foreign what's up Ninja nerds in this video today we're going to be talking about asthma this is a part of our clinical medicine section before we get started if you guys like this video it makes sense it helps you please support us and you can do that by hitting that like button commenting down the comment section also subscribe I really suggest if you guys have the opportunity to go down the description box below there's a link to our website there you can find notes you can find illustrations you can even find developing courses that we're making as exam prep courses for step one step two for the pants Etc also check out some of the merchandise we have there without further Ado let's talk about asthma asthma in itself is a very interesting Disorder so it's a part of your obstructive lung diseases right so when a patient comes in with asthma I think it's important to have an understanding of what would their historical Chief complaint be so they come to the clinic they come to the emergency department whatever it may be their common Chief complaint is usually in some way shape or form dyspnea so Disney is a very common historical feature now we'll talk about why here in just a second another one is that when you're actually examining them on the physical exam you're using your stethoscope you're auscultating you may hear wheezing that's very very common so I really want you to think about these two particular findings is wheezing distena what is dyspnea Disney is the Sensation that you feel like you're short of breath right other things that you may find if you really want to add this to the mix is sometimes if you do take the step and do do percussion you may hear this thing called hyper resonance to percussion We'll add that one in there just to be extra all right so hyper resonance on percussion so with that being said if a patient comes and they have dyspnea wheezing on auscultation maybe some hyper resonance to percussion maybe they even have a cough sometimes that may also be a presentation you can start thinking about asthma the questions you have to ask yourself is why are they having dyspnea why are they having wheezing why are they having hyper resonance to percussion and why is there the possibility of a cough if I take a sliver here so I take a section of this bronchus and I start zooming in on it I'm going to show you the pathophysiology here so what happens here is I'm taking a section of the bronchus and these patients have so much bronchial wall edema that's one of the big primary issues here is they have so much bronchial wall edema there is a massive amount of inflammation within the bronchial wall now if you think about that if there's a lot of inflammation that's narrowing the airflow so you trying to get Co2 out and move oxygen in is going to be impaired so that's one particular problem so one of the reasons why the patient's can have dyspnea and wheezing is the dyspnea may be either having difficulty getting airflow in and they're having wheezing and Hyper resonance to percussion because they're having difficulty getting air out all right cool another concept is they have lots of mucus all right so the inflammation activates goblet cells and goblet cells start secreting mucus that's just the natural inflammatory response so if there's a lot of mucus within the Airways this is another really bad problem so we have lots of mucus we have lots of wall edema think about it same concept you're narrowing the airway it's going to be difficult to get air out and it's going to be just as difficult to get air in if you're having difficulty getting air in that's going to precipitate dyspnea and if you're having difficulty getting air out you're an air trap causing wheezing hyper resonance percussion and last but not least the common feature here is bronchoconstriction or bronchospasm this is where the smooth muscle within the bronchial wall is Contracting down like a mofo this sucker is clamping down so you see how the smooth muscles kind of encroaching in here as it encroaches in here it encroaches into the Lumen and now it makes it harder for air to be able to flow in and out of the lungs again precipitating Disney if you can't get the air in precipitating wheezing in hyper resonance to percussion if you can't get the air out the other thing with the mucus is that mucus can definitely irritate a lot of certain types of receptors within the airway and so can inflammation that may precipitate a cough reflex very common when there's inflammation within the airway either way all of these things are doing what all of these things are leading to a common theme and that is they are leading to Airway obstruction if this doesn't make sense let me explain it to you in another possible way here here we have a bronchus this is going into little bronchials and this is going into the alveoli the problem in this patient is they have bronchialedema mucus and bronchoconstriction in this scenario I'm having difficulty being able to get oxygen into this alveoli now I can't provide a gas exchange process and the same concept I'm having difficulty getting CO2 out of the airway because of this bronchoconstriction and bronchial wall edema some of the things that happens as a result of this is if I can't get air in but even worse I can't get air out this becomes really problematic and what we find is is that it's actually more difficult the expiration process is actually going to be much much worse and because of that this leads to the next step where they undergo what's called air trapping if I can't get this air out because there's so much bronchoconstriction or inflammation air stays Within These alveoli and they balloon up and this is what we refer to as air trapping now here's what I want you to think about that this is because of the airway obstruction so these are all the airway obstruction