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Foreign, what's up, Ninja Nerds? In this video today, we are going to be talking about obstructive lung diseases. There's so much to cover in this one. It is going to be a monster, but it's probably going to
Comprehensive overview of obstructive lung diseases including COPD, asthma, bronchiectasis, their causes, pathophysiology, and treatments.
Key Takeaways
- COPD consists of chronic bronchitis and emphysema with distinct pathological features.
- Tobacco smoke is the primary cause of COPD, with alpha-1 antitrypsin deficiency as a genetic factor.
- Inflammatory cells release enzymes and reactive species that damage lung tissue and cause airway obstruction.
- Bronchiectasis involves structural airway damage often triggered by infections or other insults.
- Pulmonary function testing and imaging are essential for diagnosis and management.
Summary
- Introduction to obstructive lung diseases focusing on COPD, asthma, and bronchiectasis.
- Detailed explanation of COPD as a combination of chronic bronchitis and emphysema.
- Pathophysiology of emphysema involving neutrophilic proteases and elastase destruction of alveolar walls.
- Common causes of COPD including tobacco smoke and alpha-1 antitrypsin deficiency.
- Role of alveolar macrophages and neutrophils in inflammation and tissue damage in COPD.
- Mechanisms of mucus overproduction, bronchoconstriction, and airway obstruction.
- Discussion of bronchiectasis triggers and pathology.
- Clinical features such as hypoxemia, hypercapnia, and physical signs like tripod positioning.
- Pulmonary function tests including flow volume loops and DLCO for diagnosis.
- Treatment approaches including bronchodilators, steroids, and symptom management.
Chapters
- 00:00Introduction to Obstructive Lung Diseases
- 13:01Pathophysiology of Emphysema and COPD Causes
- 25:38Bronchiectasis: Triggers and Pathology
- 38:34Clinical Signs and Complications of Obstructive Lung Diseases
- 51:17Pulmonary Function Testing and Diagnostic Tools
- 65:43Imaging and Diagnosis of Bronchiectasis
- 77:51Treatment Strategies and Symptom Management
- 90:48Summary and Clinical Implications
Full Transcript — Download SRT & Markdown
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be one of the most important ones that we'll talk about in the pulmonary or respiratory system. So, we talk about obstructive lung diseases. We're going to go through specifically talking about the types, the causes, and the pathophysiology of obstructive lung
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diseases. There's three particular types of obstructive lung diseases that we'll talk about. One is COPD, the second is asthma, and the last one that we'll talk about is bronchiectasis. One of the common causes that you guys may be
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tested on in the exam is cystic fibrosis. So, we'll talk about all of those again, their particular causes, the pathophysiology, because the pathophys is extremely important to the clinical features, the complications, and even the treatment processes. All right, so first
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thing, when we talk about COPD, what I want you guys to understand is COPD, chronic obstructive pulmonary disease, is really two disorders in one, and those two disorders are chronic bronchitis and emphysema. Now, the way that we differentiate these is kind of based
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upon a small definition. So, chronic bronchitis is a type of chronic obstructive pulmonary disease where they have lots of productive cough. They have lots of mucus within their airways, and whenever they're coughing and coughing and coughing, it's just a very productive
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cough with lots of that mucus. And when we say whenever that productive cough has been greater than three months, so here's what I want you to remember: greater than three months for two plus years. That is somewhat of the definition
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as diagnostic of chronic bronchitis. Now, the other flavor of COPD is emphysema. Emphysema is more of a structurally defined type of COPD, and what that means is, and we'll go through the pathophys here, is that there is a lot of
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neutrophilic proteases and elastases that are actually released. And what these molecules do is, so imagine here I have a neutrophil. This neutrophil is going to release very nasty types of what's called elastases, and these elastases, what they're going
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to do is they're going to cause destruction of some of the elastic tissue within the alveolar walls and the bronchial walls. So, imagine here, and this actual kind of like a red color here, imagine that I have some type of
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elastic tissue, and this elastic tissue is important because not only does it form like septa of the alveolar walls, but it also gives some strength to the actual bronchioles in the alveolar walls and prevents them from collapsing. What
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happens is I'm going to destroy some of that actual elastic tissue, and I'm going to make the actual alveoli much, much bigger, and I'm going to cause destruction of the septal walls, and I'm going to destroy some of the elastic
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tissue in the bronchials. And so, the end result is that the bronchioles will collapse, and you'll have these big large air sacs with a decreased surface area. And this is one of the key features that would remember for specifically
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emphysema. Now, when we talk about COPD, we know chronic bronchitis, emphysema. What's particularly this the trigger, the cause for these particular disorders? The most common cause is going to be tobacco smoke. Ninety percent of the time, it's going to be due to some type of tobacco
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use. In small other cases, it could be due to environmental pollutants, but that's going to be less common. There's also one more cause that we'll talk about when we get into emphysema specifically, something called alpha-1 antitrypsin deficiency. So, we'll put down one other
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particular cause here that I do want you guys to potentially remember here as a trigger or a cause behind COPD. We'll mention it, and this one is called alpha-1 antitrypsin deficiency. So, it's called alpha-1 antitrypsin deficiency,
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and this is specific to emphysema, and we'll talk about that. All right, but how does all of this actually take place? We have a patient who has COPD, whether it be chronic bronchitis or emphysema. Patients can actually have both of them, so both of
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them can coexist in one patient who has COPD. They're exposed to tobacco. This could even be secondhand, so it could be them actually smoking, or it could be exposure to it in a secondhand process, or it could be pollutants, or they could have
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this specific type of genetic condition. Either way, let's say that they're exposed to this tobacco, there's a pollutant situation. How does this trigger the COPD process? So, imagine here I'm going to have some type of tobacco smoke. When I inhale it, it gets into the
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airways. In the airways, you have these special types of immune system cells called alveolar macrophages, and these alveolar macrophages will get picked up by the specific type of trigger, which is all of these that we just talked about
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over here. So, here's our trigger. Could be the actual tobacco smoke. They'll take up, phagocytose some of the actual inhalants. Once they do that, they become stimulated. When they become stimulated, they start releasing lots of cytokines, and some of
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the cytokines tend to be things like leukotrienes, like leukotriene B4, or interleukin-8, and there's all these other different types of chemokines that it's releasing. And what this does is, is this really helps to be able to jank up the actual
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inflammation process. So, it really increases the inflammatory process. One of the big things that actually happens as a result of this is that these chemicals can really stimulate very specific immune system cells to come to the area of the lungs where the
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actual bronchioles and the alveoli are and cause these white blood cells to actually move into this area, or all of these cytokines and triggers are. And these are called your neutrophils. Now, once the neutrophils come into this actual area, they start
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releasing a lot of very specific molecules such as reactive oxygen species or other types of free radicals that you can potentially see, and they also release lots of what's called proteases. So, these could be matrix metalloproteinases. These could
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also be elastases, but they're breaking down tons and tons of different types of proteins. And so, what you're going to see is you're going to see these things starting to damage the actual respiratory walls. And what you'll see is
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you'll start—you see how we have within this actual imagine we're zooming in on one of the actual bronchials. If I zoom in on one of the bronchials here, you're going to have an epithelial layer. So, here's my epithelial layer. Then
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underneath it, I'm going to have like a little basement membrane made up of like proteins and elastic tissue. And then after that, I'm going to have a smooth muscle layer. What happens is from all of these inflammatory mediators, they can also act
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on the smooth muscle and trigger the smooth muscle to undergo bronchoconstriction. Plus, the neutrophils will come to this area and release lots of reactive oxygen species, free radicals, proteases, and what that's going to do is that's going to start causing
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destruction of some of the elastic tissue. So, here, this is actually going to be elastic tissue. We're going to destroy some of the elastin. On top of that, we're also going to stimulate these types of mucus-producing cells. We're going to stimulate
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these mucus-producing cells, and if we stimulate these mucus-producing cells, we're going to have them make a ton of mucus. And all of this mucus layering is trying to be a protective barrier, if you will. If I have a lot of mucus, that's
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going to be trying to barrier between the actual epithelial lining and this trigger. It's supposed to be a protective mechanism, right? But unfortunately, you can clog up the bronchioles. So, what I see is trigger stimulates macrophages, causes inflammation.
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Inflammation can cause bronchospasm. They also can release cytokines that attract in neutrophils. Neutrophils release reactive oxygen species, free radicals, proteases. That's going to cause destruction of the elastic tissue within the...
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producing cells to increase the amount of mucus with inside of the Airways to act as a protective barrier but the problem with all of this is this can start leading to a lot of inflammation and destruction of the
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bronchial walls and you know what happens is whenever these epithelial cells are constantly exposed to this trigger this actual tobacco they start releasing things like transforming growth factor beta and what this does is this stimulates fibroblasts and fibroblasts are like okay I got to
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come in there because there's so much destruction and inflammation going on that I'm going to have to start laying down lots of fibrous tissue and this starts leading to fibrosis because they're going to start increasing the fibrous tissue deposition
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help with a lot of this inflammatory process so the end result out of just one exposure to this particular tobacco smoke consistently causes immune system activation inflammation leading to bronchoconstriction so therefore we're gonna have lots of bronchospasm because
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the inflammation is going to actually cause leukotrienes to stimulate these particular types of receptors histamines are also released lots of molecules that are going to stimulate these types of receptors and cause the bronchial smooth muscle to undergo bronchoconstriction
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this is going to be bronchospasm the second thing is that lots of this inflammatory mediators cause neutrophils to come to the area releasing reactive oxygen species free radicals proteases which causes an increase in the mucous production as a protective reflex but it
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clogs up the airway subsequently it also starts destroying some of the elastic tissue with inside of the actual bronchial and alveolar walls and if that happens it starts actually losing some of the actual elastic tissue within the bronchi and they collapse
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on top of that we destroy some of the alveolar SEPTA and make these big big large alveoli with a really reduced surface area this process here where there's lots of proteases destroying the elastic tissue is very specific to which
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type of COPD which one we see this more specifically in chronic bronchitis or emphysema emphysema so this process is definitely more specific of emphysema as compared to chronic bronchitis and then the last thing is whenever there's this repeated exposure and damage to the
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epithelial cells of the airway they release factors that trigger fibroblasts to come to the area and produce fibrosis this is leading to irreversible changes of the bronchial Airways and that's one of the big differences between COPD and asthma's once we start causing lots of
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fibrosis and chronic inflammation the damage has already been done and it's relatively irreversible and that's an important concept to understand all right so we have the concept of COPD we know that there's two types chronic bronchitis emphysema you can have both
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of these that coexist we know the differences between these one productive cough four greater than three months for two plus years and one is structural changes due to damage to the actual elastic tissue within the bronchial walls and the alveolar SEPTA causing
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decreased surface area we know the triggers is tobacco pollutants and there can also be another thing called alpha-1 antitrypsin deficiency we use the most common cause tobacco as the trigger here to activate the immune system causing lots of cytokines lots of elastases free
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radicals to be released which leads to what types of effects bronchospasm increased mucous secretions within the airway destruction of the actual alveolar SEPTA and bronchioles can start to collapse because they lose their elastic tissue and fibrosis of the actual bronchial
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tree the last thing that I want to talk about here with emphysema is whenever we start destroying some of the actual um specifically or some of these like connective tissue the elastic tissue with inside of these actual bronchials
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and some of the actual alveolar SEPTA we start ballooning them up so imagine here we actually start ballooning these into these big big large like sacks so here's this big big large Airway sack what happens is you may think oh this is
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great for like alveolar surface area but it's not when we start destroying some of the alveolar septal walls and we create these large like big sacs this actually decreases the total surface area for gas exchange so we decrease the
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total surface area for gas exchange and that actually makes worse gas exchange process causing VQ mismatching but here's the big thing this big large sack now that was actually a form due to breaking down the oval receptor walls is
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called an acinis and where these a Sinai form helps us to delineate if the emphysema that's actually present in this patient is due to tobacco use or if it's due to alpha-1 antitrypsin deficiency so here's what I want you to remember
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whenever you have a bunch of these sacs or Sinai that are forming in the upper lobe is towards the Apex the upper aspect of the lungs this is likely due to smoking remember smoke Rises and so in this situation for centrilobular
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emphysema meaning it's affecting more of the top of the lungs the apex of the lungs in this situation it's likely due to tobacco smoking but if you have a patient who has lots of these a Sinai and these biggest nir
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forming in the actual lower lobes the base of the lungs then this is unlikely due to smoking and it's more likely to be due to Alpha One antitrypsin deficiency and this is called panacena emphysema so pan acid or emphysema meaning it's
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affecting the basis of the lungs where they're having lots of alveolar septal and bronchial elastic tissue destruction if it's occurring in the base of the lungs it's Panasonic or due to alpha-1 anti-trypsin deficiency if there's alveolar wall septal and bronchialastic
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tissue destruction causing big acina to form in the tops of the lungs the apex of the lungs it's more likely due to tobacco smoking let me quickly explain to you what the heck alpha-1 antitrypsin deficiency is and how it causes this
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and I remember I told you that neutrophils will release these things called elastasis and elastasis will basically cause the destruction of the alveolar walls they'll start breaking down this elastic tissue within the bronchials and within the alveolar SEPTA okay and the overall
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effect here is if I break down the actual elastic tissue within the bronchials the bronchials will subsequently do what they'll collapse they won't be able to maintain that actual airway open and patent so they'll collapse on top of that they'll form
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this big ascendi which decreases the total surface area and affects gas exchange now elastic is the one responsible we have a very specific protein that we actually make in our body and this is called Alpha One anti-trypsin and what
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alpha-1 antitrypsin is supposed to do let's actually do this one in purple here imagine here is this cute little enzyme here and this is called Alpha One antitrypsin okay here's Alpha One antitrypsin what it does is is it's
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supposed to be able to inhibit the elastasis so it's supposed to inhibit the elastasis so they don't actually destroy the alveolar walls but in these patients due to some type of mutation they have a absence or deficiency of alpha-1
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antitrypsin and so because of that if they have less of this enzyme are they able to inhibit the elastasis from causing destruction of the ovular walls no and because of that you lose the ability to inhibit so this inhibition That was
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supposed to be present is gone and now there is an increased destruction of the alveolar walls but where does it actually predominantly destroy does it destroy the apexes or the bases the bases of the lung so that's important to
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remember Plus patients who have alpha 1 antotrips in deficiency not only does it affect lungs guess what else it affects the liver so one of the other things that I want you guys to remember as if a patient has Alpha One isotrips
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and deficiency and they have the bases of the lungs that have emphysema you can also suspect that they may have some type of underlying liver disease as well so think about that in a patient with alpha-1 antitrypsin deficiency as a
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potential cause of emphysema all right we've talked about COPD my friends now let's move on to asthma let's talk about asthma now with asthma there's very straightforward causes behind this one so we already know that COPD is due to
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some type of tobacco smoke or pollutants could be off one antitrypsin deficiency we also know that that's usually an irreversible type of reactive airway disease so there is damage to the airway lots of inflammation lots of bronchospasm and usually there's lots of
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fibrosis and Asthma it's also believed to be somewhat of a reversible obstructive airway disease and the particular triggers there's a much longer list unfortunately but it's straightforward it's either there's some exposure to an allergen dust pet animal dander pollen and then think about
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patients who have other risk factors and so we call this the atopic Triad so patients who have allergic rhinitis and atopic dermatitis are also at very high risk of developing asthma what's called allergic asthma so those are big things to be thinking
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about but don't forget the atopic try they could ask you that on the exam saying what are three parts of the atopic Tria that put patients at high risk of asthma allergic rhinitis atopric dermatitis and therefore high risk of
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allergic type of asthma now the non-allergic causes are also very important what the most important one that I want you guys to think about here is going to be viral upper respiratory tract infections this is definitely a very huge trigger for these
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patients again there's some type of virus that causes inflammation of the airway and what we'll talk about is that's already a problem for patients with asthma and Asthma their bronchial smooth muscle it's just waiting to be irritated and if you irritate it boom
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it's going to bronchospasm and cause massive amounts of constriction and bronchialedema so they're very very sensitive the other thing is cold air if you have exposure to cold air or you're exercising so you're running outside again those particular situations may be
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enough to be able to cause the bronchial smooth muscle to just get agitated enough and bronchoconstrict other things could be ger the underlying mechanism isn't completely understanded about this but it could also be a trigger and the other one that I want
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you to think about is beta blockers remember beta blockers are important because you know within the actual Airway your bronchial smooth muscle has beta adrenergic receptors beta 2 adrenergic receptors and if you stimulate the beta-2 adrenergic receptors what should they do it'll
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bronchodilate if I give a drug that blocks the beta 2 receptors will they bronchodilate anymore no what will they do they'll bronchoconstrict and the Pagano has very sensitive bronchial smooth muscle if you give them that drug they may bronchoconstrict more intensely
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than a normal individual and that's the important thing so again don't forget viral upper respiratory tract infection exercising a cold air gerd beta blocker is the big one and the other thing they may ask you is that a patient here has
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at higher risk for some type of asthma exacerbation and what particular scenarios if they have asthma they also have a nasal polyps lots of nasal polyps and you give them aspirin they can develop a massive asthma exacerbation as
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well so this is called Sanders try so they have aspirin hypersensitivity nasal polyps and Asthma big things to think about here so don't forget these two Triads now what I want to do is I want to tell us now we have exposure to one
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of these particular triggers where it's a non-allergic cause or an allergic cause what would be the early responses in a patient who has asthma and that will be the late responses to a patient who has asthma all right so the question
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that you may have is how do these particular allergens or triggers whatever it may be lead to the problematic issues that we see with asthma and the problematic issues that we see with asthma is that they develop an intense bronchospasm right so their
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bronchials will constrict narrowing the Airways on top of that they may also have a lot of Edema and swelling of their airways which also Narrows the actual Lumen of the bronchioles and then later in the disease their bronchial
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smooth muscle is so hyper responsive that just a little agitation to it is enough for it to intensely constrict and cause a massive asthma exacerbation and then again last but not least later in the stage the edema can get really
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really bad and then on top of that they start secreting a mucous lining that is trying to be a protective response for the actual Airway but again can cause more obstruction of the airway so how does all of this happen so you have the
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particular trigger here right it's within the Airways once once this actual trigger is exposed to a patient who is at risk for asthma will happen is they'll get taken up and phagocytosis by what's called dendritic cells within our
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Airway these dendritic cells will take this and phagocytose this particular antigen and then present it on its actual cell surface on what's called an mhc2 complex you see that pink protein here that it's expressing it on this is called a
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mhc2 protein it'll express it on that mhc2 complex the antigen then what it'll do is this dendritic cell will expose it on its surface on the image to do complex and take it to something called a t helper cell so here's going to be a
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t helper cell this T helper cell will have what's called A T Cell receptor that'll recognize that antigen and then what's called a CD4 protein that'll recognize the mhc2 complex once this interacts it activates these two cells specifically the T cell and the T Cell
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will start releasing very types with various different types of cytokines one of those it may release is what's called interleukin for and also May release something called interleukin-5 now when it releases interleukin-4 and interleukin-5 what happens is this
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specifically will activate another type of cell called plasma cells now you know plasma cells are basically these antibody producing factories when this plasma cell is activated it'll then release or secrete what's called antibodies and the very specific type of
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antibody that it actually releases is called i g e antibodies now the ige antibodies are very important because what they will do is they will come and bind onto a mast cell so here's going to be what's called a mast cell
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and once they bind on with the Mast Cell this can activate the mast cell and also Imagine they bind onto the membrane and let's say here once it binds onto the membrane here's again an exposure due to this particular trigger whether it be an
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allergen or a non-allergen it'll bind onto this ige receptor on the Mast Cell activate the Mast Cell guess what this mass is all going to do it gonna get crazy and it's going to start releasing massive amounts of
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leukotrienes massive amounts of prostaglandins massive amounts of histamines and what these are going to do is this is all going to act on the blood vessels that are supplying the bronchial walls and it's going to act on the bronchial
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smooth muscle and it may even act on some of the glands and the result of this is that you're going to vasodilate and increase the capillary permeability if I vasodilate these little vessels and I increase the capillary permeability
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fluid that's in these vessels are going to start leaking out into the actual bronchial wall what is that going to lead to bronchialedema on top of that some of these cytokines are going to go here and stimulate the smooth muscle here's our
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smooth muscle layer and it's going to activate particular receptors that are going to cause the bronchial smooth muscle to undergo bronchoconstriction this will lead to bronchospasm and this is going to narrow the Airways look at all that edema in the airway it's going
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to narrow it and then the bronchospasm is also going to narrow the Lumen that's going to be a difficult time for being able to get air in or out that's an important concept all right so that would be the thing
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that happens in the early phases now what happens later as patients who deal with this disease again let's say that they're exposed to these allergens right these allergens what can happen in the same kind of process here can get taken up by the
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dendritic cells when they're taken up by the dendritic cells the dendritic cells will phagocytose them and put them into these things called phagosomes Express them on their mhc2 complex after the express of the mhc2 complex they take it
