradient is usually due to a problem where I'm not moving oxygen across the actual you know through the alveolar through the bronchial system it's not crossing the alveolar capillary interface or there's a clot within the actual pulmonary capillary that's not actually pushing blood to the alveoli or there's a massive shunt and then lastly uncommon there's a diffusion problem so how do I weed these patients out I don't want us to focus too much on this one I want us to focus mainly on these two so we've come to the patient we come to the bedside we see that they have a low spo2 we appreciate their ABG and say okay they have hypoxemia here so they have a low pao2 we then go ahead we utilize our calculations we get an AAA gradient comes out to be increased a gradient so the number that you do when you take paob big little a O2 minus P little a O2 you get a very high number in comparison to what you estimate which all you do is you take their age divided by 4 plus 4. if the number that you calculate from this is higher than this they have an increased a gradient that leaves you with these three differentials once you do that what I want you to say is okay give the patient a hundred percent oxygen so if they're on some type of oxygen supplementation like high flow nasal cannula or non-rebreather crank it up to 100 fio2 what you're looking for is to see is this a shunt or is this a VQ mismatch in shunts it doesn't matter how much oxygen you give these patients all of these alveoli are clogged up with fluid pus blood or all of the alveoli are not being ventilated because there's a massive mucus plug and so no matter how much oxygen you try to be able to give this patient there's no good alveoli that can pick up the oxygen so whenever I try to send oxygen to this alveoli to this alveoli to this alveoli the diffusion is going to be the same it's going to be poor I'm not going to get a lot of oxygen inside of the blood here because there's nowhere for me to vasoconstrict and send blood to to pick up better oxygen because all of them are poorly ventilated same thing in this situation no O2 is getting to these alveoli so no matter how much oxygen I try to increase to better ventilate that entire lung all I'm going to do is just shunt it over to the right lung so I make it a little bit of ventilation but still this entire left lung is not going to get ventilated and so because of that I'm going to develop a massive drop and the O2 because I'm not going to be able to pulmonary vasoconstrict any of the actual vessels to redirect to other areas of this left lung it's just I'm going to have most of the blood going to the right lung all the blood going to the left lung is going to become deoxy that's going to produce a massive hypoxemia despite you giving them a hundred percent fio2 so if you give them 100 fio2 and they do not bump their oxygen upwards it is a massive shunt so it's due to massive ards pulmonary edema big socked and pneumonia or a massive mucous blood causing an entire lung atelectasis if you think that they have some type of cardiac sign get an echo study with a bubbles to look for bubbles to cross get a CT angiogram to look for some type of like pulmonary AVM if you give them a hundred percent fio2 and they do improve their hypoxemia so they do bump their oxygen that means it could be a mismatch what that tells me is that maybe there is a little mucus plug here and I'm not getting a lot of oxygen to this one but if I try to really pump up the amount of oxygen I'm sending to this alveoli I can still get a more improved ventilation in here and more option to this alveoli and more option to this pulmonary capillary blood so even though there's very little oxygen getting into this pulmonary capillary blood if I increase my O2 I can send more of it to other well-ventilated alveoli and so that may increase my O2 a little bit same thing if I have this area that's either socked up with fluid or blood or pus or it's atelectatic I'm not getting very good O2 coming into this pulmonary capillary blood but if I some other area of lung tissue which is well ventilated I can send more of the oxygen there and I can help to be able to improve my oxygenation last situation here I have a clot that's actually right here pulmonary embolism even though both of these guys are getting well ventilated all the auction I sent to this one it's not going to be involved right it's not going to help because no matter what there's not going to be any gas exchanges occurring here so there's going to be a low O2 because I'm not sending any blood here but if I really well ventilate the other alveoli that there's not a clot going to that alveoli then I'm going to send more oxygen into that pulmonary capillary blood and bump their oxygen so think about that in situations such as a small mucus plug bronchospasm small alveolar filling like a mild or moderate pneumonia ards pulmonary edema or atelectasis or a pulmonary embolism you can give them oxygen they'll improve but if it's a shunt a big terrible pneumonia a full-blown severe ards severe atelectasis severe types of situations like that no matter what you do it will not improve it or if they have an intracardiac shot or pulmonary AVM last situation here the only thing that I want you guys to remember for this one is that if you get them 100 fio2 they don't change it's a shunt if they do it's some type of vehicle mismatch if it occurs only when they're exerting themselves it's interstitial lung disease that's it don't make this too complicated to just