DIP Episode 421 - Pulmonary Pathophysiology Series 11

Alright, welcome. This is episode 421 with the Divine Intervention Podcast. In today's podcast, we'll continue our Pomonaire Path of Physiology series. This is gonna be series 11. We're gonna stop right where we left off. So last time we met, we said that, at least that's in episode 419, we said that when you're talking about EE Gradient, you can have hypoxemia with a normal EE Gradient and hypoxemia with elevated EE Gradient with a high EE Gradient. And I give you one central principle I said that whenever you have a problem that is intrinsic to the lungs, when you have hypoxemia as a result of it, you're going to have an increased EE Gradient. On the flip side, when you have a problem that is extrinsic to the lungs, you're gonna have hypoxemia with a normal EE Gradient. And I remember the last time we talked about this hypoxemia, we spent some time dilinating normal EE Gradients and what makes sense. Now let's talk about hypoxemia with a high EE Gradient. So again, as I said, hypoxemia with a high EE Gradient means there's a problem that is intrinsic, a problem that is native to the lungs. Now, to go a little deeper on that concept, you can think of hypoxemia with a high EE Gradient, being indicative of a problem in the alveoli or in the pulmonary vasculature. If you really think about it, the two underlying principles behind most causes of hypoxemia with a high EE Gradient are either you having problems, you know, getting the oxygen already in the alveoli into the pulmonary vessel.

So the oxygen is in the alveoli. But man, for some reason, it just cannot get into the pulmonary vessels, into the pulmonary capillaries. So your PBG02 cannot be transformed adequately to P-little A02. The other cause of hypoxemia with a high EE Gradient, or in terms of mechanism, is if the blood escapes the well ventilated alveoli altogether. So you have blood, and for some reason, it just doesn't contact the alveoli, the well ventilated alveoli. So if you think about it, blood that gets to the lungs, you know, comes from the pulmonary arteries, to the pulmonary capillaries, the blood getting to the lungs, naturally has a low P-little A02. Why? Because literally, that blood is the oxygen-fed blood, it's coming from the right side of the heart. So since the blood coming from the lungs, and coming from the rest of the body into the lungs, has a naturally low P-little A02. Any problems at the level of the alveoli, any problems at the level of the alveoli, will make the spread between PBG02 and P-little A02 wider, which is literally what constitutes the AA gradient. So what are some high yield causes of hypoxemia with a high EE Gradient? Well, it's going to be things like pulmonary fibrosis, things like shunts, things like v-cumus matches. So let's maybe talk about pulmonary fibrosis first. So obviously, pulmonary fibrosis, the big problem is diffusion distance. Remember, if you have fibrosis in your lungs, those things don't transmit oxygen very well.

The diffusion distance is just increased. It's too thick. Literally, alveoli membrane is too thick. So the P-little A02 will never fully equilibrate with the PBG02. So the PBG02 is what we have in the alveoli. The P-little A02 is what we have in the pulmonary capillaries. So by the time blood gets to the end of the pulmonary capillaries, full equilibrium will not have happened. So the spread will be bigger. If we look at a shunt, which I'm going to spend quite a bit of time discussing today, with a shunt, blood completely escapes well ventilated alveoli. There's literally a viola with oxygen to oxygen-aid blood. But that blood just doesn't get to those alveoli. The alveoli just do not see that blood. That's a shunt. So in a shunt, blood completely skips well ventilated alveoli. So if you think about it, again, since this blood just never gets to hang out with a good alveoli, the oxygen tension is very similar to those carried by the veins from the different organs of the body. So again, think about it. When you're getting to the lungs, you encounter an alveoli. Alveoli have all these great oxygen they want to give you because you are a deoxygenated head blood. But if the blood skips those alveoli, they never hang out together. Then that blood is going to have this very low p-little A02. And the alveoli is going to have this very high p-little PBG02. The spread is going to be bigger. So how can blood skip the lungs? Well, blood can skip the lungs in one of two ways.

