everyone. I think we'll go ahead and get started. We have a really good panel of experts and really what better venue to be talking about both deep diving and and high altitude than Hawaii, right? I mean you have the best trekking here, the best diving here, and so this is really a great venue and a great match in terms of the topic. And so basically the flow here will be we'll talk about high altitude and pulmonary physiology by Mary Turets, then we'll go to scuba diving where we have Dr. Lindholm, and then we will sort of finish it up with more of a clinical evaluation, you know, patient that you see in the clinic and how do you certify them to be fit for either diving or for high altitude exposure. So without further ado, we'll have Dr. Turets come here and talk about high altitude and pulmonary physiology. Thank you guys for joining at 3 p.m. because I think we are the last session between maybe some lower altitude hiking and some shallow snorkeling. I'm going to be talking about high altitude and pulmonary physiology and this is really going to be a review of physiology. My name is Merida Turets. I'm from New York City. I have nothing to disclose and my task is really to review the physiologic responses to high altitude and to hypoxia in that setting. I'm going to talk about the acute high altitude illnesses and really all of this is setting the stage so that we can then talk about how to approach our patients who have underlying medical conditions, lung disease, etc. when they come to us in order to fly or climb. So first, exposure to high altitude is very common and just as a reminder, many people classify the definition of high altitude as starting at 2,500 meters. It was very difficult to go between meters and feet and meters or feet so just to remember you can multiply by 3.3 and get meters into feet. So 2,500 meters is sort of the beginning of high altitude and that's the altitude at which altitude related illness typically starts. And about 200 million people visit these regions per year, so 200 million over 1,500 meters and 40 million visit regions over 2,500 meters, whether that's for work or recreation. Some people are slowly climbing up to these heights. Other people are flying into great heights. Other people are maybe just taking a very steep, you know, tram all the way up. So people are getting to these heights in different time sequences. And more common than that is obviously air flight, so about four and a half billion air passengers per year. And with increasing altitude, there is a nonlinear decrease in the barometric pressure and that ends up leading to a decrease in the ambient partial pressure of the oxygen and subsequently a decrease in the partial pressure of oxygen every step along the oxygen transport cascade. So reduced inspired oxygen, reduced oxygen in the alveolar spaces, in the arterial blood, in the tissues, and in the venous blood. And you can see here at sea level we're about 760 millimeters of mercury. Commercial aircraft typically pressurized to 2,400 meters, 570 millimeters of mercury, all the way up to Everest, which is 29,000 feet and 253 millimeters of mercury. And if we remember that the fraction of oxygen in the air is always 21 percent no matter how high how we are, and that the saturated water vapor pressure is always the same at 47, the inspired oxygen is related to the barometric pressure. And so in a healthy person at sea level that's 150 millimeters of mercury. On an aircraft about 110 and all the way to Everest 43 millimeters of mercury. And so obviously when we are that high and the partial pressure of oxygen is reduced, and particularly as people are exercising and require more oxygen delivery, tissues end up becoming hypoxic and we can develop hypobaric hypoxia. Because flying is more common, I'm just going to comment on that first, healthy adults do drop their saturations with flight. Planes typically are operating at 9,000 to 12,000 meters but they're pressurized for a cabin altitude of about 2,400 meters. And that's just about before we start falling off the oxygen dissociation curve. So typically we're usually okay with sat still in the 90s in that area. This was a study done in 2007 where there was a simulation of a hypobaric chamber simulating different altitudes from 650 feet all the way up to 8,000 feet, which is where about planes are pressurized for. And people, a healthy group of people typically drop their oxygen saturation by four percentage points and this was maybe a little bit lower with exercise and lower with with sleeping. And there have been another couple of studies which have looked at cabin crews and other healthy individuals have dropped below 90%. So people can drop their saturations to about 90% and even healthy people even a touch below. Obviously if you were to be deposited at the top of Everest right now you would very quickly lose consciousness and die. Typically the acute neurologic effects of hypoxia are even felt at about you know 1,500, 2,400 meters. People can get change in their vision and as they go up you know decreased energy, lassitude, dizziness or tingling, seizures, twitching, all the way up in the 7,000 meter range to loss of consciousness. And again depending on how high you are, how high the altitude is, within minutes people can approach death. But obviously people do climb these mountains. People climb mountains without oxygen and so many hundreds of million people live at high altitude areas. So our bodies are able to acclimate and adopt to these low barometric pressures and low oxygen settings. And how do we do that? We don't climb a mountain in leaps and bounds but we take it slowly. We try to go slow so that we give our bodies time to acclimate and be able to adapt to the low oxygen environment. And so being in that low barometric pressure, low oxygen state triggers a whole series of compensatory physiologic responses in many different organ systems in the body over different time courses ranging from the minutes to the two weeks. And so again I'm just going to go through some of them. The most important is that the low partial pressure of arterial oxygen ends up triggering the peripheral chemoreceptor activity. This