Asthma | Clinical Medicine

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0:06what's up Ninja nerds in this video

0:08today we're going to be talking about

0:10asthma this is a part of our clinical

0:11medicine section before we get started

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0:35there without further Ado let's talk

0:36about asthma

0:38asthma in itself is a very interesting

0:40Disorder so it's a part of your

0:41obstructive lung diseases right

0:43so when a patient comes in with asthma I

0:46think it's important to have an

0:46understanding of what would their

0:48historical Chief complaint be so they

0:51come to the clinic they come to the

0:52emergency department whatever it may be

0:54their common Chief complaint is usually

0:56in some way shape or form dyspnea so

0:58Disney is a very common historical

1:00feature now we'll talk about why here in

1:03just a second another one is that when

1:05you're actually examining them on the

1:06physical exam you're using your

1:07stethoscope you're auscultating you may

1:09hear wheezing that's very very common so

1:12I really want you to think about these

1:14two particular findings is wheezing

1:16distena what is dyspnea Disney is the

1:19Sensation that you feel like you're

1:20short of breath right other things that

1:23you may find if you really want to add

1:24this to the mix is sometimes if you do

1:26take the step and do do percussion you

1:29may hear this thing called hyper

1:31resonance to percussion We'll add that

1:33one in there just to be extra all right

1:36so hyper

1:37resonance

1:40on percussion so with that being said if

1:44a patient comes and they have dyspnea

1:46wheezing on auscultation maybe some

1:48hyper resonance to percussion maybe they

1:50even have a cough sometimes that may

1:52also be a presentation you can start

1:53thinking about asthma the questions you

1:55have to ask yourself is why are they

1:57having dyspnea why are they having

1:59wheezing why are they having hyper

2:00resonance to percussion and why is there

2:02the possibility of a cough

2:03if I take a sliver here so I take a

2:06section of this bronchus and I start

2:08zooming in on it I'm going to show you

2:09the pathophysiology here so what happens

2:12here is I'm taking a section of the

2:14bronchus and these patients have so much

2:17bronchial wall edema that's one of the

2:19big primary issues here is they have so

2:22much bronchial wall edema there is a

2:25massive amount of inflammation within

2:27the bronchial wall now if you think

2:28about that if there's a lot of

2:30inflammation that's narrowing the

2:32airflow so you trying to get Co2 out and

2:36move oxygen in is going to be impaired

2:38so that's one particular problem so one

2:41of the reasons why the patient's can

2:42have dyspnea and wheezing is the dyspnea

2:44may be either having difficulty getting

2:46airflow in and they're having wheezing

2:48and Hyper resonance to percussion

2:49because they're having difficulty

2:50getting air out all right cool another

2:53concept

2:54is they have lots of mucus all right so

2:56the inflammation activates goblet cells

2:59and goblet cells start secreting mucus

3:01that's just the natural inflammatory

3:02response so if there's a lot of mucus

3:06within the Airways this is another

3:08really bad problem so we have lots of

3:10mucus we have lots of wall edema think

3:12about it same concept you're narrowing

3:14the airway it's going to be difficult to

3:16get air out and it's going to be just as

3:18difficult to get air in if you're having

3:20difficulty getting air in that's going

3:22to precipitate dyspnea and if you're

3:24having difficulty getting air out you're

3:25an air trap causing wheezing hyper

3:28resonance percussion and last but not

3:30least the common feature here is

3:32bronchoconstriction or bronchospasm

3:35this is where the smooth muscle within

3:38the bronchial wall is Contracting down

3:41like a mofo this sucker is clamping down

3:44so you see how the smooth muscles kind

3:45of encroaching in here as it encroaches

3:48in here it encroaches into the Lumen and

3:51now it makes it harder for air to be

3:53able to flow in and out of the lungs

3:55again precipitating Disney if you can't

3:58get the air in precipitating wheezing in

4:00hyper resonance to percussion if you

4:02can't get the air out

4:03the other thing with the mucus is that

4:05mucus can definitely irritate a lot of

4:07certain types of receptors within the

4:09airway and so can inflammation that may

4:11precipitate a cough reflex very common

4:14when there's inflammation within the

4:15airway either way all of these things

4:17are doing what

4:19all of these things are leading to

4:21a common theme and that is they are

4:25leading to Airway

4:27obstruction

4:29if this doesn't make sense let me

4:31explain it to you in another possible

4:33way here here we have a bronchus this is

4:36going into little bronchials and this is

