DIP Episode 393 - Pulmonary Pathophysiology Series 2

Okay, welcome. My name is Divine. This is episode 393 of the Divine Intervention Podcast and in today's podcast I'm going to be going to a Pominary Path of Physiology series 2. Pominary Path of Physiology series 2. So let's just jump right in. What if they give you a question about a patient? They tell you that this patient had blood area two weeks ago and that now this patient has been having a you know that they've been immobile for the last two days and now we're having shortness or breath. What's going on there? Maybe they give you some other stuff in the question that tell you that you know they have like a pomodal functioning the low extremities and things like that. They even ask you for your next best-step in management. What really hope you're saying? Divine, let's go ahead and get an endotracheal intuition down. This person has Guillembré syndrome, right? Remember Guillembré syndrome? It has a strong association with an infection on Campilo-Bacteria G. J.9 but to be honest with you for imbimic sample purposes you just want to be careful about just thinking it's only C. J. J.9. Pretty much every mucus of infection, so you can be a respiratory infection, can be a lung infection, can be a GI tract infection, can precipitate Guillembré syndrome. So this person, there is in the way mobile, right? Obviously Guillembré syndrome is a problem with your shuan cells. So you must have the shuan cells, you're going to have demolination, right?

They have a symmetric ascending paralysis. So they will not be able to use the other extremities but it's going to keep going going going going going going, right? And you can have that for a chronic paralysis. When you have that that's obviously not a good thing. So your next best step for this person is endotracheal intubation, right? So how does all of this relates to pulmonary pathophysiology? Or remember the diaphragm is important. Every now and then our friends at the imbim is they're throwing some diaphragm questions on exams, right? It's literally a muscle that is involved in both inspiration and expiration. Whenever you're doing quiet inspiration and expiration, for the most part your diaphragm is the thing that's helping you out. Now remember the diaphragm don't forget that it gets its nerve supply from the frenic nerve, right? So you probably remember the pneumonia C345 keeps the diaphragm alive, right? So it gets its innervation from the frenic nerve, right? So during inspiration your diaphragm is going to go down, right? During inspiration your diaphragm goes down. If you think about it, if you remember bones law from chemistry in college, since your diaphragm is going down, your thoracic cavity volume is going up. If volume is going up, then pressure should come down. Remember volume and pressure for the most part are inversely related. So the pressure, intrathoracic pressure goes down.

That's why venus return increases when you take in a deep breath, when you inspire. So mobile load is going to come to the right side of the heart. Because again, the intrathoracic pressure is down because the intrathoracic volume is up because the diaphragm has been depressed, right? So again during inspiration your diaphragm goes down, during expiration your diaphragm goes up, right? And one thing our friends at the imbim is love to do is they love to give you sometimes they will give you an image and you notice that wow, one diaphragm is much higher than the other, right? That's a pretty classic presentation of a person having diaphragmatic paralysis on imbimim exams. Again you can get paralysis of the diaphragm if you have a long cancer, right? That has involved the bricchio plexus like you know something around C345. You can have paralysis of the diaphragm if you have the ombariz syndrome, right? So those are just all things you want to keep at the back of your mind for purposes of imbimim exams. Now the thing is with pulmonary pathophysiology I think one thing that's always helpful is being able to understand like the earways and things like that and how drugs affect them. You may notice you may be like wow, define this, what guess is kind of odd in its direction, right? But again the thing with poem most times on imbimim is if you have the understanding almost everything is like easy to learn.

poem is one of those things where memorization is not going to get you far at all. You know maybe the long infections but other than that really like poem is something where you either the study or you don't understand it. So I will say probably the primary pulmonary disease you want to worry about in terms of treatment of pharmacotherapy, right? It's COPD and asthma, right? So maybe let's hit up asthma first. So we know that asthma is characterized by episodic reversible bronchoconstriction. Episodic that's one so it doesn't happen all the time. Reversible that's two bronchoconstriction that's three, right? Episodic reversible bronchoconstriction that's the big thing. And many times these people also have a lot of airway inflammation, right? And then they form all this mucus that can plug up their earways, right? The thing is if you really look at it most of the therapies for asthma are targeted towards these three symptoms, right? They have the bronchoconstriction, they have their air way inflammation and they have all these mucus plugs, right? So you target those three pathways for the most part in dealing with asthma. So remember that asthma is generally regarded as an obstructive lung disease, right? So kind of like COPD, regards COPD as an obstructive lung disease, we also do in fact regard asthma as an obstructive lung disease, right? And remember obviously you're going to find the elevated FVU, I mean the decrease or whoops, the decrease FVU want to have this ratio.