say if they have a decreased diffusion only with exertion it's interstitial lung disease I don't want us to go too crazy down that rabbit hole so how do we go about determining this if we get to the point where it's an increased a gradient we do this test here with 100 fio2 and we figure out oh it's a shunt how do I determine it get a chest x-ray CT to look what's going on with the lungs might find a big mucus plug severe atelectasis there's my answer big sock-up pneumonia bilateral infiltrates with some type of like ards kind of picture or they have definitely cardiogenic pulmonary edema or they have a big kind of diffuse alveolar Hemorrhage or get a CT scan if you can't see it very well if you think that they have some type of cardiac sign get an echo study with a bubbles to look for bubbles to cross get a CT angiogram to look for some type of like pulmonary ABM if you think again here mucus plugging you can do a bronc or do a chest x-ray looking for a little bit of atelectasis or bronchospasm here chest x-ray CT here ctpa to look for a pulmonary embolism these are the ways that you can go about that oftentimes with paco2 with the hypoventilation it's a clinical diagnosis you kind of get it based upon use with sifting out through their history and physical exam this one super rare all right we've talked about all of the Diagnostics now we've got to do is briefly go through the principles of treatment all right so we talk about treatment for these now I don't want us to go too crazy down the depths of like mechanical ventilation and non-invasive like you know ventilation I don't think it's that important what I really want you to get is a core concept to treating hypoxemia and to treating hypercapnia obviously the basic concept here is what do you do to really treat these patients you treat the underlying cause if it's a brain catastrophe you're likely going to have to intubate them and treat that disease until they can actually start breathing well on their own reverse the sedation if it's some type of like you know drug or particular medication reverse that flumasinal for benzos and naloxone for you know potentially like um some type of like opioids if it's a disease of the chest wall trying to treat that if it's a disease of the pleura thoracentesis if it's a disease of the nerves obviously treat those muscles Etc if you have to treat the underlying disease itself to really fix the acute hypoxia and acute hypercapnia the UN the background stuff while you're treating the underlying disease you're providing supportive measures which is the core concept here that I want you to understand and that may be using non-invasive measures high flow nasal cannula BiPAP or endotracheal tube intubation with mechanical ventilation but the concept Remains the Same and that is if a patient is hypoxemic treat the underlying cause of the hypoxemia but in the interim how do we fix the hypoxemia well one way is I can try to increase the amount of oxygen the amount of inspired oxygen that is going to my alveoli if I increase my fio2 the amount the of inspired auction I might be able to bump the amount of oxygen that's diffusing across the alveolar capillary interface and increase the oxygen within the blood so think about increasing fio2 to be able to increase your O2 but be careful because there is a risk of hyperoxia so sometimes whenever you start seeing patients who are on very very high fio2 levels so sometimes normal room air is 21 so you can go up to 100 but that's very very high risk of putting the patient of hyperoxia worsening their VQ mismatch so we prefer not to go greater than 60 percent so try to keep it less than 60 percent so you say Okay Zach I have a patient who's on optiflow BiPAP or they're being and they're intubated and unventilating them on the ventilator and I have them and their spo2 is 85 and I have them on 60 and I can't go any greater than what do I do how do I help to be able to treat this patient well obviously treat the underlying causes but guess what else you can do sometimes the problem with these patients is that they have what's called D recruitment so you remember how I told you that sometimes there can be a lot of fluid here or they can have diseases which are actually come like they can be compressing on the alveoli or you're not filling air into the alveoli from like a mucus plug or you're having diseases that are washing away their surfactant and increasing the surface tension collapsing the alveoli either way they are d recruiting imagine you're trying to take a deep breath when you try to take a deep breath you have to reopen up these alveoli all right so you take a deep breath and you have to open up these alveoli when you try to open them up then you go to this stage here all right so you try to take a deep breath and when you take a deep breath you try to reopen up and re-stent these alveoli that takes a lot of effort because imagine you have multiple alveoli that are collapsed and now what you have to do is take a deep breath to work really hard to take air in and open up those alveoli it takes a lot of work a lot of effort so because of that imagine what I could do to be able to maybe at the end of expiration so after the patient takes a deep breath in they fill those alveoli open guess what will happen if they exhale they'll go back to this and they'll de-recruit so in this situation you have D Recruitment and here you have recruitment and this may happen during inspiration and this may happen during expiration wouldn't it be very