4:38going into the alveoli

4:39the problem in this patient is they have

4:41bronchialedema mucus and

4:43bronchoconstriction

4:44in this scenario I'm having difficulty

4:47being able to get oxygen into this

4:51alveoli now I can't provide a gas

4:54exchange process

4:55and the same concept I'm having

4:57difficulty getting CO2 out of the airway

5:00because of this bronchoconstriction and

5:02bronchial wall edema some of the things

5:05that happens as a result of this is if I

5:06can't get air in but even worse I can't

5:09get air out this becomes really

5:11problematic and what we find is is that

5:14it's actually more difficult the

5:16expiration process

5:20is actually going to be much much worse

5:23and because of that

5:26this leads to the next step where they

5:28undergo what's called air trapping if I

5:30can't get this air out because there's

5:32so much bronchoconstriction or

5:34inflammation air stays Within These

5:36alveoli and they balloon up

5:39and this is what we refer to as air

5:41trapping

5:42now here's what I want you to think

5:43about that this is because of the airway

5:45obstruction so these are all the airway

5:47obstruction process here it leads to

5:49expiration being super difficult they

5:52air trap then their lungs become

5:54hyperinflated

5:56and here's what I want you to try to

5:58imagine

6:00so whenever a patient has really big

6:03hyperinflated lungs

6:05their lungs are literally filled because

6:07they can't get air out I want you to

6:08take a second take a deep breath in

6:12and then at that deep inspiration hold

6:14it your lungs are completely filled or

6:16at least decently filled try to take a

6:18deep breath on top of that that's what

6:20it's like having asthma it's their lungs

6:22are hyperinflated and they can't take

6:24these deep breaths in because their

6:26lungs are super super big and puffy and

6:29that's because they're super obstructive

6:31we have hyperinflated lungs we now have

6:33to ask ourselves the question what in

6:35the heck is leading to all this wall

6:37edema what's leading to all this mucus

6:39production what's leading to all this

6:40bronchospasm that's then precipitating

6:42an airway obstruction and all these

6:44Downstream effects so as we come down

6:46here here's what I want you to truly

6:47understand

6:48the reason for all of these mechanisms

6:51usually comes down to a couple

6:52precipitating factors one is allergies

6:56allergies are a huge trigger here and

7:00something that comes up on your step two

7:01or your pants exam is really important

7:04is this Triad if you will

7:06we call this the atopic Triad and the

7:08atopic Triad is very important to

7:10remember in the sense that if patients

7:11have allergies they probably also have

7:14some type of atopic dermatitis and they

7:17probably also have asthma and those are

7:19three common findings that are part of

7:20this atopic Triad so look for that in

7:23your clinical vignette they may try to

7:24throw that in there some way

7:27another one which is really odd is

7:30certain medications and one of those is

7:32aspirin for some reason aspirin may

7:35affect some of the

7:37let's say inflammatory Pathways which

7:39we'll get into a little bit more detail

7:40down here such as the leukotriene

7:41pathway that may increase the amount of

7:43leukotrienes

7:45and that may kind of exacerbate patients

7:46who have asthma and one of the processes

7:49that you need to understand is that

7:50there's a Triad another one called

7:51Sanders Triad and it says that patients

7:54who have asthma probably likely also

7:56have some type of like aspirin

7:58sensitivity and probably also have nasal

8:01polyps so that's another thing to

8:03consider

8:04other things that could be triggers for

8:06this increased wall edema mucus and

8:08bronchospasm could be other drugs so

8:11beta blockers tend to be a really big

8:12trigger here

8:14and another one

8:16is actually going to be the probably one

8:18of the most common is infections and

8:21usually the most common infections are

8:23usually viral infections so usually

8:25viral upper respiratory tract infections

8:27are really really big triggers

8:28and the last one I would say would be

8:30cold air and exercise a lot of the cold

8:34air and exercise may be through some

8:36mechanism trigger a lot of these

8:38processes so now that we've gone through

8:41that here's what I really want you to

8:42understand

8:43we get exposed to one of these

8:45particular things and I'd say out of

8:46these the high yield ones are going to

8:48be this one

8:49and this one here you're exposed to

8:52these things what happens is let's draw

8:54a little allergen here

8:56here's my allergen or we're going to

8:58call this my trigger

9:00this thing you get exposed to in the

9:02body when you're exposed to it you have

9:04specific cells called dendritic cells

9:06and these dendritic cells will then

9:08sense that trigger they'll exp Express a

