DIP Episode 129 - Targeted Pulm Review 1 For The USMLE Step 2CK (also useful for Step 1 and 3)

Okay, welcome. My name is Divine. I am our resident and this is the 129th episode of the Divine Intervention Podcasts. In today's podcast I'm going to be doing a targeted review relating to poem. This is something I know that poem is just one of those subjects that just appears to be harder for decent number of people but on step one, on step two, CK, on step three and stuff like that. Now this podcast I'm designing a primary for people that are taking step two CK because again I've gotten a lot of requests in recent weeks that please Divine can you make a step two CK focus the podcast for poem, right? Again, obviously I can make everything in one podcast because again my goal sort of going for it is I don't want to make these podcasts like super super long. So this I will unfortunately have to break up some but again I this podcast will probably be very useful for a person that's trying to learn poem well for step one or like step three, right? Even if you're a medicine resident this will also help you quite a bit because the thing is to be perfectly honest. One question on the USMLA exams they're usually essentially the same. Like the amount of stuff that the USMLA tests on step two CK relative to step one for poem is not very different.

Yeah they may not ask about like some specific mutations in like some disease or whatever but pretty much that it's the same body of knowledge that they test every time and the thing that makes poem kind of difficult for people is one poem in what's being able to tell things apart, right? So like things that are very closely related would have like subtle differences and unfortunately those subtle differences are not always emphasized or people don't usually focus on those things while they're learning the material so that could be a problem. Second problem with poem is poem involves a lot of thinking, right? So again I'm not going to try to ruffle any feathers here or see anything that will make people think of me like a weird or a different way but just in general I suspect that many met students think that poem physiology is a little bit on the hard end of the spectrum than the physiology in some other systems of the body. I won't mention any specific ones so no one comes after me but that's basically what I'm gonna say here. Poem physiology just is on the hard end of the spectrum compared to other kinds of physiology and the thing is if you really buckle down and understand poem physio then many of the questions that you see on exams are like auto-click questions, they're like very easy. They are hard to the uninitiated eye but if you have the understanding, right? Many poem questions then become super easy, right?

So that's one thing I created my med school poem curriculum with. It was a very tough block but the teaching was extremely good, right? And in that block I was able to learn a lot of very useful things like how to think about the respiratory system and that does that that foundation right? It's essentially like carried me through a lot of stuff that I've seen in the intervening years. So really in this first first-stop poem podcast again targeted mostly for people taking step two because I'll try to bring in some high-yield step two integrations but really if you're a person that's studying for step one or studying for step three or studying poem for like your medicine exams or whatever this will also be very useful because again poem there is not much in the well-veheration again I'm not gonna go into like oh poem boards or anything like that no but if you understand this thing I'm talking about it will make it very easy for you to approach most pretty much any USMLE question you see on poem. So let's kind of begin right? So let's and again I'm not gonna talk about like extraneous basic science of stuff that you may not necessarily need to know. I'll focus more on the stuff that's clinically relevant right? So the first thing I guess I'll go ahead and start with the the PFT's right? The PFT's so your Pomonari function tests. So just as kind of like the name goes right? A PFT is a Pomonari function test it's a test of what? Of Pomonari function.

So the thing is these PFT's the way you kind of want to remember them for your exam is you want to think of them as the appropriate next best step in management on the certain classic USMLE scenarios right? So for example if a person has like a personally give you a question about a person that has like a cavitory like a long-term smoker has a cavitory lesion on chest x-ray and then they find you don't CT and this person's calcium is high right? You know right over the body you think it about like squamous cell cancer of the lungs right? Remember squamous cell cancer of the lungs can make a PTHRP in a perinuoplastic fashion right? So because you can make PTHRP in a perinuoplastic fashion it can cause hypercalcemia right? So parthoid hormone-releuthypeptide but let's assume this person doesn't have met so you know you want to do surgery for this person right? And then your friends at the MGM you can ask what's your next best step in management? The thing is your next best step in management for these people is to strongly consider getting PF Ts okay? Especially the FVV1. The FVV1 is kind of like your big target okay? The reason I say this is if you resect up you want to calculate the person's FVV1 because you want to essentially give yourself an idea okay what kind of long function does this person have now? And what kind of long function will this person have? After I resect like a lobe of the long girl, a half one half of his lungs right?

So you want to figure that out right? because you want to make sure that the person will have enough FVV1 after the surgery that's kind of like compatible with life right? So if for example a person's FVV1 is like 500ccs after like your resect their lungs right? Those people are probably not going to be able to live they're probably going to die in surgery or something weird like that right? So you want to like sort of ensure okay like make sure this person's FVV1 is like one liter or you know something reasonable it kind of varies by institution but generally like one two liters is kind of what you want to have after you've resected a person's lung so that can be the next step in management for that or they can give you a person that has COPD this is more like the upper level exams but COPD and you plan to do like long volume reduction surgery right? Again you want to estimate FVV1 before you do those things so you want to again know what the FVV1 is before the surgery know what percent of the lung function is controlled by like whatever good lung they have and then try to like use that percent over the total if you want to figure out okay this is how much FVV1 you have after surgery I think I can clear you for surgery right? So again that's one with the contest that on the USM at least and then obviously right your PF Ts you kind of use them to distinguish between obstructive versus restrictive lung disease right?

That's kind of part for the course and again I'll talk about certain high-year things you want to keep in mind with those and then another way that your friends at the MBME can test this whole concept of our of our know your PF Ts they can test it as the next best step in management prior to a person studying a drug that is pulmonary toxic right? So for example they can give you a question about a person that I don't know let's say they have rheumatoid arthritis right? And they about to start them on methyl trixate for example remember methyl trixate is a dihydrofolio reductis inhibitor prior to those people are studying our methyl trixate right? It means it's to go ahead and get some PF Ts like some baseline PF Ts so that you can sort of one-third them with time I mean this is a nice way your friends at the MBME can integrate palm with other subjects right? So I mean you know other you know other medications that are pulmonary toxic right? That can cause like pulmonary fibrosis so things like methyl trixate is a big one right? I mean remember it's your class three anti-rhythmic right? your buisulfen and your bleom and your bleomisin right?

Those anti-cancer agents prior to studying someone on those things you may want to again get like baseline PF Ts especially if they have like some kind of predisposing a risk factor let's say they have like bats, you know something you want to go ahead and like look at their PF Ts to kind of have a baseline to see if they're if their PFT like if their long function is for example worsening with therapy then you know okay maybe it's a good time to go ahead and stop the stroke right? So those are ways they can integrate all those concepts together and then one other way they can also test this right? Like you're they can test this like if for example they give you a question about a person that they had like a bloody barrier a couple of days ago and then now they're beginning to have like shortness or breath right? I would hope on that those circumstances you're thinking about some your muscular problem right? Like like Guillain-Barré syndrome So on that those circumstances right? For person with Guillain-Barré syndrome I mean classically they'll have like the symmetric is and then also paralysis blah blah blah blah but in addition to that those people will also if the thin begins to involve their early right? Then you begin to think okay maybe it's time to go ahead and into be this person right?