One way is when there is some kind of hole in the heart that allows blood to make its way directly from the right ventricle to the left ventricle. Now, here's one thing I think I want to say that you really need to be careful with. So many people will be like, yes, divine VSD. But the thing is, remember, most VS Ds are not shunts. Let me explain. We know that if you have a VSD of ventricular septal defect, blood is going to flow from the place that has higher pressure to the place that has lower pressure. So it's going to flow from the left ventricle because it has much higher pressures than the right ventricle. Since the left ventricle is at higher pressures than the right ventricle, blood is going to flow in that direction. Flow is determined by the gradient. The gradient of flow is from the left to the right ventricle because they are much higher pressures in the left ventricle. Now, when that blood hits the right ventricle, think about it. The blood in the left ventricle, what kind of blood is that? That's oxygen-ethyl blood. So when the blood hits the right ventricle, it's like very well oxygen-ethyl already. So it's like, wow, going to the lungs to get another many merry go-round. So if you really think about it, when you have a VSD, most times it is a-sionotic. It is a-sionotic. However, the thing is, when a person has a VSD and it goes on for long to enough, especially when you have a large VSD, the right ventricle is now receiving preload from two sources.

Normally, it's just one source. Normally, your right ventricle receives preload from the right atrium and that's it. But when you have a VSD, the right ventricle receives preload from the right atrium and from the left ventricle. It's getting preload from two sources. When you get preload from those two sources, the right ventricle is now beginning to handle more blood than it normally does. Since it's now handling more blood than it normally does, over time, because it's built to be a low pressure system, not a high pressure system. Over time, your pulmonary vessels to handle those increased levels of blood, they'll have to start having smooth-module hypertrophy and things like that. Over time, you're going to develop pulmonary hypertension. When you develop pulmonary hypertension, then the pressures on the right side of the heart will progressively begin to increase. When they increase sufficiently enough to overcome the higher pressures in the left ventricle, then that flow of blood across the VSD from the left ventricle to the right ventricle will reverse. It will then become flow from the right ventricle to the left ventricle. That's what's known as isymengers syndrome. So the blood is now going to flow from the right ventricle to the left ventricle and obviously, the blood in the right ventricle is deoxygenated. It's flowing to the left ventricle, then pumping to the rest of the body. Guess what has happened there? That's a shunt. That's a shunt.

So again, it's not every VSD that is a shunt, but in isymengers, you do have a shunt because now, with the blood flowing directly from the right ventricle to the left ventricle, you're pretty much skipping the pulmonary arteries, the pulmonary capillaries and the pulmonary veins. So oxygenation is not happening. Think of tetralogy of fallow. That's another example of a shunt because you have profound paumonics stenosis and you have a preexisting VSD, then blood is going to be flowing from the right ventricle to the left ventricle. That's an example of a shunt. That's an example of a shunt. Now, what's another way you can get a shunt? Well, under way you can get a shunt where blood basically skips the lungs. So, what's another way is where you have blood getting to the lungs, but the blood is in countrain of your life that have no oxygen at all. So think, for example, if you have like a collapsed ovulus, because if you have a pneumothorax, your your life are going to collapse. If they collapse, then blood may be getting to the lungs, but that blood is skipping oxygenation in the lungs because their your life hanging out with, have no oxygen in them. Because they've been collapsed. This is one of the reasons why new needle respiratory distress syndrome is not a good thing. Because they have that surfactant deficiency, surface tension between the ovulus goes up. So the ovulus are going to collapse more.