process here it leads to expiration being super difficult they air trap then their lungs become hyperinflated and here's what I want you to try to imagine so whenever a patient has really big hyperinflated lungs their lungs are literally filled because they can't get air out I want you to take a second take a deep breath in and then at that deep inspiration hold it your lungs are completely filled or at least decently filled try to take a deep breath on top of that that's what it's like having asthma it's their lungs are hyperinflated and they can't take these deep breaths in because their lungs are super super big and puffy and that's because they're super obstructive we have hyperinflated lungs we now have to ask ourselves the question what in the heck is leading to all this wall edema what's leading to all this mucus production what's leading to all this bronchospasm that's then precipitating an airway obstruction and all these Downstream effects so as we come down here here's what I want you to truly understand the reason for all of these mechanisms usually comes down to a couple precipitating factors one is allergies allergies are a huge trigger here and something that comes up on your step two or your pants exam is really important is this Triad if you will we call this the atopic Triad and the atopic Triad is very important to remember in the sense that if patients have allergies they probably also have some type of atopic dermatitis and they probably also have asthma and those are three common findings that are part of this atopic Triad so look for that in your clinical vignette they may try to throw that in there some way another one which is really odd is certain medications and one of those is aspirin for some reason aspirin may affect some of the let's say inflammatory Pathways which we'll get into a little bit more detail down here such as the leukotriene pathway that may increase the amount of leukotrienes and that may kind of exacerbate patients who have asthma and one of the processes that you need to understand is that there's a Triad another one called Sanders Triad and it says that patients who have asthma probably likely also have some type of like aspirin sensitivity and probably also have nasal polyps so that's another thing to consider other things that could be triggers for this increased wall edema mucus and bronchospasm could be other drugs so beta blockers tend to be a really big trigger here and another one is actually going to be the probably one of the most common is infections and usually the most common infections are usually viral infections so usually viral upper respiratory tract infections are really really big triggers and the last one I would say would be cold air and exercise a lot of the cold air and exercise may be through some mechanism trigger a lot of these processes so now that we've gone through that here's what I really want you to understand we get exposed to one of these particular things and I'd say out of these the high yield ones are going to be this one and this one here you're exposed to these things what happens is let's draw a little allergen here here's my allergen or we're going to call this my trigger this thing you get exposed to in the body when you're exposed to it you have specific cells called dendritic cells and these dendritic cells will then sense that trigger they'll exp Express a piece of it on their actual cell membrane and take it to a t helper cell that t helper cell will then become a little bit more specialized and become what's called a t helper 2 cell it'll then release particular cytokines such as interleukin-4 interleukin-5 there's other ones as well but these are probably the pertinent ones and when these are released they go and stimulate other particular cells such as eosinophils and eosinophils are Sons of Guns man they can act directly on the bronchial smooth muscle and cause bronchoconstriction or bronchospasm it also can stimulate plasma cells B cells who turn into plasma cells and then these plasma cells release antibodies different types of antibodies but usually the primary one is ige and there's also some IGG antibodies these antibodies will then go and interact with what's called mast cells in mast cells will then degranually see all these like kind of like baby blue granules here they'll actually release those out when they release these things out these are really potent chemicals these are things like histamines and these are things like leukotrienes so I'll with leukotriines there's so many different types I won't go through all of them but there is many different types what these chemicals then do is they also go to the actual bronchial wall and cause increased bronchial wall edema increased secretion and bronchospasm as a result all those things happen and what does the patient develop Airway obstruction and then as a default to that Airway obstruction what is the precipitating findings difficulty getting air out difficulty getting air in they wheeze if hyper resonance auscultation maybe they cough because of the inflammation they have dyspnea and again that is the process that I want you to understand now here's the next concept what if a patient who has asthma really has intense bronchial wall edema they have intense bronchospasm they have intense mucus production that it literally obstructs the airway so significantly that they develop scary complications from it let's talk about that next all right Engineers so now we're going to talk about the complications associated with asthma so we now know a patient who comes in with some dyspnea they have some wheezing some hyper resonance to percussions to potentially some coughing all because of that Airway obstruction from the mechanisms we went through and I told you again usually these patients can kind of live in that area where they