So spirometry believe it or not is a classic thing that's used in many health systems just to monitor the progression of Guillain-Barré syndrome if the if you notice the person's FVV1 is beginning to drop or something and you're like okay it's probably time to go ahead and you know let's go ahead and get you into be it right? So that again you don't want those patients to die in your hands and so those are kind of like some big things you want to keep in mind with you want to keep in mind oh what is the next best step in management? Some kind of PFT or spirometry or something could be the next best step in management for these are specific situations and then the next big topic I kind of want to discuss are long volumes right? So long volumes the big thing you want to remember about long volumes are think about again restrictive versus obstructive disease right? So if for example a person has restrictive disease let's say let's use the classic post-to-child restrictive disease pulmonary fibrosis. For person who has pulmonary fibrosis right? The lungs are fibros kind of like scarred down so remember that word down to help you remember that those people have decreased the long volumes right? It's almost like those people's lungs are being shrink wrapped essentially right? Versus obstructive disease where for the most part those people tend to have big long volumes right? So high long volumes right?

So for example like on image in a chest x-ray you may see that manifest as like a flatten diaphragm or like a hyperinflated lung those things all tell you that okay this person's long volumes are big because and the reason behind that is those people tend to have like air trapping right? Air trapping remember I kind of think of it this way and I've described this phenomenon in many of my cardiology or podcasts right? So I talk about this whole concept of volume overload right? A volume overload so volume overload is just you're chronically exposed to increased volumes is almost like a general concept in the body that we're in a particular organ is chronically exposed to increased volumes of something it begins to dilute in response okay it begins to dilute in response so in the heart for example if a person has like if a person has like aortic regurgitation where blood is chronically going from the from the order to the left ventricle the way those people kind of respond is the left ventricle is kind of get bigger right? They get like eccentric hypertrophy if you make so they get a dilated cardiomyopathy that ultimately causes systolic dysfunction right? Because remember in eccentric hypertrophy you're adding like cardiac myocytes in series right?

But those things have lucy-gussy associations with each other they don't have like very tight connections so those people have problems contracting and spewing blood out of the lungs I mean sorry out of the heart so the thing is if you take that same construct and put it into our poem right? If a person because they have like airway disease like COPD they begin to have chronic like air trapping that air right? I mean air is essentially like humidified fluid right? So the thing that can happen is that chronically increased volume on the lungs I sort of think of it as something that can cause those people to die late like their lungs are dilating dilating dilating dilating dilating over time and if a person's lungs begin to die late right? Kind of think of it as oh on expiration expiration is almost like the systolic of the lungs on expiration those people will not be able to contract enough or something to send air out okay? And you may see it's kind of a weird explanation but I promise you it actually makes physiologic sense when you think about it if you think about inspiration as the diastole of the lungs when the lungs is lungs are filling with air right? So the fluid the lungs are filling with this air versus expiration where the lungs are contracting that's like systolic right? Whenever a person has a dilated problem like dilated cardiomyopathy they have systolic dysfunction if a person has a dilated problem of the lungs right?

So like air trapping they can ultimately get like a systolic lung dysfunction so a problem with expiration where it's hard for them to get air out okay? So it's almost like oh like long long failure with decreased ejection fraction if you may okay? So those people tend to have bigger lung volumes than normal okay? Very high you to know those things and I mean your lung volumes right? It's like oh let's say you sit down and take in all the air you can take right? That's your total lung capacity right? And then if you say you know what? Let me know that I've taken in as much air as I can possibly take I hold it and then I try to blow all of it up right? All that air you're blowing out if you blow blow blow to you can blow out air anymore right? That's like your vital capacity. The thing is you can never blow out all the air in your lungs right? Even like you probably be dead you can't really do that so the thing is all that pentop air that you had from taking in all the air you could possibly breathe in that's your total lung capacity. If you subtract all the air you could possibly blow out that's like your vital capacity the thing that's left behind is called like your residual volume right? Those are kind of like your big high-yield lung volumes you want to keep in mind. Well here's the deal if you say you know what I've taken a complete deep breath and I've hit my total lung capacity and now I want to blow out all the air it possibly can but you know what?

Instead of just blowing it out for funsies how about I go ahead and have like some kind of timer with me that I can use to say you know what? Here as I'm blowing out this air let me just be tracking how much air I'm blowing out with a timer right? When you do that you're essentially getting all those forced lung volumes basically the word forced when you see like forced respiratory volume, forced vital capacity, forced this, forced that, forced this, forced that basically what the meaning is you are measuring it against time. So instead of just measuring the volume you're actually saying oh okay this how much happens in one second in two seconds in three seconds in four seconds those are your forced volumes. So for example if you essentially plot your vital capacity against time on a graph right and you say oh okay how much of this vital capacity have I blown off in one second that's essentially your FVV1 right? Again pulmonary poem is not that hard you just kind of need to understand what you're doing right? So that's kind of like your FVV1 right but obviously right like I said again you blow out all that air and I mean think about it I mean like in fact if I practice it right now I'm like taking a big breath right if you notice in that first second that's where I blow out most of the air right? So usually for most people you blow out like 80% of like the maximum amount of air you can blow out in one second right?

So most people's FVV1 tends to be like you know like 80 90% of your total FVC right? So that's again kind of like a high-yield thing you want to keep in mind right? So the thing is if a person has obstructive lung disease right they can again like I said they have like systolic dysfunction of their lungs right? They can barely blow out anything in that first second right? So their FVV1 is going to drop and also just because again they have this generalized systolic dysfunction of the lungs right? The total amount they would be able to expel right? So like the ejection fraction of their lungs will be crap as well. So their FVV1 is going down a ton right? Their FVC is also going down a ton but the thing is if you kind of think about it right? Like if you see you know dude try try try try try try and blow out as much air as you can right? With enough time they may be able to blow out a decent amount of not the maximum amount but a decent amount of air out of their lungs but if you're like oh dude it won't say come blow out as much as you can no they really can do that. So their FVV1 is dropping with the FVC the FVC is dropping but not as much. So overall the thing that happens in a person that has obstructive lung diseases their FVV1 to FVC ratio kind of goes down okay? Now contrast this with restrictive disease. Restrictive disease the thing is those people don't necessarily have problem getting air out right?