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to a t helper cell the T helper cell will release cytokines so specifically one of them may be interleukin five interleukin 5 May activate very specific types of cells you know when you release interleukin-5 what it actually does is
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is it activates your bone marrow and says hey bone marrow I need you to make more very specific types of white blood cells and these types of white blood cells that I want you to make are called EO
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cenophils and these eosinophils are going to come to the area where all this actual inflammation is occurring and these eosinophils are released release different types of molecules called major basic protein and what's called cationic peptides and the problem with these particular
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molecules is that they love to cause tissue destruction and inflammation so these molecules will come and actually attack and Destroy parts of the bronchial smooth muscle wall and cause massive amounts of inflammation that inflammation that they're going to cause
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is going to lead to even more intense bronchospasm now the bronchial smooth muscle is going to be so sensitive that any particular trigger will cause it intensely spasm and really narrow the airway on top of that we're going to
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cause the edema to become even worse and we're going to really really ramp up these mucus glands to try to produce a very thick mucous layer to protect them from these allergens or certain types of triggers by creating a thicker barrier
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for these things to have to move across to damage the epithelial cells or agitate the epithelial cells and this is a problematic issue when we talk about this okay so now we have an understanding what happens in the early
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phase of asthma what happens in the late phase of asthma we understand the pathophysiology this is truly important especially this component of the diagram because when we talk about treatment we're going to Target very specific steps here okay now let's talk about
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bronchiectasis all right so let's talk about bronchiectasis now with bronchiectasis this is another type of obstructive lung disease but this one's classified by massive amounts of chronic inflammation dilation of the actual bronchioles excessive fibrosis of the bronchials and so this is a really
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really interesting type of disorder with bronchiectasis we have to understand the primary triggers or the reasons why this happened and it actually really does make sense so imagine here I take one of the bronchials and I zoom in on it and
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really focus in on it the reasons why someone would have bronchiectasis is the primary problem is that these patients can't clear mucus mucus just builds up within their airways and that mucus is a problematic thing because it can lead to chronic
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inflammation that chronic inflammation can lead to all the things that we'll talk about down here below now what would be the reason why I can't get mucus out of my Airways well one of them is think about the structures that
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are responsible for moving mucus what are these little guys inside of your Airways remember we have what's called pseudostratified ciliated columnar epithelial tissue that's cilia as responsible for beating the actual mucus up so we can spit it out or
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swallow it unfortunately but that's the whole concept what if the silly are all jacked up they're not functioning well so I have a pack of mucus that's sitting right here here's a pack of mucus and these cilia are naturally supposed to be
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able to beat this mucus upwards so that we can spit that mucus out or swallow it if the Cilia aren't able to perform that function such as beating the actual mucus upwards this does not take place the mucus won't move it'll stay in that
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area build up what's a disease that causes a decrease of the ciliary function you know there's a disease called primary ciliary dyskinesia sometimes we also refer to this as Cartagena syndrome and usually what happens in this disease is that they
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have cilia that are actually not functioning and on top of that during the actual development you know the heart the Apex is supposed to be shifted two-thirds of the left of the midsert a line and patients who have this type of
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disease cardigan or syndrome primary cellular dyskinesia their heart can be shifted to the opposite side so they have dextrocardia or they may have other organs that were supposed to be on one side switch to the other side and so we
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can see something called cytosine versus and so that's another thing to think about who patients who have decreased ciliary function so they have this bronchiectasis and they have organs switched to the opposite side situs and versus think about that disorder
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another reason is imagine that maybe the Cilia are intact but the mucus that you have here is just so thick it's really really thick meaning that there is a very little amount of water inside of these bad boys all right and there's
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very little chloride in these bad boys chloride is supposed to be able to help to pull water into the secretions but what if you have a disorder where there's a very special type of transport protein and this transport protein which
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is called the it's a cystic fibrosis transmembrane protein what it's supposed to do is supposed to pump chloride out here and pump water out here but if this transporter is defective can you pump the chloride out into these actual
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secretions and thin them out by yanking water into them no and so because of that the mucus the secretions get super thick to the point even if you have normal ciliary function you can't clear the dang mucus so it builds up and
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causes this type of bronchiectasis problem so think about that the next thing is what if I have normal ciliary function okay I have thin mucus no crazy thick mucus but I have a I don't know some type of massive form body whether that
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be a tumor so here's going to be a massive tumor that's going to be sitting inside of the actual Airway and what's supposed to happen is that this mucus is supposed to be moved upwards but I have this big foreign body or tumor that's
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obstructing the actual movement of the mucus out of the airway to be spit out or swallowed if that's obstructing it all the mucus that's going to be distal to that tumor or form body will build up and so all of this mucus
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just distal to this actual form body or tumor will build up and build up and build up so think about that in patients who have some type of tumor whether it be an intra like luminal tumor or extra
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luminal tumor so maybe you have like a lymphoma that's pressing on the bronchus from the outside compressing it narrowing the airway and you can't get the mucus upwards or you have a tumor inside of the bronchial Airway which is
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obstructing it or I don't know you swallow like a you know a dime or something like that and it gets stuck in the airway and it's obstructing the mucus from being able to get upwards okay so those are things to think about
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the last one is maybe it's not mucus as the problem maybe the mucus is being produced as a response to a chronic inflammation there's some type of microbe you know one of the big big microbes that are worth mentioning here
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there's a disease called allergic bronchopulmonary aspergillus this is a nasty fungal infection and this microbe can stay here and just cause nasty amounts of inflammation of the airway that inflammation of the air what's a protective response to inflammation mucous secretion and so
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what will happen is in response to a lot of this actual inflammation due to this infection you'll increase your mucus production as a protective response what if I have a disease that causes like autoimmune attack and this autoimmune attack occurs to
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multiple different tissues including the actual bronchial Airways and this inflammation as a response to that what do they do they produce mucus and that increased mucous secretion occurs due to Chronic inflammatory States whether that be locally due to infections and one of
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the big ones here is allergic bronchopulmonary aspergillus or systemic inflammatory diseases such as rheumatoid arthritis or SLE socimic lupus erythematosis all right so this is the concept that I want you guys to understand so again when you think about COPD it's
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bronchospasm it's increased mucous secretions emphysema predominantly there's destruction of the alveolar SEPTA the alveolar walls and the actual elastic tissue in the bronchial walls that causes a collapse decreased total surface area and then also fibrosis in asthma there's bronchospasm in the later
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stages the bronchial smooth muscle becomes super hyper-responsive lots of Edema of the walls and potentially mucus that accumulates there and bronchiectasis there is a little massive amounts of mucus that are accumulating within the Airways due to these particular causes or there's a chronic
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inflammatory assault to the airway that's causing an increase in amount of mucus to accumulate now what does that increase mucus lead to what's the problem let's talk about that so here we have all this mucus that's just accumulating
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when mucus accumulates what do you think it's supposed to kind of like trap in it imagine you have a big thick mucus plug here guess what's unfortunately sometimes trapped in this little area here lots of microbes and if these microbes get trapped into
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this area not only can they cause infection but they could potentially cause inflammation as well and this could cause agitation or inflammation or damage to the actual bronchial epithelium when that happens it causes immune system cells to come to
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the area where this actual destruction or inflammation is occurring what kind of immune system cells come to the area one of them is neutrophils and guess what neutrophils release they release tons of reactive oxygen species and proteases that should sound familiar these T cells
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come to the area so different types of lymphocytes come to the area and release lots of cytokines multiple different types of inflammatory cytokines and then on top of that these epithelial cells whenever they're inflamed they release something called transforming growth
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factor beta that we talked about that within COPD and that tells the fibroblasts to make what's called fibrous tissue so now all of these things type start to occur reactive oxygen species and proteuses what do you think they start
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doing they start causing destruction of the elastic tissue within the basement membrane what do you think a lot of these inflammatory cytokines do they also cause inflammation guess what that does that causes Broncho constriction on top of that these cytokines
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also stimulate your mucus producing cells to increase and worsen the already present mucous production and then on top of that the fibrous tissue starts laying down fibrous tissue around the actual bronchial walls to again be more of a protective response
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from that massive inflammation what does this start to look like look at this poor little bronchial this poor little bronchial has elastic tissue destruction around the walls what's elastic tissue supposed to do well normally it allows for you to be able to kind of stretch
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and then also recoil but if I lose that ability for this the actual structure to be able to recoil naturally it can start to balloon out and as it starts to balloon out due to the elastic reduction what happens to
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the actual Airway in this area you get a localized bronchodilation but on top of that here's the problem maybe between those areas of the destroyed elastic tissue guess what I have a lot of tissue laid down here fibrous tissue
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and so all this fibrosis maybe cause narrowing of the Airways so you may have narrowed portions and bronchodilated portions on top of that what else did I say was happening because of a lot of the cytokines that are being released what happens to the
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smooth muscle it undergoes massive amounts of bronchospasm and because we already have lots of mucous production but the inflammation worsens the mucous production there's going to be so much mucus that it's absolutely insane so these are the really important
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pathophysiological features that I want you to understand for bronchiectasis now let's start talking about what do these diseases look like alright guys so now let's talk about the features and complications of these obstructive lung diseases we're going to first start with
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COPD and one of the important things that you may be asked about on the exam even though they can coexist it's important to remember this they can coexist and it may be very difficult to delineate them for your exam you should
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be able to understand the difference between chronic bronchitis and emphysema which is again a part of the COPD category so we know that these patients have some type of tobacco use or excessive exposure to pollutants or if they have emphysema with the pan acid or
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pan lobular emphysema affecting the bases it could be alpha-1 antitrypsin deficiency but either way one of the big things here how to differentiate these two especially on the exam with chronic bronchitis we call these patients blue bloaters let me explain why
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and patients who have chronic bronchitis they may have what a bloated type of look and the reason for this bloated type of look is a couple different reasons one is if you think about it if a patient has COPD one of the problems
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is that they have a lot of bronchospasm they had a lot of mucus in the Airways and that's obstructing air from being able to get out of the lungs if you obstruct air from getting out of the lungs what happens to the lungs they get
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bigger because you can't exhale out the CO2 so these patients may have what's called hyperinflation of their lungs if you hyperinflate the lungs what that may do is is push the diaphragm down imagine this entire thoracic cavity is just
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filled with air because the lungs are hyperinflated it can push the diaphragm down and cause all the abdominal organs to protrude outwards giving somewhat of this obese type of appearance if that's not enough to make them look bloated on
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top of that we'll explain this in a second but patients who have chronic bronchitis they're a higher risk of what's called hypoxemia and hypercapnia meaning that they have low oxygen levels in the blood and high CO2 levels in the blood now
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explain why later but because of that when you have low oxygen levels in the actual blood and high CO2 levels in the actual blood what happens is that it's usually because of some type of problem in the actual
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alveoli they're not getting enough ventilation to particular alveoli so we don't send blood to that alveoli and so the way we don't send blood is we constrict the blood flow to the poorly ventilated alveoli and that puts a lot
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of stress on the right side of the heart to the point where the right heart starts to fail when the right heart fails what do we know about this from our Cardiology section if the right heart fails blood backs up via the
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superior vena cava causing jvd so then you get some swelling potentially of the upper neck area then on top of that it also moves inferiorly via the inferior vena cava causing swelling of the liver hepatomegaly causing fluid to accumulate
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in the abdomen ascites and then causing fluid to accumulate interstitial spaces in the lung causing pedal edema this collectively and we'll talk about this in a little bit whenever you have jvd hepatomegle and edema this is collectively due to right heart failure
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and this is secondary to what's called corpoma now which is due to some type of chronic bronchitis so you may see this so the reason why they have this type of blue bloater they look bloated is because the obese Factor because of their
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abdomen being pushed out by their abdominal organs being pushed out because lungs being hyperinflated and the second reason may be due to right heart failure the other thing for these patients is that they may have the bluish discoloration because of the point of
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what's called cyanosis and I'll talk about that in just a second the other key points that you want to remember for patients who have chronic bronchitis is some of the other features what did I tell you about their airways
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they have lots of mucus chronic bronchitis by definition is a productive cough for greater than three months for Two Plus consecutive years so one of the key features in differentiating these is that patients of chronic bronchitis have a very productive cough in comparison to
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emphysema where they have more of just like a mild cough it's not super you know productive and consistent that's one of the big differences the other thing is when you have all of this mucus accumulating within the airway imagine
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that a patient takes a deep breath in when they take a deep breath in air has to flow through this Airway and through this mucous plugged Airway when that happens it produces this kind of like snoring sound and that's called rhonchi
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and if you have the patient kind of really cough and cough it may clear that actual mucous secretions out of the airway and the wrong kind May potentially disappear so that's one potential thing that you can see because
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of the mucus in their airways the second thing is when they exhale the air that's actually having to be leaving the lungs and going out into the atmosphere has to move outwards through that tiny little mucous Airway and that air that's having
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to move to that tiny little Airway is going to cause wheezing so we'll hear wheezing potentially on expiration and maybe rhonchi on inspiration and they'll have a very very productive cough in comparison to emphysema and then the bloated appearance is due to right heart
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failure and abdominal obesity due to the diaphragm being flattened and pushing the abdominal contents forward okay with emphysema we call these patients pink puffers and the reason why they're pink puffers is pink meaning that they don't have a
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significant degree of cyanosis and again I'll explain the cyanosis on the bottom part of this diagram but again emphysema patients they don't have cyanosis meaning that they're not super hypoxemic and they're not Super Hyper capnic okay where does the puffer part come into
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play the puffer comes into place because if you imagine like a if you're trying to breathe out very very slowly you're breathing with pursed lips one of the key features that you may see in the clinical media for a patient who has
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emphysema is that they breathe or they Exhale by purslip breathing and the reason why is very actually pretty cool imagine that you breathe and exhale very slowly what happens is you allow for the pressure in the lungs to stay high so
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what this person of breathing does is is it keeps you know it increases the airway pressure and that's a really cool concept and the reason why is if you think about these patients bronchioles think about them if you think about
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these patients bronchioles and whenever they're trying to Exhale out air whenever they're trying to get air out of their lungs right what did I tell you is that tissue that's on the outer part of the bronchials that helps them to prevent
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them from collapsing elastic tissue what happens in emphysema you destroy that elastic tissue so whenever they exhale guess what happens to their tiny little bronchioles they collapse and when they collapse it's hard to be able to get air out so what happens is
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if they breathe really really slowly through that pursed lips it helps to be able to increase the pressure in their airways to see keep these bronchials just a little bit more open to allow for more air to Exhale out that's a really
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cool thing so look for per slip breathing in patients with emphysema by trying to keep their airway pressure open to keep their bronchial somewhat open okay the other thing is again big differentiating factor mild cough productive cough for chronic bronchitis
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they'll also have some wheezing because they may also have a little bit of mucus within their airways which can be again reducing the amount of air that's flowing out of the lungs during expiration here's the real big thing
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though because they're getting little air out they're alveoli and their lungs get super hyperinflated they get crazy hyperinflated because again we're trying to trying to get the air out but we can't because the bronchials are collapsing and this is
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just reducing the amount of air that's getting out so they have massive air trapping because of the air trapping their lungs get huge and because of that imagine having all of these large lungs when you're trying to listen it's very
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difficult to be able to hear very good breath sounds because their lungs are so large they're so large so whenever they actually have to take a breath and they can't very take in very much air because their lungs are already really big so
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imagine having big lungs pretty much almost already filled and you have to try to bring air into those already filled lungs it's very difficult and so oftentimes they'll have decreased breath sounds so again big thing both of them
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may have wheezing this one will have bronchi chronic bronchitis and productive cough this will have a mild cough and low or decrease breast sounds because of massive hyperinflation of their lungs the other thing is that these patients are super dysnic imagine how difficult
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it would be imagine your lungs are already filled they're already filled really really you know pretty good you have to take a breath in but the breath that you can take is very small so you're breathing super quickly over time
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you're going to become very short of breath and that shortness of breath is going to lead to you having having to breathe and breathe and breathe at a fast rate for long long periods of time and that exerts a lot of energy and as
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you use and use and use tons of energy guess what starts to happen to these patients they start to become cachetic and thin so that's one of the big things that's why whenever you see a patient who's has emphysema they're more likely
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to look cachetic and thin appearing and then their chest is barrel chest so if you were to look from a side view their diameter from anterior to posterior is gargantuous and the reason why is their lungs are super hyperinflated so it
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causes their chest to actually Barrel outwards and again anteriorly and posteriorly so they have what's called an increased anterior posterior diameter which we also refer to as a barrel chest and they're thin because of the amount of work or breathing that they have to
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do to be able to compensate for a little air that they can bring in pretty interesting all right so now that we understand this the basic concepts of how they physically present what I want to understand is a little bit more about
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the bluish so when we say blue bloaters they're cyanotic so there's a degree of hypoxemia and hypercapnia I want to understand the difference here but that you can see between chronic bronchitis and emphysema and then we'll talk really
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quickly about some of the complications that you can see with these two all right so here's the really interesting thing with Chronicle so still we're talking about chronic bronchitis over here emphysema over here so again I want to keep having some differentiations
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even though they can't coexist it's important to know the difference between these on the exam so we have the basic kind of like physical exam and symptomatology types of presentation here to go a little bit more into the
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concept of the bluish or pinkish type of like situation for pink puffers and blue bloaters we got to kind of zoom in into the alveoli bronchial area what we know about chronic bronchitis that there's a lot of mucus right lots
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of mucus within the Airways some bronchospasm so we know these Concepts here so there should be a degree of mucus accumulation and bronchospasm the problem with that is what well one of the problems here is that if I want to bring oxygen into this Airway
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I have to try to push it through this like mucus plug it's going to be really difficult to push oxygen into this alveoli in comparison look how easy it would be to push oxygen into this alveoli so if I
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were to compare which one is going to have more oxygen in this alveoli the one with the mucous plug leading to less oxygen or the one with that's just wide open pretty obvious right this one will get well ventilated and this one will
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get poorly ventilated because of that mucus okay the other concept here is CO2 so CO2 has to be exhaled so it has to cross the actual capillary blood and then move out here and then again move out of the
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lungs and then over here same thing has to move across the pulmonary capillaries and then out of the lungs which one would it be able to move easily out from this alveoli area or this alveolar area in this situation there's going to be
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less CO2 that's leaving through this area and so CO2 will build up in the blood in this particular scenario and then you'll have less CO2 in this area of the blood because it's going to easily clear the CO2 from this
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particular area okay pretty straightforward concept so in this alveoli that has a big mucus plug or bronchospasm less oxygen getting in less CO2 getting out now here's the cool thing our lungs are really smart in a way that it likes to
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make sure that we send blood to an alveoli I send blood to the alveoli that's well ventilated I don't want to send oxygen or blood particularly to an alveoli that's poorly ventilated out of these which one is poorly ventilated this is the poorly
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ventilated one so because this is poorly ventilated and this one is well ventilated I'd want to increase the blood flow through this one and then decrease the blood flow through this pulmonary vessel how do I do that I have to intensely
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vasoconstrict this vessel and divert the blood away to this vessel that's one of the things that happens in this situation and the reason why is you're going to get less movement of oxygen so if there's less oxygen coming into this
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alveoli that means that there's less oxygen it's going to move into the blood here that means that the oxygen inside of the blood in this particular situation will be low what is that called whenever you have low oxygen in
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the blood it's called hypoxemia what is it called whenever you have high CO2 levels within the blood that's called hypercapnia so these are the potential situations that I could see I could see a patient developing hypoxemia and I could see them developing
