Acute Respiratory Distress Syndrome (ARDS) | Clinical Medicine

foreign what's up Ninja nerds in this video today we're going to be talking about acute respiratory distress syndrome also known as ards this is part of our clinical medicine section and if you guys like it please support us and you can do that by hitting that like button commenting down the comment section please subscribe also if you guys get a chance go down the description box below I really urge you guys to go to our website become a member there we have a lot of cool stuff we got nodes illustrations we're developing question Banks we're

even developing exam prep courses for those of you who are taking your boards and we got some cool merchandise so go check that out how do we Define this this is an interesting type of disorder usually in these patients they have some type of very particular findings and you can remember that via ards there is acute hypoxemia there is acute hypoxemia so that spo2 is usually either less than what 90 in patients who develop acute respiratory failure or their pao2 is less than 60 millimeters of mercury if you're getting it off of an ABG the

other finding is that they're exhibiting potential other signs like what well one of the other particular things is they're exhibiting signs of a ratio that is determining of the degree of their hypoxemia and we'll talk about this a little bit more in the diagnostic section but we say that the ratio which is determining their PF ratio has to be less than 300 to also consider these patients to have ards so they have to have acute hypoxemia meaning it developed within at least in less than a week let's also add that in less than one week

since the particular trigger a ratio that's determines the severity of their hypoxemia which is a PF less than 300 and they have to have diffuse infiltrates in their chest so there has to be diffuse bilateral infiltrates what the heck that mean that means if you look at these patients chest x-ray or their CT scan you're going to see all of these like white types of opacities all throughout both of the actual lung fields now whenever you see that you see all these like bilateral opacities on Imaging on top of that hypoxemia that developed within less

than a week a PF ratio off their ABG that suggests that it's less than 300 you then need to say could it be cardiogenic pulmonary edema that we're seeing how do I really rule that out well the most definitive test is that you do what's called a swan guns catheter and that places this into the pulmonary capillaries and gives you a wedge pressure and if that pulmonary capillary wedge pressure is less than 18 that is the most definitive way of saying that there is no cardiogenic pulmonary edema so this would say that there is no

cardiogenic pulmonary edema there is other ways and I would suggest that you do other things before going to a swan usually these are going to be things like an echocardiogram that would also probably be the more likely thing but again this is one of the most definitive ways that say that there's no cardiogenic pulmonary edema now this patient has these particular findings this is what we call the Berlin criteria they already asked but we have to then go and say okay we have a cute hypoxemia develop within less than a week it shows a PF

ratio less than 300 they have diffuse infiltrates and they have no cardiogenic pulmonary edema that's causing these bilateral infiltrates what in the heck is going on why are these infiltrates here causing all these problems let's see here we take an alveoli here's a normal alveoli has Type 1 type 2 alveolar cells all of a sudden we decide to cause some diffuse alveolar damage we injure the type 1 cells the type 2 cells the pulmonary capillaries we jack all these things up and we're going to represent that by what's called a diffuse alveolar damage we also

sometimes just abbreviate this as Dad so diffuse alveolar damage is going to occur here when this occurs we're going to damage different types of cells let's say in this scenario we go down this pathway and we damage the type 1 cells you know the type 1 cells are squamous cells they're supposed to participate in gas exchange and they maintain a good barrier between the alveoli and the pulmonary capillary if you destroy them soccer is now guess what fluid can easily leak out here and right into what right into this poor alveoli and this thing can

start filling up with fluid right so let's lay down some things that it can actually start filling up with it may start layering up here and filling up with fluid that's one particular thing it may start layering up with proteins it may start accumulating a lot of different types of immune system cells that'll accumulate in this particular vicinity and then on top of that there may be a lot of protein so we'll put some proteins here within this kind of like this pinkish color so now you end up with all this filling that occurs within

this actual alveolus So within this first injury here what happens you end up with what's called of a lot of exudate Alaska date oxidative phase and what this means is is you're taking and filling these alveoli with tons of fluid and cells and a bunch of other types of chemicals and this thing starts getting super super filled what's the problem with that well imagine here we take this scenario where you fill this alveoli up and now it's filled up with fluid and cells and back you know maybe other kinds of things as well can you