interesting at the end of expiration instead of them actually completely collapsing I push a pressure into their lungs and keep them open so that way whenever they take a deep breath during their next inspiratory cycle they won't have to work as hard to bring air in that'll keep them open and keep them able to bring oxygen into them and then allow for better diffusion of oxygen into the pulmonary capillary blood so what do I call this when I push pressure into their alveoli at the end of expiration to keep them stented open to keep them recruited and to not de-recruit that's called Peep and so what I will do is I'll apply a pressure here at the end of expiration and I'll increase what's called my positive end expiratory pressure and what that'll do is that'll inhibit D Recruitment and that'll keep the alveoli stent it open so that oxygen can easily move into these and I can breathe easier it decreases my work of breathing so it'll increase your O2 and it'll decrease the work of breathing and then I can allow for better oxygenation so the questions that they usually will ask is patient has hypoxemia you've increased their fio2 up to 60 percent they are still hypoxemic should you increase the fio2 more or should you increase the peep you increase the peep because it'll keep these alveoli from de-recruiting keeping them open and prevent hyperoxia okay the next concept here is hypercapnia so we have a patient who's hypercapnic the basic concept that I told you guys and I really wanted you guys to remember is that hypercapnia Pac paco2 is dependent upon what it is dependent upon the tidal volume and the respiratory rate so if I want to clear CO2 in other words I want the patient to be able to get Co2 out of their body I want them to Exhale more CO2 out how do I get them to Exhale more CO2 out well I have to increase their meta ventilation well that means I have to increase their respiratory rate and I have to increase their tidal volume and collectively when I increase both of these that's increasing their minute ventilation how in the world am I going to do that sometimes with these patients what we may do is treat the underlying cause my friends if it's hypoventilation you treat it so if it's a CNS disease you're probably going to have to intubate them because they're not going to be able to protect their Airway you're going to have to do it for them if it's a sedation reverse the sedation if it's a chest wall plural disease treat that if it's a neuromuscular Junction disorder treat that if it's some type of lung or Airway type of obstruction upper Airway obstruction or lung Airway problem then what do you do I can treat that what happens to be kind of the most beneficial thought process behind this is we can use something called BiPAP so BiPAP tends to be a beneficial entity for patients with neuromuscular Junction disorders or COPD and asthma because what we've found is is that this can really help to clear CO2 reduce air trapping and really help to reduce the work of breathing in patients and so this may be an entity that we utilize in patients with severe hypercapnia secondary to COPD asthma or neuromuscular Junction disorders especially like myasthenia gravis Guillain-Barre syndrome where they kind of act just like this disorder these tend to be very beneficial to be able to maintain good tidal volumes and respiratory rate that are actually helping the patient to ventilate properly while you're treating their underlying disease same thing there's only really one situation where BiPAP can be used for acute hypoxemic respiratory failure that actually has been beneficial if you really wanted to remember that we can use BiPAP up here and acute hypoxemia particularly in what's called pulmonary edema secondary to heart failure so we call that cardiogenic pulmonary edema and if you guys remember from our heart failure lecture where we talked about this we went over how it really decreases the right the right side of preload and how it really helps to increase the right ventricular afterload and to decrease the left ventricular afterload and by doing that the whole concept is that you reduce the filling to the right side of the heart and you increase the blood flow out of the left side of the heart the whole concept is is that you're getting blood flow out of the heart and it's not backing up into the lungs that's the concept that we would use so BiPAP is really good as a non-invasive measure in patients with COPD asthma neuromuscular Junction disorders where you can control their respiratory rate their tidal volumes their overall Mena ventilation while treating their underlying disease and then it's also good for pulmonary edema that's due to heart failure where you reduce their right side of preload and decrease their actual left side they're left-sided afterload and that really helps to improve blood flow out of the heart and decrease inflow into the heart and that'll really help to reduce the pulmonary edema but this is the concept my friends that I want you to understand for acute respiratory failure let's do some cases now all right my friends let's do a case here we have a 65 year old male presents with an spo2 of 80 on room air and also complains of pluritic chest pain okay very interesting so when we do this we're evaluating for the cause or what type of acute respiratory failure they have so we do a physical exam their heart rate's 120 so they're slightly tachycardic the respiratory rate's 32. their temp is 101.2 so they're febrile interesting and the spo2 is 80 so