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hypercapnia now the way that I can try to be able to protect this from happening is I can vasoconstrict the pulmonary vessel to this poorly ventilated alveoli because of the mucus or the bronchoconstriction and then send the blood to this good
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alveoli because it's going to get lots of oxygen moving into the blood here and not have any hypoxemia and I'm going to clear the CO2 out of the blood here so I'm not going to have hypercapnia this is a very interesting type of
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concept so I want to undergo what's called pulmonary vasoconstriction to this particular area I want a pulmonary vasoconstrict the poorly ventilated area and then increase the blood flow to the well ventilated area now in patients who have chronic
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bronchitis this hypoxemia is very severe and their hypercapnia is very severe because of that when you're hypoxia making your hypercapnic that leads to that cyanotic appearance that bluish discoloration if you want to think about it because if you have hypoxemia you're
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not giving enough oxygen to the tissues and so the oxygen content of the hemoglobin within the blood is decreased there's lots of deoxyhemoglobin and therefore more of a cyanotic type of appearance and patients who have emphysema there's not as much
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of that type of problem and I'll explain why in a little bit but because a patient becomes hypoxemic what happens they're less ventilated alveoli is what the brain starts to think it says oh there's less oxygen in the blood you
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know what I should probably do I should have the patient breathe faster and breathe deeper and so they develop dyspnea and they develop tachypnea in a way to be able to increase their oxygen and decrease their CO2 that's their
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compensatory mechanism that they're thinking is going to happen but instead it just makes the patient have to work harder to breathe that's one of the clinical features here to think about and then they may have cyanosis because of again that decrease oxygen and that
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increase CO2 but more particularly is the decrease in oxygen okay now that's a really interesting type of concept now the other thing that you want to think about here is that what can this do to the heart because remember I told you they can
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develop right heart failure this is why the reason why is is if let's say that here this alveoli has a big mucus plug right so here's a big mucus plug in this alveoli and then here there's a big
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mucus plug in this alveoli and a patient has chronic bronchitis if I have little oxygen getting into this alveoli and little oxygen getting into this alveoli do I want to send blood flow to these alveoli no and so what will I do
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pulmonary vasoconstricts I'm going to clamp down on these vessels I'm going to squeeze these vessels to make sure that blood is not going to these poorly ventilated alveoli when I do that I increase the pressure inside of the
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pulmonary circulation what does that do to the right side of the heart makes it have to work harder if the right heart starts having to work harder it'll originally start to hypertrophy but that hypertrophy will eventually lead to right heart failure
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because it won't be able to maintain that contractility over time and that'll cause blood to backflow into the Supreme vena cava causing jvd backflow into the inferior vena cava causing hepatomegaly ascites and pedal edema and this is what
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we call Core pulmonal right heart failure due to underlying pulmonary vasoconstriction due to an underlying lung disease such as chronic bronchitis One More Concept that we also have to understand if I have a lot of mucus that are
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plugging up this Airway what does that do can I clear bacteria can I clear bacteria if there's a bunch of mucus that's just clogging up the airway that's actually let's see there's bacteria in this area of the alveoli and
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I want to be able to clear that bacteria I can't because the mucus is blocking me from clearing it and so that can increase the risk of bacteria accumulating just distal to where the mucus plug is leading to bacteria
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increasing colonizing thriving and infecting the actual respiratory tissue increasing the risk of pneumonia so when patients who have chronic bronchitis they're at high risk for pneumonia they're at very high risk for core pulmonal and right heart failure and
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there's one more thing they're high risk for whenever a patient is persistently hypoxemic so they have low oxygen levels within the blood what it does it tells our kidneys and says hey there's very low oxygen levels in the blood maybe
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another problem is not only the patient is not breathing fast enough so that's why they get discipnic but maybe they need more red blood cells so why don't you make more erythropoietin and erythropoietin will tell the red bone
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marrow to increase the production of red blood cells and if I have more red blood cells I have more things to carry oxygen and maybe that'll improve it but it doesn't instead it causes these patients to develop something called
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polycythemia so they increase the number of red blood cells so in patients who chronic bronchitis look for some of the big differences between that and emphysema core pulmonal which is right heart failure increased risk of pneumonia and again
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secondary polycythemia as well as a productive cough is a very characteristic feature and a bloated type of appearance and what that means is jvd hepatomegalyosites petaledema and abdominal obesity due to the diaphragm pushing down and pushing the abdomen
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forward okay and on top of that they have the bluish discoloration due to hypoxemia the cyanosis due to very little oxygen getting into poorly ventilated alveoli okay when we compare that and a patient who has emphysema an early emphysema they don't have that
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degree of hypoxia and hypercapnia they have very mild very mild hypoxemia and very mild hypercapnia the reason why is their problem is not as much mucus so remember that you will have a little bit of mucus production and emphysema so
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there will still be a little bit but it's going to be nowhere near the amount that you would have in a patient who has chronic bronchitis so that's one of the big differentiating features but there still will be some mucus
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the problem here is that this actual bronchial will be open during inhalation during inhalation it'll be open right so you'll be able to bring what into the alveoli easily you'll be able to bring oxygen to this alveoli and oxygen into
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this alveoli okay and because of that oxygen will be well ventilated in this one and properly ventilated decently in this one so oxygen will be able to move into the blood relatively easy and you'll get increased oxygen the blood
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increase oxygen of the blood that's not the problem the problem is when the patient exhales when they exhale the elastic tissue that's supposed to burn the bronchials from collapsing no longer prevents them from collapsing so when they exhale what
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happens my friends what happens here is the bronchioles collapse really powerfully during exhalation so oxygen got in pretty well into the alveoli during inhalation but now CO2 which is supposed to be cleared is not going to be exhaled as easily and so
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what happens to the CO2 within their bloodstream that does rise so the CO2 will rise within their bloodstream so these patients will have a degree of hypercapnia they won't have a very significant hypoxemia one of the reasons why they may have a very mild hypoxemia
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is not due to the amount of oxygens getting into the alveoli what's the problem with emphysema what happens to their total surface area their total surface area decreases and if your total surface area decreases that means that less gases are
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potentially exchanged across the alveoli so the amount of oxygen getting into the alveoli is normal but maybe the amount of oxygen that's moving across the actual respiratory membrane into the blood is a little less and that's where you get a little bit less oxygen so they
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have a very mild hypoxemia not because they have difficulty getting oxygen into the actual alveoli because they have a problem being able to diffuse it across the alveoli into the blood so that this is due to a decreased total surface area
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and they have increased CO2 why because the bronchioles collapse during exhalation which traps the CO2 in the alveoli I hope that makes sense because they have so much air trapping in their lungs imagine their lungs are filled with air every breath that they
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have to take they have to add more air into their already filled lungs so imagine you're already filled up you're having to take these little breaths of air and so it causes this degree of dyspnea and to kidney to try
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to be able to properly ventilate but again your lungs are already hyperinflated so that's why these patients will have dyspnea into kidney it won't be due to their hypoxemia because it's very very mild it'll be due to their air trapping and they're having
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to work very hard to breathe in small volumes still ventilate but again it's a problematic issue for them one of the big problems for these patients because their airways are so hyperinflated is they have a significant degree of air trapping and when they air
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trap imagine all this air starts kind of ballooning up and causing these things called bulay or blebs they're like these little kind of like pimples popping off of the lung these things are very high risk so now for whatever reason a
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patient's under positive they're being mechanically ventilated they take some type of deep breath whatever may happen sometimes it can be completely spontaneous no trigger whatsoever this thing can pop and if it pops it'll push air directly from the lung into the
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pleural space and all that air will start to accumulate into the actual pleural space and start pushing on the lungs what is this called a pneumothorax so patients with emphysema do their air trapping effect or at very high risk for
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pneumothorax not so much hypoxemia leading to right heart failure core pulmonal and secondary polycythemia in the later stages of emphysema really late stages they may have hypoxemia and they may have worsening hypercapnia which could lead to right heart failure but not
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commonly in the early to mid stages their primary complication is pneumothorax so please understand the differences between these two because now let's talk about asthma all right so now let's talk about the features and complications of asthma so and the
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patient known as asthma what's the basic kind of trigger there's either allergic or non-allergic causes we went over viral upper respiratory tract infection cold air exercise beta blockers gerd we went over the samters Triad which were aspirin use and then we talked about all
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the allergens right from the atopic Triad so either way we know that those are the triggers patient develops an intense bronchospasm so they have bronchial smooth muscle constriction on top of the day of bronchial edema which also Narrows their Airway when you have
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that intense bronchoconstriction bronchial demon in the later stages even some mucous secretion this is really going to narrow the actual Lumen of the bronchioles what happens with that is that whenever these patients are trying to Exhale they have a severe wheezing so they have a
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significant expiratory wheezing where it's even worse and louder at the end of expiration so indexpiratory wheezing is a very common feature for these patients also they will have a cough they're cough though because theirs isn't an intense amount of mucus in comparison to
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COPD shouldn't be a very intense productive cough it should be more of a dry cough because it's a lot of bronchialedema and an intense bronchial smooth muscle constriction in the late late stages they may have a little bit
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of mucus production as a protective response but primarily bronchialedema and bronchoconstriction which will produce an intense expiratory wheezing now what is a very ominous sign is a silent chest when you go to listen to the patient you hear almost no air flow
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moving in or out that means that they have a severe obstructed Airway that means it is so obstructed that literally no air is getting into the chest or they're so hyperinflated because they're trapping so much air so imagine this
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imagine like I have here just here's my bronchial and imagine all of this is all the air in the alveoli here I am trying to get Co2 out but I cannot because it is so bronchoconstricted and so edematous it is literally impossible to
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get Co2 out so no CO2 is moving out of the airway because of that these lungs are already hyperinflated they try to take a breath in they can barely take any air in because their lungs are already super inflated and on top of
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that their airways are so obstructed that it's very very difficult to be able to get O2 into the actual lungs so this is a very scary finding when you have a patient who has a silent chest this is a
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very severe bronchoconstriction very severe bronchial edema and a very severe asthma exacerbation so again think about these as a particular particular findings of a patient with asthma now what are some other things that I want you guys to
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understand let's come down and talk about that now when a patient has very severe asthma we know that there is going to be an intense degree of bronchospasm this intense degree of bronchospasm prevents CO2 from being able to be exhaled right
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so CO2 wants to be able to move from the blood into the alveoli and then be exhaled out that's the normal pathway for CO2 but in this situation it's being prevented because these bronchioles are so constricted that it's going to reduce
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CO2 outflow and that's going to cause hyperinflation that hyperinflation is a problematic issue because the reason why is when your lungs are already hyperinflated it's very difficult to be able to bring air in on top of those already filled lungs and so because of
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that they take in smaller amounts of air in on top of that if you have an intense bronchoconstriction it's also going to reduce the oxygen coming into the alveoli so they may have a reduction of air coming into the alveoli and if
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there's a reduction of o2 coming into the actual alveoli and a reduction of oxygen moving into the blood this may cause particularly what's called hypoxemia so these patients may have a degree of hypoxemia plus we want CO2 to get out if
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it's being trapped the CO2 will build up in the bloodstream and that is called hypercapnia so these are some of the potential features that you can see in a patient who has a very severe asthma exacerbation and what we know is that
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hypoxemia will activate our sympathetic nervous system and our sympathetic nervous system will say oh we're hypoxemic and we're hypercaptic we must not be breathing good enough we're not must not be taking in deep breaths and breathing fast enough I'm going to have
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them breathe deeper and breathe faster work harder to breathe and so what that does is that causes dyspnea and tachypnea and increases their work of breathing it says okay you won't have to work hard Boy And So It causes the
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patient to have to use all accessory muscles like what way it might cause them to flare their actual Nares to open up the airway there it may cause them to use some of the accessory muscles like their scalenes and sternocleidomastoid
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to help with their inspiratory and expiratory response it may cause them to use some of their actual abdominal muscles to help with the mix their expiration and so you start to see a lot of work of breathing and one of the
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biggest things is looking for them to have tachypnea dyspnea and an increased work of breathing these are scary signs lines because this could be indicative of a very severe exacerbation so look for these particular things such as nasal flaring
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tripoding accessory muscle use abdominal muscle use these are all concerning signs so these could be things that you could see as a patient has hypoxemia and hypercapnia due to massive amount of air trapping for hypercapnia and because of
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the air trapping little air can be brought into the lungs so less ventilation to the alveoli and on top of that the intense edema and bronchoconstriction reduces the amount of airflow into the lungs and again this can lead to reduced ventilation and
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therefore reduce oxygen accumulation within the blood leading to hypoxemia less CO2 being able to escape hypercapnia the other thing that these things can do particularly hypoxemia is it can also increase our heart rate and so you may have a patient Who develops
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something called tachycardia so look for that as well as a very concerning sign of an exacerbation so these are big things to think about but you know what else is really important for these patients and patients who have asthma they also
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can have uh when we think about this concept of here's a normal lung so here's a normal lung and a patient who has asthma they have intense bronchoconstriction bronchialedema that leads to less CO2 being exhaled so less CO2 is going to be exhaled out
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of the lungs because of that this is going to cause air to be trapped in the lungs so there's going to be lots of air trapping Whenever there is lots of air trapping what's really interesting here is whenever you have less CO2 being exhaled
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you're going to cause this air trapping effect this air trapping it causes the pulmonary vessels which are supposed to take blood back to the left side of the heart to be pinched so imagine these lungs are actually being super inflated
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and air trapped what it does is it pinches on the pulmonary veins so the blood the actual vessels that are supposed to take blood back to the left side of the heart so pinches on the pulmonary veins if you pinch on the
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pulmonary veins you're going to reduce the venous return to the left side of the heart so the venous return to the left side of the heart is going to be reduced so you have a reduced left ventricular filling
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if you don't fill the ventricles very well right so you have a patient who their lungs are super air trapped whenever they are super air trapped especially during inspiration they're so filled they compress and squeeze on the pulmonary veins and again in these
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patients their lungs are filled all the time during expiration and inspiration because they're hyperinflated because they're so hyperinflated especially during inspiration they squeeze in the pulmonary veins when they squeeze in the pulmonary veins less blood flow comes into their left ventricle and again this
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is all during inspiration so during inspiration there is a massive pinching of the pulmonary veins because we're going to expand them even more compressing the pulmonary veins reduce the left side of the venous flow if we reduce the left ventricular filling what
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is going to happen then to the left ventricular cardiac output if you have a reduced left ventricular feeling mean that you have a reduced preload that's going to lead to a subsequent reduction in cardiac output if you reduce the cardiac output you
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could potentially reduce the patient's systolic blood pressure if I reduce the patient's systolic blood pressure during inspiration greater than 10 millimeters of mercury this is called pulses paradoxis this is a very important thing that you can see in asthma and not really in any of these
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other obstructive lung diseases so think about this and what this would look like is if I had an arterial line on the bottom part here is the diastolic pressure on the top part here is the systolic blood pressure here's what
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their actual arterial pressure waveform would look like during expiration and during inspiration you would see that there's systolic blood pressure would drop 10 millimeters of mercury or more during inspiration and what's the reason why that it would do that because the
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patient's lungs are already hyperinflated at the end of expiration you try to take air in take more air in on top of those already inflated lungs they're going to expand and squeeze on the pulmonary venous vasculature reducing the actual amount of blood
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coming back to the left heart if I don't get blood coming back to the left heart we get a reduction in left ventricular preload during expiration a reduction in left ventricular cardiac output during inspiration and a reduction in their
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left ventricular systolic blood pressure during inspiration and if it's more than 10 millimeters of mercury that's called pulses paradoxis so don't forget that as a potential complication of a patient who has asthma all right so we know with
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asthma they have dry cough and expiratory wheezing a silent chest is an ominous signing of a very severe bronchospasm they also have dyspnea to kidney and increased work of breathing especially during exacerbations because they're super bronchoconstricted less CO2 getting out
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causing air trapping making it difficult because their lungs are hyperinflated it's hard to bring more air into a hyper-inflated lung plus if the bronchials are super constricted it's hard for airflow coming in less ventilation to the alveoli less oxygen
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moving into the blood hypoxemia the hypoxemia creates a compensatory response where the patient has to breathe harder and faster to try to bring more air into the lungs that leads to dyspnea tachypnea and increased work of breathing and hypoxemia also try to
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make their heart beat faster leading to tachycardia all right my friends now let's move on to bronchiectasis alright guys so now let's talk about bronchiectasis now this one may sound similar to chronic bronchitis but there is some couple
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different features that will help us to really delineate and differentiate between those two with bronchiectasis what I tell you was the big thing obviously they have bronchodilation due to the elastic tissue destruction they also have fibrosis do a lot of
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fibroblast activity they have lots of lots and lots of mucus production that's one of the big things and they also have bronchospasm so because of that we can see a lot of the similar features between that and chronic bronchitis
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except their cough is going to be very productive and very foul smelling okay so a very productive and foul smelling cough due to an excessive mucus production I think it's one of the big key things to remember about
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bronchiectasis is that there is a massive amount of mucus that is accumulating and that's one of the kind of driving factors behind the disease so productive foul smelling cough they'll also have wheezing because you're going to have mucus that is obstructing the
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actual Airways air is supposed to be leaving the actual lungs so during expiration we'll hear a wheezing during inspiration you may hear a lot of kind of a snoring sound because again there's a narrowing of the airway and when air
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is trying to move past the actual mucous filled Airway it may cause this snoring sound which may disappear if you have the patient kind of really cough and expectorate some of that mucus up it may clear the airway and you might not hear
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the wrong guy anymore the other thing it's not patho mnemonic it's important to remember that but in patients who have bronchiectasis they also have a degree of hypoxemia and that chronic hypoxemia may cause a change in the configuration of the nail bed to
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where it kind of really bulges out and causes clubbing of the digits it is not path of mnemonic but it's something to think about that you may see more calmly in the clinical vignette for bronchiectasis than all of the other
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obstructive lung diseases another really big feature here that differentiates is hemoptysis now remember I told you that there's lots and lots of mucus within this patient's Airway because of that it causes lots of inflammation lots of inflammation of the
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bronchial walls and then bronchodilation really thins out the bronchial walls well you know you have these blood vessels here you know these are called These are called your bronchial blood vessels because you know there's a dual blood supply to the actual lungs there's
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the pulmonary vessel Supply and there's the bronchial Supply which these as you have lots of inflammation of the bronchial walls it can get very close to the little bronchial vessels that are feeding the actual bronchial tissue and if it just is enough to erode its way
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into the actual bronchial wall and cause these bronchial blood vessels to get eroded and eaten at it can cause blood to enter into the Lumen of the actual bronchus and this can lead to hemoptysis which is coughing up of blood so you may see this
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in patients with bronchiectasis the other thing here is because they have all of these mucus that is actually accumulating their airways again what are they going to have a hard time being able to eliminate from the actual bloodstream
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CO2 CO2 will not be exhaled as well so CO2 will build up in the bloodstream what is that called This is called hypercapnia so they may have some degree of hypercapnia on top of that it's also going to cause
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less oxygen to be able to come into the alveoli because of these bronchial is being obstructed and occluded with all this mucus and also having degree of bronchospasm so less oxygen will be able to get into the alveoli and less will pass into the
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blood and if there's less oxygen in the blood what is this called my friends this is called hypoxemia and so in these patients you may see a degree of hypercapnene hypoxemia and let's see if you guys can remember what
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does the compensatory response to hypoxemia to increase your respiratory rate so it has them breathe harder to keep nail breathe faster and breathe harder and cause some shortness of breath dyspnea and it may also cause a compensatory increase in the heart rate
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so these are potential things that you can see in these patients okay now the other really big thing here just like in chronic bronchitis is because you have this mucus that is just plugging up the Airways what is it one
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of the big functions here is that we don't want bacteria to kind of really colonize right but if all this mucus is plugging up so let's imagine here that the mucus is getting clogged up all right here these bacteria that are supposed to be
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moved upwards and cleared stay in this area and because of that they can colonize they can multiply and then they can start leading to an infection and if they lead to an infection this will lead to pneumonia so patients with bronchial