9:11piece of it on their actual cell

9:13membrane and take it to a t helper cell

9:16that t helper cell will then become a

9:18little bit more specialized and become

9:20what's called a t helper 2 cell

9:22it'll then release particular cytokines

9:25such as interleukin-4

9:27interleukin-5 there's other ones as well

9:29but these are probably the pertinent

9:30ones and when these are released they go

9:33and stimulate other particular cells

9:35such as eosinophils

9:38and eosinophils are Sons of Guns man

9:40they can act directly on the bronchial

9:43smooth muscle and cause

9:45bronchoconstriction or bronchospasm

9:48it also can stimulate plasma cells

9:51B cells who turn into plasma cells and

9:54then these plasma cells release

9:56antibodies different types of antibodies

9:58but usually the primary one is ige and

10:01there's also some IGG antibodies

10:04these antibodies will then go and

10:06interact with what's called mast cells

10:09in mast cells

10:11will then degranually see all these like

10:13kind of like baby blue granules here

10:15they'll actually release those out when

10:18they release these things out these are

10:19really potent chemicals these are things

10:22like histamines

10:24and these are things like leukotrienes

10:27so I'll with leukotriines there's so

10:30many different types I won't go through

10:31all of them but there is many different

10:34types

10:35what these chemicals then do

10:38is they also go to the actual bronchial

10:40wall and cause increased bronchial wall

10:42edema increased secretion and

10:45bronchospasm as a result all those

10:47things happen and what does the patient

10:49develop

10:50Airway obstruction and then

10:53as a default to that Airway obstruction

10:56what is the precipitating findings

10:58difficulty getting air out difficulty

11:00getting air in they wheeze if hyper

11:03resonance auscultation maybe they cough

11:04because of the inflammation they have

11:06dyspnea

11:07and again that is the process that I

11:09want you to understand now here's the

11:11next concept what if a patient who has

11:13asthma

11:14really has intense bronchial wall edema

11:17they have intense bronchospasm they have

11:20intense mucus production that it

11:22literally obstructs the airway so

11:23significantly that they develop scary

11:25complications from it let's talk about

11:27that next all right Engineers so now

11:29we're going to talk about the

11:30complications associated with asthma so

11:32we now know a patient who comes in with

11:34some dyspnea they have some wheezing

11:36some hyper resonance to percussions to

11:37potentially some coughing all because of

11:39that Airway obstruction from the

11:41mechanisms we went through and I told

11:43you again usually these patients can

11:45kind of live in that area where they

11:46don't have these severe complications

11:48they can just live with a little bit of

11:50wheezing a little bit of dyspnea but

11:53usually it's in you know in response to

11:55particular triggers allergens very big

11:58one is pollen seasonal changes viral

12:00infections right but in unfortunate

12:03patients who they have a lot of

12:06particular exposure to a really bad

12:08viral infection a really bad allergen

12:10exposure they may have a massive

12:12increase in bronchial wall edema and

12:14increasing mucus production and

12:16bronchospasm like it's going out of

12:18style and what happens is is when that

12:20occurs in a patient who really gets hit

12:24hard they can develop respiratory

12:25failure sometimes we see this in severe

12:27asthma exacerbation sometimes we also

12:29call this like status asthmaticus

12:32what happens is is now look I can't get

12:35Co2 out of this patient's lungs all

12:37right because it's so clamped down how

12:39am I supposed to get any stinking air

12:41through there so CO2 will actually start

12:43building up inside of the lungs

12:45the other concept here is that look am I

12:48going to be able to get O2 in here for a

12:51couple reasons one is a little bit from

12:53the bronchospasm but a second reason I

12:55told you guys before imagine a patient

12:56with asthma take a deep breath in hold

12:59it that's what they're living like right

13:00now now try to take a deep breath on top

13:02of that that's how hard it is so they're

13:03hypoventilating so it's difficult to get

13:06both air in

13:08and air out but I would say it's way

13:10more difficult to get air out so this

13:12process is inhibited and this process is

13:15inhibitive and as a result you develop

13:18an increase in CO2 within the lungs air

13:20trapping and you develop hypoventilation

13:22decrease O2 coming into the lungs

13:26so what happens effectively is if you're

13:29not getting air out and you're getting

13:30very little air in particularly in this

13:33process these patients develop what's

13:34called hyperinflation we already talked

13:37about that