That's why when people have NRDS, they tend to have lungs that are operating at low-long volumes. So they have those low-long volume lungs and the ovulus have collapsed. So blood may be flowing through those lungs, but there's no oxygen that have your life to, in the ovulus, to oxygenate it. So the person becomes hypoxic. The person becomes hypoxemic. So the thing is, it's ridiculously high to know that if you give oxygen, it will not correct a 100% shot. The good thing is, most times, it's very rare to have a true 100% shot. But if you have a 100% shot where blood in your vessels do not encounter oxygen in the ovulus, if you have a 100% shot, giving supplemental oxygen is not going to help. So literally the blood is not going to the ovulus. It's not having any real contact with the ovulus. So even if oxygen shows up, there's going to be no blood to oxygenate. So again, if you have a 100% shot, they are dangerous with this statement. It is very high yield. If you have a 100% shot, it will not improve with the administration of supplemental oxygen. But if you have a shot that is less than 100%, it will be improved with the administration of extra oxygen. So let me explain how they will test this on an exam. If our friends at the NBM Es give you a question. They give you a question about a person that is hypoxemic. And they give you some values, you notice, wow, they tell you, they give you the O2 tension before the person gets supplemental oxygen.

Obviously, the person is going to be hypoxic. And then they give you the O2 tension after the person has gotten supplemental oxygen. And you notice that, wow, the A-igridients has not changed. The O2 sats and stuff have not changed between administrations. The most likely cause of that person's hypoxemia is a shot. The most likely cause of that person's hypoxemia is a shot. They love to even test this. Some people almost, they don't even realize this. But these things drop a lot on the peach shop for whatever is our reason. They tell you that, wow, this is this newborn had these low abgars at birth. And then the newborn is becoming hypoxic. And then they start giving supplemental oxygen. And you notice that the O2 sats don't budge. There is some kind of a shot operating in that child. The child has some kind of sanitary congenital heart defect that is literally causing a shot. For example, if you have transposition of the grid vessels, that's a shot. That's a shot. Think about it. When you have transposition of the grid vessels, because what's the normal situation? The normal situation is that blood flows from right atrium to right ventricle. And then from the right ventricle, it flows into your pulmonary arteries. And then from your pulmonary arteries to your pulmonary capillaries. Your pulmonary capillaries to your pulmonary veins. Pulmonary veins to the left atrium, left atrium to left ventricle, left ventricle to the atrium, the atrium to the rest of the body.

And then all the way back to the right atrium. So normally, the right ventricle is empty by the pulmonary artery. Normally, the left ventricle is empty by the atrium. But when you have transposition, look at the term transposition of the grid vessels. So those vessels, the grid vessels are your pulmonary arteries are your yoder, they become transposed. The right ventricle is then now drained by the yoder. The left ventricle is then now drained by the pulmonary artery. You can clearly see that that's not a good thing. Let's look at things from the right ventricle's perspective. Blodding the right ventricle is, you know, is deoxygenated. That block from the, that deoxygenated block from the right ventricle is going to drain into the yoder. And then that block from the yoder is going to drain to the rest of the body. And then is going to come back to the right atrium through the SVC and then back into the right ventricle and then back into the yoder. And then back into the rest of the body and then back into the right atrium right ventricle. That's a shunt. That's literally a shunt because the blood from the right ventricle is literally not going to the lungs. It's literally skipping the lungs is literally going into the yoder. You're essentially recirculating around the body deoxygenated blood. You're going to notice that those kids are not going to live very long in those circumstances. That's a shunt. That's a shunt.

So many of these really bad nasty, salinity, continental hard defects are examples of shunts. I'll say that again. The examples of shunts, the examples of shunts. And the thing is our friends at the NBA, I think I want to kind of really delve deep on this because this is actually something they love to test a lot. On NBA means they'll tell you that this child was normal for the first few hours of birth and then like day two, day three, they start becoming hypoxic and you're like, wait, if this child had the sanitary continental hard defect, that was a shunt, how did they survive? Well, the reason they survived is that there was some mixing. The shunt was less than 100% in ureth. And the shunt was less than 100% when they were born. Let me explain. The thing is, say for example, a child has transposition of the greed vessels. That's not great. However, don't forget that there's this structure that exists in ureth, known as the doctors arteriosus. The doctors arteriosus is a pipeline. It's literally a blood vessel that transmits blood from the in uterine. When you're in uterine, it transmits blood from the pulmonary artery to the yoder. And that's not a problem. That's what happens in uterine. But after you're born, obviously the left side of the heart has much higher pressures. So blood is not going to be flowing across that doctor's arteriosus from the yoder to the pulmonary artery.