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bronchiectuses are at very high risk for pneumonia nearly there's a very special bug especially in patients who have cystic fibrosis because cystic fibrosis is a very high risk uh you know cause for patients with bronchiectasis what is the very specific bug that they can
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actually accumulate and can cause a lot of problems do you guys know what it's called it's called pseudomonas originosa so patients who have bronchiectasis are a very high risk for pneumonia infections due to a nasty pathogen called pseudomonas originosa so this is
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a big thing to think about for these patients so again with bronchiectasis very productive foul spelling cough wheezing bronchi hemoptysis increased risk of pneumonia they may have a degree of hypoxemia and hypercapnia that cause them have some degree of dyspnea to
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keepnia maybe even a little bit of tachycardia here's the one big thing that I want you guys to remember though in a patient who has bronchiectasis one of the classic things that they're going to present on the exam is due to cystic fibrosis
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that's going to be the common cause okay if a patient has cystic fibrosis think about some of the other features that they may present in the clinical vignette that they're trying to point you towards bronchiectasis in this situation if a patient has
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cystic fibrosis we already know that this is due to a defect in the transmembrane Protein that's supposed to pump chloride out into the secretions and yank water into it but because of they're not doing that they're not pushing chloride and pushing water into
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the secretions the secretions get thick and that can happen not just in the lungs you know when a baby is very young sometimes the secretions that actually are supposed to help with the actual bowels eliminating something called the
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meconium which is the first stool of the baby can get really really stuck inside of the actual bowels and because that can cause a bowel obstruction this is called a meconium ilius so if a baby had a previous history of what's called a
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bowel obstruction due to meconium ileus that's something to think about really really young right where whenever they're actually just born on top of that because the pancreatic ducts also make lots of pancreatic secretions if the pancreatic ducts actually are trying to make these
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secretions and they can't actually push chloride and water into it and the secretions get too thick that they get stuck in the pancreatic ducts can you see creep pancreatic enzymes into the actual intestines no so that builds up causes Auto digestion
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and inflammation of the pancreas and eventually that can lead to the pancreas starting to fail causing pancreatic insufficiency you'll look for them to have malabsorption malabsorption syndromes lots of kind of nasty diarrhea as well the other thing is it can cause mucus to
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accumulate within the Airways causing those bronchials to get obstructed causing mucus to accumulate and bacteria to colonize and leading to bronchiectasis and leading to the dilation of the bronchial fibrosis bronchospasm and all that mucous production last but not least you know uh it's also
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important particularly within the development of the vas deferens and in patients who have cystic fibrosis they don't form their vas deferens they're going to be able to pass sperm on to the other actual sex no and because of that
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that leads to the actual increased incidence of male infertility so a cystic fibrosis not only is important to be able to remember that it is one of the causes of bronchiectasis in the clinical vignette they may ask you a
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patient has bronchiectasis okay due to cystic fibrosis what may be some of the other features and complications that you would expect besides productive foul smelling sputum wheezing bronchi hemoptysis increased risk of pneumonia mild degree of hypoxemia and hypercapnia
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what look for increased incidence of meconium ilius pancreatic insufficiency we already know bronchiectasis and male infertility all right now that we've talked about all the features and complications we move to the next big part which is understanding how to differentiate an
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obstructive lung disease versus something we haven't talked about yet called a restrictive lung disease and other diagnostic tools all right guys so I don't poop yourself I know that this is a lot of stuff it looks pretty scary
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but I promise it's actually not too bad it's going to make pretty good sense now one of the important things I think that is really really essential for your step two exam is being able to not only differentiate some of the obstructive
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lung diseases from one another but it's also really important to be able to differentiate obstructive lung diseases from restrictive lung diseases and we'll have a separate lecture on that but for right now I want to just quickly take
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the time that while I'm talking about some of these different things called pulmonary function tests we should not only discuss obstructive lung disease but throw in a little bit about restrictive because it's going to help you in the overall end game when it
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comes to talking about these on your exam all right so first thing we talk about pulmonary function tests we're going to do some things called spirometry and what we're going to try to determine is we're going to look at a couple
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different parameters when we take a patient who has normal lungs in comparison to obstructed lungs versus restricted lungs we're going to look at three particular things with the pulmonary function test what I want you to understand is when a patient is
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breathing okay they have normal healthy lungs when they're breathing normally normal quiet breathing taking a breath in taking a breath out that normal quiet breathing is this purple kind of line that's oscillating here that's called your tidal volume now whenever a patient
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decides to take a deep breath in beyond their normal tidal volume inhalation so that's called their inspiratory Reserve volume so it's the amount of air that they can forcefully Inspire beyond their tidal volume inhalation that's the Irv the next one is the amount of air that
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you can forcefully exhale beyond your tidal volume exhalation that would be your Erv so I'm a little dumb here but go [Applause] that amount of air that I blew out beyond my tidal volume exhalation is called my expiratory Reserve volume the
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amount of air that remains in my lungs at the end of that forced exhalation is called the residual volume that's the amount of air that kind of keeps the alveoli open and prevents them from collapsing that's important concept and
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what I'm going to do is is we're going to take and look at this graph and compare it what happens to the Irv the TV the Erv and the residual volume in obstructed and restricted lungs but before we do that we have to talk about
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one more thing there's another terminology which you guys see here called Force vital capacity and total lung capacity what I want you to remember is that Four's vital capacity fvc is the combination of your inspiratory reserve Volume Plus your
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tidal volume plus your expiratory reserve volume this is called your forced vital capacity your total lung capacity is your Force vital capacity Plus your residual volume so if I go all the way from here down to my residual volume this is called my
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total long capacity what I want us to Now understand is what happens to all of these volumes in a patient who has obstructed lungs versus restricted lungs let's take a look here so when a patient has an obstructed lung
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disorder what is the classical feature whether it's asthma whether it's COPD whether it's bronchiectasis there's a problem being able to get air out so because of that air stays trapped in the lungs they hyper inflate their big old
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chunky lungs because they're big compliant very large lungs what would we expect we would expect that they're going to have really big chunky lungs now here's what I want you to think about if a patient has really really big lungs
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imagine how hard it would be to take in to imagine my lungs are already filled here right and I'm going to try to take a deep breath in beyond my normal tidal volume how hard is that going to be to
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take in a large volume of air when my lungs are already hyperinflated imagine the lungs being already filled almost and you got to try to take in a lot of air it's not going to happen so in these
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patients they're inspired to a reserve volume the amount of air that they can forcefully inhale behind their tidal volume inhalation is very low so that is reduced in patients who have structure lung diseases because you can't take in
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a large volume of air because they're already super puffy and inflated their tidal volume actually doesn't become affected though thankfully right so that's relatively normal the amount of air that they can breathe in during normal inhalation and exhalation is the
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same their expiratory Reserve volume the amount of air that they have available that they could forcefully exhale after the title volume exhalation is insane because look how puffy these Dangs lungs are they're huge and so because of that
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their expiratory Reserve volume is increased and their residual volume the amount of air that they remain have remaining in the lungs after exhalation is also increased they're air trapping so they have a very high residual volume we sometimes use a very special term here
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which I want to write down here for a second it's called functional residual capacity so the functional residual capacity FRC is elevated in patients who have obstructive lung diseases okay now let's use this concept of what force vital capacity is and what total lung
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capacity is then right and patients of obstructive lungs their lungs are hyperinflated so the amount of air that they have available to be able to Exhale is large the amount of air that they have sitting in their lungs
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after they exhale forcefully exhale is large so their functional residual capacity is large the amount of air that they can try to bring in forcefully is very little because their lungs are already hyperinflated think about how much air their lungs can
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occupy at an entire time so total lung capacity is the Irv plus the TV plus the Erv plus the RV in this situation my RV is massively increased my Erv has increased my title volume stays the same I inspired to
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reserve volume will reduce a little bit if that's the case this is actually going to cause the lungs to have a very very large total lung capacity the total lung capacity for obstructive lungs is increased significantly okay and that is
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in part due to these two factors the Erv and the RV significantly increase just to put it in perspective let's give it a double arrow let's give this a double arrow here and let's give this a double arrow here
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okay and therefore the functional residual capacity is going to increase okay The Four's vital capacity is the Irv plus the TV plus the Erv well the Erv is increased the Irv decreases so the FEC May decrease but it almost may
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be normal so sometimes in these patients it can vary from where it can actually be relatively normal to mildly decreased it can be normal to mildly decreased usually in the early stages of obstructive lung disease it's relatively normal as they get later and later and
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later into the disease their fvc starts to decrease so that's what I want you guys to remember the fvc may be relatively normal in the early stages and decrease as we get to the later stages okay that's this component here for
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obstructive lungs now let's go to the restrictive lungs for the restrictive lungs look at the size oh my gosh big old suckers baby suckers right and restrictive lung diseases we haven't talked about this yet but in their situation they're very very fibrotic
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they're super super kind of like elastic and they just don't want to be able to expand and they just want to collapse naturally they just don't want to be able to bring air in and they collapse really easily so it's really hard to
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fill these lungs and they don't have a lot of air in them they're very very tiny so because of that imagine this how hard is it going to be able to bring air into these stiff non-compliant lungs very difficult so being able to
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forcefully inhale a ton of air do you think I'll be doing a good job at that no so these patients Irv is reduced tidal volume doesn't really change thank goodness that's relatively straightforward the amount of air that they can bring in normally during quiet
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breathing and out during quiet breathing is the same they're Erv look how little their lungs are they don't have a lot of air that are available for them to Exhale so because of that their Erv is reduced and then the residual volume the amount
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of air that they'll have remaining in their lungs at the end of a forced exhalation is also really little so there's a residual volume will be reduced and the combination of these two which is called r forced our functional residual capacity
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will be reduced if we take all of this into consideration and look now at the total on capacity which is all of these things added up there's a lot of down arrows my friends so what do I expect to happen to
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the total loan capacity if I added all of these up I expect it to be low so I'm going to have a very low total loan capacity Four's vital capacity is the Irv plus the TV plus the Erv two down arrows and
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one's kind of normal I expect the actual FEC to be low and so in this situation I want you to remember that the fvc is really this is why I want you to stress this fvc is really low in patients with
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restrictive lung diseases in obstructive lung disease that can be normal to slightly decreased okay that's one of the big features to understand here now we've had a basic concept of these numbers whenever we're having a patient breathe into what's called a spirometer
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so basically all of these things we're taking a patient as normal lungs obstructive lungs restrictive lungs having them breathe into the spirometer apparatus and then give us all of these particular things and help us to be able to kind of
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determine based upon these volumes where they kind of fall within the obstructive versus restrictive versus normal lungs we can further extrapolate this and really what happens when we do these spirometer devices we actually get these things called flow volume loops
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so what this is going to show us here is on the x-axis here we're going to have volume on the y-axis we're going to look at the flow of air on the top part it's going to be expiration on the bottom
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part it's going to be inspiration okay and then here's zero liters 2 liters four liters 6 liters eight liters so when a patient takes a breath in normal lungs they're going to inhale when they inhale they're going to potentially
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inhale beyond what they already have in their lungs so here this patient's going to start taking in air and it's going to go from two liters during their inspiratory process to about seven liters during their inspiratory process then during expiration they're going to
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have a normal flow outwards and then again that will start to decrease and take them back to their original volume okay now what this gives us is kind of a couple different things from this point here from the moment of inspiration all
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the way here expiration all the way here this is going to continue this think about this I take a deep breath in beyond my tidal volume inhalation this would be my Irv and then I take and I breathe out as much air as I forcefully
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can during exhalation this would be my Erv and then the volumes that are actually just going to be during the normal quiet breathing process my tidal volume so my tidal volume plus my Irv plus my Erv is my Force vital capacity
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right Irv plus TV plus Erb is force model capacity so from this point here to this point here is what's called my Force vital capacity the amount of air that remains in the lungs after I've exhaled all the air
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that I possibly can is what my residual volume and then if I were to take the residual Volume Plus the force vital capacity what would this be this would be my total lung capacity this entire thing here this is for normal lungs so what I
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want us to do now is imagine this is what the normal flow volume Loop will look like in normal healthy lungs if I have a patient who has obstructive lungs what do I know what do I know about these particular
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parameters and a patient knows obstructed lungs well they're hyperinflated if they're hyperinflated they're going to have a high residual volume we know that if they have a high residual volume what's that going to do what we know is an increase in residual
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Volume Plus an increase in their expiratory Reserve Volume Plus a normal title volume and a mild decrease in their Irv causes their total lung capacity to increase and we said that their Force vital capacity which is their Irv plus their TRV plus their Erv
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can do what it can be somewhat normal to slightly decreased so if I were to kind of do this it would be here to here okay so somewhere between normal to slightly decrease what would that look like in comparison to the normal
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graph which is here in Black well now I would expect my Force vital capacity to be what potentially the same but I would expect my residual volume to be increased so what I'm going to do is look where my graph starts here now I'm
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going to take a deep breath in beyond my normal title volume inhalation and then I'm going to Exhale as much as I possibly can during exhalation beyond the title volume exhalation so this is going to be my entire force vital
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capacity so from here to here is my Force vital capacity if I think about that one in comparison to that one it might be normal it's almost slightly decreased in comparison to normal but here's the big thing the amount of
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air that remains in the lungs after that forced exhalation is called what as a residual volume so my residual volume is what in this in this diagram it's super increased because my residual volume increases it shifts the actual curve of
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this graph to the left that's an important thing to be able to remember so when you're given a graph on your exam and comparing to say which one of these do you think this lung disease is based upon the flow volume Loop is it
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obstructive or restrictive if the graph is shifted to the left in comparison to the normal lungs it's an obstructive lung disease and in these situations due to a massive increase in their residual volume and what will happen to their total loan
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capacity look at this look at this son of a gun it's gargantuous they have a massive total lung capacity that's increased and on top of that you know what else is really cool about these patients look for this as well
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sometimes and these patients who have obstructive lung disease they have this little like coving that you can see sometimes within their graph and that's because they have a kind of a reduction in their Peak expiratory flow rate and
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so sometimes you'll see this kind of reduction this little coving in thing and that's an important thing to be able to differentiate between obstructive and restrictive so if you see the curve shifted to the left with a very massive increase in residual
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volume and an increase in total lung capacity you're looking at obstructive lung disease now compare that to restrictive for restrictive here's again our normal and black and in blue we're going to talk about restrictive in this situation what do we know about
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their volumes we know the residual volume is decreased we know that all of these are decreased so therefore their total lung capacities decrease and we know their Irv and their Erv is decreased and the tidal volume stays the
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same but since both of these are decreased we see their Force vital capacity decreases okay look at their curve if I take a deep breath in with this blue line here a deep breath in Beyond normal tidal volume inhalation and then I breathe out
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as much as air as I can forcefully Beyond title volume exhalation then from here to here from this point here to this point here is my Force vital capacity so from here to here this is my fourth vital capacity look how small
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that son of a gun is in comparison to obstructive versus normal that's a tiny Force vital capacity and then look at this look how much like I might even overshot it I might have to kind of go like right here from here to
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here is there residual volume the amount of air that remains in their lungs after a force exhalation look at that that's their tiny little residual volume and then look if I take the force right out of capacity in the residual volume
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combine this is the total lung capacity look how tiny it is so in a patient who has restrictive lung disease if they show you the graph what will you see the curve do you'll see that the restrictive Curve will shift to
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the right so restrictive the curve shifts to the right obstructive the curve shifts to the left and maybe has a little coving in of the expiratory Curve that's what I want you to remember the last thing that we have to talk
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about here when you look at these graphs the next thing that we can do is we can take and look at whenever they're forcefully taking in air and pushing out air what we can do is we can look at the
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very specifically the volume of air that they are exhaling so they take a deep breath in from the moment I begin exhaling until the moment that I stop exhaling I'm going to monitor that volume and that's going to be on the y-axis on
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the x-axis is going to be the time that it takes for me to start exhaling until I stop exhaling what I want to know is what is the maximum volume of air that I can actually exhale during that entire
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breathing process the maximum amount of air which is at the peak point of the Y so on the y-axis wherever I hit the top the peak point that is my Force vital capacity that would be this point here okay at
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one second let's say that somehow I breathe for I don't know five seconds okay so during that five second period that was the maximum volume that I could actually reach that was my Force vital capacity at one second in the inspiration
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expiration process I want to know how much air I was able to forcefully exhale we call this the forced expiratory volume of one second what you need to be able to take from this my friends is this ratio where we
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actually say fev one over the fvc this is a particular ratio that we're going to use in this example let's say that the amount of air that I could forcefully exhale in the first second was four liters then that's going to be four liters
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divided by the maximum amount of air that I could forcefully exhale throughout the entire time period let's say that that kind of curve goes around 5 liters-ish so five liters 4 divided by 5 is going to be about 0.8
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multiply that by a hundred and I'm going to get 80 percent that's about what the normal ratio is between fev1 and fvc what I need to be able to determine now is what would that look like in an
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obstructive and what would that look like in a restrictive lung disease let's take a look in obstructive lung disease what we notice here is in this red curve here is that the fvc can be reduced there could be a reduction in FEC we said that it
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could be anywhere from normal to decreased okay so we see that that is potentially reduced a little bit so let's actually put a down arrow for the FEC the fev-1 though that's the worst situation here look at their fev-1 in comparison to this one so
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here's their fev-1 let's just kind of I'm going to make up numbers I'm going to say that in the normal patient was about four liters and this patient oh my gosh this is terrible actually this might be somewhere around like two
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so now this patient's fev1 is approximately somewhere around two liters what in the heck happened I dropped their fev one significantly so when patients who have obstructive lung diseases their Force expiratory volume and one second is significantly reduced whereas their fvc can be just
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normal to almost slightly reduced if that's the case and I take into consideration this ratio what will I get in comparison to 80 if a normal fev1 to FEC ratio was four over five liters which is eighty percent and I went from Two and I
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would drop my fvc down let's just say to four liters I'm definitely going to be less than 80 if that was the norm if the norm was 80 you can tell me that 2 liters and four liters what would that give me that would give
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me like 50 percent so my fev one over fvc ratio was definitely less than 80 percent that's what we see in obstructive lung diseases important to remember that very reduced fev1 and mildly reduced or normal fvc all right so now let's talk
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about restrictive now it's very interesting here right so again we're going to take the normal curve here that's their fev one at one second that's their Force vital capacity right for the normal patient now here's the patient who has a restricted lungs look
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what happens to their fuv1 it drops but not a crazy amount right in comparison to the patient who is the norm one or in comparison look at this look at the fev one here for the restricted and the
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obstructed lungs massive difference right so restrictive not a crazy reduction in fev1 we'll just give it like one arrow down okay their fvc though does actually reduce and so in comparison here was about five liters if I'm kind of like
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this is about four liters because that was their fev one there was about four liters here their FEC is about five liters I'm gonna say it's like somewhere around like three three and a half all right so I'm just kind of extrapolating
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so their fvc definitely dropped maybe like about 3.5 liters and their fev1 it's just mildly dropping even a little bit below that one so let's just like extrapolate that to about three liters if that's the case their fvc definitely was the one that
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dropped remember what did I tell you was the big big Factory here for the restrictive lung disease is what happens with their fvc drops pretty significantly so what I'm going to do is I'm going to drop my fvc by two arrows and obstructive I
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dropped my fev-1 by these multiple arrows so now if I were to just kind of extrapolate here that I had 3 divided by 3.5 that's definitely going to be greater than 80 percent or at least about same close to it so maybe about