even ventilate this alveoli no you can't ventilate this dang alveoli so because of that there's going to be very very poor ventilation there'll be almost no ventilation and if there's no ventilation and somewhat normal perfusion what do we have here we have the most extreme low VQ mismatch that's what we call a shunt and if ventilation can occur are you going to be able to get any any oxygen into this actual capillary bed no and so what happens is blood is flowing through here because the perfusion remains relatively normal when it leaves because NOAA gas

exchange is actually even occurring here what's going to happen to your pao2 or your O2 it is going to drop and these patients will have profound hypoxemia what do patients look like when they have significant hypoxemia well they start breathing really really fast and so what happens to the respiratory rate it goes up what happens to the work of breathing it goes up how do they feel they feel very short of breath and so these are very very common features that usually occur as a result of the patient's hypoxemia all right so we see one

way that they can develop profound hypoxemia and filling this is an infiltrate if this happens in multiple multiple alveoli in all parts of the lungs do you see why this can cause this diffuse infiltrates here's another thing that's not the only thing it causes diffuse alveolar damage it hits the type 2 cells so let's come down and see what it does there this thing jacks up the type 2 cells and if we jack up the type 2 cells you have to remember what do the type 2 cells do these are cuboidal cells and they make

a molecule here called surfactant it's supposed to code this but if all of a sudden you start leading to less of these type 2 cells do you keep all that surfactant that coats the inner parts of the alveoli and make sure that what it doesn't collapse no so when you have type 2 cell injury what happens is is you lead to a decrease in the surfactant and if you decrease the surfactant you then have surface tension begin to rise and as surface tension begins to rise in combination if you're having both of these cells being

damaged fluid will also begin to accumulate here so you're going to have fluid from what we just talked about Above So now imagine having fluid here and then on top of that imagine having less surfactant what's going to happen is the alveoli will start to collapse because the surface tension Rises and then you're going to get here an example of a pulmonary shunt because what you're going to have alveolar collapse and now you're going to have this problem where the alveoli can't stay open because the surfactant is pretty much lost and it's going to be

filled with a bunch of fluid if you collapse these alveoli pretty intensely what's going to happen are you going to get any ventilation at all into this poor little alveoli no as a result perfusion could be somewhat normal running through here but if the ventilation is poor are you going to be able to get any Oxygen over here no and so because of that the ventilation is lost even though the perfusion remains somewhat normal and so because of that they'll have a significant drop and they're oxygen because of no ventilation and relatively normal perfusion and

as a result the patient's respiratory rate will go up their work of breathing will go up and attempts to be able to hopefully increase their amount of oxygen but if the disease doesn't improve that won't help and this will just make them look like they're more distressed so now we have an understanding here this patient they're developing shunting because of two processes one they're developing a shunt because of alveolar collapse because of decreased surfactant or they're developing a pulmonary shunt because of an exudative phase and if there's an increase in this exudated phase this will

cause this alveoli to get filled and if the alveoli fills that'll cause that shunt so there's also going to be again alveolar filling and that alveolar filling is what is precipitating this pulmonary shunt we have to then ask ourselves the question okay what is causing the diffuse alveolar damage what's leading to this type 1 and type 2 cell injury which is causing shunting of oxygen where you're not getting oxygen moving across the alveol into the blood the primary problem is that we're having some direct lung injury or indirect lung injury and it is massive what's

the direct lundering injury causes it's something that we're inhaling or we aspirate and this comes down here and it directly injures these alveoli all these alveoli type one type two they get all jacked up and even some of it even spreads out here and hits some of these capillary bets will be some things that could actually be inhaled or aspirated into our Airway all right I just gave you kind of the answer one is pneumonia this is a huge one you guys know which pneumonia is really really a big one now SARS cov2 are used

to be kind of a big one and the other one here is going to be aspiration aspirations a really big one and then finally inhaled toxins so if you have inhaled toxins this is another really big one for example like a a fire there's a fire in a house when you inhale a lot of that sudden that can definitely do that so these are two big three big things here that I want you guys to remember that can directly damage these cells if you damage them you see the result that can occur but you have

to damage a lot of them the other one is not being inhaled or brought in via the lungs it has to be spreading through the bloodstream and then as it spreads through the bloodstream it diffuses out into the lung area and damages the capillaries here and damages the lung tissue this has to be something systemic what kind of systemic features would cause this type of massive inflammation I can already tell you a bacterial infection systemic bacterial infections which we call sepsis another one is a massive inflammatory condition that we call pancreatitis and another one that