they are hypoxic so the hypoxicon room air they're slightly febrile they're a little bit to kipnic and they're tachycardic when you look at their chest and you examine their chest their chest is completely normal you have no evidence of any consolidation any Pleural fluid kind of problems or anything like that so that's very interesting right off the get-go makes me think that it's a VQ mismatch likely from no true kind of like consolidative cause so in other words it's more of like a perfusion problem like a PE but nonetheless let's go to the next step which is obtaining an ABG when we attain the ABG what we see here is when we actually look at the patient's a a gradient it is actually much higher than the estimated aa gradient okay so we kind of went through and we've talked about all of this already but if we see that the AAA gradient that we calculate is way above the estimated that's an increase a gradient that tells me that it's either a VQ mismatch or it's a shunt or again it could be like an interstitial lung disease process as well but I think it's important to remember so we've already narrowed it down it's not a ventilation problem it's not a low fio2 problem this is likely a VQ mismatch or it is a shunt process okay so with that being said let's look at the other aspect here their pH at 7.5 so slightly alkalotic the reason why is because their CO2 is 22 they're breathing probably pretty fast they're breathing at a very high rate so they're blowing off CO2 trying to bring in more air but unfortunately they're dropping their CO2 causing a respiratory alkalosis and then their pao2 is 45 so that's pretty low so they definitely have a pretty good hypoxemia here so the patient has an increased aa gradient supporting a VQ mismatch or a kind of like shunt process and so that would tell me that this is likely a type 1 respiratory failure and I can tell that it's a type 1 because look how hypoxemic they are their spo2 is significantly low 80 percent and on top of that their pao2 is very low 45 and so this is definitely in support of an acute hypoxic respiratory failure or type 1 respiratory failure all right so what would be the differential to a cause of a VQ mismatch or a shunt well remember I told you think about is it the bronchus is it the alveoli is it the interstitial fluid or is it the pulmonary capillaries that are the problem and so we kind of go through that process whether it's a VQ mismatch a shunt problem or a diffusion problem which was the last one that we talked about which is like an interstitial lung disease issue but I think the next thing that's really important here is when we think about this if we think that it's a VQ mismatch or we think that it's a diffusion problem we could actually give these patients a hundred percent fio2 and generally what it'll do is it'll actually improve the patient who has a VQ mismatch but it will not improve the oxygen saturation of those who have a shunt so if they have a shunt in other words they have a intracardiac shunt they have a vsd they have some type of PDA they have a um you know atrial septal defect or something of that nature where they're kind of like mixing blood that would be an intercardation they have a pulmonary AVM they have significant like mucous plugging of like a primary bronchus they have massive ards or they have like extreme severe pulmonary edema or pneumonia in those situations you can give them a lot of oxygen if they don't improve it's a shunt but if it's like a little bit of mucus in the Airways like a mild kind of mucus plugging kind of like atelectasis or if they have a little bit of like fluid within their alveoli like mild pulmonary edema or a little bit of pus in their alveoli like in you know a pneumonia or if they have a little bit of blood in the alveoli like a diffuse alveolar Hemorrhage or they have a little bit of kind of like fibrosis and fluid in the interstitial spaces like interstitial lung disease or they have a a clot in their pulmonary artery that can also cause like a pulmonary embolism those kinds of situations are VQ mismatch you can give them oxygen and they'll actually improve their oxygen saturation so if I gave them a 100 and improved it supports a VQ mismatch so in this patient we're actually going to give them 100 oxygen and guess what they actually improved and so that helps me to support a VQ mismatch versus a shunt so go through your differential is it the airway so in other words do they have severe COPD asthma um there was nothing on their actual exam or their history to suggest that alveoli do they have any Consolidated findings no they didn't do they have any kind of like clear you know crackles or rails and auscultation no atelectasis did they have any kind of like decreased expansion on one side any kind of like decreased tactile fremitus any kind of dullness or percussion anything that would suggest that no so could it be a PE I think it could be a pulmonary ambulance especially with the patient's tachycardia that also is in support of that especially with a normal lung exam and then the next thing their chest x-ray shows no evidence of pneumonia pulmonary edema diffuse alveolar Hemorrhage or atelectasis they have no wheezing on auscultation they don't smoke they have no history or remote history of COPD you get a ctpa and there it is Boom a big saddle embolus kind of straddling the right and left pulmonary artery so we know that the patient has a proximal pulmonary embolism and that's their cause all right so let's move into the next case here