The thing is their lungs have just been shrink wrapped so their lungs cannot retain as much oxygen as a normal lung right? I kind of think of it like if you shrink wrap something right then you won't be able to you won't be able to accommodate as much volume. So if you're accommodating very little volume from the beginning even if you're working I sort of think of it this way right? So let's say let me give you an easy analogy. Analogies help a ton in pulmonary physiology right? So let's say you tell someone you know what or let yeah let's say tell someone you know what 80% of my income I will give it to you every year regardless of how much I earn I'll give you 80% of my income. If so let's say in a year you earn a million dollars right? That means you're gonna give that person 800 thousand dollars and it's pretty big outcome if you really think about it but let's assume your income then drops to a thousand dollars a year right? Yes what you can only give that person 800 dollars 80% of that thousand dollars. So if you sort of think of it that way it's like you're still able to give the same fixed percent between those two incomes the only problem is the nominal amount of those fixed percent change because you just have lower capacity with you being earning like less money right? So that's kind of like the way I want you to think about it and if you want to make parallels with cardiology right? If for example a person has like hypertrophy cardiomyopathy right?

Their hearts get like big and beefy right? There's less space in the heart to accommodate blood it's almost like again their hearts are almost like shrink wrap shrink wrapped yeah you're saying yeah divine hypertrophy cardiomyopathy their heart hypertrophies yes that's true but the thing is just with the way the sacramir is added those people's hearts don't have enough room to take in as much blood right? So they have a dastolic dysfunction so the thing is those people's hearts it can still eject the decent percent in fact you may be able to eject a normal percent right? But because they just don't have enough capacity in the first place whatever the eject is still gonna be small because they don't take in enough in the in the initial instance when a dastol is happening so kind of like the same thing with restrictive lung disease the lungs can still you know the ejection fraction of the lungs right? kind of like heart failure would preserve the ejection fraction the ejection fraction of the lungs under those circumstances is great works really well but the only problem is you eject in from a smaller study amount because your lungs have been shrink wrapped okay? Again if you can understand the salient points it would just make your life very easy as I continue to go with as I continue to go with this okay?

So in general the FVV1 to FVC ratio is normal or mildly increased in a person that has restrictive lung disease the FVV1 drops the FVC drops but it cannot drop proportionally it's like you're getting little in when you're inspiring and feeling the the lungs with air so you're gonna give little out all right? Because you just started with little right? if you start with a thousand dollars you can only give up 800 you start with a million dollars you can give out 800 thousand right?

That's kind of like the same thing with with a restrictive lung disease so those are again high-ealth things you want to keep in mind so the FVV1 to FVC ratio is decreased for sure in an obstructive lung disease but the FVV1 to FVC ratio is normal or mildly increased in people that have a restrictive disease and then the thing is for the higher exam so like for step two CK step three your friends at the NV Me may give you this weird value called like the F-E-F 25 to 75% just sort of think of it as kind of like a nice surrogate again there are some subtle difference from like FV FV1 to FVC ratio but and I won't go into those details because it's not very necessary for these exams but this F-E-F like fast-expertory flow in from like 25 to 75 just think of it as a nice FVV1 to FVC surrogate for obstructive disease okay think of it again this is again a simplified lecture because I know I'm kind of gauging the audience I'm giving the spot cast too so this is kind of like a simplified measure for for obstructive lung disease FVV1 to FVC ratio so if your F-E-F 25 to 75 is down okay on an NV Me exam then that tells you that you're dealing with obstructive lung disease again you may see I'm not divine it's kind of weird I've never heard of this before I promise you it's high up to actually know it for for the USML is especially step two CK and step three so again it's decreased in a person that has that has an obstructive lung disease and then one thing you may see on NV Me is that me sort of throw you for a look is you may see like percent predicted percent predicted you may feel like divine what is percent predicted basically percent predicted is almost like a population measure is almost like a population population a measure just the good number you want to remember with these percent predicted is like from 70 to 80 percent right if you're kind of like higher than that 70 to

80 percent threshold you're a normal person okay but if you're less than that's like basically if you're like less than 70 percent in like FV1 for example like 70 like you're less than 70 percent predicted that means you have problems right that means you probably have some kind of lung pathology although being like 120 percent of predicted for something is not necessarily good right take for example if a person has like a total lung capacity that is like 120 percent of predicted that means those that person has higher than normal lung volumes so under those circumstances you begin to think about again some kind of obstructive lung disease and then the next thing the next I guess concept I'll talk about is like this whole thing of DLC right DLC the way you think about it is I kind of think about it as like a gas exchange test for the lungs right so like how well is the how well how like how good of a job does the lung perform with a gas exchange right so what do I mean by that if you kind of think about it right then what what's that what does what what your lungs what do they need to true what does what does oxygen need to traverse to get into your blood stream right it needs to traverse the aviola membrane right and it needs to traverse the walls of the pulmonary capillaries and then it gets into your it gets into the blood that runs through your runs through your your blood vessels right so that's the normal circumstance if you kind of think about it this way if you have anything that gets in the way right because again oxygen right it can only diffuse efficient universe like a certain distance right if you begin to put more road blocks in the way right I kind of think of it as again as a person trying to like jump over an obstacle right you know they're for the most part like an able body 20-year-old guy can probably jump over like an obstacle of a certain length

right but when you begin to like make it longer longer longer you kind of like exceed his capacity to jump over reasonably right so that's kind of the same thing here so say for example if a person has like fibrosis right if a person has like some kind of a restrictive lung disease like pulmonary fibrosis it's like you're putting more stuff in the way right it's like you're putting more distance distance distance distance distance because the lung like the aviola membranes right I'll feel like a like a fiber tissue you're putting more distance so the fusion is less efficient because you increase in the diffusion distance right so that'll be associated with a decreased dlcl right but the thing is many people sort of take the serenius thinking to exams that oh the only thing that causes a decreased dlcl and mbm is is if a person has like pulmonary fibrosis no that is actually not true okay another thing that classically on mbm is can actually cause like a decreased dlcl is if a person has emphysema right because remember yeah you want diffusion of stuff to happen from like you know from your viola to your pulmonary capillaries but the thing is you do need those membranes for the diffusion to sort of occur across right you need those membranes for those things to happen so if you literally have like no viola right you literally have no surface area for diffusion to happen which is what happens in emphysema because remembering emphysema you have a destruction with those with those proteases right or if you have like alpha one antitrips in deficiency where you have like a deficiency of antiproduce right you essentially have like a destruction of your of your longer parenthesis you destroy like your viola membranes so you're basically getting the rate of the surface area that you need to be able to have diffusion happen right so under those circumstances your dlcl will als

o be decreased as well right and then if you sort of go with the extreme example you'll be like um divine okay is anything that can cause a higher than normal dlcl on an mbm exam right this quest whenever these questions pop up and again they don't pop up often on mbm is whenever they pop up almost everyone is almost like uniform most people um willing to wager get those questions wrong right but the thing is again let's think about this for a second right so let's assume they give you a question about a person that has a defect where antibodies are made against like type 4 collagen right so let's say they have good posture syndrome right or let's say they have uh webinars right to remember webinars is like the sinusitis the kidney problems right like the C&C positive uh glomerulina fritis and then they have like him obtuses right whenever people have all these problems right they tend to have an increase dlcl so you may see and if I have those that work think about it if a person has him obtuses right usually it means that they have like blood in their lungs somewhere like literally the blood is in the alveoli right so I sort of think about it this way normally for oxygen to get to your blood it needs to traverse the alveoli membrane and then it needs to traverse the membrane of the endothelium of your pulmonary capillaries and then it gets to blood but think about it if for example your blood the person has bleeding to their lungs right um let's say they have like again like webinars or good pastures they've bleeding to their lungs if essentially cut out the middle man it's like the blood is not in your vessels anymore it's like literally inside your your alveoli right so you've cut out the middle man so it's like there's all it's like as the oxygen is coming from the atmosphere it's like literally like bathing your blood right directly if cut out the middle man und