is potential but I would say it's relatively less common but it is something to think about for your boards is when a patient gets a transfusion and they have a significant reaction to that and it really really injures the lungs and we call that a trolley a transfusion Associated lung injury these would be the particular things where these are going to massively increase inflammation systemic inflammation so let's put that here this is systemic inflammation and that systemic inflammation just happens to run through the capillaries in the pulmonary area and lead to this diffuse alveolar damage

whereas direct lung injury will cause direct local injury that's the concepts I want you to understand about ards now that we've gone through ards the particular definition the pathophys the causes what are some of the potential complications that can happen either from this disease or the things that we do to treat this disease all right my friend so the patient who has ards acute hydroximity less than a week PF ratio less than 300 they have diffuse infiltrates and their Swan our Echo suggests non-cardiogenic pulmonary edema they have these bilateral infiltrates that are causing refractory hypoxemia

and now with their signs of respiratory distress we're going to have to notice potential complications that can arise Within These patients one of the big ones that I think is important to remember because there is a treatment process that we can use for this is pulmonary hypertension and patients develop ards what happens is they have this intense refractory hypoxemia and that hypoxemia that happens as a result of them having these you know pulmonary shunting process leads to intense and I mean intense hypoxic vasoconstriction so what happens is this comes over to these pulmonary vessels and

these things clamp down so they develop an intense Vaso constriction so that's one of the things that hypoxia can do is it can really intensely contract down on these pulmonary vessels if I stimulate this intense pulmonary vasoconstriction what happens as a result is the pulmonary vessels get really really small and narrow and that increases the pulmonary vascular resistance right so now my pulmonary vascular resistance will go up the pulmonary artery pressures will go up as well so what will I notice the pulmonary vascular resistance will go up and the patient can start having high pulmonary

artery pressures which is called pulmonary hypertension one of the downstream effects of this is twofold one is if these pulmonary vessels are super vasoconstricted what does that do to the perfusion to those alveoli it reduces it so that can actually worsen VQ mismatch that's one Downstream effect but the other thing is if this becomes persistent this can really affect the right heart and this can start causing patients to develop things like right heart failure how does that look well if the right heart fails to pump blood forward and it can't fill in these particular scenarios

the central venous pressure begins to rise and the blood will back up via the vena cava and if it backs up via the vena cava what will that look like well one thing is it can cause jugular venous distension it may cause hepatomegaly it may cause ascites and it may even cause pedal edema so there's potential of right heart failure precipitating these findings and a patient Who develops severe RDS causing intense vasoconstriction but again I want you to remember that if resistance is really high the other problem here is that this can worsen VQ mismatch

this can actually increase your VQ mismatch and that can worsen the hypoxemia so that's the other kind of Downstream effects of this and this is very very common in patients develop ards the other thing that I really want you to remember is these patients are usually if they develop severe ards they're intubated all right they're going to be working hard to breathe they're going to have refractor hypoxemia and there's just not going to be enough to manage these patients usually with non-invasive ventilation which we'll talk about but to get intubated what are the downstream effects

that happens when the patients are intubated are at least greater than two days and if it's longer obviously there's a higher risk is this tube is a piece of plastic it's foreign to the body when you have something formed within the body it creates an opportunity for bacteria to grow and bacteria can stick and form biofilm on this thing and then what happens is these bacteria bacteria can spread to multiple parts of the lung tissue and now I have an opportunity where this ventilator tube has spread bacteria to multiple parts of my lung tissue and

now the downstream effect of this is these bacteria can lead to an infection and if I cause an infection of these particular lungs now that's related to the ventilator that's called a ventilator Associated pneumonia the problem with this is these are some really nasty bugs and usually nosocomial infections the ones that you really want to watch out for here is going to be things like pseudomonas they can really grow some nasty bugs here pseudomonas and another one called staphylococcus aureus especially the MRSA type more of the MRSA category these are very common as potential you