case study number two get a 45 year old male status post opioid overdose presents with spo2 of 88 on room air so physical exam heart rate's 50 respiratory rate six okay they're not breathing I'm not breathing very much at all attempts normal spo2 is a little bit low because they're not breathing very well GCS is seven so they definitely have like a decreased level of Consciousness likely because they probably you know took way too much opioids and they're having a degree of CNS depression and sedation so with that being said let's obtain the ABG utilize that to help us to determine the AAA gradient and then what other kind of problems they have so we look at the pH 7.24 so slightly acid why are the acidotic is the CO2 going to be high or is the bicarb low bicarb is appropriate but the CO2 is 62 that's elevated so they're not really breathing very much so their minute ventilation is low the respiratory rate's low so they're not actually exhaling as much CO2 so CO2 is increasing bringing the pH Down po2 is actually a little bit low but nothing crazy but it's mildly low so it's likely mildly low because they're not ventilating as well and so because they're not actually taking inadequate amounts of ventilation they're probably not bringing in as much oxygen into the bloodstream so they also have a little bit of a hypoxia as well in this situation but then we go to the AAA gradient so we calculate the pao2 we utilize that to calculate the a gradient and we obtain that that's 7.5 the estimated is 15.25 so it's not increased above the estimated so it's not an increase a a gradient therefore it is not a VQ mismatch therefore it is not any type of problem with a shunt physiology or diffusion problem this is either a low fio2 that they're inhaling because they're at high altitudes or it's hypoventilation because they're not generating an adequate respiratory rate in depth which is likely because they took too many opioids suppressing the respiratory drive they have a decreased respiratory rate in depth they're not adequately ventilating properly so that would likely be the potential cause for this patient since they have a normal a gradient and this is definitely going to be an acute hypercapnic respiratory failure or type 2 respiratory failure so what's the differential we already said that it's likely going to be either due to low fio2 maybe there's some kind of like problem where they're not having enough oxygen in the tank or you're not breathing enough fio2 via the device that you're using or you're at high altitudes um or the other potential etiology is that there's hypoventilation so in this patient they're not taking adequate tidal volumes this could be due to a decreased respiratory drive like a CNS depression or seen as disease or stroke seizures brain masses something of that effect or there's a problem with the nerves going from the spinal cord to the actual skeletal muscles so something like ALS or something like a spinal cord injury it could be Guillain-Barre syndrome so actually like demyelination of the axons there it could also be due to myasthenia gravis so there's neuromuscular Junction problems or it could be due to myopathy so muscular dystrophy or it could be due to a myopathy of the muscle or even sometimes it could be due to weakness or fatigue of the muscles in other words the patient's been breathing heavily and fast and deep for a long time and those muscles are fatiguing out because they can't maintain this adequate kind of like this High respiratory rate so those would be things to think about as a potential etiology here for this patient so it's likely hypoventilation is the potential cause and then again we can go through and think about all the reasons as to why they would have this potential problem here and again we can say it could be due to a CNS disease of depression it could be due to a nerve problem or a neuromuscular Junction disorder another thing is it could be due to a chest wall or pleural disease so I didn't mention this but sometimes if a patient has like Ankylosing Spondylitis or some type of like abnormality in their rib cage where they aren't able to adequately take deep breaths because of their Anatomy that could be a potential problem or if they have big huge whopping pleural effusions that are compressing down on the lungs or big pneumothorax that are compressing down in the lungs if they try to take a deep breath they can't take a deep breath because it's not going to allow for the lungs to expand because they have this restriction of the lungs or they have obesity so sometimes if you have obesity it actually restricts the lungs from being able to properly expand so that could be a potential issue and then the only other thing that could be is an obstruction of the airway so generally if they have an obstruction of the airway that'll allow for Less air to come into the lungs as well so those are things to think about I think that the patient's etiology is CNS depression though all right so if that is the case and it is CNS depression or opioids how do we treat that we reverse that usually give them something like naloxone to reduce or reverse the actual effects of the opioids and generally the patient should improve all right my friends so that covers acute respiratory failure I hope it made sense I hope that you guys enjoyed it love you thank you and as always until next time [Music] thank you [Music] foreign

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Length: 68min 44sec (4124 seconds)

Published: Tue Mar 28 2023