er those circumstances in circumstances of like pulmonary hemorrhage your DLCO will be will be increased okay so again again you may say divine you're kind of going a little slow here but I just want to make sure you have the solid background especially if you're going to internal medicine in the future you do need to have the solid background because again you'll help you understand things as you go along so under those circumstances you'll have an increased DLCO but um so let's get to more testing things with this whole DLCO business right the thing is your friends on the mbme right if they want to again really get a little nitpicky they can try to give you questions where you need the DLCO to tell certain diseases apart within the same class right so I mean let's talk about first like the two big classes of lung disease right so like restrictive lung disease right many people again the erroneously going to mbme exam saying that oh you know what for every strict for every restrictive lung disease the DLC is always low that is not true right if a person has fibiotic lung disease for sure yes they'll have a decreased DLCO but the thing is if you have an extra pulmonary cause of restrictive lung disease you will actually have a normal DLCO the lung itself is working well the only problem with an extra pulmonary causes you may have something that is physically compressing the lung remember I told you in restrictive disease you have your lungs are smaller than normal because they've been shrink wrapped well your lungs can be shrink wrapped because it's fibiotic right so your lungs get very elastic so they are like they almost have like no compliance right that's one reason why your lungs can be shrink wrapped another thing that can shrink wrap your lungs is if literally the things that surround your lungs so your lung itself is fine but it's like you're almost like closi

ng in on your lung itself right so I give you an example if a person is like morbidly obese right remember like from your neck to your pubic synthesis I kind of think of it as one fixed box right but that fixed box is being like there are two competitors there are two people that are competing for space in that fixed box right it's like your thoracic cavity is competing for space your abdominal cavity is competing for space well if your morbidly obese your abdominal cavity wins that battle if you have don't know cavity wins that battle there's less space available in the thoracic cavity that can actually cause a restrictive lung disease but again that's restrictive lung disease with a normal DLCO now another way you can sort of like another nice fancy way that your friends at the endemic can introduce this is if for example a person has like a problem with their spine right so let's say a person has like really bad scoliosis again if you have an abnormal spine like spine curvature again your restricts like the expansion of your lungs right so that can cause again restrictive disease with a normal DLCO or they can again they can like your friends at the endemic they love giomba re for whatever bizarre is there right like giomba re syndrome ALS right those are kind of like neuromuscular problems where the diaphragm doesn't work as well it cannot like contract or relax as it should for you to expand your lungs again that can be another cause on mbm's of restrictive lung disease with a normal DLCO right so earlier on I said that emphysema right is like you have a normal DLC I mean you have a decreased DLCO but it's an obstructive lung disease well are there obstructive lung disease that may potentially have like a normal DLCO well I would hope you're thinking about like things like chronic bronchitis for example right so again your mbm friends they can write questions whe

re a person has like you know all the classic markers of obstructive lung disease and then they give you an answer choice that says oh chronic bronchitis or another answer choice that says infezima the way you can tell those things that part is you ask yourself okay between these two diseases which one is associated with a reduction in surface air for diffusion of oxygen in the lungs well that's emphysema so emphysema will be an example of an obstructive lung disease with a decreased DLCO versus chronic bronchitis where it's an example of an obstructive lung disease with a normal DLCO so again you want to be able to differentiate these things again yes I know like I'm taking my time here but the thing is on the USMLE is ready if all you had to do was memorize crap right then you crush the exam everyone will crush the exam but unfortunately that's not what happens right so you need to that's why I kind of like giving these podcasts is you want to know the concept right so I try to explain it first but then I try to give you scenarios on how they will test that concept like oh okay you know what you know this concept well how can you apply it these are ways your friends at the mbme kind of expect you to apply that concept but now let's assume so let's I guess sort of jump over to the next bit of knowledge here so let's assume you get an mbme question you know person has you know you suspect the person has asthma and you perform spirometry like man yeah asthma is obstructive lung disease this person is if you want great specific is great and all that stuff right it's like you're getting kind of like getting equivocal tests from your spirometry the next thing you kind of want to do actually is to do something called a metacoling challenge right so what is metacoling metacoling right is a most grainy receptor metacol is a most grainy receptor antagonist hope I'm thinking a

bout that correctly no no no whoops scratch that metacoling is a most grainy receptor agonist so by being an agonist by being an agonist right it essentially causes bronchoconstriction right causes bronchoconstriction but again in most people causes pretty you know trivial symptoms like the kaffaton you're like they feel like crap for a short while but if a person has reactive airway disease like asthma for example they will have a profound bronchoconstriction because there are early is a kind of like touchy touchy right so they will have like a profound bronchoconstriction with the administration of a metacoling right so if you notice that a person's FV1 drops by like 20% or more with the administration of metacoling so you're almost like trying to like provoke asthma symptoms in those people that tells you that a person has asthma right I kind of want to parallel this with this like Ergonovina challenge right so or I guess some people call it like the Ergonamine challenge right so here for example a person has like virion tangina like prince metal right one way you can provoke and sort of like figure out like this person has prince metal and you know is to give them again in a cath lab right you're not gonna do this on the bedside because the patient could literally have an M.I.

and that you don't want to do that right so you'll do this probably like in a cath lab where you give them like Ergonamine like a very delude concentration of Ergonamine in many people if you give them that Ergonamine Ergonamine is like a visual constrictor right many most people don't get M.I.s if you give them like small amounts of Ergonamine but if a person again has like again blood vessels that have again touchy touchy right like a person has like a visual spastic coronary disease like prince metal or virion tangina right that small amount of Ergonamine can provoke visual constriction like coronary visual constriction trigger like M.I. symptoms so that's like a positive test that's like a almost like a confirmatory test for for prince metal and genna and again you may notice you're like you're making all this parallel between cardio and poem cardio and poem I'm doing it for a reason right again I want you to be able to see links across different systems and then one other thing again that your friends at the M.I.M.E.

can do is they can again give you a guiding variety question about a person that you know has asthma for example has some kind of obstructive lung disease and then they tell you that oh you give this person a bronchordialidr right and you notice that oh by giving let's say you have like I can see them giving this as an like experimental question right where you give person A a bronchordialidr the F.E.V.1 jumps significantly you give person B a bronchordialidr like our butterone the F.E.V.1 barely budges or you changes but only by a little amount the person that had this big jump in F.E.V.1 right with a with like the administration of a bronchordialidr that tells you that those people have some kind of reversible lung disease right so what kind of reversible obstructive lung disease will the M.I.M.E. be going after well I hope you're telling me asthma right so again that's kind of like a nice way that your friends at the M.I.M.E.