Well, if you think about it, if you think about it, the blood in the yoder is oxygenated blood normally. The blood in the pulmonary artery normally is the oxygenated blood. Although, as you'll see, that relationship is not what happens in uterine. In uterine, because you're literally banking on mom for oxygen, that blood that is coming into the right side of the heart for a fetus is already oxygenated. So it makes sense one uterine that blood can flow from the pulmonary artery through the doctor's arteriosus to the yoder. And that's not a big deal. Even if the blood is coming from the pulmonary artery, it has already been oxygenated at the umbilicus, at the placenta, sorry, at the placenta. So the baby is fine. After the baby is born, think about it. Walk with me here. This baby has transposition of the great vessels. So the right ventricle is being drained by the yoder. The leventricle is being drained by the pulmonary artery. So blood is going from left ventricle to pulmonary artery. Obviously it's going to go to the pulmonary capillaries, get oxygenated even more, go to the pulmonary veins, and then come back to the left atrium, left ventricle, and then again into the pulmonary artery. So think about this. Walk with me here. When a person has transposition of the great vessels after they are born, after they are born, after they are born, which vessel has oxygenated blood? Think about this. Pause this podcast and think about it. Don't just memorize stuff.

You can work this out in your brain. Think about this. Which vessel has oxygenated blood? The vessel that has oxygenated blood is going to be the pulmonary arteries. It's going to be the pulmonary arteries. The pulmonary arteries are going to still have oxygenated blood. Because the pulmonary arteries are draining the left ventricle and then they are sending that blood. So pulmonary artery draining the left ventricle, sending that blood to the pulmonary capillaries to get more oxygenated, sending that blood to the pulmonary veins, and then the pulmonary vein is draining back to the left atrium. So the pulmonary arteries still contain oxygenated blood. But your ayurter contains the oxygenated blood. Because the ayurter is draining the right ventricle. And from the right ventricle, the oxygenated blood is going into the pulmonary, into the ayurter, because it's been transposed. The right ventricle is draining the oxygenated blood into the ayurter. And that the oxygenated blood is going around the body and then going back through the SVC to the right atrium. But when you think about it, because there's a doctor's arteriosus, a pipe that connects the pulmonary artery to the ayurter, there's going to be some mixing of blood in the ayuric system. With blood in the pulmonary arterio system. So that mixing makes the shunt less than 100%. But we know that after a child is born, what is one of the first things that happens in the heart is the closure of that doctor's.

So when the child is immediately born, the doctor is still open. So they still mix in. So the child may not have any initial problems. But over time, over time, when that doctor's arteriosus starts to close, the shunt will begin to approach the patient. And then the doctor's arteriosus closes completely. Then that shunt is perfectly 100%. Giving supplemental oxygen is not going to help in those circumstances. That is why many times when you get an NV Me question on a child that has a cyanotic congenital heart defect. And the child is becoming hypoxic. Many times the right first step in management is to administer a drug known as our prostitial. Our prostitial is a prostaglanding E1 analog. By giving that prostaglanding E1 analog, it's a visual dilator. And the doctor's arteriosus is literally a vessel. It's going to dilate the doctor's arteriosus and keep that shunt at less than 100%. Because the thing is when you actually administer oxygen, you're not slowing down the closure of the doctor's arteriosus. So you're not really helping the child in those circumstances. So again, if you need to replay this and think through this, I think it's a smart idea to do that. This stuff I just described is extremely high yield. If something you're going to see on USML exams, on shelf exams, especially the Pete's shelf. I'm telling you, in fact, if you want to maybe raise some more with Pete's cardio, I will encourage you to listen to episode 326 on the website.