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like 80 86 percent so in that situation here what do I notice about my ratio if I look here and my numerator is really small but my denominator is even really small what happens to the overall number it's going to be large because my
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denominator is really small and so in this situation theirs will be greater than or equal to 80 percent so in patients who have normal lungs what was theirs about 80 percent and the patient was a restrictive lung disease there's about greater than or
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equal to 80 percent but for a patient who has obstructive lung diseases theirs is less than 80 percent very important to be able to remember that and the reason why theirs is less than 80 is because they're fev1 at one second
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is significantly reduced and their FBC is only mildly reduced or almost normal and the patient with restrictive lung disease they have a mild decrease in their fev one at one second but their FBC is the one that really
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drops so their denominator drops even though both of them drop their denominator drops even more which allows for their overall number to still be high at least greater than or equal to 80 percent that's what I need you to remember about
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normal versus obstructive versus restrictive when it comes to the spirometry to put this in a quick little algorithm let's come down and talk about that all right so we compare obstructive versus restrictive we're looking at this ratio that we just talked about the fev at one
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second over the FEC for a patient who's obstructive what did we just say their fev1 is very very low we know that so because they have a very low fev1 and a really mildly decreased or almost normal fvc what do we expect the ratio to be
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less than 80 percent so because of that they'll be less than 80 they'll have a decrease ratio and a patient who has restrictive lung disease which is the primary problematic issue here which one is it fev1 or fvc
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the fvc is the primary one that's actually reduced if the denominator is small and the numerator is only mildly small what's going to happen to the overall number it's going to be large so theirs will be greater than or at least
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equal to 80 percent that is the big differences so when you're looking at a patient and you're given here's their fev1 here's their FBC determine their ratio if it's less than 80 percent this is likely obstructive and again the primary problem with this
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is which one of those actual variables the fev of one second versus restrictive their primary problematic issue that caused them to be greater than or equal to 80 is they have a very low fvc all right great now that we've talked
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about that there's a couple other things that we can do with these pulmonary function tests we're going to talk about something called dlco we'll talk about some bronchodilator tests and then we'll do some other additional tests as well
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all right guys so now we're going to talk about is the next thing that we can do within pulmonary function tests and so what we do is we can use something called the diffusion of carbon monoxide and it's a really interesting type of
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test and I think it's actually something that you should know especially for your exam especially when you're trying to differentiate certain obstructive lung diseases from one another now what we do is we actually give a patient a tiny amount of carbon monoxide
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and what we're trying to determine is how much of that carbon monoxide diffuses across the alveoli into the blood and then basically we basically measure how much we give them versus how much we exhale and the difference in between
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there's how much actually diffused into the blood and that's what we're trying to determine now the diffusion of the carbon monoxide is very dependent in the same way like oxygen CO2 is upon very specific factors one is the total
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surface area this is one really important one that I want you to know so the total surface area by which the gases are supposed to be exchanged is very significant it's directly proportional the diffusion of carbon monoxide the higher the total
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surface area is the higher the amount of diffusion of carbon dioxide there is the lower the less diffusion that's really important especially for one of those diseases which one was it emphysema that actually has a very low total surface
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area what do you think that it does to the dlco the amount of carbon monoxide that would diffuse across this alveolus into the blood just think about it low total surface area what would that do to the dlco it would
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decrease the dlco we don't see that in chronic bronchitis because there is no effect with chronic bronchitis on total surface area this here is just a kind of like a constant it's a coefficient this here is the pressure gradient and
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here's the thickness of the respiratory membrane thickness is really important when it comes to situations such as interstitial lung diseases you know under social lung diseases are part of restrictive lung diseases they have very thick respiratory membranes if they have
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very thick respiratory membranes so let's imagine here that I added another another class into this let's just say I added interstitial lung diseases into this class here we already know that with emphysema there is a decrease in the total surface area because of the
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destruction of the alveolar septal the walls the bronchial elastic tissue and so we know that they have a reduced dlco and interstitial lung disease what happens to the thickness of the respiratory membrane it increases this is a type of restrictive lung disease if
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the thickness increases what will that do to the dlco it would decrease the dlco so dlco may not be super beneficial in being able to differentiate restrictive versus obstructive lung diseases but what we know is that this would have a decrease
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in the dlco because it's inversely proportional to the dlco now if we compare emphysema to chronic bronchitis there would be a difference there then so we could say oh this patient more likely has emphysema because they have a reduced dlco chronic
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bronchitis is a normal dlco what about asthma this one's variable and I just want to mention it because it is something that you may see on the exam and I don't want you to be too confused about and patients of asthma one of the
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theories is that because they're so intense bronchoconstriction and lots of bronchial edema if they have intense bronchoconstriction and bronchialedema what happens is they have air trapping right they have air trapping so air is not able to exhaled out so CO2 can't be
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exhaled out and so because of that their alveoli may become hyperinflated if they're more hyperinflated what happens to their total surface area it may increase a little bit if their total surface area increases a little bit what made that due to the
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dlco it may increase the dlco so in patients with asthma they may have a normal two slightly increased dlco so these are things that I want you guys to understand okay so that is an important concept so I hope this makes
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sense when it comes to DLCs if you have a patient you go through the pulmonary function test you obtain their fev1 or FEC ratio and you say oh less than 80 percent likely and obstructive which one is it is it asthma is it emphysema or is
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it chronic bronchitis well how would I determine that maybe look at the dlco if the DLC is low it's likely emphysema if it's normal it could still be asthma or chronic bronchitis and then if I really wanted to in certain scenarios and
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Asthma when they're really hyperinflated it may be increased and then for interstitial lung disease it wouldn't really help us if we just did this on its own we would have to say oh they're fev1 over fvc was greater than or equal
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to 80 percent and then we checked a dlco and it was low that's more supportive of interstitial lung disease okay now that we've covered that the next thing that we can also do with the actual pulmonary function test is test the degree of
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reversibility this is really cool I'm confused if someone has COPD versus asthma I don't really know they have obstructive lung disease because they're fev1 over FEC ratio is less than 80 percent I do the dlco it doesn't really
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help me so I'm trying to figure out okay what else could I do to really differentiate between these two this is really cool I can give the patient a bronchodilator so I'm going to give them something called a beta Agonist and what this is
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going to do is it's going to open up the bronchioles by causing them to dilate and what this will do is it'll open the airway up a little bit and make it easier for air to be exhaled and patients who have asthma
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there is a reversibility that's one of the key things it's reversible and patients with COPD It's relatively irreversible so I'm going to give them a bronchodilator and what I'm going to do is I'm going to measure their fev1 prior
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to the bronchodilator and then post bronchodilator and what I want to know is what happens if I bronchodilate it open up the airway more it should be easier for air to be exhaled theoretically right so what I want to do is I want to put
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post post fev1 post fev1 what would I expect I would expect an increase I would expect a increase in the fev one for both of them but here's where it gets a little tricky you have to be greater than or equal to
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12 increase in the fev1 to be considered reversible which is more indicative of asthma if you don't reach greater than or equal to 12 it is not likely a reversible type of disease and it's more likely COPD so if it is greater than if
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it is increased but it's less than 12 percent it's likely COPD if it's increased post bronchodilator and it increases greater than equal to 12 percent it's more likely asthma that's what I want you to remember Okay so we've gotten the pulmonary
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function test to determine if it's obstructive versus restrictive we use the dlco to maybe help us differentiate between emphysema and chronic bronchitis we use the bronchodilator test to really help us to differentiate between asthma and COPD and then what if we're really kind of
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confident that the patient has asthma but they're not symptomatic we want to really kind of see is this patient really having asthma but they haven't had an exacerbation lately I can actually induce a patient who is non-symptomatic into
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having maybe a little exacerbation to test and see if they do have asthma because not only is asthma reversible but it's inducible I can actually cause them to have a hyper responsiveness you know bronchial smooth muscle and normal patients you give a
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methylcholine they'll bronchoconstrict a little bit but nothing crazy and a patient with asthma they go on Broncho constrict and they'll do it very intensely and if they bronchoconstrict you're going to have them really really narrow their Lumen imagine how difficult it's going to be
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to be able to get Co2 out and exhale air through a very tiny Lumen more than normal what would I expect to happen to my fev1 so if I measured it pre before I gave the methylcholine and then I measure it
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post after methylcholine I would expect what a decrease in my fev1 because I'm going to bronchoconstrict if the decrease in the fev1 is greater than or equal to 20 percent that is indicative of bronchial hyper-responsiveness which is supportive
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of asthma remember that all right the next thing that I want us to do is let's take a look here instead of us actually looking at kind of writing things down on the actual whiteboard of what a chest x-ray or CT
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would look like for a patient with COPD or chronic bronchitis or emphysema or bronchiectasis let's take a look at a couple images so you guys can have more of a visual representation of what these actual images look like for patients
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with obstructive lung disease all right so let's go ahead and take a look at some images here so the first one that I want you guys to take a look at here is here's a chest x-ray of a patient that
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definitely classifies as a COPD or this is definitely pretty obvious so what you'll see is you'll see some massive hyperinflation of the lungs these really tall looking lungs and this is like a PA chest x-ray so if we were we were
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looking at a kind of a posterior to anterior view if we were to turn them into do a lateral view their anterior posterior diameter would be massive so again you see these really tall hyper-inflated lungs and you see
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something called hyperlucency so whenever you have air on the chest x-ray it appears very dark so look how much air is trapped in these lungs because they're very hyper loose and they're very dark that's one thing so two things
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so far hyperinflation the second thing is very hyper loosened lungs very dark on the chest x-ray the other thing is look at the diaphragm they're supposed to be a right Hemi diaphragm that bulges up and a left hip diagram that's
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supposed to bulge up the dang thing's flat so I got a flat diaphragm that's it because there's so much hyperinflation it's pushing the diaphragm down the other thing that's really important here for these patients is if you look
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sometimes the ribs almost appear somewhat straight that's not the most obvious sign but whenever they're very hyperinflated their ribs can kind of have almost a horizontal or straight like appearance so a big couple things to be able to remember for these classic
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in this situation COPD patients more likely emphysema predominant will have hyperinflation on the PA or AP chest x-ray if you get a lateral to have an increased AP diameter like a barrel chest look they'll have hyperlucency of their chest feel due to a lot of air
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trapping they'll have flat diaphragms and on top of that they may have these flat or almost horizontal appearing like ribs alright so that covers our COPD chest x-ray likely emphysema predominant all right so we're taking a look here at
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a CT scan and again this is of a patient who has COPD one of the really interesting things that you see out of this is again here's our right Hemi diaphragm right here and here's the left Hemi diaphragm right here so we have the
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heart in this position what you're noticing on this is this is all lung paring and you see how there's a line right here and it looks like a little septal per tissue here a little septal tissue here a little septal tissue here
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this is also parenchyma it's just air filled and these air filled sacs have become so enlarged because of alveolar wall destruction that they become these huge air sacs near the pleura remember what I told you happens in patients who
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have emphysema they form these big things called Bole or blabs and they have high risk of rupturing and then emptying air into the pleural cavity which you can't really see here which would cause a big pneumothorax so this
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is not a pneumothorax but it can lead to one because again this is an air filled sack just a really large one due to alveolar wall destruction and copders and again you can see some of these very very large walls here all right that's
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our COPD again patient but more particularly one of the complications such as boole that we see in emphysema predominant patients all right so we're looking here at another CT scan right hemidiaphragm left hemidiaphragm heart here in the center and what you're
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looking at is you're seeing the he's like these are your bronchi so these are actually like your bronchioles and you can see them kind of extending out to the periphery now if you notice something look how huge they are they
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should not be this obvious and this dilated whenever they have this very large dilated appearance to them we see this in patients who have bronchiectasis this is actually called what's called tram tracking and they're just these big huge dilated bronchials that you'll be
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able to see on a CT scan most predominantly you may be able to see them on chest x-ray but you'll definitely be able to pick these up on CT scan for bronchiectasis alright so the last image that I want you guys to
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take a look at is again here's another CT scan right Hemi diaphragm left Hemi diaphragm here's the heart and again here's going to be the vertebrae but what you're seeing here is again you see all lung parenchyma lung parenchyma but
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we're seeing the cut sections of the actual bronchi or bronchioles you see how first off they're very dilated but you know what else is really interesting in some of these especially this one you see how it's very dilated and and then
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it has like this little like nugget coming off of the edge of it it almost takes on the appearance of a ring but we call this a Signet ring so if you guys ever take a picture of a Signet ring it
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also looks like just this little big pearl on top of a normal kind of like ring and so it's really really interesting we call this the Signet ring sign so you see one here if we were to try to find another one potentially we
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may be able to find one maybe right here here you're going to see the dilated bronchial with again this like kind of little Pearl thing coming off the edge but this is a very common finding in bronchiectasis these dilated bronchioles
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with these little edges coming off here which we call the Signet ring sign we see this in bronchiectasis all right that covers all the images for our obstructive lung diseases let's get back to the Whiteboard all right so we've
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talked about chest x-ray and CT the next thing that we also should talk about is sometimes it may be beneficial remember I told you what is the complication of a patient who has chronic bronchitis they may have something called core pulmonal
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due to again intense pulmonary vasoconstriction due to again having less perfusion to the poorly ventilated alveoli and good perfusion to the well ventilated alveoli and because you may have poorly ventilated alveoli all over the lungs you may have intense pulmonary
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vasoconstriction put a lot of stress on the right heart and cause right heart failure we may be able to pick that up on Echo so if we're doing an echo of a patient with COPD what you could be
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looking for is right ventricular hypertrophy our right heart failure secondary to core pulmonal and that may be helpful if you're thinking of a patient has this due to something like COPD secondary to which one more likely more likely due to
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chronic bronchitis in comparison more commonly than emphysema usually emphysema we see this in the later stages all right my friends the next thing we have to talk about is a couple other additional tests they're not as high yield but I want you to
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understand them so let's come down to talk about CBC and ABG all right the next thing is with a CBC if a patient has something like chronic bronchitis or they have bronchiectasis in these situations what I want to remember again
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more likely chronic bronchitis and maybe bronchiectasis they have lots of mucus plugging and narrowing of the Airways which reduces ventilation to their alveoli because of that they may have less oxygen reaching their actual bloodstream what is that called when there's less oxygen in the
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blood hypoxemia hypoxemia chronically May stimulate your JG cells in the kidney to make something like which are the proximal convoluted tubular cells not JG cells the proximal convoluted tubular cells to make something called erythropoietin erythropoietin will then stimulate your
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red bone marrow and say hey there's less oxygen maybe if we make more red blood cells we can have more oxygen carrying capacity and that may help and so sometimes in patients with chronic bronchitis or bronchiectasis you may see
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that they have an increased number of red blood cells so they have an increase in their hemoglobin and they have an increase in their hematocrit which is called polycythemia you may see that in these patients with COPD primarily
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chronic bronchitis predominant or bronchiectasis the last thing that I want to talk about is an arterial blood gas I don't think this is as valuable as people may think but it is something that you may be asked about on your exam when a patient
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is having an exacerbation of their asthma or their COPD it's important to be able to kind of think about this if the patient's really breathing fast and very very very to kipnik because whatever the trigger may be for them
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there was a trigger and they have a worsening of their COPD or they have a really severe episodic asthma attack in those situations they may breathe really fast because they may have hypoxemia they may have hypercapnia and so they're
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trying to compensate for the hypoxemia or hypercapnia by breathing really fast so if I have a patient who has respiratory alkalosis right it would be it would make sense it's likely that they are having an increase respiratory rate and the reason why is
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maybe they have a significant mucus plugging that's reducing oxygen getting into the airway reducing the amount of oxygen getting into the blood causing hypoxemia less CO2 being able to be exhaled so CO2 is building up in the blood
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and then the response to this is to increase your respiratory rate if you increase the respiratory rate what happens as a result of this you try to breathe faster to breathe off more CO2 and bring in more oxygen
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if you breathe faster you're going to Exhale more CO2 theoretically if you exhale more CO2 what is that going to do to the actual equation you guys remember that equation I know you guys do CO2 plus water yields
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carbonic acid which disassociates into protons and two bicarb if a patient is exhaling lots and lots of their CO2 then this amount is decreasing and so Le chatley's principle says you want to shift the reaction this way to the left
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so what would happen is we would actually shift this reaction to the left and what would that do to the number of protons that would decrease the number of protons if you have less protons inside of the bloodstream what does that do to
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the pH it increases the ph and so as a result we would have an increase in the ph and so this would be called an alkalosis due to a respiratory problem where the patient is breathing really really fast we can see this and maybe
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exacerbation so think about it that's why sometimes abgs may not be as helpful as your exam if a patient sitting in the room and breathing at a respiratory rate of 50 breasts per minute you'll likely be able to know what their ABG is going
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to tell you it's likely going to tell you that they probably have a very severe respiratory alkalosis their pH is going to be high and their CO2 is going to be low and it may also show a hypoxemia but we
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can also pick that up off the O2 saturation on their finger right so it's important to be able to consider these things and this may not just be due to a mucous plugging in situations like bronchiectasis or chronic bronchitis it
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also could be due to intense bronchoconstriction in situations such as asthma okay now the problem with this is that if a patient is breathing at very very high respiratory rates for a long period of time the concern is that this increased
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work of breathing will eventually lead to fatigue and if this fatigue occurs their diaphragm will not be able to maintain that respiratory rate their inner costal muscles will not be able to maintain that respiratory rate and they'll start
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to fatigue and if they fatigue the respiratory rate will start to drop their ability to clear CO2 will start to drop and then their ability to bring an oxygen will start to drop and they can actually develop worsening hypoxemia
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they can develop a respiratory acidosis that leads us into the next part here what is a concerning finding sometimes for patients is if their respiratory rate is decreasing and this B could be because of fatigue they've been in situations now where
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they're have to compensate for so darn long that now they can't get Co2 out you know what this is also really scary of if I have a patient who has intense bronchoconstriction intense bronchoconstriction and I'm having a difficult time being
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able to get CO2 out of the actual bloodstream into the alveoli and then exhaled in situations such as asthma in early asthma if it's not as intense of a bronchoconstriction they may still be able to get Co2 out of the lungs
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mildly and bring a little bit of oxygen into the blood right and severe asthma I'm talking very very severe asthma where the bronchoconstriction is so intense or they've been working so hard to breathe for so long that their muscles are
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starting to get fatigued and they can't generate the same rate to clear CO2 either way one of the problems we're not getting CO2 out CO2 is going to start building into the bloodstream if CO2 builds up into the
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bloodstream and we have an increase in CO2 what does that do to this equation well then we would have high CO2 and we would want to shift the reaction in the opposite direction which would increase the number of protons we know this
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equation right that if we have again CO2 plus water yields carbonic acid which breaks down into protons and bicarb we know that we're going to have an increased amount of CO2 because we're not clearing it we're either not clearing it because of a
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severe obstruction blocking CO2 out or because the respiratory rate is so low because we're fatigued because we've been working so hard so they've been doing this for so long their muscles become weak and they can't do this anymore and they start slowing down CO2
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starts accumulating or they have a massive obstruction that's not letting CO2 get out if that happens the CO2 builds up and what happens we know that if the chatley's principle says that if this side of the reaction is increased we
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have to shift it to the side where there's less and so this will shift the reaction to the right and increase the amount of protons if we increase the amount of protons what does that do to the pH
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it decreases the ph and if we decrease the pH then we now have a acidosis this is a problematic issue right and so this is why it's very very important to understand if a patient has severe asthma and their pH is actually starting
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to show signs of acidosis and CO2 retention you better be scared because this means that their patient is either fatiguing out and they're not able to continue to breathe at the rate that they've been to compensate or their