can test those are those are concepts and then one thing I would want to kind of direct you to next here is um the slides that I actually attach to this podcast so believe it or not I did actually make slides for this podcast and the thing is these slides I'm just using them to illustrate flow volume loops so I will encourage you like download the PDF I'm attaching it at the bottom of this at the bottom of the podcast and you want to kind of like try to follow along right so flow volume loops I know some people are already like hyperventilating or like shodowing internally like flow volume loops so don't panic don't freak flow volume loops I mean there's tons of them right but again this is the usm we were talking about here right and flow volume loops to be honest they actually know that already again if you've understood what I've been talking about so far you're not that hard just talk about them right so on my second slide right you see where I show a normal flow volume loop so first things first let's sort of define the axis whenever you you're confronted with a graph on an M.B.E.

me the first thing you need to do is not panic respond with a smile okay smile and then try to analyze what's going on with the axis usually if you can analyze the axis like I tell people this like people like Twitter for a step one all the time I tell them if you get a graph or even the MCAT if you get a graph on these exams right right don't hyperventilate just calm down the first thing you should do is I tell them is your first step in the analysis of any graphical question is to write down what you have on the x and y axis right write those things down like on a piece of paper and then forget the graph initially and then just tell yourself before again before looking at the graph just tell yourself okay these two quantities are written down let me go back to my knowledge box like what do I know about these two concepts what is there like ask yourself first what do I know about these two concepts and then the second thing is ask yourself what is the relationship I know between these two concepts if you can sort of establish the relationship you might like oh yeah these things these two things are really fed by this metric like oh if this one goes up this one goes up why this one goes down this one goes down oh wait if this one goes up this one goes down right if you sort of like establish that relationship in your mind and then go back to the graph the graph then on second inspection will look a lot easier than it did when you looked at it initially so that is really the way you should approach graphs write down the x what's what I mean they're not going to give you on label graphs on NV Me that can't help economy so write on what you have on the x write on what you have on the y take a step aside ask yourself what's the relationship between these two things is that a direct relationship is that a inverse relationship establish that in your mind first and then take

a look at the graph right when you do that again you'll notice that many times these graphs are much easier to understand so let's do the same thing here with these flow volume loops right so we have a normal flow volume loop here and again on the y axis we have flow the top we have x like expatory flow the bottom we have inspiratory flow and then on the x axis we have we have volume okay I should have labeled these graphs a little better but on the x axis we have volume and if you notice the volume is kind of weird it's increasing from right to left okay from like the I don't mean an atomic composition I mean like literal right and literal left it's increasing from right to left on the x axis right so basically as you're inspiring you'll be approaching the like the left side of this graph as you're expiring you'll be approaching the right side of this graph right because again when you inspire right the volume of your long should increase because you're literally taking in air but if you're expiring the volume of your long should decrease because you're literally expelling air right so that's a normal flow volume loop and again if you notice the curve and this is this part it so if if you've been kind of like zoning out you'd really want to pay attention here if you notice in this graph that I have here right I'm not studying at zero volume in the lungs because again remember what I said you can't start out at zero long volume right if not you you probably you're probably be dead right the thing is your lungs have some volume that it doesn't necessarily expire out right there's almost like some basal level of oxygen in the in the lungs right so basically if you're looking from the zero mark to like where I start like at like two liters essentially looking at residual volume with that right so so that's normal right then again if you look at the expatory part of thing

s again remember if just listen to me in this podcast Tika D-Breathin I've taken the D-Breathin and then if you notice when I'm expiring the sound is very loud at the beginning and then it kind of gets moderate as time goes on the reason is getting moderate is as time goes on in that first second is where you can expire most of your air out right but after that first second right you've expired most of your air because if you think about it right if any rate rate is a volume over time measure right if you've expired most of the volume out within that one second whatever volume you're gonna expire to then get to like your FVC is very little so because that remaining volume you're expiring is very little right and you're dividing that by by time because the numerator is going down that means that flow has to calm down right it's literally decreasing so if you notice if you see this graph I'm like labeling like oh there's an FV1 part it literally is between like five and four seconds like oh that's where you're getting read of the most amount of oxygen right and I'm using like the standard number seven again it just any I could have put any number there wouldn't make any big difference but I'm just gonna use in the standard number seven like okay you know what this is the height you want to get to right when you're getting written like this is the height in terms of flow rate right flow rate so again remember on the y-axis these are flow rates okay not volumes they are flow rates so this is the height you want to get to when you expire and again you see how steep everything is in that will first second and then you notice boom you get rid of the rest of the air I mean the rest of the oxygen pretty quickly right as you go from like as you go from like four liters to three liters like that part of the curve is really steep so I may have me spoken a second earlier where lik

e I guess like 30 60 seconds ago where I said that oh like four to five seconds sorry I mean like from five to four liters so let me track back a little if you notice between five and four liters on the expatory part of the curve right things are very steep okay that is the FV1 part of your graph okay and then if you notice from the four liter to the two liter mark things again kind of steep but they're not as steep as that FV1 part because again the flow rates go down because you've in that first second that you expired you've got in rid of most of the oxygen so I hope that kind of makes sense so now if you understand this you can already begin to predict what an obstructive long disease graph should look like and what a restrictive long disease graph should look like right so if you go to the next slide where I talk about where I talk about restrictive disease if you notice in if you notice right in in restrictive disease the thing that's happening is that you're like oh divine this curve looks eerily similar to the first one you talked about what's up with that right so notice it actually looks a lot like normal like a normal flow volume loop right for the lungs but do you see that the if you look at the expatory flow part of the curve do you see that it doesn't get up to that magic number seven that I established as a standard in terms of flow rate notice it doesn't get there right so this is again kind of like what I explained with restrictive disease in the beginning I said that with restrictive granted your flow volume looks your flow your your lungs can eject like your lung ejection fraction is is normal or it may even be greater than normal but the thing that happens is because you almost again have like that stoic dysfunction of the lungs like your lungs cannot accept enough oxygen initially because your shrink wrapped then if you're getting in less again it