don't have these severe complications they can just live with a little bit of wheezing a little bit of dyspnea but usually it's in you know in response to particular triggers allergens very big one is pollen seasonal changes viral infections right but in unfortunate patients who they have a lot of particular exposure to a really bad viral infection a really bad allergen exposure they may have a massive increase in bronchial wall edema and increasing mucus production and bronchospasm like it's going out of style and what happens is is when that occurs in a patient who really gets hit hard they can develop respiratory failure sometimes we see this in severe asthma exacerbation sometimes we also call this like status asthmaticus what happens is is now look I can't get Co2 out of this patient's lungs all right because it's so clamped down how am I supposed to get any stinking air through there so CO2 will actually start building up inside of the lungs the other concept here is that look am I going to be able to get O2 in here for a couple reasons one is a little bit from the bronchospasm but a second reason I told you guys before imagine a patient with asthma take a deep breath in hold it that's what they're living like right now now try to take a deep breath on top of that that's how hard it is so they're hypoventilating so it's difficult to get both air in and air out but I would say it's way more difficult to get air out so this process is inhibited and this process is inhibitive and as a result you develop an increase in CO2 within the lungs air trapping and you develop hypoventilation decrease O2 coming into the lungs so what happens effectively is if you're not getting air out and you're getting very little air in particularly in this process these patients develop what's called hyperinflation we already talked about that but again with the hyperinflation I want to dig into this a Teensy bit little more where if the patient's become hyperinflated the real problem here is now these alveoli are gargantuous all right and because of that what happens is they developed that problem I told you called hypoventilation all this is saying is the patient's lungs are already hyperinflated it's really difficult for them to take a deep breath in more than usual because they're already as big as they can possibly be or at least close to it so imagine that if that's the case very little oxygen is going to get in we already talked about this but even worse very little CO2 is going to get out if that happens the patient can develop respiratory failure and how would this look well one is as the CO2 starts to build up into the bloodstream what is this called whenever CO2 really builds up inside of the bloodstream it's called hypercapnia right what's it called whenever very little O2 is actually getting out here into the bloodstream that's called hypoxia so now these patients can develop kind of this weird problem here where they can have an increase in CO2 and a decrease in oxygen now let's come down for a second here when this occurs there is a type of respiratory failure that we can see beginning to form here and usually the type of respiratory failure that these patients usually exhibit is what's called a type 2 respiratory failure sometimes we call this hypercapnic respiratory failure and their characterization of this is that they're hypoventilating so they're not bringing a lot of oxygen but they're not getting CO2 out because of the airway obstruction and we classify this as high CO2 so you want to see high CO2 which is called hypercapnia and you would like to see a low oxygen but it's not going to be as bad as the CO2 okay that's one of the big things one of the primary things that happens with asthmatics is they can hold their SATs for a long time they can hold 98 to 100 percent but what's happening in the kind of behind the scenes is they are building and building and building up CO2 and that's the problem but here's the thing whenever they're hypoventilating they're not getting enough air in so they feel disc the other thing is that whenever they become hypercapnic and hypoxemic this can look a couple different ways one is the patient may try to compensate if your CO2 is building up what's the one way that you can try to get it out breathe faster and so these patients respiratory rate will go up and their work of breathing will go up they will look terrible they'll be breathing using accessory muscles nasal flaring intercostal retractions using their belly and so you'll see an increase in their respiratory rate and an increase in their work of breathing on top of that these Airways are so so inflamed and filled with mucus and bronchospastic that you're going to hear a lot of weird sounds like wheezing hyper resonance to percussion but these are the big things that I want you guys to remember real quick in a patient who comes in who maybe has mild asthma maybe it's not severe their Airway isn't super super obstructed so a little clear some of their CO2 and then they'll compensate but as the obstruction gets worse and worse and worse and we're taking the worst case scenario here as it gets really really bad the CO2 will build will build will build and the patient will develop a respiratory acidosis and association with a mild hypoxemia and that's what we call type 2 respiratory failure so one of the big things to look out for is an elevated CO2 and a corresponding drop in the ph and so when you get an ABG which we'll talk about later this is classically seen as a respiratory acidosis when you are late to the game so I'm going to put severe asthma it may be normal and like you're moderate and they may actually have a respiratory alkalosis in the mild cases because they're not super obstructed but this is the worst case scenario and you don't want to miss that okay another concept that I need