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obstruction is so severe that they're not getting CO2 out in the same way if a patient has a COPD exacerbation they could have been breathing so hard for a long period of time to compensate but again they're starting to Tucker out
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this could also be a particular reason there's one more thing to think about you know patients with COPD chronic copders they naturally have a chronic respiratory acidosis but the way that they don't actually have to breathe the way that they do is that they compensate
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from their kidneys their kidneys actually retain bicarbonate excrete protons and so they naturally help to be able to compensate for their actual low PH by retaining bicarb and so that's one of the important things is that patients with chronic COPD may have a degree of
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respiratory acidosis they may have a high CO2 but their pH will be Stone Cold normal and the reason why is they've retained bicarb from their kidneys over a long period of time so it's important to remember just because someone has a respiratory
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acidosis does not mean that it's actually an acute problem like an exacerbation like they're they're starting to fatigue out from breathing so hard they have a severe obstruction it could be that a patient has a chronic respiratory acidosis because they've had
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chronic COPD for a long time and they naturally have a high CO2 and that's kind of dropped their pH a little bit but they accumulated bicarbonate excreted protons and then help to be able to bring their pbh pH back up to
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normalize so again it's important to think about these things that's why I think sometimes the physical exam is a lot easier to follow and more important to follow than in ABG because these can vary but either way I hope this part
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made sense we've covered Diagnostics we're moving on to the last part here of our obstructive lung disease lecture let's talk about treatment all right so let's talk about the treatment of obstructive lung disease we'll start first with COPD then we'll talk about
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asthma and then we'll finish up a bronchiectasis so first things first for these disorders what I want you guys to understand is we're gonna have a specific way that we're treating them one of the big things where COPD is that
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they have a lot of bronchospasm so bronchoconstriction what we should try to do is obviously do the opposite of that bronchodilate if we bronchodilate we open up the airway more allowing for more air flow in and out of the lungs
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that's going to help these patients so primarily with symptoms it will not reduce the overall chance of mortality or death but it will help to be able to potentially reduce the morbidity the symptoms the probable issues that they
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have with this disease so how can we do that let's understand basically the pharmacology behind it so here we have the bronchial smooth muscle what we want to do is dilate to increase air flow in and out of the lungs so when we zoom in
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on one of these smooth muscle cells on these smooth muscle cells you have beta 2 receptors and muscarinic type 3 receptors now basic concept here is that whenever you have a beta 2 receptor whenever you stimulate this beta tube
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receptor it'll naturally cause bronchodilation whenever you act on a what's called a muscarinic receptor or an M3 receptor and where acetylcholine would bind onto that it'll actually produce bronchoconstriction so we want mainly bronchodilation so I want to give a drug
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that will potentially act as a Agonist and stimulate this receptor to be able to increase bronchodilation and I want to give another drug category that'll act as an antagonist and inhibit this receptor and help to be able to increase
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decrease bronchoconstriction so decrease bronchoconstriction so if I inhibit this receptor I'll inhibit the bronchoconstriction and decrease the activity there and therefore if I decrease bronchoconstriction I may allow for a little bit of bronchodilation so I need to give muscarinic antagonist and
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beta adrenergic receptor agonists you know the best way to deliver this drug to the smooth muscle inhaled so I'm going to give inhaled bronchodilators in the form of beta2 receptor agonists which is going to promote bronchodilation we can give it
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short act short acting and this would generally be an acute scenario so whenever a patient maybe is having an acute COPD exacerbation I can give them a drug like Albuterol and more of a long-acting so long-term chronic management of the patient who
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has COPD I can give them more of a longer acting beta 2 Agonist and this would be something like selmeterol from motorol volanterol all of these different types of drugs okay but the basic concept is they'll produce bronchodilation long acting just
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remember it's salmeterol for Motorola valenterol and the main one remember for the short acting is Albuterol okay these will bronchodilate the other drug category is the M3 receptor antagonists they're going to inhibit this receptor prevent bronchoconstriction and therefore cause
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bronchodilation the drugs that I could give is short acting or long-acting the short acting would obviously be during acute exacerbations of their COPD whereas the long acting is for more of the chronic management of these patients you know what actually is really
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interesting I can give a combination of the short acting beta Agonist and a combination of the short acting muscarinic antagonist and a combination during acute COPD exacerbations so we write these as as we can do a short acting beta Agonist
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Plus a short acting muscarinic antagonist short acting muscarinic antagonist these are actually a common thing that we can give and we call this a Duo neb and a Duo NAB is a combination of a Albuterol and a sama
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short-acting muscarinic antagonist the most common one to remember is a protopram bromide so this is a very common Duo neb combo that we give to patients during their acute exacerbations now in Long acting this would be more of
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the chronic treatment of the COPD we could give a muscarinic antagonist and that would be diatropium so remember these things so bronchodilators we can give beta agonists muscarinic antagonists you can give short acting as a combo doing ebb during acute
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exacerbations and then long term you can do a lava a long-acting beta Agonist like salmeterol for motorol volanterol or a long-acting muscarinic antagonist a llama like diatroprium all right beautiful that covers that part the next thing that we also want to
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consider here for these patients is that sometimes these patients are at high risk for pneumonia especially chronic bronchitis right so because chronic bronchitis is definitely a high risk for pneumonia what we may be able to do is give a very specific drug that may
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reduce inflammation and prevent exacerbations of COPD causing high risk of pneumonia what is that actual drug azithromycin azithromycin has been shown at it can be one antibiotic that you could give to patients okay especially if they have lots of exacerbations if
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they had at least three plus exacerbations then you should consider giving them something like azithromycin to prevent further exacerbations and things like pneumonia okay that's an important thing to consider the other thing that's really important for these patients is something called
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oxygen therapy giving them oxygen not all COPD patients are candidates for oxygen therapy meaning that they have to wear oxygen like 16 liters a day I mean 16 uh 16 hours a day they may have to get a couple liters two to three liters
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about 16 plus hours a day and those patients what are the category what is the actual patient population that would be qualified for that long-term oxygen therapy every day one of the particular reasons here would be that they have some issue where
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during rest during exercise whenever if their spo2 is less than 88 percent or the amount of oxygen that makes it into the alveoli crosses the actual capillaries and it crosses the the alveolar membrane into the across the capillary membrane and gets into the
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blood the pao2 is less than 55 millimeters of mercury in this situation they would qualify for oxygen if a patient again has an spo2 of less than 88 percent or a Pao to a 50 less than 55 millimeter mercury
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during rest during exercise they qualify for long-term oxygen the other situation where you may be a little bit more stingy and say you know what I actually would accept even a higher oxygen Target that they would need it because less than 80 is actually
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pretty low right and when you consider this a normal human being we would be even a little bit more likely to say hey man I'd even have a lower threshold for other patients to start oxygen therapy because they're at higher risk and
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patients who have already right heart failure due to core pulmonale long-term COPD or they have an increase in their number of red blood cells do they have polycythemia that tells me that they've had hypoxemia for a long period of time
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and they're at high risk for further hypoxemia so what I need to do for these patients is treat them a little bit earlier so maybe they don't make 88 but and these patients they're at less than 90 percent if they reach less than 90
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percent or the amount of oxygen that reaches their alveoli and Crosses into the pulmonary capillary blood so the pao2 the partial pressure of arterial oxygen is less than 60 millimeters of mercury so you see how the goal you have to be a
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lot lower in this category who does not have right heart failure does not have polycythemia you have to have a way lower oxygen saturation and a lower pao2 to start oxygen in this category you can have a higher oxygen saturation a higher
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pao2 but you also have to have right heart failure or polycythemia to be a candidate for oxygen therapy so remember that again one more time less than 88 pao2 less than 55 no right heart failure no polycythemia candidate
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for oxygen therapy patient spo2 less than 90 or pao2 less than 60 have right heart failure or polyzeidemia oxygen candidate all right now that we've talked about bronchodilation antibiotics oxygen therapy the next thing I really want you to understand is out of these
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three that I've just mentioned which one of these have actually been shown to produce mortality in patients with COPD only one of these oxygen therapy so I want you to remember that oxygen therapy is one of those types of treatments that
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actually do have the ability to reduce mortality okay let's come down and talk about the other ways that we can treat COPD all right so the next thing we have to talk about with COPD is that we can
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actually reduce some of the inflammation remember I told you that there is a chronic degree of inflammation remember that process let's see if you guys do remember we have the tobacco smoke or the pollutants whatever it may be
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triggers the macrophages macrophages release leukotrienes they also can release maybe some degree of prostaglandins they can also release certain types of interleukins like interleukinate that can attract in neutrophils but what we know is that these leukotrienes and prostaglandins that
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they may work to be able to cause bronchoconstriction they may also ramp up and amp the inflammation which may cause some degree of increased mucous secretion so a little bit more mucus that's produced all of these things that
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we understand right on top of that neutrophils are also going to be coming into the area and they start releasing things like reactive oxygen species they start releasing proteases and this starts causing an increase in the inflammation right starts destroying
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some of the elastic tissue with inside of the actual bronchial walls increases the mucous production even more and then on top of that if these epithelial cells are damaged from repeated exposure to the tobacco smoke they'll activate fibroblasts that will cause fibrosis
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what if I had a drug that would potentially be able to inhibit the macrophages from releasing some of these cytokines and saying hey macrophages shut up totally all these cytokines that's going to cause this massive inflammatory response causing
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bronchospasm elastic tissue reduction increased mucus and fibrosis that would be a pretty cool thing right so guess what these are where corticosteroids come into play there is basically helped to be able to shut off something called the arachidonic acid pathway without going
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crazy into detail you guys need to know that arachidonic acid is the precursor to making things like leukotriines making things like prostaglandins which are kind of like the alert molecules but that are released by The macrophages to tell that there's inflammation going on
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telling the neutrophils to come to the area if we inhibit the actual arachidonic acid pathway we would actually reduce leukotriene's reduce prostaglandins and all these other cytokines that kind of trigger the inflammatory response and maybe reduce bronchospasm reduce mucus
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production potentially reduce fibrosis wouldn't that actually be relatively helpful and maybe even reduce some of the actual further breakdown of the elastic tissue as well this is actually pretty beneficial concept so in hail corticosteroids things like budesonide or fluticasone we would generally use
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them in combination with a bronchodilator but more specifically since this is more of a chronic management we've used this more specifically with a lava so long-acting beta Agonist or a llama a long-acting muscarinic antagonist so very important now in patients who have very severe
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acute you know exacerbated COPD so they're having a COPD exacerbation an acute exacerbation maybe they inhaled corticosteroids will not be enough and in those situations we may want to give them po we want to give them systemic corticosteroids very high
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levels of anti-inflammatory mediation and we would use IV or po steroids more likely IV especially if you're having a patient having difficulty breathing probably going to be difficult for them to swallow a pill we'd likely give them IV methylprednisolone or if they can
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tolerate a pill po prednisone to be able to really increase the corticosteroid levels to really try to shut down the inflammatory response so we would use this in an acute COPD exacerbation all right my friends that would cover
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this component now the next thing that I want to want us to talk about is preventing infections these patients with COPD especially which one chronic bronchitis especially patients with chronic bronchitis because of the mucus that's accumulated within those Air
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Raids that can cause a colonization of bacteria increasing the risk for pneumonia so now imagine that the patient is already at high risk for pneumonia and you have them being exposed to the most common types of factors that cause
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pneumonia a Streptococcus pneumonia or a h influenza so homophilus influenza virus so if they are exposed to I'm sorry influenza virus or they're exposed to streptococcus pneumonia which are too common microbial agents that can lead to pneumonia in a patient who's already
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high risk for pneumonia this can definitely increase the mortality for these patients so because of this they're already at high risk for pneumonia these patients with chronic bronchitis now if they get infected by streptococcus pneumonia or influenza this will definitely increase
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the mortality rate because what it'll do is it'll definitely increase the risk of pneumonia worsen their ammonia and increase mortality from the pneumonia so what we want to do is make sure that these patients get vaccinated against these very common pathogens such as the
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pneumococcal vaccine protecting them against streptococcus pneumonia and the influenza vaccine protecting them against influenza because influenza not only does that actually cause a really nasty pneumonia but it also can increase the risk of patients developing a pneumonia due to staphylococcus aureus
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remember influenza definitely increase the risk of staphylococcus aureus infections especially in the elderly so think about this okay now this is a very important thing if I give these patients vaccines I can potentially reduce their mortality so it's important to be able
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to give this very important instruction to your patients because this is a mortality benefiting effect the next thing what if I remove the dang cause of the patient's trigger the trigger was the tobacco smoke which activated our macrophages which
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activated the neutrophils and caused all this inflammatory mediators which destroyed cause bronchospasm cause destruction of the elastic tissue increased mucus production cause fibrosis the dang tobacco was the primary cause what if I get rid of that wouldn't that prevent the further
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progression of the disease and therefore help to be able to maybe reduce mortality of the patient Absa stinking lutely so smoking cessation will definitely be a factor that you want to try to push your patients to follow because it can reduce mortality so
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whenever you're telling a patient here's what I want you to do for their COPD the things that you need to consider that actually have mortality benefits smoking cessation making sure they're vaccinated against the pneumococcal of bacteria and influenza
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and if they need oxygen therapy make sure they get the oxygen therapy if they fit the category that we talked about above the last thing that I want to talk about is more specifically for the acute exacerbation of COPD so someone has an
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acute COPD exacerbation and that situation sometimes these patients really we need to work to eliminate their CO2 and just provide them kind of a ventilatory support so really what we could actually find benefit from in these patients that actually can reduce
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mortality in these acute exacerbations of COPD is putting them on something called positive pressure ventilation and this would generally be BiPAP so BiPAP has been shown to be able to reduce mortality and these exacerbating situations and if they fail bipapath
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then we would perform endotracheal tube intubation and then we would mechanically ventilate them invasively okay but we don't want to have to do that generally we would try to do what kind of things if a patient has an acute
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exacerbation of their COPD give them a bronchodilator the short acting ones and the combination of a duaneb give them IV steroids right on top of that if they have any need because they have a pneumonia that caused this treat the
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underlying pneumonia and then on top of that also provide good ventilation support particularly BiPAP if they fail BiPAP then you can consider something such as endotracheal tube intubation okay we talked about the treatment of COPD let's now move into asthma all
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right guys so let's talk about the treatment of asthma so asthma is relatively similar to COPD we're going to try to bronchodilate reduce inflammation give some ventilatory support and then we'll talk about the stepwise regimen and chronic asthma
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management if a patient has asthma it's the same exact thing that we talked about before we don't really use the muskrenic antagonist as much you can consider it there's nothing wrong with it it's just it's easier to be able to keep it
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separate on your minds for you know COPD but in a patient who has asthma they're going to benefit more particularly from the beta 2 receptor agonists if you guys remember we want to promote bronchodilation so we want to be able to
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have agonists that stimulate the beta2 receptors to be able to increase the bronchodilation response to open up the Airways get more air in and out the other concept here is that smooth muscle has calcium channels on them we
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can give a particular drug that actually will bind around these calcium channels and block calcium from being able to get in so they inhibit calcium entry and the calcium comes into the smooth muscle cell it activates the cross bridge and
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activates the whole troponin tropomyosin type of process and leads to contraction in this situation we block calcium entry therefore we block the actual smooth muscle contraction therefore we block bronchoconstriction therefore we decrease bronchoconstriction maybe promote bronchodilation so there's two drugs
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that I want you guys to remember the ones that stimulate the beta 2 receptors are called the beta agonists we've already talked about these the short acting ones in acute scenarios or maybe a patient is having like an
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acute exacerbation or they're having a little asthma episode we can give them Albuterol and like a nebulizer or potentially even an inhaler and long acting would maybe be more of the chronic management and these patients okay and again
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remember albuterol is the short acting beta Agonist the Saba salmeterol from motorol volantrol those are more of the actual long-term beta agonists more for The Chronic management I'll teach you guys the stepwise fashion of how to know how to add a Saba then which one do I
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add next and when do I add a lab Etc I'll explain all that in the stepwise fashion the other situation is magnesium magnesium is going to act like a little calcium channel blocker on the smooth muscles if magnesium blocks these
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calcium channels it prevents calcium entry and prevents bronchoconstriction which will allow for bronchodilation so magnesium and an IV bolus form is a great during acute exacerbations of asthma so sometimes the patients have coming in they're having a really bad
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asthma exacerbation we can give them a short acting beta Agonist like Albuterol and IV magnesium to really get a good bronchodilation response and help to be able to open up the Airways to allow for more CO2 to come out more oxygen to come
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in really great concept there all right now the other concept is remember the pathophysiology one of the reasons that patients have asthma is really intense bronchoconstriction the second is that they have lots of inflammation and edema what if I had a way of being able to
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reduce some of the inflammation and reduce some of the bronchialedema and reduce some of the bronchoconstriction even more let's talk about that now right so remember the pathophys guys you have some type of trigger whether it's an allergen so pollen dander dust right
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or the again if you think about the the patients who have high risk of allergic types of reactions by the the atopic Triad atopic dermatitis allergic rhinitis and asthma or the non-allergic causes viral urti some type of beta
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blocker cold air exercise gerd or again we even talked about the samters Triad so patients who have nasal pops and Asthma you should be very careful with giving them aspirin now if they're exposed to this particular trigger we already know that it gets
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taken up by the dendritic cells so it gets phagocytos by the dendritic cells when it gets phagocytosis by the dendritic cells it'll actually take a piece of it and expose it on its mhc2 complex when it exposes on the mhc2
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complex it activates the T cells the T cells will start to release cytokines like interleukin for an interleukin five we know the interleukin-4 more specifically stimulates plasma cells plasma cells will make antibodies do you guys remember what kind of antibodies it
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makes the more specific one is i g e antibodies the IG antibodies will bind onto the mast cells and then when the actual specific trigger binds onto the IG antibodies connected to the mast cells the mast cells which have these
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like little things here you see these like little green dots these are called granules what are these little things here called they're called granules once they're stimulated by the allergen binding onto the IG antibody it causes these granules to undergo degranulation
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meaning that they just basically fuse with the membrane and release all of their contents what are some of the things that they release they release things such as leukotrienes prostaglandins histamines and what do these things do they cause vasodilation
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of the actual capillaries in the bronchial walls causing increased leakage of fluid which causes edema they also cause bronchoconstriction so they cause the smooth muscle constriction and that is an important concept because now what I can do is I can Target specific steps in
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this pathophysiological process remember why I talked about it so dang much this is why what if I gave a drug that acts like a monoclonal antibody and just blocks up so you're exposed to the particular trigger you have this
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response where you release cytokines and then you make antibodies but I give you a drug called amalzamat which is a monoclonal antibody and it binds up these iges so that they can't bind onto the mast cells so then they can't
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degranulate release these cytokines cause bronchoconstriction bronchial edema that's pretty cool who would I give this to mainly those patients with allergic rhinitis or atopic dermatitis or very refractory allergic asthma so it's more for the allergic type of asthma or very severe in stage like
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stage six or stage five asthma okay then now that one doesn't actually be the one that you want to the Target let's say I Target the degranulation step you know when I take the granules they're stimulated by the allergen binds
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to the IG antibody tries to come and stimulate these granules to degranulate what if I gave a drug that stabilized the mast cell membrane and prevented these granules from being releasing these molecules like leukotrienes prostaglandins histamines that cause the
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vasodilation increased capillary permeability edema and bronchoconstriction that'd be a great drug this is where we can use things like chromal and sodium which is a mast cell stabilizer and the primary indication is for prophylaxis against exercise induced asthma so we can give
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Mast Cell stabilizers which prevent degranulation of these cytokines and exercise-induced Asthma or Mal's map to block the IG antibodies in allergic asthma or severe refractory asthma the next situation is corticosteroids we already talked about this a little bit
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remember that in order to make things like leukotrians and prostaglandins what do I need I need something called arachidonic acid and arachidonic acid will be acted on by different enzymes like the Cox enzymes and the Lipo oxygenase enzymes to be able to make
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different types of molecules like prostaglandins or leukotrienes if I give corticosteroids they help to be able to inhibit this arachidonic acid pathway and so then I don't stimulate the Cox enzymes the Lipo oxygenase enzymes and I decrease my prostaglandins