13:39but again with the hyperinflation I want

13:41to dig into this a Teensy bit little

13:43more where if the patient's become

13:45hyperinflated the real problem here is

13:48now these alveoli are gargantuous all

13:51right and because of that what happens

13:53is they developed that problem I told

13:55you called

13:57hypoventilation all this is saying is

14:00the patient's lungs are already

14:01hyperinflated it's really difficult for

14:04them to take a deep breath in more than

14:07usual because they're already as big as

14:09they can possibly be or at least close

14:11to it so imagine that if that's the case

14:13very little oxygen is going to get in we

14:16already talked about this but even worse

14:18very little CO2 is going to get out

14:21if that happens

14:24the patient can develop respiratory

14:25failure and how would this look

14:27well one is as the CO2 starts to build

14:31up

14:32into the bloodstream what is this called

14:34whenever CO2 really builds up inside of

14:37the bloodstream it's called hypercapnia

14:39right

14:40what's it called whenever very little O2

14:43is actually getting out here into the

14:45bloodstream that's called hypoxia so now

14:48these patients can develop kind of this

14:50weird problem here where they can have

14:52an increase in CO2 and a decrease in

14:55oxygen

14:56now let's come down for a second here

14:59when this occurs

15:01there is a type of respiratory failure

15:03that we can see beginning to form here

15:06and usually the type of respiratory

15:08failure that these patients usually

15:09exhibit is what's called a type

15:122

15:13respiratory failure sometimes we call

15:16this hypercapnic respiratory failure

15:18and their characterization of this is

15:21that they're hypoventilating so they're

15:23not bringing a lot of oxygen but they're

15:24not getting CO2 out because of the

15:25airway obstruction

15:27and we classify this as high CO2 so you

15:30want to see high CO2 which is called

15:33hypercapnia

15:35and you would like to see a low oxygen

15:38but it's not going to be as bad as the

15:42CO2 okay that's one of the big things

15:44one of the primary things that happens

15:46with asthmatics is they can hold their

15:48SATs for a long time they can hold 98 to

15:52100 percent but what's happening in the

15:55kind of behind the scenes is they are

15:57building and building and building up

15:58CO2 and that's the problem

16:01but here's the thing whenever they're

16:03hypoventilating they're not getting

16:04enough air in so they feel disc the

16:07other thing is that whenever they become

16:08hypercapnic and hypoxemic this can look

16:11a couple different ways one

16:13is the patient may try to compensate if

16:16your CO2 is building up what's the one

16:18way that you can try to get it out

16:19breathe faster and so these patients

16:22respiratory rate will go up and their

16:25work of breathing will go up they will

16:27look terrible they'll be breathing using

16:30accessory muscles nasal flaring

16:32intercostal retractions using their

16:34belly and so you'll see an increase in

16:36their respiratory rate and an increase

16:38in their work of breathing on top of

16:40that these Airways are so so inflamed

16:43and filled with mucus and bronchospastic

16:45that you're going to hear a lot of weird

16:46sounds like wheezing hyper resonance to

16:48percussion

16:50but these are the big things that I want

16:51you guys to remember

16:53real quick in a patient who comes in

16:56who maybe has mild asthma maybe it's not

16:59severe

17:00their Airway isn't super super

17:02obstructed so a little clear some of

17:04their CO2 and then they'll compensate

17:06but as the obstruction gets worse and

17:08worse and worse and we're taking the

17:09worst case scenario here as it gets

17:11really really bad the CO2 will build

17:13will build will build and the patient

17:15will develop a respiratory acidosis and

17:18association with a mild hypoxemia and

17:21that's what we call type 2 respiratory

17:22failure so one of the big things to look

17:24out for is an elevated CO2 and a

17:26corresponding drop in the ph and so when

17:29you get an ABG which we'll talk about

17:30later this is classically seen as a

17:34respiratory

17:36acidosis when you are late to the game

17:39so I'm going to put severe asthma it may

17:43be normal and like you're moderate and

17:45they may actually have a respiratory

17:46alkalosis in the mild cases because

17:49they're not super obstructed but this is

17:51the worst case scenario and you don't

17:52want to miss that

17:54okay another concept that I need you

17:56guys to understand here with these

17:58patients who can have respiratory

17:59failure is

18:00it's not only going to be their work of

18:01breathing the respiratory rate their CO2

18:04building up and taking short small

18:06breaths

18:07it's also going to be other features

18:10they're going to have profound wheezing