It's a podcast I made back in the day, but it's a super high yield podcast to know, for example. So just remember, when a child has a sanitary congenital heart defect like transposition of the grid vessel, that's the model that I used in utero. The child is fine because blood is flowing through the doctor's arteriosus from the pulmonary artery, which contains oxygenated blood, because which is weird for an adult, but normal for a fetus. Because that blood has been oxygenated from the placenta by mom. So blood is flowing through the doctor's arteriosus from the pulmonary artery to the pulmonary vein, I mean to the to the yoder. So that's fine. And that blood from the yoder flows to the rest of the body, not a big deal. But after that child is born, you know, the child may be fine the first few hours, first one or two days, because they still that mixing of blood. The shunt is less than 100%. But as the child leaves long enough, that doctor's arteriosus that is allowing mixing that is making the shunt less than 100% will close. When it closes, when it closes, when it closes, that's going to be a problem for that child, because now the shunt is going to be 100%. Because literally your recirculating the oxygenated blood throughout the body and your recirculating oxygenated blood throughout the lungs, that's literally what you're doing in translation of the grid vessels.

That's why in those circumstances, many times the right first step is to give prostaglandin E1, our prostadil, to help keep the doctors open, to keep the shunt at less than 100%. Until you can take the child for cardiac surgery. So again, I can already imagine in my mind how the imbini's can literally make a plethora of questions from this one concept that we just discussed. They can, because think about it, how can you make a translation of the grid vessels question harder than it needs to be? Easy way, I mean, if I read the imbini's a simple smart way to accomplish this is to just start bringing in this shunt physiology. Just to see people really understand it, because people are very good at memorizing, oh, if you see this kind of heart on X-ray boom, that's transposition. Okay, you can memorize the buzzwords for the imbriology. But if you want to really see if people can think and reason, just write a few multiple choice questions, where do you have to work these things out in their mind? And again, you don't have to memorize anything if you just understand what I just said in the first place. So to wrap up, because I want to make sure I finish this a-agridient business. So I said that causes of hypoxemia or the high-a-agridient we said that you can have this kind of problem if you have a shunt or if you have like pulmonary fibrosis, the diffusion distance is just not good. And then I said the final thing that can cause this is what is known as VQ mismatch.

Now, VQ mismatch is something that people make harder than it needs to be. So what's the easiest way to think about this relationship? Think about it in fractions. Think about it as a fraction. V over Q. V represents ventilation. Q represents perfusion. Now, what other way to think about this is I think of it as impute equals outpute. And think of the impute as being ventilation and the output as being perfusion. So the ventilation you bring in that's your impute. It would make sense that it should match the perfusion for it. That's the Q that's your output. So under ideal circumstances, think about it. You want it to be a one-to-one ratio. You want your ventilation to, you know, you want an off-blood, taking off that oxygen you are bringing in. You want the ventilation and the perfusion to match up as good as possible. You want the VQ ratio to be one. But that's not the case because again, the body is an amazingly efficient machine. But it is not a 100% efficient machine. Under normal physiologic conditions, the value is approximately 0.8. It's approximately 0.8. So in general, you have more perfusion than adequate oxygenation for that blood coming in. Let me put it this way. Let's say you have like one unit of blood coming in. It's only like 0.8 units of that blood that gets oxygenated. In the next Poinier Pathophysiology series, I'm going to talk about why that relationship holds. Because you may be like, divine, why is it no one-to-one? There is a reason.

But to discuss that reason, we'll have to discuss long zones. I'm not going to go into long zones today because I feel like that's just going to be a little much for one podcast. So, under normal physiologic conditions, the ratio of V to Q is 0.8. So that means the denominator is bigger than the numerator. The perfusion outmuches the ventilation. Now, whenever you have a huge deviation from this relationship, that's how you get hypocsemia. For example, if you have a VQ ratio that is much less than 1, let's say you have a VQ ratio that's like 0.5. It means one of two things. It means that your numerator has gotten too low. Either the ventilation has decreased, or the denominator has gotten too high. That means you have too much perfusion for the amount of ventilation that you're getting. So, the key thing here is that blood is getting to areas without enough oxygen to completely saturate it. Blood is getting to areas without enough oxygen to completely saturate it. Now, what if you have a VQ ratio greater than 1? A VQ ratio greater than 1 can arise from one of two reasons. It can arise because the numerator is too high. You have wasted ventilation. You have a lot of ventilation. But the blood is not taken advantage of all that extra, extra ventilation. Alternatively, you can get a high VQ ratio, a VQ ratio that's greater than 1, because the denominator is too low. So, you're not having adequate perfusion for the amount of oxygen coming in. Well, why is that happening?