know factors here that could cause these types of infections so again that's one Downstream effect patients with ards usually they're intubated for a long period of time and the longer they are intubated for more than two days the higher the risk of bacterial colonization the higher the risk of infection and then therefore VAP and that's definitely going to worsen their Arts as well okay next particular scenario here is a patient can be intubated when they're intubated not only does VAP potentially arise but another thing is that they can actually have ventilator-induced lung injury so not

just the pneumonia what happens these patients is usually something that we're doing so when we hook them up to the ventilator we we set particular components of the ventilator modes and pressures and volumes and Peep Etc that we'll talk about but one of the biggest complications is patients who have ards they have very low lung compliance and whenever we give them very high pressures maybe that's in the form of Peep right so whenever you increase the patient's peep maybe a little bit too much and this isn't a patient with decreased lung compliance so their their

lungs just don't really want to expand so they don't really aren't very fond of getting all of this pressure what can happen is the pressure inside of the Airways can get Pretty stinking high and when the pressure inside of these Airways start getting to the point of what we call the plateau pressure so when the P Plateau is greater than 30 that is enough that this can actually cause a lot of trauma and can start dissecting the alveolar walls if you dissect the alveolar walls what can start leaking out air and where will that air

leak out into the pleural cavity and guess what you just increased the risk of a pneumothorax so this is a potential complication where these patients can develop as a result things like a pneumothorax or it can leak into the mediastinal which we call a pneumo mediastinum so a pneumothorax or a pneumo mediastine are potential complications from having just way too much peep or high Airway pressures within the lungs that distend in dice and slice these alveoli and then these could potentially result as a result of that complication all right so you can develop things like

a normal media assign them or pneumothorax all right cool that's one thing we got to watch out for when we put patients on these high high modes of pressure on the ventilator is really watching out to not get these Plateau pressures too high what about volume trauma right so you take an alveoli that's diseased decrease lung compliance right so same concept here but what I'm going to do is I'm going to give them very high volumes so I'm going to try to increase their tidal volumes but the problem is this is a patient who has

very decreased on compliance they do not like their lungs to get all this volume and all this stretch and so what happens is you push this title volume into them and their alveoli will get all this volume and it'll over distend and so now look at this alveoli you have an over distended alveoli now you might be like oh same thing Zach right it's going to blow this puppy no in this patient when you over distend these alveoli you actually injure the type 1 and type 2 alveolar cells and what that does is that causes

these cells to start releasing more inflammatory mediators and so now you get a increase in inflammation you're like what how the heck yeah and if you increase your inflammation what do you think you're going to do to this patient you're going to make them have more alveolar edema more alveolar collapse and you're going to decrease their lung compliance even more so this is going to be potentially a worsening factor here so giving them too much volume can increase inflammation and can actually worsen their lung injury and on top of that stimulate an even worsening of

decreasing lung compliance so this is the thing that you got to stay away from stay away from way too high tidal volumes and stay from way too high of an airway pressure the other thing that you want to do is you want to make sure that you don't give them too little pressure so you're like what is that how am I supposed to I got to keep this happy medium all the time yeah it's really difficult but I don't want to give them to the point where I don't have enough peep so here's a normal

alveoli all of a sudden I take a patient and I really really decrease the peep when you decrease the peep in these patients who have very very low lung compliance what do you think is going to happen it's going to collapse and we call that D recruitment so now look at this poor little alveoli it collapsed so this is going to be an example of alveolar collapse or alveolar we call this alveolar D recruitment so this is what happens when you really decrease the peep now here's the thing whenever you take an alveoli and you

go from this to this what do you think is going to happen now the patient has to take an even deeper breath in and they're going to have to work a lot harder to reinflate that alveoli the problem with this is this will definitely increase a couple things it'll increase their work of breathing and believe it or not that constant going from flayed inflated to deflated inflated to deflated increases inflammation you're like man I can't get away with anything here so you're going to increase inflammation which is going to do what that's going to decrease

the lung compliance even more and if you decrease the lung compliance and you have Low PEEP it's going to cause again them to de-recruit so they're going to have to work harder you're going to cause and become more inflamed and decrease their lung compliance so don't have too high of airway pressure don't have too low of an airway pressure and don't give them too much tidal volume the last particular scenario here which is kind of seems paradoxical is but you don't want to give them too much oxygen you're like what the they got a little