18:12sometimes in worst case scenarios if you

18:15think about it these patients their

18:16chest could literally not move at all

18:18because they're not even taking in a

18:19deep breath so it could get from that

18:22all the way to a silent chest this is so

18:25ominous and this would pucker my stank

18:27hole so quick if I saw something like

18:29this so this is terrifying all right the

18:32other thing here is that they'll have

18:34that hyper resonance to percussion

18:36but you're going to notice that they'll

18:37take these short Inspirations and their

18:40expirations will be super long and so

18:44what we say is they have what's called a

18:46i e ratio that's really weird where

18:50they'll have

18:52a very short

18:53inspiration

18:55and a very prolonged expiration so they

18:57have a decrease I to e ratio

19:00these are the things that you want to

19:01watch out for

19:03if I see a patient with a silent chest

19:05evidence of a decrease IE ratio increase

19:08respite increase worker breathing and

19:11then I see this other finding I'm

19:12terrified for this patient that's called

19:14pulses paradoxis what can happen is in

19:18think two things one is the patient has

19:20an increase in their right heart venous

19:22return and the reason why is because

19:25these patients have a negative

19:27interpleural pressure their desire to

19:29take a deep breath and is so strong so

19:31they have a very negative interplural

19:32pressure

19:33the second concept is their lungs are

19:35hyperinflated and so it's pushing on the

19:38left side of the heart and reducing the

19:40left ventricular filling

19:42so this is being impaired this is being

19:45increased if the heart fills with blood

19:47on the right side during inspiration

19:49what's it going to do to the septum

19:52shift it over

19:53so now you shift the septum over and

19:56that's going to impede the left

19:58ventricular filling if you impede the

20:00left ventricular feeling during

20:01inspiration what happens the blood

20:03pressure drops so these patients can

20:05have a 10 point drop or more and there's

20:08a solid blood pressure during

20:09inspiration and we call this pulses

20:12paradoxis

20:14this is something that you can also see

20:17and a patient who has cardiac tamponade

20:19but you can see it in severe asthma

20:21all right my friends that's how I would

20:23cover respiratory failure in a patient

20:24who is a very severe status asthmaticus

20:28the last one here I would say that this

20:30is somewhat common but not as common

20:32is a pneumothorax so this could be a

20:34cause of what's called secondary

20:36pneumothorax if you really want to think

20:37about that this can be a cause we'll put

20:39this down here secondary pneumo

20:43thorax and I'll explain what I mean here

20:45in a second secondary unit with orexes

20:47are because you have an underlying lung

20:49pathology and these patients their lungs

20:51are already hyperinflated all right and

20:54the reason why is you have an airway

20:55obstruction air can't get out so now the

20:57lungs that let's say this is normal size

20:59now look as a result because of all that

21:01air trapping because they can't get the

21:03air out because of the bronchospasm

21:04mucus bronchialedema all that Airway

21:08obstruction leads to the lungs becoming

21:09hyperinflated

21:11now as they hyperinflate

21:15the apexes become super high risk

21:18so here's some hyper inflation

21:21now these lungs are gargantuous

21:23and now the Apex become a little bit

21:25high risk

21:26and they can bleb up

21:28and what happens is sometimes if these

21:31puppies rupture

21:33air can leak right from the lung

21:35parenchyma into the pleural cavity

21:38if air leaks into this pleural cavity

21:40this is now referred to as a

21:42pneumothorax but the reason for the

21:45pneumothorax was because of an

21:47underlying lung disease secondary to

21:49hyperinflation and a patient with severe

21:51asthma

21:53you see this a lot

21:54when the patient has what's called

21:55Dynamic hyperinflation or they're if

21:57they're on the ventilator and they're

21:58bucking the ventilator and they're

22:00really having the hard time getting air

22:01out they can have what's called Auto

22:02Peep and that can just distend and

22:04distend to stand their lungs and they

22:06can literally cause a pneumothorax

22:08so you want to watch out for this and

22:09listen for any absence of breath sounds

22:11on one side and the evidence of tracheal

22:14deviation any hypoxemia that quickly

22:16develops this is a possible complication

22:19that can rise in patients with severe

22:21asthma all right my friends we've talked

22:23about the asthmatic very detailed now

22:26what I want us to do is go through a

22:27diagnostic approach to asthma all right

22:29so now that we've gone through that we

22:30now need to say okay we have a patient

22:32who I think has asthma based upon maybe

22:34they present with an exacerbation or