you guys to understand here with these patients who can have respiratory failure is it's not only going to be their work of breathing the respiratory rate their CO2 building up and taking short small breaths it's also going to be other features they're going to have profound wheezing sometimes in worst case scenarios if you think about it these patients their chest could literally not move at all because they're not even taking in a deep breath so it could get from that all the way to a silent chest this is so ominous and this would pucker my stank hole so quick if I saw something like this so this is terrifying all right the other thing here is that they'll have that hyper resonance to percussion but you're going to notice that they'll take these short Inspirations and their expirations will be super long and so what we say is they have what's called a i e ratio that's really weird where they'll have a very short inspiration and a very prolonged expiration so they have a decrease I to e ratio these are the things that you want to watch out for if I see a patient with a silent chest evidence of a decrease IE ratio increase respite increase worker breathing and then I see this other finding I'm terrified for this patient that's called pulses paradoxis what can happen is in think two things one is the patient has an increase in their right heart venous return and the reason why is because these patients have a negative interpleural pressure their desire to take a deep breath and is so strong so they have a very negative interplural pressure the second concept is their lungs are hyperinflated and so it's pushing on the left side of the heart and reducing the left ventricular filling so this is being impaired this is being increased if the heart fills with blood on the right side during inspiration what's it going to do to the septum shift it over so now you shift the septum over and that's going to impede the left ventricular filling if you impede the left ventricular feeling during inspiration what happens the blood pressure drops so these patients can have a 10 point drop or more and there's a solid blood pressure during inspiration and we call this pulses paradoxis this is something that you can also see and a patient who has cardiac tamponade but you can see it in severe asthma all right my friends that's how I would cover respiratory failure in a patient who is a very severe status asthmaticus the last one here I would say that this is somewhat common but not as common is a pneumothorax so this could be a cause of what's called secondary pneumothorax if you really want to think about that this can be a cause we'll put this down here secondary pneumo thorax and I'll explain what I mean here in a second secondary unit with orexes are because you have an underlying lung pathology and these patients their lungs are already hyperinflated all right and the reason why is you have an airway obstruction air can't get out so now the lungs that let's say this is normal size now look as a result because of all that air trapping because they can't get the air out because of the bronchospasm mucus bronchialedema all that Airway obstruction leads to the lungs becoming hyperinflated now as they hyperinflate the apexes become super high risk so here's some hyper inflation now these lungs are gargantuous and now the Apex become a little bit high risk and they can bleb up and what happens is sometimes if these puppies rupture air can leak right from the lung parenchyma into the pleural cavity if air leaks into this pleural cavity this is now referred to as a pneumothorax but the reason for the pneumothorax was because of an underlying lung disease secondary to hyperinflation and a patient with severe asthma you see this a lot when the patient has what's called Dynamic hyperinflation or they're if they're on the ventilator and they're bucking the ventilator and they're really having the hard time getting air out they can have what's called Auto Peep and that can just distend and distend to stand their lungs and they can literally cause a pneumothorax so you want to watch out for this and listen for any absence of breath sounds on one side and the evidence of tracheal deviation any hypoxemia that quickly develops this is a possible complication that can rise in patients with severe asthma all right my friends we've talked about the asthmatic very detailed now what I want us to do is go through a diagnostic approach to asthma all right so now that we've gone through that we now need to say okay we have a patient who I think has asthma based upon maybe they present with an exacerbation or maybe they present with some of the classic findings then I have to say Okay how would I diagnose it when a patient comes in short of breath naturally you get a chest x-ray ECG and an ABG you just don't want to miss anything so this is a classic Triad or the Holy Trinity of Disney or chest pain work up generally Disney and so the chest x-ray it's usually not very specific it's usually normal sometimes if you catch them in a really bad exacerbation they could show hyperinflation ECG is usually not specific as well it's not going to give you anything particular it's usually normal and that's the big one there ABG this is the one that you really want to be careful for if it's a mild so maybe even like moderate asthma exacerbation their CO2 is usually kind of like downtrended or they're in a respiratory alkalosis because they're breathing so fast they're bloating their CO2 off but if they get to the point where the air obstruction is so bad they can't get Co2 out they will start to build up CO2 and it'll normalize and then worst case scenario it'll increase and so a sign of a very severe asthma exacerbation is respiratory acidosis where the pH is low and that pco2 is really high that's very concerning now if a patient is