oxygen I got to give them oxygen you don't want to give them too much so if you give a patient just these crazy high levels of what's called fio2 so the fraction of inspired oxygen so you give them way too much oxygen when you give them very very high levels of fio2 the problem with that is that some alveoli that are actually somewhat healthy will take that and these oxygen molecules will start getting turned into free radicals and these little poppies here will start causing what do you think more damage to the alveoli so what

do you think is going to happen as a result with these free radicals if you have morphe radicals you're going to increase tissue destruction increase tissue destruction leads to increase inflammation plus weirdly and not enough having too much oxygen actually can act as a pulmonary vasodilator and that can worsen your VQ mismatch so another concept that you actually want to watch out for is if you give way too much oxygen oxygen can also cause increased VQ mismatch because it acts as a pulmonary vasodilator so the concept that I want you guys to take away from

all of this is a patient has ards really the complications that come from these patients is when we put them on the ventilator because we can do a lot of harm if we're giving them way too much airway pressure and their plateaus go up we give them too much title volume we don't give them enough peep or we give him way too much fio2 so it's important to make sure that we don't allow these things to happen as to prevent the actual continued destruction of those lungs and worsening RDS now let's talk about how to

diagnose it and treat it so then we move into the next one we have a patient who maybe we think has ards how do we determine that well one of the biggest things you have to have a patient who has been acutely hypoxemic and it usually has a onset has been for at least less than a week it hasn't been chronic it's been within less than the past usually sometimes 48 hours you get an ABG when you get an ABG you look at the PF ratio and this is basically what it says you take the

pao2 off the ABG and you divide it by the fio2 how much oxygen percentage of oxygen you're giving them if it's less than 300 that's really suggestive of the RDS let me give you a little bit of an example here so again po2 you get from the AVG fio2 is usually anywhere from 21 on room air to 100 depending upon the way that you're providing the oxygen if I give you an example I have a patient who has a Pao 2 of 50 off their ABG their fio2 is 80 you'll take this divided by 0.8

and it'll give you their PF ratio which is 62. what the heck does that mean well if you look at the patient there's a PF ratio than less than 300 we can kind of divvy this off into severity if it's anywhere from 200 to 300 that's mild if it's 100 to 200 that's moderate and if it's less than 100 that's severe so this patient right here would have would be considered to be severe ards so you have to have acute hypoxemia less than a week you have to have a PF ratio less than 300 and

again depending upon where it is it'll tell you the severity what else do you need you need to then check and say okay I want to make sure that this patient doesn't have any kind of like hypoventilation or something weird like that this would usually be what ours is a type 1 respiratory failure so this means it would be like a VQ mismatch or a true shunt so in this particular scenario it would definitely be suggestive of a kind of a shunt process so what I would do is I would get a chest x-ray or

a chest CT and what would I see on the chest x-ray you would see a lot of like diffuse bilateral opacities you see how it's all white here it should be a lot darker so this patient has diffuse bilateral opacities all right or bilateral pulmonary infiltrates same thing on the CT scan here's the right hemithorax here's the left hemithorax you can see all of this kind of diffuse white patchiness and a little bit of a plural effusion here this is really really suggestive of diffuse bilateral pulmonary infiltrates so the next thing you want to say

is okay I have acute hypoxemia PF ratio less than 300 I'd have diffuse bilateral pulmonary infiltrates how do I know that that's not from cardiogenic pulmonary edema patient is in CHF and they're having fluid back up elevated pulmonary capillary wedge pressure is causing this you can do a lot of different things one of the best things to do is get an echo does their Echo suggest that they have a normal left ventricular ejection fraction greater than 50 do they have a normal left ventricular in diastolic pressure they don't have any diastolic dysfunction it's probably not

cardiogenic pulmonary edema but if you're like I still don't think that's good enough then you can go the far you know extreme and most invasive way and do what's called a swangon's catheter or a right heart catheterization you take a catheter put it down through the right IJ into the pulmonary vessels and then eventually you're going to get a pressure off the pulmonary capillaries and if that pulmonary capillary wedge pressure is less than 18 it is again suggested that it's not cardiogenic pulmonary edema so this is not from the heart therefore this patient likely has