22:36maybe they present with some of the

22:37classic findings

22:38then I have to say Okay how would I

22:40diagnose it when a patient comes in

22:42short of breath naturally you get a

22:43chest x-ray ECG and an ABG you just

22:46don't want to miss anything so this is a

22:47classic Triad or the Holy Trinity of

22:49Disney or chest pain work up generally

22:52Disney and so the chest x-ray it's

22:54usually not very specific it's usually

22:57normal sometimes if you catch them in a

22:59really bad exacerbation they could show

23:01hyperinflation

23:03ECG is usually not specific as well it's

23:06not going to give you anything

23:07particular it's usually normal and

23:10that's the big one there ABG this is the

23:13one that you really want to be careful

23:14for if it's a mild

23:17so maybe even like moderate asthma

23:18exacerbation their CO2 is usually kind

23:21of like downtrended or they're in a

23:23respiratory alkalosis because they're

23:24breathing so fast they're bloating their

23:26CO2 off but if they get to the point

23:27where the air obstruction is so bad they

23:29can't get Co2 out they will start to

23:31build up CO2 and it'll normalize and

23:34then worst case scenario it'll increase

23:35and so a sign of a very severe asthma

23:38exacerbation is respiratory acidosis

23:40where the pH is low and that pco2 is

23:42really high that's very concerning

23:45now if a patient

23:46is not exhibiting a asthma exacerbation

23:51pfts are usually pretty good if they're

23:53not super symptomatic at that point in

23:55time so we can do something where we

23:57obtain what's called an fev1 and FEC

23:59ratio and this is really helpful in

24:01determining if it's an obstructive

24:03airway disease and what you'll notice

24:05for these patients is that they have

24:06very low fev ones and a very minorly

24:09reduced fvc but their fev1 is really

24:12really reduced so their ratio is less

24:14than 70 percent

24:16the next thing is you know that that's a

24:18suggestive of an obstructive lung

24:19disease based upon pfts but you have to

24:21say Okay how would I prove that it's

24:23asthma

24:24generally what we do is we say okay

24:25let's check the fev1 see where it is

24:28that kind of gives you the severity of

24:30their asthma and then what we do is we

24:31want to see if it's reversible

24:34so we'll give them what's called uh in

24:35particular scenarios methacholine if

24:37it's if it's in a scenario where we want

24:39to see if it's inducible or reversible

24:41so if it's inducible and I give this

24:43patient methacholine it will worsen

24:46their fev1 because it'll constrict the

24:48bronchi and their fev1 should plummet

24:50and it should drop more than 20 percent

24:52all right and if it does that's really

24:54really suggestive of asthma so that

24:55suggests inducibility

24:57the other thing is I want to see if

24:59there's reversibility so I give them a

25:00bronchodilator like Albuterol I'd

25:03recheck their fev1 and what I should

25:05expect is is in the same way that those

25:07Airways are inducible and they can

25:08Bronco constrict and reduce the fev1 if

25:11I give them a bronchodilator it should

25:12open up the Airways and improve their

25:14fev-1 and if it does and it's greater

25:17than 12 that's even more suggestive of

25:19asthma in comparison to COPD so these

25:22are ways that we could definitely

25:23diagnose asthma

25:25now in a patient who has asthma and

25:28they're having an exacerbation these PFT

25:30tests probably wouldn't be the best what

25:33would be better is to check what's

25:34called their Peak expiratory flow rate

25:36which you see here you have these like

25:38kind of little this little thing here

25:39you have them take a deep breath in and

25:40then exhale and it'll give you kind of a

25:42volume that they're able to generate and

25:45based upon their age their sex their

25:47gender you get like a predicted value

25:49that they should be able to get to and

25:51if that Peak expiratory flow rate is

25:53less than 40 percent of the predicted

25:54that's suggestive of a really bad asthma

25:57exacerbation one of the interesting

25:59things that you can do with this though

26:00is you can treat them for their asthma

26:02so you can give them things like

26:03bronchodilators and steroids and Trend

26:06their Peak expository flow rate and see

26:08is it getting any better that could

26:10suggest that they're either improving or

26:12they're not improving at all

26:14the last thing that you could do is if

26:16you really want to go the extra step

26:17especially we talked about this in pfts

26:19you can check a dlco this is the

26:21diffusion limitation

26:22sometimes in patients who have asthma it

26:24may or may not be helpful because it can

26:26be normal but it can be increased

26:28because it may change the surface area

26:30of the alveoli but again big thing here

26:34is it could be somewhat helpful in