's the 1000 example if you're getting in a thousand dollars instead of a million dollars whatever you expel will be smaller than normal okay so if you essentially see a smaller version of a normal flow volume loop that tells you a dealing with restrictive disease and then one thing that can essentially help you clinch the diagnosis is look at the x axis part of this graph right look at the volume right if you notice if you track back to the first normal flow volume loop remember we started at like two liters right which was again basically our zero volume and then after taking in a full inspiration we ended up at five liters now look at my restrictive disease graph you're like hey the values they're not a letter and you're filling up to four liters remember in restrictive disease the hallmark is you have grossly decreased lung volumes right so you can essentially like basically if you look at the graph you can essentially deduce essentially what's going on right so if you notice this person's residual volume in restrictive diseases like one liter but in the normal flow volume loop I have in the second slide the residual volume is like two liters right so you're seeing that this this curve is smaller than normal right and it's right shifted whenever you see a right shifted flow volume loop that tells you for the most part on MBMS again there are many more causes of a right shifted loop but again that's not your concern for the MBMS this is what I want you to know if you see a flow volume loop that looks normal right compared to like a standardized normal they give you it looks normal but it's right shifted and you notice that many of these volumes are like lower than normal that tells you pretty much on MBMS that you're dealing with you're dealing with restrictive lung disease remember the R in right shifted for the R in restrictive disease right and then now if you j

ump to the next one right so this if you jump to the graph of restrictive lung disease you see this looks grossly abnormal right so first things first if you notice it's smaller than normal right it's smaller than normal and if you look at the expatory flow part of this graph right you notice that the slope is not as steep as what obtains for normal in that FVV1 part of the curve right so remember the part I labeled like the FVV1 part right you see it's not as steep and then you also notice that you have like almost like a scalloped or like super shallow intro like next part of your expatory flow loop right if you notice it's like oh you get to your crest and again you see your crest is much less than seven like if you're even comparing this with restrictive disease or restrictive disease you're like oh okay you know what I'm sort of kind of approaching seven and like kind of like maybe like at a five or a six obstructive disease notice you're kind of like at a three right your FVV1 drops like crazy in obstructive lung disease right so these people have just massively decreased flow so the FVV1 is like in the toilet and then if you notice their graph like gently tippers down if you see a gently tippering down portion of an expatory flow loop you're very likely dealing with obstructive lung disease on an MBA right and then notice another thing here notice another thing if you compare to the initial normal graph right that I had earlier I studied the residual volume at two liters notice you I'm studying the residual volume of three liters right and notice the total lung capacity in the first graph was five liters but in this graph here it's seven liters right I'm just essentially telling you that you have increased this is just a different way again graphs are just means of expressing thoughts that are logical right this is just the a graphical wealth telling you that l

ong volumes are increased in people that have obstructive lung disease right long volumes are increasing people that have obstructive lung disease so if you see again a graph that has like a very tapered like a slowly tapering expatory flow like portion but you notice that the graph is left shifted okay a left shifted graph tells you that you're dealing with obstructive lung disease right or you may say okay if I how do I remember this just remember right shifted restrictive lung disease the R's match and then the other one has to be the other one okay that's kind of like a nice way to keep those things strict and then the final graph this is just something I want you to memorize it's just a classic pattern you can miss it if you see it but if you see a box shaped flow volume loop that tells you a dealing with like a fixed like a fixed like operator obstruction for example and again these ones really show up but it's just something you want to keep at the back of your mind okay again there are many other flow volume loops this is again supposed to like sort of get you get you started on what you need to know for the USM Ls chances are if you see a flow volume loop it's probably going to be one of these four that I illustrate in this in this presentation so hopefully hopefully hopefully hopefully this makes a perfect sense to you again fixed error obstruction can be like some kind of foreign body in the lungs for a person has like a like a like a like a trick else the noses let's say they've had like they've been intubated for a while remember one of the biggest complications of prolonged intubation is trick else the noses right so again they can sort of present it to that with a flow they can present it to you on an NV Me exam with a flow volume right so again those are ways to kind of keep all those things straight and then I realize that this podcast is you know sort

of going in this super long direction so I'm going to try to I guess go ahead and go ahead and round things up but I think to sort of again get your basis solid with the lungs let me just discuss if you can permit me let me just real quick discuss one or two other quick lung pathologies and I guess more like like lung physiology but discuss them in the context of like exam questions right so one of the classic concepts that seems to give people again quite a bit of trouble on exams is this fancy shmancy oxygen delivery equation right so the thing is this is like PEMFODER like many attendants love to PEMP people on this this is an equation you probably should memorize if you're taking step one maybe not so much if you're taking step two but the thing is if you actually understand the equation it makes many things easy to remember right because there again there are many pathologies they can integrate here right so you've heard of the oxygen you've probably at some point in your life heard of oh oxygen delivery equation well what is it the oxygen delivery equation is basically your cardiac output right multiplied by your hemoglobin right multiplied by your like the saturation of oxygen in hemoglobin so like your O2 set and then multiply by some small number 1.34 so this is one this is one like one part of the equation and then to all this stuff I've mentioned you just basically add 0.0031 right times your P little AO2 right so you'll hear me keep saying P big AO to P little AO2 so let me describe what those things mean okay your P big your P big AO2 means the like the partial pressure of of the oxygen that you find in your vial line okay the partial pressure of oxygen that you find in your vial line now your P little AO2 refers to the partial pressure of oxygen that you find in your blood vessels like in your pulmonary capillaries for example okay so that's a big thing

you want to kind of want to keep straight so in this oxygen delivery formula and referring to the P little AO2 basically the arterial oxygen partial pressure okay so again I'll repeat it again cardiac output times your hemoglobin times your percent saturation again again of oxygen that's bound to hemoglobin right times 1.34 and then to that you add 0.0031 times your P little AO2 so you may say okay so define how can they test this crap on exams right so let's think about this for a second right if a person has anemia right in fact let me let me establish this concept right so your body always wants to try to maintain homeostasis right your body wants to try to maintain like a fairly consistent oxygen delivery right so how can they test this concept let's think about this for a second if a person has a profound anemia so let's see a person's hemoglobin is like four for example right because hemoglobin is a big part of this equation if you have a bad anemia okay fine your hemoglobin drops right because your hemoglobin has dropped your overall oxygen delivery will drop so your body is like how can I compensate for this bad bad bad anemia well excuse me one way your body can compensate is by raising your cardiac output right it can try to bring up that cardiac output number a lot because as hemoglobin is going down you want your cardiac output to go up to again maintain a constant oxygen delivery if you may well think about it if that hemoglobin is chronically decreased and your cardiac output is chronically increased to meet to sort of counterbalance and keep your oxygen delivery like at a fairly constant value after a while of chronically increased cardiac output right you can already begin to see how a person can have high output heart failure with that right so that's one way that again you can sort of see like oh wait this equation can actually help me reason through