ards so what are the four things that you need to diagnose ards you need an acute onset less than one week you need a PF ratio that is actually less than 300 you need diffuse bilateral infiltrates on chest x-ray or CT scan and this last one just to help it make it work is you need to Swan guns catheter that shows the pulmonary capillary wedge pressure less than 18 all this is telling you is it cannot be cardiogenic in origin you don't have to do a swan you can do an echo but again those are

the ways that we're going to diagnose a patient with ours which is a type of one of the worst types of respiratory failure that leads to the next step if I have a patient on the ventilator how the heck am I supposed to know how to manage them well the first things you want to know is what's the mode that we have the patient in I think what's called CMV or controlled ventilation so this is a mechanical ventilation strategy where we actually set the respiratory rate that we want for the patient to have and we

set the amount of tidal volume the volume that we want to deliver into the lungs this is usually good for a patient who is not taking spontaneous breaths and the other scenario if a patient is taking spontaneous breaths we should let them breathe on their own don't let them be dependent upon the ventilator and so this is usually what we call PSV so it's called pressure support or patient controlled ventilation where you can actually allow for the patient to breathe at their own respiratory rate and their own tidal volume all you do is you set

the peep and the fio2 that leads to the next step oftentimes in the exam they may say okay you have a patient who is being ventilated their pco2 is really high what do I do to reduce their pco2 well I want you to remember two things one is respiratory rate and tidal volume if you increase the respiratory rate or you increase the tidal volume it'll drop the pco2 if you have to pick between the two respiratory rate is going to be the more effective one same way test your knowledge if the pco2 is low what

do you need to do then you need to decrease the respiratory rate or decrease the tidal volume because that will help to bring it up you're just trying to reduce their ventilation so pco2 is tied to respiratory rate and tidal volume the next one is pao2 what if it's too high well if the po2 is too high that may sound dumb but what do I want to do I don't want their oxygen to be really high no it's actually kind of dangerous you want to reduce the peep or the fio2 and that'll reduce the po2

same scenario pao2 is low increase the peep or increase the fio2 that'll increase the pao2 the concept behind peep is that here's an alveoli it's not getting good ventilation you give them a lot of pressure at the end of expiration and they don't collapse they stay stented open and big so now they can perform good ventilation and they can actually perform gas exchange but if you take the people away they'll de-recuit go back to that small size and they won't perform good ventilation so this keeps the alveoli stinted open and it'll be able to perform

gas exchange that's one of the big things about peep what about Pip this is called positive inspiratory pressure or Peak inspiratory pressure if the Pips are really high that means that there's a lot of resistance to airflow through the ventilator tube maybe it's a small tube maybe it's kinked maybe there's a lot of mucus within the tubing or they're having intense bronchospasm that's important to remember if the Pips are low that means that there's probably something wrong with the ventilator circuit there's probably an air leak somewhere the big one here that I really want you

to remember is called the plateau pressures Plateau pressures are a measure of kind of the if you take an inspiratory hold it kind of gives you the pressure within the airway at the at the end of inspiration so it's really important for helping to determine the risk of lung injury if Plateau pressures are really high that means that the lung compliance is not very good a patient likely has ards or pneumonia or things to that effect or they're air trapping a lot and so this is really dangerous and so whenever patients have very very high

Plateau pressures it's important to reduce the tidal volume so you don't cause Barrow trauma to the lungs the last thing I want to talk about is whenever you have a patient who maybe is was intubated for a particular issue and you improve that underlying issue you don't want them to be on a ventilator forever so you want to get them liberated from it and so what we do is we do is called sbts or spontaneous breathing trials and we look at a couple different things did they resolve the reason why they were intubated if they

did good that's one thing second thing is is there fio2 requirements very very minimal okay good is there peep really really minimal good is there risby which is their rapid shallow breathing index are they breathing really really fast and not taking very good deep breaths these are all things that would say that a patient would likely succeed and be able to be extubated if they don't meet these criteria you should probably not activate them because they'll have a high risk of being re-intubated big things that I really want you to remember is ventilating a patient

comes with complications if you have really high tidal volumes in these patients especially in ards a really high Plateau pressures you can really rupture those alveoli and cause bear trauma that's one really big thing it can cause what's called ventilator-induced lung injury you want to avoid that the other thing is that you don't want to give them too much oxygen because if you give them too much oxygen you cause VQ mismatch and you cause a lot of free radical formation a lot of inflammation that can also worsen the actual lung disease so avoid that and