26:36suggesting asthma but I would go off of

26:37everything that we talked about here for

26:39stable everything we talked about here

26:41for exacerbation

26:43I just really want you guys to take away

26:45from this that when a patient is

26:46presenting with dyspnea wheezing

26:48increased work of breathing and

26:50complications like respiratory failure

26:51especially in a younger patient so in a

26:54younger patient I would really be

26:55thinking about a patient with an asthma

26:57disease rather than a COPD type of

26:59picture

27:01with that being said how do we treat

27:03asthma I really want us to go back a

27:04little bit and talk about some of this

27:06kind of pathophysiology because it links

27:08it together

27:09one of the best things that you can do

27:10for these patients is give them

27:12bronchodilators reduce this bronchospasm

27:14and cause those Airways to open up

27:17and one of the ways that we can do this

27:18we can give drugs called beta 2 agonists

27:20these are going to be things like

27:21albuterol or you know for motorol

27:24there's a bunch of different types and

27:26we'll talk about those

27:27all right the other thing that we can do

27:30is we can really reduce a lot of the

27:31inflammation because this is an

27:33inflammatory Cascade and usually giving

27:34steroids are really great they suppress

27:36the T cells they suppress the cytokine

27:39release and so this may reduce a lot of

27:41that Downstream effect of bronchial wall

27:42edema bronchospasm and mucous production

27:45things like corticosteroids are usually

27:47good here

27:49leukotrienes are usually a very

27:51particular area which they are a bit

27:53beneficial but it would make sense if

27:54you were to think about these if you had

27:56a receptor antagonist like leukotriine

27:58receptor antagonists they would block

27:59leukotrienes which would block a lot of

28:01the bronchial wall edema the mucous

28:03secretion the bronchospasm and so they

28:05can be used in certain scenarios and so

28:07that's the other things that I want you

28:08guys to remember

28:09the last one is histamines if we could

28:11block this part of the pathway we could

28:13also reduce again a lot of the same

28:14effects and so using histamine blockers

28:17may also be helpful as well like chromal

28:19and sodium

28:20the last thing is if we could

28:22potentially block these ige antibodies

28:24we would reduce these cytokine releases

28:26so wouldn't that also be beneficial 100

28:28so giving things like a malazimab is a

28:31potential drug that could block this

28:33Cascade so I want you to think about

28:34this pathophysiology and think about

28:36where we could utilize drugs to block

28:37this pathway

28:39with that being said

28:41I want us to go through a stepwise

28:42asthma treatment a patient comes in they

28:44have asthma you need to be able to think

28:46about how you're going to start their

28:47treatment process especially on your

28:48board's exam the questions that you

28:50should be asking the patient is how many

28:52times do they have this daytime symptoms

28:53during the week and if it's greater than

28:55two check that off in your head are they

28:57having greater than two nighttime

28:58symptoms per month check it off in your

29:00head are they having greater than two

29:02exacerbations at some point time in

29:04their life check that off in your head

29:05so 222 the last thing is do their pfts

29:08suggest that there's an abnormality

29:10there that they're less than 80 percent

29:13if that does you have a patient who no

29:15longer has what we consider intermittent

29:18asthma it's not that this is actually

29:21going to be what persistent asthma and

29:24this is usually how we kind of get an

29:26idea of treating these patients

29:28so and a patient who has intermittent

29:30asthma you're going to start off just

29:32with a Saba so that bronchodilate or a

29:35short-acting bronchodiler like a

29:36Albuterol and use it whenever they're

29:38having symptoms

29:40but if this is a persistent asthma then

29:43we're going to step two all the way down

29:45and so we start treating these patients

29:47a little bit more aggressively and we

29:49say okay let's use something to reduce

29:50the inflammation there was like a low

29:52dose inhal corticosteroid

29:54have them come back and reevaluate are

29:55they still symptomatic

29:57up the dose of the inhaled corticostero

29:59to a medium dose or if that's not

30:01something you want to do you can keep

30:03the dose the same and add on a

30:05long-acting bronchodilator like some

30:07Adderall okay

30:09have them come back are they still

30:10symptomatic oh they are

30:13add the dose up so go to a medium dose

30:16inhale corticosteroid if you were at

30:19this scenario here or if you were at a

30:22medium dose inhale corticosteroid add on

30:24a lava so it's one of the other so by

30:26this point you should have a lava and a