That's happening, for example, if you have a PE, a pulmonary embolus. Literary pulmonary artery is obstructed. So, if you're still oxygenating the lung just fine. Well, you know, you're bringing oxygen into the alveoli. That oxygen doesn't see any blood to partner up with, because the blood is literally not getting to the pulmonary capillaries, because the pulmonary artery has been obstructed. Really, this is pretty much a dead-space situation. It's pretty much a dead-space situation. There's enough oxygen in the area, but there's no blood there to take off that oxygen. So, I think I'm going to pause here. Again, I'm telling you this is one of those podcasts where if you have the time, just go back and release into it and make sure you really understand. But we then talk about lung zones. You'll put together so many concepts we have already talked about. So, this is why this is a series. Just follow it and you should be in good shape. So, I'm going to wrap up here. And I'm going to wrap up with a small life lesson as well. I do offer one or one tutoring for all the USMT exams. Step one to three, complex one to three, pre-clean cool medical exams, 30th shelf exams. The only thing I don't do to is OMM. I also have review courses, a 20 hour review course for step two and step three and complex two and three, an NV Me testing and strategy scores and a biostatistics bootcamp.

And then I have these podcasts on the three major podcast apps, Apple podcasts, Google podcasts and Spotify. And I have a You Tube channel, Divine Intervention, USMT podcasts and videos. That's where I can find the videos that I make. And then I also help with Eras applications and mock interviews and things of that sort. If you're interested, shoot me an email. And then finally, I have a website called Divine Intervention Lifelesses.com. Many people have told me they love the life lessons that I put at the end of my podcast. So I made a separate website where every week I post two podcasts that from a biblical perspective, address a common problem faced by people. So Divine Intervention Lifelesses.com, there's an Apple podcast associated with that. It's called Divine Intervention Life Lessons Podcast. We have more than 120 podcasts I believe right now. So what's my life lesson today? My quick life lesson for today is to not wait until it is too late. Don't wait until it is too late. The thing is, many people are failures in life because they just wait for the last minute. They are not prepared. The thing is, when you're prepared, the life does not just heat you suddenly. Even if an emergency arises, you're better able to handle an emergency when you did not wait till it's too late. Because you see many people, for example, just looking at a met student. They know that the USMT exams are coming up a year from now. What's the smart prudent thing to do?

The smart prudent thing to do is to be like the aunt mentioned in the Bible. Start stocking up food in the summer when windtroll arrives. The winter in this case is when your USMT exams are coming. The summer in this case is when you're a year out from your exams. Why don't you spend time studying calmly, not breaking your back to study? Because you're like, oh, my school is hard. Don't get me wrong, my school is hard. But the thing is, people don't learn from the aunt. Because they don't learn from the aunt, they don't get in a lot of trouble. If you're studying like, oh, you know what, I'm going to put in an hour every day consistently. Then when your dedicated period comes, that's not where you're doing the bulk of your learning. Like, to be honest with you, when I was studying for, I'll see pretty much each of my USMT exams. Most of my learning was not done during my dedicated period. Most of my learning was done months before my dedicated period even started. Because I had prepared. So I was like the aunt in that situation. When it was summer, when all the conditions were good and easy, I was stocking up stocking up stocking up stocking up knowledge. And then when the winter came, when the USMT exams came, by the grace of God, I was able to do well on those exams, because I was well prepared. But you see some people, they're not like the aunt. I mean, there's it for people that I want to, where is this aunt's story coming from?