lastly is that these patients are at high risk the longer they remain intubated the longer there is the risk for them to develop a VAP a ventilator-associated pneumonia so you want to try to liberate them as soon as you can from that we've talked about how we treat respiratory failure let's hope let's kind of change gears and go to the worst case we have a patient who has ards how do we treat this one of the biggest things is that these patients are likely going to be intubated all right and when they are intubated they're

going to be really air hungry they're going to want to breathe really really fast and take a lot of deep breaths so you want to sedate these patients and get them to be synced up with the ventilator you want them to be in CMV where you can control the ventilator so heavy sedation via propofol or my dad's lamb is going to be the best way to go here you also want to avoid them getting fluid overloaded so you want to keep a normal volume status because you don't want to worsen any edema within those alveoli

and the last thing that you want to do here is that you really want to and aim for what we call low tidal volume ventilation this is important because we want to make sure that the tidal volumes that they're taking based upon studies to be less than six CC's per kilogram of ideal body weight and if they're above that they're at high risk of worsening their actual lung injury we also want to make sure that their peep is decently High because that keeps those alveolites stented open and doesn't cause them to collapse so that's really

really important to go back to that concept we don't want these we don't want this process here deep recruitment we only want recruitment so that's a really really important thing because we've seen that with this strategy we've been able to reduce ventilator-induced lung injury and reduce mortality High peep same thing you reduce trauma and you reduce mortality so it's really important to employ this step because it shows that you can reduce mortality the next thing is let's say that the patient is getting heavy sedation they're trying to maintain you bulimia you're putting them in this

low tidal volume ventilation strategy to reduce mortality but they're really breathing over the set ventilator rate or their PF ratio showing that it's getting worse at least less than 150. now we have to escalate and what we do now is we paralyze the patient we don't allow for them to breathe above what we want the ventilator to give them because it can injure them so this is designed to reduce ventilator to synchrony and generally we do this again when a PF ratio is less than 150 and we've failed the other measures above and it's been

shown that if we can do that we potentially can reduce mortality now let's say that the patient again is on ventilator uh they're on neuromuscular blockade you should always have them sedated you should always can treat their pain you don't want them to be paralyzed and be aware or in pain and so that's really really needed if you have them on a neuromuscular blocker which we already do the next concept here is if we have this patient on neuromuscular blockade heavy sedation gold uvulimia low tidal volume ventilation strategy and they're still having a PF less

than 150 the data says you should prone these patients and the reason why pruning is really important is it reduces the dependent atelectasis it's so kind of interesting here so we do this when the PF ratio is less than 150 and they've failed everything above because it's been shown to reduce mortality so we want to do mortality reducing things if you look at a patient who's laying on their back all this area here in the posterior portions is being compressed and this is the areas that really really we want to get good ventilation for so

if we go ahead and we flip them over and now we open up these areas here and you're going to get good ventilation and good gas exchange again you're seeing the component here that as we do this pruning and then supine them we see the effect of how we're kind of just moving the actual lungs and opening up these dependent posterior portions and that's really going to improve oxygenation and reduce mortality all right now if the patient has pulmonary hypertension and they have RV dysfunction there has been things that you can actually dilate those pulmonary

vessels and that may be somewhat helpful in refractory hypoxemia despite proning neuromuscular blockade low tidal volume ventilation golu bulimia and heavy sedation so you can consider this if they have pulmonary hypertension RV dysfunction and refractory hypoxemia and if you've done all of those and the patient is still hypoxemic VV ECMO or Vino venous ECMO is usually the best thing to do in these patients what happens here is you take a catheter you run it in Via a big vein and go into this portion near the right atrium you take another catheter and you're going to

take the blood out through this pump through this kind of like the console here you're going to oxygenate the blood and you're going to return that back into the patient's bloodstream and so if you look here you have blood coming out you're going to run through oxygenate it and then send it back in so you're basically performing the job of the lungs this is usually the thing that you do in the last case scenario when the patient is not able to improve but there's just no good trials that suggest that this would be beneficial but

I have seen patients who have had this done and they've been able to improve and and get off the ventilator eventually so that's something that you would do in these patients I hope it made sense hope that you guys enjoyed it and as always until next time [Music] thank you