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I decrease the leukotrienes I decrease the vasodilation increased capillary permeability and I decrease the bronchoconstriction that's a really interesting process and so for corticosteroids we're trying to be able to inhibit the cytokine release from the mast cells by inhibiting the arachidonic
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acid pathway that occurs in them we can use these in two forms the inhaled form what do you think we use this in more of the chronic States and we use it in the same way we use in COPD we use it with a
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lava but we don't use lammas too much or muscarinic antagonists and Asthma that's primarily for COPD so whenever you give someone an inhal corticosteroid it has to be used with a long-acting beta Agonist which is a bronchodilator we can also give it IV or Po in the same
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situation we would give it during COPD when was that when a patient is maybe a little bit sicker and in those situations we need to increase the levels of the corticosteroids to really maintain a good anti-inflammatory effect we would use that an acute exacerbations
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of asthma so if someone's having an acute asthma attack we would use IV preferably because if a patient's breathing really fast you think they're going to be able to take a tablet it's going to be very difficult so I give them a big slug of IV
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methylprednisolone if somehow they can tolerate po prednisone you could also consider that but that's what we would do in very severe acute asthma attacks all right the next thing is if we didn't Target the antibodies that kind of trigger the
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mast cells we didn't inhibit the granules from being able to release these cytokines we didn't we didn't inhibit the actual arachidonic acid pathway that makes these particular molecules what if I inhibit the receptor which leukotriene is supposed to be able
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to bind to so this is a leukotriene receptor where it's supposed to bind onto the smooth muscle of the bronchials or the capillaries that are in the bronchial walls and proto-edema and bronchoconstriction if I give a drug it'll inhibit these particular receptors
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if I give corticosteroids it'll inhibit the rachidonic acid pathway if I get Mast Cell stabilize their inhibit degranulation if I give a malzimab it'll inhibit the IG antibody from fusing with the mast cells so if I give these leukotriene receptor
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antagonists like mantelucast it'll block the leukotrians from being able to bind to these particular receptors inhibit vasodilation increase capillary permeability inhibit bronchoconstriction allow for bronchodilation and less bronchialedema who do I use this in I use this in Aspirin induced asthma and
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exercise induced asthma so exercise induced asthma prophylaxis is which one you guys remember Mast Cell stabilizers treatment in aspirin-induced asthma and exercise induced asthma is leukotriene receptor antagonist amalgamab and allergic asthma do in the situations like allergic rhinitis atopic dermatitis or
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severe refractory allergic asthma and then corticosteroids you can use inhaled and asthma in any stage particularly but again usually it's used with a lava in asthma that's more chronic and then we use this more as an ivpo version and
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very acute asthma attacks okay we talked about the ways they can we can reduce inflammation now let's talk about what do we do with a patient that we've started them on bronchodilators we've given them anti-inflammatory agents so we've a patient that comes in with an
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acute asthma attack they're breathing really fast they look terribly look at they collapse at any moment you started a short acting beta Agonist so you give them Albuterol inhalers you gave them IV magnesium you gave them IV steroids now
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you're moving on to the next step which is trying to improve their ventilation how do we do that let's talk about that now all right so we have a patient who has an acute asthma exacerbation we start them on a short-acting
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bronchodilator like albuterol all right so really like nebulized we have Mighty magnesium we give them an IV steroid like maybe methylprednisolone if they somehow tolerate po prednisone would be another option and again it's not saying that you can't give them a short-acting
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muscarinic antagonist like ipertropium it's just it's easier to be able to delineate this in your head that you would do it more likely for COPD but you can give muscarinic antagonists in asthma it's just more commonly remembered and easier to remember for
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your COPD ears so we started them on that but they're still really like having shortness of breath they're still disc they're still working really hard to breathe what else can we do to ease their work of breathing we can do
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positive pressure ventilation so in these patients we can do positive pressure ventilation and one of those things just like we did in a patient who has COPD would be BiPAP bi-level positive airway pressure this is going to help to be able to Exhale the CO2 and
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generate enough pressure to push air into the Airways so I think this is a really great tool and if the patients fail they aren't able to tolerate BiPAP they fail BiPAP they're continuing to get worse you can then transition them
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into an endotracheal tube intubation and then subsequently mechanically ventilate them that way which would likely require a decent degree of sedation for these patients all right we've talked about the treatment of asthma but one of the big things that I think is
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really important is how to be able to stepwise approach these patients so you have a patient out outpatient wise that you're managing and they're starting from the beginning they have mild asthma what is the treatment that you would
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start with and as their asthma let's say progressively gets worse from mild to moderate to severe to maybe refractory what kind of Agents am I adding on in sequence or modifying in sequence because you may get a question on this
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so you have a patient whose first one very mild you're going to start them on a short-acting beta Agonist and it's just PRN so you only do this PRN so whenever they're having little kind of like wheezing episodes shortness of
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breath maybe a tight chest take a hit a couple puffs of your Albuterol and see if that provides Improvement if it does you can stop there if the patient comes back and says hey I'm still doing my albuterol I'm using
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it a lot and I'm still not getting any better I'm still having wheezing I'm still having shortness of breath I'm still having some tightness in my chest what can I do now then the next thing we can do is we can escalate up the
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treatment and we can add something on well we would add on next is we would add on very low dose inhale corticosteroid so we would start off you can still have a Saba use that in during your exacerbations but every day I want
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you to take a low dose of an inhaled corticosteroid which are going to represent as a down arrow and halocorticosteroid if the patient continues to get worse despite that then what you can do is and say okay you're coming in you're being
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used in your albuterol when you need to yeah you've been taking your inhaled corticosteroid the low dose every day yep okay now we're going to do is keep doing that Saba whenever you're having symptoms but what we're going to do is
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is we're going to add on a long-acting beta Agonist so now we're going to add on for motorol salmeterol volanterol to your actual daily regimen so now you're going to still have a low dose inhaled corticosteroid but we're going to add on
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a long acting beta Agonist to that okay then from there patient comes in says hey I'm still getting worse I'm still having these problems you're still using your Saba yep you're still using your low dose and helicorticosteroid in your
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lava yeah okay up the dose of your inhaled corticosteroid to a medium dose and keep doing the lab every day so then we're going to go to a medium dose inhale corticosteroid and we're going to keep using the lava patient comes and
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says hey I'm still having worsening symptoms okay dang it all right let's increase the dose of the inhaled corticosteroid keep the lab and keep using your Saba as needed so then we're going to do a high dose and hail
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corticosteroids and we're going to keep the lab up patient comes in and they're saying hey man I've done everything he asked me to do and I'm still having these worse wheezing and shortness of breath and you know difficulty being able to breathe
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this tight chest what do I do okay what we're going to do is we're going to keep the inhaled corticosteroid a high dose we're going to keep the lava but I'm going to add in a oral steroid and they should be able to tolerate this
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oral steroid because in these patients they shouldn't be so they shouldn't have such an acute asthma exacerbation where they can't actually even breathe or speak in between sentences if you have a patient who's having difficulty being able to speak in full sentences that's
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an acute asthma exacerbation and from there we're going to do something like an IV steroid again short acting beta Agonist magnesium and again trying things like ventilation support now if a patient goes through all of these in state step five and in Step six
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we may consider an additional thing that we can add on especially if the patient has allergic asthma if they have allergic asthma and step five and step six you can add on something called a malism map because this can be used in severe
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refractory Asthma as well as asthma which has some type of allergic component to it so in step five and in Step six you can add a malazimab onto these patients if they're having refractory asthma or even better features of allergic asthma okay all
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right I hope that made sense for asthma we talked about the treatment of asthma we got one more obstructive disease talk about and then we'll get into some cases let's talk about bronchiectasis all right so let's talk finally about the
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treatment of bronchiectasis okay so we have a patient broncheck this is what's the primary issue the primary problem that I wanted you guys to remember is that the mucus there's excessive amounts of mucus that they have very productive
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very foul smelling blocking up the Airways so one of the most important or easiest ways to remember these is going to be mucolytics and we'll talk about that but the other problem is that they have bronchospasm right so they have
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some degree of bronchospasm so we'll talk about ways that we can bronchodily reducing the bronchoconstriction but I want you guys to remember what was the primary trigger so obviously for asthma we avoid the particular triggers the pollen the animal duster dander the
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particular types of things that may trigger an exacerbation of an atopic dermatitis allergic rhinitis or an allergic asthma exacerbation staying away from getting viral urtis not running in the cold maybe trying to improve our gerds staying away from beta
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blockers staying away from aspirin etc for COPD not smoking those are the things that we can avoid for patients who have bronchiectasis it's trying to treat the underlying disease and what was one of those that I told you was
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really important cystic fibrosis unfortunately you can't reverse that you can try to be able to manage the symptoms which is what we're going to try to do when they have bronchiectasis managing the symptoms for other situations like primary ciliary
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dyskinesia cardiganer Syndrome again there's nothing we can do about that we can't reverse that it's already happened it's a mutation for other situations like things that we can potentially fix like if you have a tumor that's protruding into the Lumen of the bronchi
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you might be able to remove that tumor if you have a foreign body you might be able to remove that foreign body if you have an extra luminal tumor that's compressing like a lymph node tumor compressing on there maybe you can
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remove that and that will allow for mucus to be able to you know be expectorated and prevent it from building up right if it's chronic inflammatory situations like allergic bronchopulmonary aspergillus treated with antifungals if it's a systemic inflammatory disease put them on
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steroids or dmards to improve that disease so treating the underlying disease is definitely the thing that's going to prevent the further worsening and progression of the disease but it has to be something that can be potentially treated or reversed
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we've done that then we talk about ways that we can help to be able to reduce bronchospasm it's straightforward it's everything we talked about before same thing for COPD what do you want to do we want to give
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drugs that antagonize the M3 receptor which helps to decrease the bronchoconstriction we want to give agonists that stimulate the B2 receptors beta 2 receptors that actually help too bronchodilate the same concept if it's short acting you would give albuterol if
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it's long acting at some Adderall from Motorola okay if you want to be able to work short acting and block the M3 receptor it would be a petropium if you want long acting it would be titropram very straightforward the whole point is
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to bronchodilate reducing the bronchospasm in these patients the next thing that I want you guys to understand is that these patients have very high risk of infections these bronchi are getting so clogged up with mucus that it creates an opportunity
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initis for bacteria not to be able to be moved through those bronchi and be expectorated and so it accumulates accumulates accumulates and then leads to a nasty infection and so these patients are very very high risk for pneumonia and so what do we do to be
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able to reduce their risk for even further exacerbations pneumonia and therefore leading to high mortality rates well one of the things that we can try to be able to do is make sure that we maybe give them vaccines that prevent
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further chances of having infections due to the most common pathogens that are bacterial and viral same thing we would do for COPD make sure that they get their pneumococcal vaccines that they don't develop a pneumococcal pneumonia and then also make sure that they get
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their influenza vaccine to make sure that they don't get some type of pneumonia due to influenza remember influenza especially in elderly patients increase the risk of staphylococcus aureus pneumonia so this is an important thing and then because there are high
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risk of pneumonia what did I tell you was the primary pathogen was this scary pathogen especially in cystic fibrosis patients they have very high risk of pneumonia secondary too pseudomonas so you have to be able to consider that
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that when you're giving them antibiotics it has to be antibiotics that are guided towards pseudomonas and if you're unsure about the particular pathogen what would be a way that you could test for the pathogen that could be causing that
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pneumonia maybe consider plus or minus some sputum cultures to be able to test for what type of pathogen it is after you start them a more broad agent you can narrow it down to whatever the pathogen may be but on
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your vignettes clinical vignettes that you're going to see on your exam it's most likely going to be pseudomonas so remember the antibiotics that you can use to treat pseudomonas okay the next thing that we'll talk about is called hemoptysis so with
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hemoptysis coughing up of blood in these particular patients why does this happen remember I told you it's because they have so much inflammation that's eroding through the thin bronchial walls that it just chews into the bronchial blood vessels and causes them blood to
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actually enter into the Lumen of the bronchus and then they cough up that blood what if I had an ability to either resect out the disease section so what if I could actually take and resect out this disease section that could be one
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particular way so I could do a very specific type of lung resection of the most disease portion of this patient who has bronchiectasis or what I could do is I could take a catheter find the bronchial vessels that are
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actually being eroded into and the ones that are feeding into the Lumen of this bronchus and I could embolize it and if I embolize it I prevent further blood from being able to enter into this Lumen and I stop the actual hemoptysis this is
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called bronchial artery embolization bronchial artery embolization and these are some of the things that we can do to these patients here so again what I want you to remember is the same kind of cause up here treat the underlying cause
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give Bronco dilators to produce bronchospasm prevent further infections by giving the vaccines and treating their potential exacerbations or high risk of pneumonia what's the big pathogen not forget pseudomonas originosa and again prevent kind of episodes of hemoptysis such as bronchial
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artery embolization or resection of the massive disease segment in these patients or bronchectasis what else what was the big thing I told you for these patients they're a high mucous production we can give them drugs that'll break up that mucus and make it
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easier to expectorate preventing that chronic inflammation let's talk about that all right so for mucolytics for these patients it's basically the whole design is to be able to break up the mucus and make it easier for the patient
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to expect to remember they got thick mucus right whether it be due to the Cilia being problematic whether it be the thick mucus due to cystic fibrosis whether it's because you have some type of obstruction of the airway or whether
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it be due to chronic inflammation regardless of the cause we need to be able to make sure that we provide good hydration to the patient if we hydrate the patient we might be able to push more water are into these actual
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secretions and if you increase the water in the secretions it may thin them out a little bit and help to be able to make it easier to cough them and move them along so they're not obstructing the airway the other thing is chess PT so
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this could be due to like many different ways one it could be vest therapy so sometimes they put this vest around the patient and just have it like beat the patient's chest a little bit to be able to kind of help the expectorate or break
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up some of the actual mucous secretions you can literally like turn the patient on their actual stomach and then kind of hit their back a little bit any way that helps to be able to kind of move like
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postural drainage maybe laying in a particular position having giving some hits and beats onto the chest can help to be able to move some of those secretions and break them up and make them easier to be able to cough up
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the other ways we can give nebulizing medications so one of them is called in acetylcysteine in acetylcysteine is a really interesting drug that basically helps to be able to break up certain types of bonds that are in the mucus
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that make the mucus strong it helps to be able to break up some of the disulfide bonds and all those things that make the mucus really tough and thick and by doing that it thins the mucus out a little bit and the other one
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is we can give hypertonic saline nibs so three percent hypertonic saline nibs and what this does it helps to be able to kind of draw fluid into the secretions as well thin them out and make them easier to expect a rate so these are
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things to remember for the mucolytic function one hydrate two physiotherapy maybe that's someone beating on the back of someone's chest and having them lean forward to allow for postural drainage or putting like a vest on them that kind
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of like beats their chest continuously for a certain amount of time to break up some of those actual secretions make it easier to expectorate and give them nebulizer treatments of things like enocl system which breaks up disulfide bonds within the actual mucus making it
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thinner easier to expectorate or three percent hypertonic saline nibs which pulls fluid into the actual mucus and helps to be able to thin the mucus out making it easier to expect three all right the last thing is that sometimes in
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these patients unfortunately really sad their lungs are really damaged they have lots of mucus and usually this is in patients with cystic fibrosis that there is a high chance that they may need a lung transplant so in patients with
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bronchiectus is secondary to cystic fibrosis there is a very strong chance that these patients will not be able to prevent the progression of the disease and have a high likelihood that they'll require a complete lung transplant all right my friends we did it even
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though this took a massive amount of time and I'm so exhausted I I we did a really good job by covering all this information but believe it or not we're not done we got to get to the cases we
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got to really understand the stuff even more so head on over and let's do some cases on obstructive lung diseases all right fam we're gonna go ahead and do some cases now on some obstructive lung diseases let's see if we guys can we can
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all come together and really understand this topic now so we got first case 75 year old male presented an engineering Clinic with dyspnea so shortness of breath and his usual productive cough that he's had for about more than three
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months for the past two years consecutively it's a very high clinical year Pearl there was it does that kind of like lead me to think COPD but which one more predominantly more likely chronic bronchitis predominance all right past medical history hypertension
Speaker A
tobacco use tobacco use is going to be one of the most common causes for patients with COPD like chronic bronchitis and emphysema okay cool physical exam we go to examine the patient and what do we appreciate well first thing is when we go we actually
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use our stethoscope we listen we hear some inspiratory wrong guy so whenever they're taking a breath in we hear kind of like a snoring respiration kind of within their Airways and then we ask them to cough and it kind of disappears during
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expiration we hear some wheezing that's one thing okay so inspiratory ronkai wheezing so in the expiratory Wonka is probably telling me in the expiratory wheezing is tell me that there's some kind of like mucus that's accumulating within the airway or some type of
Speaker A
narrowing of the airway that's obstructing the airflow in and out they have abdominal obesity so they're a little bit puffy they also have some jvd Peter demon a paddle magley what did I tell you on the Whiteboard that those
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three things plus abdominal obesity due to the diaphragm hyperinflation pushing the diaphragm down kind of pushing the abdominal contents forward giving this patient that puffish type of look um what does this usually signify those blue bloaters due to right side heart
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failure right so core pulmonal so this is kind of showing me core pulmonal hyperinflation pushing the diaphragm down to getting that abdominal obesity look okay definitely again more supportive of chronic bronchitis because you don't see corepolinal too often and emphysema
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until it's in the late severe stages Vital Signs hypoxic right so 86 they're definitely hypoxic at rest without any kind of like supportive supplemental oxygen on them respiratory rates 26 so just a little bit decapnic um heart rate's 104 so they're slightly
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tachycardic and then blood pressure is just you know just a Teensy bit below the actual elevated point of uh 140. so I'd say with that being said main vital concerning science is a hypoxemia myotagipnia and a slight tachycardia
Speaker A
okay let's move on to the next thing so given tobacco use which obstructive disease do you really suspect out of all of these so again we got to go back is it asthma is this bronchiectasis or is this some
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type of like COPD where it's chronic bronchitis or emphysema or kind of like a mixture of the two it's sometimes really difficult to be able to kind of point out that that kind of like mixture oftentimes they do coexist but we're
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trying to be able to separate them to some degree and I don't think it's asthma and the reason why is that this patient is relatively older asthma can present in older individuals but how commonly you're going to see it in
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younger individuals and usually they don't have this like productive cough for three months out of the two years it's usually episodic right so I don't think it's that one bronchiectasis it could be they do have a productive cough
Speaker A
um it could be that it's hard to say but I don't you know think that it's necessarily the case because usually what I told you guys to think about is it's usually that purulent foul smelling type of cough that they have
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um with the nasty smelling sputum um I didn't really mention that there so it still could be that but you know I'm kind of leaning more to like a COPD and between these I think it's more of a
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blue bloater type of appearance chronic bronchitis and emphysema so we could say it could be chronic bronchitis could be bronchiectasis maybe we need a little bit more information but really parse out which one of those is but I
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definitely think it's more likely a COPD or than a bronchiectasis kind of patient okay and again bronchiectasis remember you got to think about those cause it's going to be a tumor could it be a form body could it be a primary ciliary this
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kinase or cystic fibrosis usually you'll see those a little bit in the younger ages um so or is it kind of like a chronic inflammation of the airway or systemic inflammation so I do definitely think this is a more supportive
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um of COPD chronic bronchitis predominant but we can still think possibly bronchioactic this all right let's move forward again we kind of like really put together this really interesting concept that whenever they have that really high pulmonary artery pressure due to the
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intense conveys or constriction of the pulmonary vessels due to multiple alveoli kind of being hyperinflated or not actually being utilized during ventilation they can get this intense pulmonary vasoconstriction um because maybe the alveolar are plugged up or they're not actually
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ventilating the alveoli properly because there's lots of mucous plugs and bronchoconstriction so either way those ventilation to the alveoli is poor and so you want to decrease the perfusion of those alveoli so you cause pulmonary artery vasoconstriction that increases
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the pressure in the pulmonary arteries puts a lot of stress on the right Heart Right heart failure ensues and then develop jvd hepatomegaly and pitting or pedaledema all right boom roasted with that one all right next thing here
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is when we talk about these patients other complications that they're definitely at risk for besides core pulmonal chronopharyngitis wise is there at high risk of pneumonia right we said that if you have these mucus that's accumulating within the bronchials all