30:28medium dose inhale corticosteroid have

30:30them come back are they still

30:31symptomatic increase the dose of the

30:33inhale corticosteroid to Max have them

30:36come back are they still symptomatic

30:37add-on and oral steroid but keep them on

30:40the lava and keep them on the high dose

30:42inhale corticosteroid so that's

30:43generally the way that we go about this

30:44determine how many times a week Daytime

30:47Nighttime symptoms how many

30:48exacerbations if it's two more than two

30:50two two you already are in the

30:52persistent Camp if that's the case

30:54you'll have the Sabbath but you're

30:55already going to start your step two all

30:57the way down to stack step six based

30:58upon their symptoms if they don't have

31:01any of those then you're more in the

31:02intermittent camp and you can just do

31:04the albuterol PRN

31:06all right

31:08if the patient has particular things

31:11that may benefit those leukotriene

31:13receptor antagonists for example if they

31:15have aspirin-induced asthma or allergic

31:17asthma you can consider a leukotriene

31:20receptor antagonist

31:22you can also consider xylitolin which is

31:24again going to be in cold and exercise

31:25induced asthma and you can consider a

31:28malazimab an allergic asthma or patients

31:30who whenever you test them they have

31:32very very elevated levels of ige

31:34antibodies

31:36okay the last thing I want to talk about

31:38is a patient who comes in they have a

31:39really bad asthma exacerbation they are

31:41huffing and puffing they have intense

31:44bronchospasm they have intense Airway

31:46edema they're really working hard to

31:48breathe they're to kipnic they're disc

31:50they're really looking bad maybe they're

31:53even hypoxic their ABG shows respiratory

31:56acidosis they're having a silent chest

31:59and these signs this is a very scary

32:01patient you want to get on top of them

32:03right so you don't use the same

32:04treatment we just talked about

32:06what you do for these patients is you

32:08give them bronchodilators right away and

32:10you focus on only two types short acting

32:12you're going to give them a Saba a

32:14bronchodilator that is acting on the

32:16beta tube receptors and a sama a

32:19muscarinic type of Locker

32:21this is going to be a petroprium both of

32:23these in combo we call them duonebs they

32:26promote a good amount of bronchodilation

32:30then IV magnesium has also been shown to

32:32be potentially beneficial because it

32:34also may cause smooth muscle relaxation

32:35so you're getting a lot of

32:37bronchodilation with these drugs so

32:38you're going to hit them with a duaneb

32:40and give them IV magnesium after you've

32:42done that the next thing is to reduce

32:44inflammation inhale corticosteroids are

32:47not going to be enough you have to give

32:48them systemic steroids so po if they can

32:51tolerate it if they if they're really

32:53hard working hard to breathe you might

32:54have to do IV so that would be the next

32:56thing that's the difference there

32:58the next concept is I really want to

33:00reduce their work of breathing I don't

33:02want these patients to look bad I don't

33:03want to have to intubate them these are

33:05the last patients that you want to

33:06intubate they're really scary so BiPAP

33:08is oftentimes somewhat beneficial the

33:11concept behind this is this is really

33:12the cycle of asthma and COPD patients at

33:14the air trap because they're so having

33:16so much Airway obstruction they

33:18hyperinflate they hypoventilate they

33:19build up their paco2 and drop their pao2

33:23and they continue this process so how

33:25can I stop this cycle I initiate BiPAP

33:27and that keeps the airway stented open

33:30that will allow the lungs to deflate

33:32properly and allow for them to reduce

33:35their work of breathing improve their

33:38gas exchange and then again reduce the

33:40air trapping and that's the concept that

33:42we see here

33:44intubation is really the thing that you

33:46would only do if you've tried everything

33:47above and the patient is not improving

33:50lastly I always find that this is

33:52important to remember just for your

33:53Awards is that you really want to reduce

33:55anxiety in these patients they're

33:56working hard to breathe they're scared

33:57they got things going in and out of them

33:59they got this BiPAP on it's really

34:01uncomfortable sometimes relaxing them a

34:03little bit with something called

34:04ketamine may be helpful because you know

34:06what else is nice about this drug it's a

34:08bronchodilator so you get a little

34:09bronchodilation help them to relax and

34:12tolerate the BiPAP so that you can work

34:14them through and hopefully avoid avoid

34:16intubation

34:17all right my friends that's asthma I

34:19hope it made sense I hope that you guys

34:20enjoyed it as always until next time

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