But remember the person that has asthma, if they are not having an asthma exacerbation or anything, they have a completely normal FVU want to have this ratio. So that's just something you want to keep in mind, right? That's why again, asthmatic symptoms are regarded as episodic symptoms. That's very high you to know. The symptoms are episodic, right? And one other thing that I feel like many medical students conflict is understanding that asthma is treated very differently. If you have an acute exacerbation where the patient's life is in immediate danger, they're going to be dying soon. If you don't do anything versus chronic asthma management, right? Generally in chronic asthma management, your goal is to decrease the number of attacks they have and try to keep them symptom free for as long as it's humanly possible, right? Now one physiological thing that will be helpful to understand for asthma is the metacoling test, right? The metacoling challenge test. So the thing is we know that the virus and pathetic nervous system, so metacoling by the way is a most chronic agonist. Let's put it that way. Okay, it's a most chronic agonist, right? So we know that the virus and pathetic nervous system mediates bronchoconstriction. So the thing is if you give a most chronic agonist at a very low concentration, you know, in most normally individuals that don't have high percentile airways, they don't have any problems.

But if you give it to a person that has asthma, a person that is susceptible, a person that has hyper reactive airways, that low concentration of the most chronic agonist metacoling is going to cause a profound powerful bronchoconstriction, right? You get a profound powerful bronchoconstriction, right? So even those little metacoling concentrations, they have market effects in these people, right? And I guess I'll take a quick segue before I continue talking about asthma. If you're taking step two, CK or step three, or complex level two or three within the next two, within the next few weeks, I would encourage you to attend my courses that I have this month. I have an NV Me test taking strategy scores. That's going to be from five to seven, 30 p.m. Pacific standard time. And that's going to be on Friday. That's literally two days from now. It's going to be held over zoom. And then I have a 20 hour review course taking place from Monday to Saturday next week. We're going to be skipping Wednesday, but there's going to be a Monday Tuesday. Thursday, Friday and Saturday from five to 90 in Pacific standard time. It's just going to be four hours each day. Again, I've had a ton of people take these classes. They've done really well. In fact, I get emails from people almost all the time, especially on Wednesdays like today. Oh, wow, divine. I attended your course. Well, my score bumped up 30 points, 40 points, right? I've had people do really well. And then I have a disk school.

Remember, I made a special podcast just on that, the 75-hours step 2, CK slash step three. Obviously, also for complex level two or three school, the version two is going to be taking place in the first two weeks of July. All these courses over zoom so you can take them from the comfort of your home. So just shoot me an email through the website. The course is on live. Shoot me an email through the website. I'll give you some more details on registration and costs and things like that. Okay, so let's continue on asthma. So we know that asthma is basically a allergic reaction of the airways. I really want to dig deep on asthma so that you can understand the path of physiology behind asthma. Right? So asthma is pretty much an allergic reaction of the airways. Right? Do you usually find it in people that have other atopic diseases? Right? So they have like all the kinds of allergies and things like that. Right? Don't forget asthma is a type one hypersensitivity reaction. It's an IGE mediated hypersensitivity reaction. Again, our friends at the NVM Es for step two, step three, they're beginning to introduce some clinically relevant basic science. Right? In fact, another thing I guess I would say, in fact, this is something I emphasize pretty heavily during my courses. The NVM Es these days, embryology is something they love to test and they love to test it from the perspective of pizza or obi-guin.

So just make sure you understand like the embryology, at least briefly, the embryology of many of those congenital pediatric disorders. So things like congenital diaphragmatic RNA, congenital diaphragmatic RNA, if I have to think of others, I will say things like thyroid development, things like brinkel cleft cysts, things like blood and allatrysia, gestional allatrysia, herchprong's disease. Just a bunch of those disorders, just kind of make sure you know like quick underpinnings, cranial firing, geomers, you know, rough keys, pouch and stuff. Just kind of keep those things in the back of your mind. But let's continue with that topic for today. Right? So again, what are the big problems in asthma? The big problems in asthma, early hyper-responsiveness, brinkel constriction, that is reversible. But contrast this with COPD and COPD, these people have like constant airway obstruction. Right? And there are many things that can trigger an asthma attack, right? Coordere. Some people exercise is what gets them going, hey, dander, animal dander. Right? And again, aspirin is also something that can trigger, that can trigger asthma attacks. That's something I'm going to talk about as we go along. But aspirin, even NSAI Ds, just in general, they can trigger asthma attacks. We'll actually call it aspirin exacerbatory respiratory disease. Most of those people tend to have nasal polyps on tests.