Just go to the book of Proverbs in the Bible. It has this part about the aunt. You can actually learn a lot of really good things from aunt. That's literally like a topic in and of itself, but anyhow. But you see some people, they wait till winter. They wait till, oh wow, they're like four weeks from the exam, before they start studying and studying hard. So you see some people, they wait like two weeks before. And then they wonder, man, why am I struggling? To be honest with you, you kind of waited till it was too late. And the thing is this does not just apply to the USMT. They are searching commitments, you know in your life, man, I need to make this commitment now. And not keep delaying, delaying, delaying, delaying this commitment. Delaying this thing. So the thing is, now is the time to start doing the right thing. Don't keep, because the thing is, you keep saying, oh, I'll start doing the right thing tomorrow. The thing is tomorrow may be too late. Tomorrow may come, and you may no longer have that opportunity anymore. So why don't you just take advantage? I mean, as a person that has been a physician, I've literally seen people that, you know, I've literally seen people that they were alive one moment. And then both minutes later, they were gone. And when your life is the time to do the right thing, because you're not guaranteed the next moment, you know, a person could be talking right now, and by tomorrow, they are just not around anymore.

So just ask yourself, what kind of life commitment? What are the right things I'm supposed to be doing? In my life, you know, look at yourself. Look at your relationships. Just look at different areas of your life. What are things that I know that, man, I'm supposed to do this thing. And you keep postponing them. Like, wow, you know, I've been telling myself that I'm going to get healthy. Okay, I'll start tomorrow. I'll start next week. No, start today. Start today. If you make good decisions today, those decisions, those good decisions have more time to compound over time. If you start doing the right thing, you can take advantage of the compounding effect of timing in making those good efforts yield strong results in the end. So I just encourage you today, just be wise. Make the right commitments. You know what the, you know that thing that you keep blowing off, that thing you keep putting off, that you know that, this thing I know is going to calm down the line for me. Why don't you just start doing the right thing now? There is no better time to start doing the right thing than now. As you do the right thing, start it now. You see your life take a turn for the better. So thank you for listening to me today. I'll see you in episode 422. Have a great rest of your day and God bless you. Bye for now.

It indicates a problem intrinsic to the lungs (alveoli or pulmonary vasculature).

The problem is extrinsic to the lungs (e.g., cardiac failure, anemia).

Shunts, Diffusion limitation (fibrosis), and V/Q mismatch.

Because the blood bypasses the alveoli entirely; increasing alveolar O2 concentration cannot fix the lack of contact between blood and air.

Approximately 0.8.

There is too much perfusion relative to ventilation (blood going to poorly ventilated areas).

Dead space physiology, such as pulmonary embolism (PE), where there is adequate oxygen in the alveoli but no blood flow.

Intrinsic lung problem (alveolar or vascular).

Pulmonary fibrosis, emphysema/interstitial disease.

Most VS Ds are not shunts because flow follows pressure gradients (left to right), but a shunt occurs when blood completely bypasses gas exchange units.

Prostaglandin E1 (PGE1); it prevents immediate 100% shunting by maintaining mixing of oxygenated/deoxygenated blood until surgical repair.

The ductus arteriosus; its closure leads to a 100% shunt, causing severe cyanosis.

The ratio of ventilation (V) to perfusion (Q); ideal is 1, but normal physiological state is ~0.8.

Pulmonary embolism (PE), leading to dead space where oxygen is present but blood flow is blocked.

Intrinsic lung problem (alveolar or vascular).

Pulmonary fibrosis, emphysema/interstitial disease.

Most VS Ds are not shunts because flow follows pressure gradients (left to right), but a shunt occurs when blood completely bypasses gas exchange units.

Prostaglandin E1 (PGE1); it prevents immediate 100% shunting by maintaining mixing of oxygenated/deoxygenated blood until surgical repair.

The ductus arteriosus; its closure leads to a 100% shunt, causing severe cyanosis.

The ratio of ventilation (V) to perfusion (Q); ideal is 1, but normal physiological state is ~0.8.

Pulmonary embolism (PE), leading to dead space where oxygen is present but blood flow is blocked.