questions on exams or think about it again if a person is like hypotensive because they've lost a ton of blood right if you give them like fluids right or you give them pressures you are sort of like artificially propping the cardiac output part of their of the oxygen delivery equation right because by giving a person fluids or blood or whatever you expand in your volume right you're giving them more preload well if you give more preload according to the Frank Stalin principle right your cardiac output will go up because your end-astolic volume is going up right so again that's something to keep in mind or if for example you're giving a person like more if you're giving a person like if you're like oh person's hypoxic in the hospital the first thing people do is boom they jump to like slapping oxygen on those people's faces right by doing that your reason like that p little ill too part of things right but the thing is if you notice that p little ill too part of things is multiplied by 0.0031 right so whenever you increase the amount of oxygen that's in people's um in people's blood right like the dissolved oxygen in their blood not in hemoglobin in their blood itself like they're the liquid part if you may have their blood you're not really raising their oxygen that you're not really improving the oxygen delivery by much because again of that 0.0031 factor right remember if you if you're giving like if you're saying like oh I'm gonna give you a third like 0.3 of one million dollars that's very much higher than oh I'm gonna give you 0.0031 of a million dollars that's much lower right so again something to keep in mind and then if you also again think of this equation like the SAO2 part like the oxygen saturation part right for a person has I don't know like carbon monoxide poisoning right your SAO2 is not is not great right your SAO2 will definitely not be great amon

g other circumstances because again carbon monoxide is just taking spots remember the hemoglobin has like four seats for oxygen carbon monoxide may be taking two of those seats right so your SAO2 goes down that's why your oxygen delivery goes down if your person has carbon monoxide poisoning so they're they're they become hypoxemic hypoxemia just means low levels of oxygen in your blood and then there are some finer points to this oxygen delivery equation but I think that's more appropriate for like a medicine resident so when I do the medicine board review and I start talking about poem critical care I will talk about the oxygen delivery equation in in a fairly different context and then I guess the last and I'll go ahead and talk about here I'm sure this is the stuff you've really been waiting for and this is actually a part way unfortunately you do need to kind of like maintain attention this is the whole concept of AA gradient right so AA gradient so it's like okay divine what does A gradient mean well A gradient basically means is essentially the spread or the difference between your P big A02 and your P little A02 right it's the difference again between your P big A02 and your P little A02 right so what do I mean by that your P big A02 remember I already defined it as the amount of the partial pressure of oxygen in your fuel line you'll P little E to remember really define that as the partial pressure of oxygen in your blood vessels right like your pulmonary capillaries your arteries and stuff so the thing is think about it where does oxygen come from it initially comes from your fuel line right it comes from I mean obviously comes from the atmosphere right oxygen comes into your lungs comes into the aviola first and then after the aviola it then goes to your bloodstream right so the way I kind of think of it right you kind of think of it this way you kind of ha

ve like normal losses as time goes on right so it's like oh let's say you make a car at a manufacturing facility you're gonna put some miles on it before it gets to the dealership right so it's like oh as you're going from big from like the like the origin of something as time goes on you begin to give up like little little bit of amounts here and there right so that's kind of like the same thing that happens your P big E to usually should be higher than your P little E to right but the thing is if you want to I mean again if you go back to business production if you want to measure how efficient the process is right you want to say okay you know what you study with a hundred and after production and blah blah blah you end up with a 95 that means you're a very efficient whatever business process so if you sort of think of it this way with the lungs if for example your lungs start out with like let's say okay this is the origin this is the oxygen getting into my aviola that amount is like a hundred right and then you look at the person's P little E to like the partial pressure of oxygen in their in their bloodstream and it's like 97 and that tells you you know what oh I only lost like three along the way that tells you that you're dealing with very efficient lungs right so for the most part the AA gradient is usually like 10 or less right again I'm sure if you read for a state or some other book you'll find some other number but just remember a simple easy number 10 okay if your A gradients is less than 10 it's great right although you may see that there are certain circumstances where your A gradients less than 10 well that's not normal still the person is still be hypoxemic and I'll talk about that in a second versus if your A gradients like 30 or 40 or 50 then that means your lungs are super super super inefficient in getting oxygen from the aviola to the pulmonary

couplers so how do we calculate big P big A or two right really the way you do it is you take like I'll just give you an equation that you should commit to memory it's like 150 minus a product okay so what's that product that product is you take a person's P little A CO2 right so like the partial pressure of carbon dioxide in those people's bloodstreams multiply that by 1.25 right and then when you take that product you subtract that from 150 and with that you get your P big A or two right so think about it right the person's the partial pressure of oxygen in I mean of carbon dioxide in most people's blood is like 40 right if you take 1.25 times 40 so that's like one and a quarter like a hundred percent and then 25 percent of 40 so that's like 50 if you take that product and subtract it from 150 that's like a hundred right so a normal P big A2 is about a hundred and then your P little A2 you just made you can measure that directly with AB Gs there's like a physiologic mechanism there kind of involves like some spectrometry but you don't necessarily need to worry about for the worry about that for the USMLE so I'm gonna gonna move on right so that's how you calculate your P big A or two and then you just directly measure the P little A or two so again the ideal situation is the spread between these numbers should not be huge right it should not be more than 10 so if and again I kind of talked about this home on factory anything where oh you know you lose some small amount so your P little A or two is usually like you know a little less than your P big A or two right the kind of like the physiologic reasoning behind that is it's not all the blood that gets to your lungs that gets oxygenated believe it or not right it's not every blood that gets to your lungs that gets oxygenated right so if you sort of add up like oh all this blood that's getting super well oxygenated th

is little amount of blood that's not getting super well oxygenated if you sort of add up the appascial pressures right you notice that it's kind of like again mildly decreased but if the spread between your P big A or two and your P little two is like super super high right then that tells you that there must be something in the lungs okay that's essentially preventing the blood from being oxygenated properly right so for example it can be if a person has like a pulmonary embolus right if a person has a pulmonary embolus they're not having enough like blood is essentially not flowing through that part of your lungs well if you're not flowing through a part of lung well the oxygen that's coming here coming through there you're not gonna see it right so you're not gonna get oxygenated that will lower your P little A or two right and that will make your A ingredient wider or if for example a person has like a right to left shunt right so this would be an example of an intra cardiac shunt okay for person has a right to left shunt right like a PFO or a VSD or an ASD where they have like isemangra physiology right that blood is essentially just directly bypassing the lungs right so because again blood is not physically contacting oxygen right then you're gonna have problems with your P little A or two is gonna go down on your A ingredient world well widened but the thing is there's this thing I'm beginning to notice that the MBM is a beginning to throne exams and they're beginning to and again it's just like a small adjustment in your thinking that you want to keep in mind but here's the thing your friends at the MBM are beginning to try to see if you can really need to find differences between things that are intra cardiac versus things that are extra cardiac right so for example a PFO or an ASD or a VSD those are examples of intra cardiac because it's literally within the