Remember, nasal polyps are things you can find in people that have asthma, especially asthma that's triggered by NSAI Ds on aspirin. You can find in people that have cystic fibrosis. You can find that in people that have Wagner's granulomatosis. Remember these days we call it GPA, granulomatosis with polyangitis. So again, you see a person that has these episodic respiratory symptoms, think about asthma. Many times there'll be an identifiable trigger in the Q-stem, right? So the symptoms come and go. Now, the thing is, the bronchoconstruction that happens during these asthma episodes, it can decrease the velocity of air that's living the lungs. Many times you may hear this referred to as decreased peak flows in people that have asthma, right? And again, that inflammation that happens in asthma, it's going to make you follow these mucus plugs in your earways. And those mucus plugs can cause airway obstruction, okay? Those mucus plugs can cause airway obstruction. Now, one thing you need to understand about an acute asthma exacerbation is that there's an early phase and there's a late phase. I'll say that again, there's an early phase and there's a late phase. So the early phase, typically, you know, you have the exposure to the allergen and then the allergen binds to IgE that's on the surface of mast cells. Remember, those mast cells have FC epsilon receptors that can bind the constant region of those IgE antibodies. So there are those and Ig antibodies are pre bound.

Well, when those antibodies bind an allerging, you're going to have cross linking. And when you have cross linking, that's going to lead to degranulation of those mast cells and those mast cells, they would degranulate and release histamine, the release local trines, which can cause a lot of wrinkle constriction, which can cause a lot of airway adema, right? And then you get those acute symptoms. But the late phase, most of the time comes from recruitment of IgE. So the thing is mast cells, besides releasing histamine, bready kinings and local trines, one thing they can release is something called IgE. So no field chemotactic factor. IgE. So no field chemotactic factor. What does IgE do? Well, the thing he does is it literally causes chemotaxis, right? So it's a chemical that causes IgE to take a taxi to the side of inflammation, right? So and those eucenophils when they show up, they're going to cause more inflammation and they can trigger the next round of really bad acut asthma symptoms a few hours after you've had the early phase. That's why many times when people come into the hospital with an asthma exacerbation, you don't just give them in heel, bronchodyte leaders, you also try to give them injectable steroids like IV steroids, because by doing that, you prevent that lead phase that can arise from eucenophils. Sometimes that lead phase reaction can be more severe than the early phase reaction. It can be pretty deadly.

So that's why many times again, in addition to the in heel, bronchodyte leaders, you're going to go ahead and give those people a IV cortical steroids. Now, the thing is these eucenophils that you recruit, you know, they'll ultimately die off and begin, you know, as those basically the debiocenophils at things that can create some histological findings. Again, histology is something that is becoming more and more big deal on MBM exams. Just something you want to watch out for. Just make sure if they are classic, you know, presentations of things. Just make sure that that's something you know and know well, for exams. I mean, that's one of the reasons why in my 75 hour disk school, one big thing we do, we do a lot of adaptive learning. We analyze a lot of pathology images, just to get you like up to snuff on many of those things. Right. So many of these histological findings like Corseman spirals, I hear about an asthma or a shock relating crystals. Those are all things that you find on histology. Basically, those are dead eucenophils. Now, one thing that you want to keep at the back of your mind is that asthma is associated with what we call pauses paradoxes. Porsus paradoxes. So the thing is pauses paradoxes is something many people know in relation to cardiac tamponad. But the thing is, you can actually have pauses paradoxes in many disorders. So they can test pauses paradoxes in many different contexts on exams. They can test it in an asthma context.

They can test it in a COPD exacerbation context. They can test it in a cardiac tamponad context. Right. And you see many people, they're like, oh, you want to memorize the list of all those things. No, it doesn't make any sense. Let me just make your life easy. If you understand certain, if you understand the core principle or the core concept behind pauses paradoxes, then you, then you, you can almost like predict situations that will be associated with pauses paradoxes. Right. So maybe let's start off with a definition. What in the world is pauses paradoxes? Well, pauses paradoxes is when your systole blood pressure drops by more than 10 millimeters of mercury with inspiration. It's basically an exaggeration of no physiology, which is in fact, pathologic. So let's explain. So if I'm seeing, oh, wow, it's an exageration of normal physiology. That means there must be a normal physiology angle to it. So typically, when you're taking a deep breath, when you inspire, when you inhale, your systole blood pressure drops will usually drops by less than 10 millimeters of mercury. What's the mechanism? Again, think about it. When you're taking a deep breath, your diaphragm is going down. It's descended. Since your diaphragm is going down, your intra thoracic volume is going to go up. And again, if you remember, balls, low from chemistry that volume and pressure are inversely related, as your volume goes up, your intra thoracic pressure calms down.