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of the mucus I'm sorry that mucus that's blocking up the bronchioles you're supposed to be able to clear bacteria right through those bronchioles up via the Cilia well if you have this big kind of like occlusion or obstruction within
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the airway you're not going to be able to get that bacteria cleared from the bronchioles and so what happens is they can get locked up in these small little alveoli and bronchial areas and lead to an infection and that can lead to
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pneumonia the other thing is because these patients do develop pretty good hypoxemia that hypoxemia over time if it's chronic will tell the actual kidneys to start pumping out something called erythropoietin and erythropoietin will tell your bone marrow to pump out more
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red blood cells so the other thing I would see is if I did a CBC I may see some increase in their hemoglobin increase in their hematocrite increase in their red blood cells so-called polycythemia all right well if we really
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want to diagnose this patient with a COPD and differentiate them from chronic bronchiectus I would start from bronchiectasis things that I would really really would want to know is okay let's do some pfts pfts would be great because it also helped me to really
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discern if this is restrictive versus obstructive especially if the picture is a little bit confusing so when I do the pfts my patient has a low fev1 and a relatively low FEC so when we put the ratio between these the fev1 is more
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significantly decreased so it drops the percent ratio to less than 70 percent we know that whenever the fev1 over FEC is low less than 70 some books will say less than 80 percent it's more suggestive of an obstructive where if
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it's normal or high it's restrictive so automatically I know that it's obstructive plus I can also see that the residual volume is really high in total lung capacity is high so they're likely having a hyperinflated lung due to an
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obstructive cause well the next thing I can do is I can actually check the dlco this in terms of the diffusion capacity across the alveoli this can be somewhat helpful in Discerning is this some type of you know
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emphysema or is it asthma or is it COPD I'm sorry it's a chronic bronchitis so generally I know that it's obstructive right when I have a dlco that is decreased usually it could be suggestive of one specific type of COPD you guys
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remember emphysema they have such a decreased alveolar surface area that it really drops the dlco because remember surface area is directly proportional to the dlco so if you if you actually cause a decrease in the total lung surface
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area you'll decrease their dlco whereas in asthma they might have hyperinflation in a slightly increased or moderately slightly to moderately increase the lco and sometimes that can actually increase I'm sorry a small to moderately increased surface area which may
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increase their dlco so you can actually see a normal to slightly increase the lco and Asthma but again I think that in this patient's population here we see a decreased lco so we may see that this might be kind of like an emphysema or
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some type of again chronic bronchitis type of case but again usually decrease the lco could be suggestive of COPD but if you're really looking to be more specific it's the emphysema predominant in that case all right but here's the real
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interesting test that we can do we can give the patient a bronchodilator when we give them a bronchodilator what this will do is tell us the degree of reversibility so remember asthma is reversible to bronchodilators so you can
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actually get their smooth muscle to relax a little bit dilate open up the airway and improve their expiratory volume so if it's COPD though that's relatively irreversible the damage is done their smooth muscle is not really going to react very well and then dilate
Speaker A
enough to increase their expiratory volume significantly so we do is we do a bronchodilator test after we've done this pfts and then look at what happens to the fev1 their expiratory volume within the first second if it increases
Speaker A
greater than 12 percent it suggests a reversibility like asthma if it's doesn't it suggests more of an irreversible type of COPD picture alright so this is again supportive of more of a COPD rather than asthma picture CBC again did show polycythemia
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supportive of more of that chronic bronchitis type of picture the echo supported more of a right ventricular hypertrophy which again suggests of more of the core pulmonale which is in the chronic bronchitis feature now again abgs aren't super helpful in these
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patients because oftentimes you can look at their exam and determine that but it can be somewhat helpful if you're concerned about a CO2 Narcosis or the patient being in an exacerbation of some type and they're super obstructive they're just not clearing their CO2 and
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their level of mental status is declining significantly but sometimes in this patient it's pretty obvious they were breathing relatively fast so I would expect that they're probably going to have some degree of like a respiratory alkalosis but here's the
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thing they may always breathe fast so in these patients it's likely that they have a chronic respiratory acidosis and copders it's usually a chronic respiratory acidosis and they likely always have a compensatory response which is for their kidneys to be able to
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respond to that so if you're acidotic you're going to want to be able to reabsorb bicarbonate excrete protons and so you would expect that their bicarb would go up to compensate for the high CO2 so oftentimes these patients are
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usually chronic respiratory acidosis with metabolic compensation all right so how do I start my treatment process for these patients well you got to address the issues for these patients with COPD one is you obviously have the patient to address the bronchospasm
Speaker A
there's a lot of inflammation within the Airways and this inflammation definitely causes a lot of bronchospasm so one thing I can do is start bronchodilators in the acute situations I can do short acting ones so things like Albuterol and
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ipritropium usually as a duaneb combo or I can do long-term outpatient management with a long-acting one so something like some metal for motorol volanterol or a llama which is a muscarinic antagonist and that would be something like diatropium
Speaker A
the next thing I'd want to do is reduce the inflammation so sometimes these patients May benefit from inhaled corticosteroids especially in use with a lab or a llama and if they're really having an exacerbation and really having a difficult time breathing and clearing
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out their CO2 we can consider things like steroids po if they're able to tolerate it IV more likely if it's a severe exacerbation to really reduce that inflammation but there's three particular things that I really think are really important to
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remember for these patients because they have been shown to reduce mortality smoking cessation obviously one of the primary things here is that this patient is a tobacco user so because of that it increased their risk of worsening damage
Speaker A
if you get them to stop you can at least prevent someone of the progression of the disease oxygen therapy is key remember spo2 less than 90 they have core pulmonal and they have polycythenia in this situation you start them on
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oxygen therapy maybe two to three liters uh for about a good chunk of the day 15 to 16 hours in the day that they're going to be on O2 so again a very very very important concept here and again if
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they don't have core pulmonary or polycythemia then it's less than 88 spo2 or less than um 55 on their ABG and then the other thing is vaccination vaccination is the only other one that also against influenza and particularly
Speaker A
the pneumococcal vaccination that reduces the mortality from pneumonia so these would be the big things to not forget all right let's move on to our second case 18 year old female presents to the engineer Clinic with dyspnea difficulty
Speaker A
speaking and full sentences dry cough in a very tight chest they have a past medical industry very particular for pet dander allergy with a recent viral upper respiratory tract infection and some exposure to a dog that's probably where
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they got that dander allergy so because of that I'm thinking that this is more asthma just because they're younger they're presenting with an episodic type of appearance where they have dyspnea difficulty speaking of full sentences so it's likely an asthma
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exacerbation a dry cough and a very tight chest the tight chest is a very a very concerning sign for asthma plus here's their triggers think about their triggers it's either allergic so some type of allergy to something pet dander
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you know maybe some type of um pollen again a lot of different things of that nature drugs whatever it may be and then again think about the atopic Triad as well so think about those patients with allergic rhinitis atopic dermatitis and
Speaker A
Asthma as well um the other thing is that what's the big triggers that are non-allergic would be viral upper respiratory tract infections so some type of cold air exercise gerd beta blockers things of that nature so I think that this patient and then
Speaker A
don't forget Sanders Triad which is that Triad of nasal polyps aspirin sensitivity and asthma but I think this definitely seems like asthma but let's go ahead and take a look here at their exam when we look at their exam we definitely see that they
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have wheezing when we're also taking the chest especially during exhalation we see a lot of nasal flaring really trying to be able to have accessory muscle use so neck muscles abdominal muscles to help them to be able to breathe so you
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see an increased worker breathing plus they're having difficulty speaking of full sentences so I definitely see a very degree of respiratory distress due to them having to work really hard to augment their breathing Vital Signs spo2 is they're hypoxic so 30 82 percent at
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rest with no oxygen on them and then respiratory rate is 36 so they're to kepnic they're really really working hard to breathe right now heart rate's 144 so they're tachycardic and then their blood pressure on inspiration is 88 over 46 and during expiration it was
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noted to be 108 over 52 which is relatively interesting because there is a degree of phenomenon there which if you guys remember what is that called whenever your blood pressure drops more than 10 millimeters of mercury during the inspiratory process it is pulses
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paradox so that's a common feature of asthma so definitely seems like asthma my friends okay so given off of these things the allergen exposure the viral upper respiratory tract infection and their history and physical exam I think it's
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more suggestive of asthma okay what are the other causes of asthma do you guys remember where they are we said allergens we said cold air we said exercise we said gerd we said beta blockers we said sampers Triad again we
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went through all of that already so how do we go about diagnosing a patient with asthma well right now we can obviously tell that they look like they're having an asthma exacerbation so pfts may not be the best situation here
Speaker A
but let's say that in the perfect world that this patient came in and we were able to somehow get pfts on this patient if we did we would see the same thing that we just saw in the COPD picture
Speaker A
that they would have a low fev1 over FEC we see a drop in fv1 we see a drop in their FEC ratios less than 70 percent and we see an increase in the residual volume in total lung capacity oftentimes
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something that we do in an emergent situation is we do something called a peak expiratory flow rate we'll use a peak flow and we'll look for their Peak expiratory flow rate to be very very low in these patients so that might be
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something that you do at bedside and then really these rough situations they won't be able to Exhale a lot of air if you were to be able to get this patient to do a dlco what kind of testing you would see that it could be
Speaker A
normal to a slightly increased dlco whereas if it's decreased it could be a more suggestive of COPD which one more predominant emphysema more predominant here's the best thing though to also consider if you were to give this patient a bronchodilator like Albuterol
Speaker A
and then measure their pfts afterward you would notice that they are reversible that they have a massive increase in their expiratory volume after getting a post-bron after getting a bronchodilator that actually increases their fev1 to greater than 12 whereas in
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COPD it did not increase greater than 12 percent so that's a big thing to remember so sometimes what we'll do is if the patient you're not usually in an exacerbation doing this you're doing a peak flow so you have them take this
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little like little apparatus take them have a deep breath in and then breathe out into the peak flow and it'll generate a volume and then you'll estimate that based upon age gender you know a lot of like uh kind of
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standardized things based upon that you're giving a bronchodilator and then after the bronchodilator you should expect that their expiratory volume within the first second should increase and so then what you'll do is is you'll have them come back and then take another blow at that
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Peak flow and see if it improves and you'll check the volume changes and so usually in those patients you would expect that their Peak flow would be low Peak expiratory flow rate will be low after the broncholide dilator you'll
Speaker A
expect an increase in their Peak expectatory flow rate now if the patient did not have any symptoms they came in and that they had you know prior episodic you know situations and they came in outpatient you wanted to test them to see do they
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have a degree of inducibility can I provoke the bronchi um smooth muscle to really raise a bronchoconstrict in response to a particular medication more than normal people would and so what we do is we do something called a methylcholine
Speaker A
challenge that's we've given this drug called methylcholine which is a cholinergic Agonist so to bind onto the muscarinic receptors and cause bronchoconstriction and so if it causes bronchoconstriction and a normal person it wouldn't cause that much difficulty in breathing but in a patient
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with asthma they're very hyper responsive and so they respond to it and they intensely block a constrict that it drops their forced expiratory volume more than 20 percent after that test and so that's a really really big one to
Speaker A
remember to induce a bronchospasm and again in these patients what will the ABG show I would likely say that this patient is working so hard to breathe that if I were to look at it it's probably respiratory alkalosis they're
Speaker A
breathing so hard they're clearing off their CO2 that it's just causing their CO2 in the blood to drop okay a question that I think would be important to add to answer is that what if the patient stopped really like
Speaker A
moving a lot of air they're you know obstruction continues to get worse that the ability that the chest became silent and they weren't able to Exhale air out of their actual chest then CO2 is going to build build
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build and they'll start having a respiratory acidosis that would be a really concerning one all right tell me that they're either fatiguing out or that they're obstructing their Airway almost completely so how would I start this patient off
Speaker A
well acute acutely you know we're going to start off a bronchodilator Saba so again albuterol is going to be the big thing give them IV magnesium because that'll also bronchodilate the area as well IV steroids because they can't even
Speaker A
speak in full sentences there's unlikely they're going to be able to tolerate taking appeal Med and then put them on BiPAP BiPAP would be a great thing to be able to kind of really help with clearing some of that
Speaker A
CO2 generating higher pressure within the Airways to in you know help to reduce the patient's work of breathing so this would be the best thing to do and if they fail BiPAP you can intubate them with endotracheal tube intubation
Speaker A
but for managing these patients outpatient wise I think it's important to notice the stepwise fashion so you start off with you know kind of this basic kind of regimen here where a patient comes in you start off with a
Speaker A
Saba okay they continue to get worse add-on inhale corticosteroid at low dose oh they continue to get worse add on a medium dose inhalocorticosteroid and then maybe add on a lava you know oh they're still getting worse okay then
Speaker A
you know you can increase their dose of the the inhaled corticosteroid and then add on a lava you can increase their dose of the anacorticosteroid add-on lab increase their dose of inhale corticosteroid add an oral corticosteroid and then again continue
Speaker A
with the lava so I think it's important to remember that stepwise fashion for patients that as they continue to get worse and you've tried things a patient comes in they start off I'm having shortness of breath some wheezing okay
Speaker A
start off with and albuterol every time you eat it use it okay I'm still using it a lot I'm not getting any better add-on in a hill corticosteroid so B that's an ivy with the flu ticker Zone something of that nature then okay I've
Speaker A
used that doesn't work okay well then add on a lava okay that didn't work okay I don't increase the dose of the nail criticus if that didn't work increase the dose of inhale corticosteroid oh that didn't work I don't know oral
Speaker A
steroid okay that actually did work so those are the things to be able to consider and it's important to be able to make sure that you either increase in a stepwise fashion to get them to the point of where they're having good
Speaker A
response and then if possible if they're on the highest type of Step here see if you can step down to reduce the amount of medication load that they're on possibly okay so these are big things to think about now to make it easier for
Speaker A
all these other kind of like Alternatives usually the best situation that you maybe asked on the exam is which medication is best for exercise induced asthma or aspirin-induced asthma that you can consider as an alternative throughout these situations and the best
Speaker A
answer would be your Montelukast okay the other one would be which one would be best for prophylaxis against those who have exercise induced asthma and you would say chromal and sodium okay and then the only other one that I
Speaker A
would actually add on here is that if a patient has severe allergic asthma or refractory asthma then you can consider a malazimab okay a severe allergic asthma that is refractory to a lot of these therapies you can add on a malice
Speaker A
map all right beautiful so the next case here in the last case is we have a 39 year old male presented an engineering Clinic with severe Disney and Mild cough past medical history of non-alcoholic cirrhosis actually this is
Speaker A
not the last case we got another one after this one all right so interesting patient here they're young and they have a very severe dyspnea mild cough and a past medical history of cirrhosis not due to alcoholism they actually couldn't
Speaker A
find an etiology for it when we look at this patient they have a very interesting type of appearance they have a barrel chest very thin cactic appearing type of look they also have decreased breast sounds on their bilateral chest walls whenever you're
Speaker A
trying to auscultate and then they have expiratory wheezing okay very interesting vital signs not very hypoxic at rest slightly very slightly to kipnik rh-84 so normal and blood pressure is pretty normal okay nothing crazy there off their physical exam other than just kind
Speaker A
of what looks like more of a pink puffer type of appearance wouldn't you agree when you have those patients who are per slip type of breathing they're very thin cactic appearing they have barrel chest log they have deep Express sounds
Speaker A
definitely more suggestive but here's one of the interesting things with patients who have that emphysema type of look you usually see it in those who are smokers and really old this patient's really young so what did I tell you to think about in a patient
Speaker A
who's less than 45 years of age has an underlying liver disease and really no tobacco use they may have tobacco use it doesn't necessarily mean that it can't also be smoking but given the patient maybe has really no tobacco use they do
Speaker A
have liver disease they have less than 45 years of age and now that looks like they have like an underlying COPD what did I tell you to think about Alpha One antitrypsin deficiency right for the COPD cause so I really think
Speaker A
that this is emphysema but I think it's alpha-1 antitrypsin deficiency so whenever you think about that you think about something very interesting which part of the lungs is most affected in patients with alpha-1 anti-trips and deficiency Who present with this
Speaker A
emphysema type of appearance it's panlobular so that affects more likely the bases of the lungs so I'd see that more in the bases of their lungs that I would see these emphysemitis changes as compared to those who smoke which would
Speaker A
be more the Apex is a upper low predilection right with that centrilobular emphysema all right very interesting and then what is a very important complication I want you guys remember from emphysema because they get all these like belay these like
Speaker A
very like large kind of like alveolar kind of like a bronchiole or kind of like really dilated look of a lung parenchyma they're very high risk for popping and causing a pneumothorax so don't forget that as well all right so when we go through
Speaker A
Diagnostics we don't need to do this we've already understood that this is an obstructive disease it should be a low fev1 over fvc okay dlco it's likely going to be decreased especially this one okay more likely emphysema predominant you're going to see a
Speaker A
decrease dlco not so much in chronic bronchitis post bronchodilator we know that they're not going to reverse it's going to be less than 12 percent what will the ABG show likely a chronic respiratory acidose with metabolic compensation same thing for copders
Speaker A
now if we were to do a like a chest x-ray or a CT scan of this patient you would definitely see that this patient would have very like hyperinflated lungs you would see some boli and the emphysemidis changes that would be
Speaker A
involving more of the bases of the lungs and what else will we test this patient send off what particular enzymatic test the alpha-1 antitrypsin deficiency so you would check to see if is there alpha one anti-tryption kind of mutation
Speaker A
they're present how would I treat this patient just as you treated the patient who had the chronic bronchitis so if it's an exacerbation Samus or sabbas if it's long-term lamelaba inhalocorticosteroid if it's an exacerbation ivrpos tell them to stop
Speaker A
smoking tell them to use oxygen if they meet the particular requirements less than 88 for this patient Plus or less than 55 millimeters of mercury of their ABG okay they don't have Corporal manal they don't have bios polycythemia so we
Speaker A
wouldn't go with the lower Target like less than 90 or less than 60 AVG and then make sure they're vaccinated because smoking cessation oxygen vaccination are the things that lower mortality all right last case 12 year old male
Speaker A
presents the ninja Clinic with Disney and productive cough with foul smelling sputum has a medical history of cystic fibrosis likely bronchiectasis that's how they're going to present in this exam so whenever you go ahead and examine the patient they do have nail clubbing they
Speaker A
have some inspiratory ronkite and expiratory wheezing lots of mucus that are kind of obstructing the air flowing in and air flowing out slightly hypoxic at Romero at rest they are slightly tokipnik normal heart rate normal blood pressure what should we think given the cystic
Speaker A
fibrosis which obstructive disease do you think it is it is bronchiectasis so what are some of the other causes of bronchiectasis remember I told you the Cilia ain't working it would be primarily cellular dyskinesia if it was some type of like situation where they
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weren't actually making a very thin mucus the mucus was super super thick due to the chloride channels being altered not pushing chloride into the mucus not pulling water into the mucus that would be cystic fibrosis if there's something obstructing the movement of
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mucus that could be a tumor form body or if there's just a massive inflammation of the airway due to it being systemic like r-a-s-le or a fungus within the airway like allergic Bongo pulmonary aspergillus that would be the causes
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what other organs does cystic fibrosis usually affect which ones did I tell you guys to think about meconium ileus pancreatic insufficiency and some degree of patients who have insterility particularly males okay uh or infertility I apologize the two
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complications that I wanted you guys remember in bronchiectasis is that because the mucus is really chalked up within those Airways and it causes so much inflammation and it can start causing bronchodilation and just the inflammation can wear and wear and wear
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through the Airways where it erodes into the nearby bronchial blood vessels and can lead to hemoptysis the second thing is that all that mucus chalks up the airway and blocks bacteria from being cleared from that mucous area just
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distal to that kind of mucous plug and so it creates a nice for infection so pneumonia would also be a very important complication as well how do you treat patients who have hemoptysis what do you do bronchial artery embolization or
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resect the really disease segment out all right Diagnostics it's the same my fam we have a low fev one over FEC ratio it's the same thing with every obstructive lung disease the DLC is going to be normal okay or the chess CT
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show this is the real big thing if you look at these patients you're going to see very dilated bronchioles so you see kind of like that you'll see like this really large thick dilated bronchial in this view called the tram track sign so
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these are big things to be able to consider so just looking at these again highlighting it there's your kind of tram track lines the other thing is you may see the Signet Rings which are like the dilated bronchials with like a
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nearby like pulmonary vessel off the edge of it so those are big things to think about for these patients how do I treat them well think about it start with the most important thing treated the underlying cause what's the
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underlying cause cystic fibrosis you can't really reverse that the only way to be able to stop this is to get a lung transplant and then supportive care is going to be the big thing so help to dilate those bronchials that are really
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kind of inflamed and hyperspastic and undergoing bronchospasm with bronchodilators mucolytics to really help to clear some of that mucus from the Airways to prevent hemoptysis to prevent pneumonia and other complications so hydrating them keeping the mucus kind of like thin chest PT so
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kind of beating on the chest postural drainage things of that nature to clear up some of that vest therapy all of those things and then sometimes nebulizers that'll help to really thin up the mucus making it easier to cough up so three percent
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hypertonic saline Solutions are nebulized and acetyl cysteine which really helps to break down some of the disulfide bonds in the mucus and then a big thing is to prevent them from developing infections so vaccinating them against pneumococcus and against influenza and then remember
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if these patients do develop pneumonia which they are at very high risk for you need to give them antibiotics that will cover pseudomonas Originals so that's a big high yield fact all right my friends next thing that we'll do is we'll talk about restrictive
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lung diseases on another lecture get there go check it out and then we'll go over some cases of restrictive lung disease uh Engineers I hope that this made sense I hope that you guys enjoyed it and as always until next time
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[Music] thank you [Music]
Topics:obstructive lung diseasesCOPDchronic bronchitisemphysemaasthmabronchiectasisalpha-1 antitrypsin deficiencypulmonary pathophysiologylung inflammationpulmonary function tests