not exhibiting a asthma exacerbation pfts are usually pretty good if they're not super symptomatic at that point in time so we can do something where we obtain what's called an fev1 and FEC ratio and this is really helpful in determining if it's an obstructive airway disease and what you'll notice for these patients is that they have very low fev ones and a very minorly reduced fvc but their fev1 is really really reduced so their ratio is less than 70 percent the next thing is you know that that's a suggestive of an obstructive lung disease based upon pfts but you have to say Okay how would I prove that it's asthma generally what we do is we say okay let's check the fev1 see where it is that kind of gives you the severity of their asthma and then what we do is we want to see if it's reversible so we'll give them what's called uh in particular scenarios methacholine if it's if it's in a scenario where we want to see if it's inducible or reversible so if it's inducible and I give this patient methacholine it will worsen their fev1 because it'll constrict the bronchi and their fev1 should plummet and it should drop more than 20 percent all right and if it does that's really really suggestive of asthma so that suggests inducibility the other thing is I want to see if there's reversibility so I give them a bronchodilator like Albuterol I'd recheck their fev1 and what I should expect is is in the same way that those Airways are inducible and they can Bronco constrict and reduce the fev1 if I give them a bronchodilator it should open up the Airways and improve their fev-1 and if it does and it's greater than 12 that's even more suggestive of asthma in comparison to COPD so these are ways that we could definitely diagnose asthma now in a patient who has asthma and they're having an exacerbation these PFT tests probably wouldn't be the best what would be better is to check what's called their Peak expiratory flow rate which you see here you have these like kind of little this little thing here you have them take a deep breath in and then exhale and it'll give you kind of a volume that they're able to generate and based upon their age their sex their gender you get like a predicted value that they should be able to get to and if that Peak expiratory flow rate is less than 40 percent of the predicted that's suggestive of a really bad asthma exacerbation one of the interesting things that you can do with this though is you can treat them for their asthma so you can give them things like bronchodilators and steroids and Trend their Peak expository flow rate and see is it getting any better that could suggest that they're either improving or they're not improving at all the last thing that you could do is if you really want to go the extra step especially we talked about this in pfts you can check a dlco this is the diffusion limitation sometimes in patients who have asthma it may or may not be helpful because it can be normal but it can be increased because it may change the surface area of the alveoli but again big thing here is it could be somewhat helpful in suggesting asthma but I would go off of everything that we talked about here for stable everything we talked about here for exacerbation I just really want you guys to take away from this that when a patient is presenting with dyspnea wheezing increased work of breathing and complications like respiratory failure especially in a younger patient so in a younger patient I would really be thinking about a patient with an asthma disease rather than a COPD type of picture with that being said how do we treat asthma I really want us to go back a little bit and talk about some of this kind of pathophysiology because it links it together one of the best things that you can do for these patients is give them bronchodilators reduce this bronchospasm and cause those Airways to open up and one of the ways that we can do this we can give drugs called beta 2 agonists these are going to be things like albuterol or you know for motorol there's a bunch of different types and we'll talk about those all right the other thing that we can do is we can really reduce a lot of the inflammation because this is an inflammatory Cascade and usually giving steroids are really great they suppress the T cells they suppress the cytokine release and so this may reduce a lot of that Downstream effect of bronchial wall edema bronchospasm and mucous production things like corticosteroids are usually good here leukotrienes are usually a very particular area which they are a bit beneficial but it would make sense if you were to think about these if you had a receptor antagonist like leukotriine receptor antagonists they would block leukotrienes which would block a lot of the bronchial wall edema the mucous secretion the bronchospasm and so they can be used in certain scenarios and so that's the other things that I want you guys to remember the last one is histamines if we could block this part of the pathway we could also reduce again a lot of the same effects and so using histamine blockers may also be helpful as well like chromal and sodium the last thing is if we could potentially block these ige antibodies we would reduce these cytokine releases so wouldn't that also be beneficial 100 so giving things like a malazimab is a potential drug that could block this Cascade so I want you to think about this pathophysiology and think about where we could utilize drugs to block this pathway with that being said I want us to go through a stepwise asthma treatment a patient comes in they have asthma you need to be able to think about how you're going to start their treatment process especially on your board's exam the questions that you should be asking the patient is how many times do they have this daytime symptoms during the week and if it's greater than two check that off in your