If your intra thoracic pressure calms down, you're literally creating a low pressure system in system in the thorax. So things from other parts of the body will want to flow to the thorax. So you'll have an influx of blood into the right side of the heart, you're going to have increased venus return by taking that deep breath because again, the heart is at a lower pressure and things flow from ears of high pressure to ears of low pressure. So the thing is venus return for the right side of the heart goes up significantly. When that happens, it's almost like your right ventricle gets engorged with so much blood. So your right ventricle has to learn to bulge. It needs to expand itself to deal with that extra volume that is coming in. So when it's dealing with that extra volume that comes in, it expands, it almost like, oh, this is some space in the thoracic cavity, you know what, let me expand into it. In addition to doing that, it also expands into the intra-interventricular septum. So you bulge through the interventricular septum. So it's almost like you're causing a mild extrinsic compression or, you know, through that interventricular septum into the left ventricle. So you're reducing the cavity size of the left ventricle. Just think of the left ventricle as having like a wall that is facing the right ventricle and a wall that is facing the thoracic cavity. The wall facing the right ventricle gets bulged in, right?

It gets it gets that bulge from the right ventricle having to deal with extra volume. So when you do that, you're going to decrease the cavity size of the left ventricle. That's going to decrease the stoic feeling of the left ventricle. And if you decrease the stoic feeling of the left ventricle, according to the Frank Stalin principle, less the stoic feeling is going to mean that your stroke volume is going to go down. So your credit card put obviously is going to go down because credit card put is equal to your heart rate times your stroke volume. So obviously if your credit card put goes down, your system liberal pressure is going to go down. But again, usually it goes down by less than 10 millimeters or mercury. Unless you have other things going on. Remember, I said that oh, you're right ventricle in doing this bulge. It bulges more into the thoracic, you know, it bulges into the interventricular septum to a degree. So you know, it inconveniences the left ventricular bit, but it also bulges a lot into your thoracic cavity, which is good. So it has multiple places it can bulge into. But whenever you have anything that is in the way in the thoracic cavity around the right ventricle, then the right ventricle does not have those other places to bulge into. So the right ventricle is going to be like left ventricle. I'm really sorry, but I'm going to bulge into you some more through the interventricular septum.

So what are some things that can make it hard for the right ventricle to bulge out? Well, if for example, you have cardiac tamponat, there's a ton of fluid in your pericardial cavity. So your right ventricle is not going to be able to bulge into the pericardial space. It's going to bulge into the left ventricle. Or if a person has like a tension pneumothorax or a pneumothorax of any sort, you have this air that is building up in the thoracic cavity. That air is literally going to be squishing the right ventricle itself. So the right ventricle cannot bulge into any other place, but the left ventricle through the interventricular septum. Or you think about a person that has COPD? People that have COPD absolutely can get pulses peridoxes. Why is that? Because again, they have hyperinflated lungs. So the lungs are taking up more space than the ordinary world. So that more space they are taking up the right ventricle does not have that extra space to bulge into. So because it does not have that extra space to bulge into, that can absolutely also cause pulses peridoxes. Right? And also, if a person has like an asthma exacerbation or something, right? Again, because they have like decreased air flow out of the lungs, their lungs become temporarily hyperinflated. That hyperinflation of the lungs, again, makes it hard for the right ventricle to be able to bulge out. Because again, all that extra space that it could normally bulge into have been taking up by hyperinflated lungs.

So that's one of the things that causes pulses peridoxes because the right ventricle cannot bulge. But another thing that also, so again, the right ventricle, since it cannot bulge into the thoracic cavity, is going to bulge more through the interventricular septum into the left ventricle. And if your bulge is more into the left ventricle, you're going to have less left ventricular feeling. And that's going to reduce your stroke volume. So your cardiac output is going to go down. So your systolic blood pressure is going to go down. But there is another mechanism that you almost never seen resources that also explains pulses peridoxes. In fact, many times two things happen at the same time. You are making it harder for the right ventricle to bulge, but another thing you typically also doing is you're squishing on the pulmonary arteries. You're squishing on the pulmonary arteries. Because again, remember, many of those pulmonary vessels literally run through the lungs. So whenever you have like increased airway resistance, and you have all this gas, all this oxygen, all this carbon dioxide building up in your lungs, those increased pressures in your lungs are going to be squishing on the pulmonary arteries. Remember, the pulmonary arteries literally bring blood from the right side of the heart.