heart that this connect like intra connectivity is going on those are examples of intra cardiac shunts a shunt is just basically a situation where blood is not seeing the oxygen from the lungs okay so that's an example of an intra cardiac shunt well here's the thing your friends at the MBM can give you a question about a person having a white like a big A ingredient but it's from an extra cardiac shunt so what's an example of an extra cardiac shunt well an extra cardiac shunt I mean there is one that's kind of like um physiologic that you find an utero it's like between the pulmonary between the pulmonary arteries and the other right through like the doctor satiriosis right that's an example of an extra cardiac shunt but another nifty one and this is very good for like like I will be surprised if your friends at the MBM don't throw this on an exam like sometimes soon because it just makes so much sense as an MBM question but it's this whole concept of like a hereditary hemorrhagic telangetija right also known as like things known as like oslo waibir or waibir randu syndrome right that's an example those people tend to have like AV Ms like AVM affirmations right remember AV Ms it's like a direct connection between like an artery and a vein so these people can get a lot of like pulmonary AVM so they have like direct connectivity between the pulmonary arteries and the pulmonary veins okay so they don't have blood traversing like pulmonary capillaries so they don't again have enough time right they don't essentially have like good gas exchange so that can be a very nifty mb example of an extra cardiac shunt okay um that can cause hypoxemia with a widening e-gredient where it's not necessarily a problem like within the heart it's more a problem like within the lungs so that's something to keep in mind so you may see okay but divine I've also heard that there are certain thi

ngs that can cause hypoxemia but they cause that hypoxemia with a normal e-gredient well again let's think about this for a second if you remember when I was talking about dlcl I told you that if you have a problem with like your native lung like your actual lung is all screwed up right you tend to get like an elevated dlcl sorry like a decreased dlcl well here's the thing if you have hypoxemia with an elevated e-gredient that usually tells you that your lungs are actually screwed up right like a PE you have an obstruction of your pulmonary capillaries right or like you have like a pulmonary AVM like I talked about with HHT right now on the flip side if a person has an extra pulmonary so they have like some cause something just weird happening outside their lungs right that's making them hypoxemic that would likely cause hypoxemia with a normal e-gredient right so think of this for example um let's assume a person overdoses on an opioid right if you overdose on an opioid well guess what happens to your respiratory rate he goes down to like four or like three well if your respiratory rate is that low right you're not gonna be getting in enough oxygen in the first place so your pb a02 will be low from the beginning right well I just explained earlier that your p little a02 right so like the partial pressure of oxygen in your bloodstream right comes ultimately comes from your pb a02 it's your vial oxygen that ultimately is the source is the creator of the oxygen you have in your bloodstream so if your pb a02 is low because you're not taking it in enough breaths because you've overdosed on an opioid well guess what your p little a02 will also be low it's like garbage in garbage out okay so opioid overdose is a classic mb example of hypoxemia with a normal e-gredient right another thing that can also be like a similar cause is let's say you go to Colorado right you go to D

enver you go to a place with like very high elevations well guess what if you go to higher elevations right your FIO2 doesn't necessarily change right but the higher you go the less oxygen content there is in the atmosphere right so again your pb a02 will be low but your p little a02 will also be low as well but the spread between them will not change there will be normal because your lungs are working just fine it's just your lungs are just getting little oxygen in to start with okay so again I really hope you understand this this is one of these like podcasts where I'm like no it well okay again I promise you if you're a medical student if you're if you're a resident this is one of those podcasts where I believe that it can truly help you like both on exams it can help you clinically and all that but again like I say these podcasts are never supposed to be useful patient care and I'm supposed to see all this just again to sort of protect protect and cover myself right but again if you really understand these concepts I've explained to you again I know it took a while right but I really do think that this will give you a very very very solid background in poem right and once you have this background basis like down path then the rest of poem is not that hard right and again poem intrinsically again it sounds hard at the beginning but if you understand it kind of like again the we have expanded here it should have very few problems going forward so as I always do at the end of every podcast I do offer again one on one tutoring for many exams right so the USM is step one step two C case step two C.S.

step three exams right and then like the pre-clinical exams in med school the 30th shelf exams the NBA shelf exams of the tutoring for all those things right and then if you're a medicine resident and you need tutoring for like the um the in training exam right like the medicine in training exam or the medicine board exams believe it or not I'd offer tutoring for those and then if you're a college student and you're studying for like biochemistry organic chemistry general chemistry physics histology physiology I'd offer tutoring for all those things and then if you're a med student applying to residency so like an ERAS application or a college student applying to med school so an AMCA application I do offer one on one advice in or I guess you can call it consultant for these things so like editing personal statements doing more interviews like preparing your entire application these are all things I've worked with tons of people on and again this past cycle that I worked with people essentially everyone I worked with uh matched into uh residency right most of them got like their first choice most people got within their first two choices so take that for for what you will and again I also have a lot of admissions committee experience right so I've been on the admissions committee of a top two med school for a year okay so again I've reviewed tons and tons of applications in fact I'm already working with a ton of people for this current application season so um if that's anything you interested in feel free to reach out to me through the website or you can send me an email at divine intervention podcasts with an essay the end at gmail.com so I hope you gain a lot from this podcast have a wonderful rest of your day and God bless you thank you

Obstructive disease shows a low $\text{FEV}_1/\text{FVC}$ ratio; Restrictive disease maintains a normal or high $\text{FEV}_1/\text{FVC}$ ratio but has reduced total volumes.

It measures the efficiency of oxygen transfer from the alveoli to the blood. Widening suggests impaired gas exchange (e.g., V/Q mismatch or shunt).

$\text{FEV}_1$ (or FVC) is used to calculate predicted post-operative lung volumes, ensuring the patient has sufficient residual capacity for survival.

The body increases Cardiac Output ($\text{CO}$) to maintain adequate Oxygen Delivery ($\text{DO}_2$) despite low Hemoglobin ($\text{Hb}$).

It physically restricts the thoracic cavity, limiting the total volume (TLC) available for lung expansion. This is a "fixed box" problem.

Hypoxemia with a widened $\text{A-a}$ gradient where the cause is outside of the heart or lungs, such as AV Ms (e.g., in Hereditary Hemorrhagic Telangiectasia).

Normal lung function; it rules out significant obstructive disease.

Pulmonary fibrosis (restrictive process).

The cause of hypoxemia is likely extra-pulmonary, such as opioid overdose or high altitude (low ambient $\text{PO}_2$).

Chest wall/thoracic cage abnormalities (e.g., scoliosis) or extrinsic compression (e.g., morbid obesity).

Intra-cardiac shunts involve defects within the heart structure (VSD, ASD); Extra-pulmonary shunts bypass gas exchange outside of the normal pulmonary circuit (e.g., AV Ms).

Airway narrowing/loss of elastic recoil prevents rapid exhalation, leading to air trapping and a low rate of flow over time.

Normal lung function; it rules out significant obstructive disease.

Pulmonary fibrosis (restrictive process).

The cause of hypoxemia is likely extra-pulmonary, such as opioid overdose or high altitude (low ambient $\text{PO}_2$).

Chest wall/thoracic cage abnormalities (e.g., scoliosis) or extrinsic compression (e.g., morbid obesity).

Intra-cardiac shunts involve defects within the heart structure (VSD, ASD); Extra-pulmonary shunts bypass gas exchange outside of the normal pulmonary circuit (e.g., AV Ms).

Airway narrowing/loss of elastic recoil prevents rapid exhalation, leading to air trapping and a low rate of flow over time.