head are they having greater than two nighttime symptoms per month check it off in your head are they having greater than two exacerbations at some point time in their life check that off in your head so 222 the last thing is do their pfts suggest that there's an abnormality there that they're less than 80 percent if that does you have a patient who no longer has what we consider intermittent asthma it's not that this is actually going to be what persistent asthma and this is usually how we kind of get an idea of treating these patients so and a patient who has intermittent asthma you're going to start off just with a Saba so that bronchodilate or a short-acting bronchodiler like a Albuterol and use it whenever they're having symptoms but if this is a persistent asthma then we're going to step two all the way down and so we start treating these patients a little bit more aggressively and we say okay let's use something to reduce the inflammation there was like a low dose inhal corticosteroid have them come back and reevaluate are they still symptomatic up the dose of the inhaled corticostero to a medium dose or if that's not something you want to do you can keep the dose the same and add on a long-acting bronchodilator like some Adderall okay have them come back are they still symptomatic oh they are add the dose up so go to a medium dose inhale corticosteroid if you were at this scenario here or if you were at a medium dose inhale corticosteroid add on a lava so it's one of the other so by this point you should have a lava and a medium dose inhale corticosteroid have them come back are they still symptomatic increase the dose of the inhale corticosteroid to Max have them come back are they still symptomatic add-on and oral steroid but keep them on the lava and keep them on the high dose inhale corticosteroid so that's generally the way that we go about this determine how many times a week Daytime Nighttime symptoms how many exacerbations if it's two more than two two two you already are in the persistent Camp if that's the case you'll have the Sabbath but you're already going to start your step two all the way down to stack step six based upon their symptoms if they don't have any of those then you're more in the intermittent camp and you can just do the albuterol PRN all right if the patient has particular things that may benefit those leukotriene receptor antagonists for example if they have aspirin-induced asthma or allergic asthma you can consider a leukotriene receptor antagonist you can also consider xylitolin which is again going to be in cold and exercise induced asthma and you can consider a malazimab an allergic asthma or patients who whenever you test them they have very very elevated levels of ige antibodies okay the last thing I want to talk about is a patient who comes in they have a really bad asthma exacerbation they are huffing and puffing they have intense bronchospasm they have intense Airway edema they're really working hard to breathe they're to kipnic they're disc they're really looking bad maybe they're even hypoxic their ABG shows respiratory acidosis they're having a silent chest and these signs this is a very scary patient you want to get on top of them right so you don't use the same treatment we just talked about what you do for these patients is you give them bronchodilators right away and you focus on only two types short acting you're going to give them a Saba a bronchodilator that is acting on the beta tube receptors and a sama a muscarinic type of Locker this is going to be a petroprium both of these in combo we call them duonebs they promote a good amount of bronchodilation then IV magnesium has also been shown to be potentially beneficial because it also may cause smooth muscle relaxation so you're getting a lot of bronchodilation with these drugs so you're going to hit them with a duaneb and give them IV magnesium after you've done that the next thing is to reduce inflammation inhale corticosteroids are not going to be enough you have to give them systemic steroids so po if they can tolerate it if they if they're really hard working hard to breathe you might have to do IV so that would be the next thing that's the difference there the next concept is I really want to reduce their work of breathing I don't want these patients to look bad I don't want to have to intubate them these are the last patients that you want to intubate they're really scary so BiPAP is oftentimes somewhat beneficial the concept behind this is this is really the cycle of asthma and COPD patients at the air trap because they're so having so much Airway obstruction they hyperinflate they hypoventilate they build up their paco2 and drop their pao2 and they continue this process so how can I stop this cycle I initiate BiPAP and that keeps the airway stented open that will allow the lungs to deflate properly and allow for them to reduce their work of breathing improve their gas exchange and then again reduce the air trapping and that's the concept that we see here intubation is really the thing that you would only do if you've tried everything above and the patient is not improving lastly I always find that this is important to remember just for your Awards is that you really want to reduce anxiety in these patients they're working hard to breathe they're scared they got things going in and out of them they got this BiPAP on it's really uncomfortable sometimes relaxing them a little bit with something called ketamine may be helpful because you know what else is nice about this drug it's a bronchodilator so you get a little bronchodilation help them to relax and tolerate the BiPAP so that you can work them through and hopefully avoid avoid intubation all right my friends that's asthma I hope it made sense I hope that you guys enjoyed it as always until next time [Music] [Music]