So if you think about it, if your pulmonary arteries are being squished by all that extra air right in your lungs, then blood cannot drain out of your right ventricle and enter into those pulmonary arteries. And guess what? If blood is not getting to your pulmonary arteries, it's not getting to your pulmonary capillaries. If it's not getting to your pulmonary capillaries, it's certainly is not getting to your pulmonary veins. If it's not getting to your pulmonary veins, it is not getting to the left atrium, it is not getting to the left ventricle. So literally, it's almost like preload for your left ventricle is also decreased by that mechanism. If the preload for the left ventricle goes down, your stroke volume for your left ventricle is going to go down, your caracal output is going to go down, your systole blood pressure is going to go down, right? It's going to go down by more than 10 millimeters of mercury. So hopefully this makes a lot of sense from a pauses, paradoxes, perspective. So that you don't have to keep just going around blindly memorizing things. And I feel like I've really hit a lot of mechanisms today. So I'm going to pause here. Again, as I say at the end of every podcast, I'll offer one or one tutoring for all the USML exams, step one to step three, complex level one to three. The only thing I don't tutor for is at the OMM questions and also the CCS cases for step three. And then again, I also offer review courses.

There's tons of people that are taking these review courses. They found it to be supremely helpful. I've had many people have big score jumps after taking my courses. So if you're interested, again, just ship me an email. And then I also help with eras applications. I know we're beginning to get into that season. I've actually started working with people already for the era cycle. Again, with personal statements, rec letters, your eras application, your supplemental applications, mocking reviews. Again, I offer all those services. And then I have this podcast on Apple podcasts on Google podcasts and on Spotify. So you're welcome to check out those apps, at least you can see the most recent 150 podcasts. If you want all the older ones from episode one, then I would encourage you to go on the website, divine intervention podcasts.com. Everything is on dates for free. You don't even need to do any sign up. But if you have a Word Press account and you sign up and subscribe to my podcast, you get an email notification whenever I make a new podcast. And then I have a new website called many people have told me, Oh, divine, I love your life lessons. So I've got in countless emails from people saying that you know, it really helped them, it really encouraged them. So I started a new website. It's a Bible based website is called Divine Intervention Life Lessons.com. And on that website, I post two podcasts every week, most of them are 10 minutes or less.

And it uses the Bible to talk about a common problem that is faced by humanity or good character treats to have. I use a biblical perspectives, but also give a lot of good examples just to help you really understand the Bible, help you really understand those points. I even have the podcast on Apple podcasts is called the Divine Intervention Life Lessons podcast. And also I have a You Tube channel called the Divine Intervention USMLE podcast and videos. That's where I post the videos that I make. So thank you for listening to me. Have a wonderful rest of your day. I will see you in the next series of Poeminary Path of Physiology. God bless you. Bye for now. Thank you.

The phrenic nerve (C3, C4, C5).

Asymmetrical elevation of one hemidiaphragm.

Type I hypersensitivity (IgE mediated).

Cardiac tamponade or Tension pneumothorax.

Early phase involves immediate mast cell degranulation; the late phase involves eosinophil recruitment hours later.

NSAI Ds (Non-Steroidal Anti-Inflammatory Drugs) or Aspirin.

The diaphragm descends, increasing the thoracic volume; according to Boyle's Law, increased volume leads to decreased pressure.

A systolic blood pressure drop greater than 10 mm Hg during inspiration.

Asthma has episodic, reversible bronchoconstriction; COPD typically involves constant/irreversible airflow limitation.

Endotracheal intubation (due to impending respiratory failure).

To prevent the late phase reaction mediated by eosinophils, which can be more severe than the early phase.

Hyperinflated lungs take up space that the right ventricle needs to bulge into, and increased airway resistance reduces left ventricular preload.

The diaphragm descends, increasing the thoracic volume; according to Boyle's Law, increased volume leads to decreased pressure.

A systolic blood pressure drop greater than 10 mm Hg during inspiration.

Asthma has episodic, reversible bronchoconstriction; COPD typically involves constant/irreversible airflow limitation.

Endotracheal intubation (due to impending respiratory failure).

To prevent the late phase reaction mediated by eosinophils, which can be more severe than the early phase.

Hyperinflated lungs take up space that the right ventricle needs to bulge into, and increased airway resistance reduces left ventricular preload.