ends up causing hypoxic ventilatory response or a marked increase in the minute ventilation. That increased minute ventilation will end up increasing alveolar oxygen, decreasing the carbon dioxide, ultimately causing a respiratory alkalosis. And that will quickly end up limiting this response. But over the next series of days with kidneys compensating, excreting more bicarb, leading to more of an acidosis, and also to the chemoreceptors becoming more sensitive, this hypoxic ventilatory response will pick back up again and be sustained. In addition to the kidneys excreting more bicarb, there's also a diuresis and natriuresis. And in addition to the increased minute ventilation, which ends up having more respiratory losses, more fluid losses to the respiratory tract, as well as this natriuresis, people can have a decrease in plasma volume. There's also increased sympathetic activity that will end up leading to an increased cardiac output. And that's all driven by heart rate. So at altitude, the heart rate will increase. Cardiac contractility will be about the same. And stroke volume will actually decrease due to that decrease in plasma volume. So this is generated through the heart rate. And very importantly, the low alveolar oxygen will end up causing hypoxic pulmonary vasoconstriction. The increase in the pulmonary vascular resistance, as well as that increased cardiac output, will end up causing an increase in the pulmonary artery pressure. There's increased EPO. So that is going to end up increasing hemoglobin concentration. Within the first days, that's due to the decreased plasma volume. And within days to weeks, the hemoglobin concentration will increase due to the EPO. And this is all designed obviously to increase the oxygen carrying capacity of blood. And then finally, there's multiple other things that are triggered by hypoxic inducible factor, including increased VEGF, causing angiogenesis, and hopefully delivering more blood to exercising tissues. So hypoxia inducible factor is a master switch for a lot of the body's response to hypoxia. So all of these responses, the acclimatization process, it varies among all the organ systems. But in the setting hypoxia, HIF-1-alpha is not degraded. It will combine with HIF-1-beta, enter into the nucleus, and end up acts as a transcription to increase genes that are related to mitochondrial pathways, anaerobic metabolism, angiogenesis, endothelial effects with increased nitric oxide, induction of EPO and erythropoiesis, and changes in the carotid body chemosensors. So this series of complex changes takes different organs, take, you know, on the order, again, of minutes to weeks. And the pattern and timing is similar in everyone, but the magnitude of these changes varies between individuals. And that ends up affecting individual tolerance to hypobaric hypoxia and the susceptibility to altitude illness. The other couple of things to remember are that sleep disturbances are very common at high altitude. There's an increased incidence of poor sleep quality, increased arousals, change in sleep architecture, increased incidence of central sleep apnea, and periodic breathing. And then oxygen, low oxygen environments clearly have effects on exercise. So the effects of high altitude on exercise, there's a decrease in the maximal oxygen consumption at work capacity, so that at any level of work people are fatigued much more easily. There's an increase in ventilation, which leads to the increased oxygen cost of breathing and the sense of breathlessness very early on. And as opposed to being at sea level, with exercise people's oxygen saturation decreases. That's a combination of the reduced gradient for diffusion with the alveolar oxygen being lower than usual, so the gradient between the alveoli and the venous blood or the capillary blood is reduced. And there's also a decreased pulmonary capillary transit time with exercise, so less time for the oxygen to hop on board. So decreased saturation is common as people are exercising. So just, you know, as we're seeing patients it's important just to let people know that there are a series of normal responses that people will feel. So travelers should expect to feel an increased heart rate at rest and with any level of exertion, an increased respiratory rate, increased frequency of urination, dyspnea and exertion that resolves with rest, poor sleep, and also positional lightheadedness. Most people when they travel to altitude do okay, but certainly people have maladaptive responses that can cause acute high altitude illness. Again, this typically starts occurring at 2,500 meters and above. Also, if people are already at a certain altitude and they climb higher it can occur, and people have underlying diseases that impact their ability to ventilate, they already have respiratory illnesses, they have anything that prevents them from having the regular responses to low oxygen, can feel these symptoms sooner. And the three things that we talk about are acute mountain sickness and high altitude cerebral edema. These are thought to be sort of different aspects of severity on a continuum with AMS being very common but relatively benign and HACE being very uncommon but lethal. And the pulmonary manifestations are seen as high altitude pulmonary edema. The other important thing to remember is that these illnesses, it doesn't matter how fit you are, how much of an athlete you are, what your prior experiences with altitude are, these can happen in anyone. But the risks, the main risks for these diseases are how high you go, how quickly you go, and people's individual or genetic susceptibility. Other things that can also act as risks are degree of exertion. So if you go quickly to a high altitude and you're exerting yourself you're going to become more hypoxic and more symptomatic and at risk quicker. If you're taking any substances that interfere with acclimatization, so you know sleeping pills, other sedatives, alcohol, and again if you have comorbidities that impact your ability to increase your ventilatory rate or if you're already compromised by low oxygen, etc. So again acute mountain sickness is the most common high altitude illness. It's diagnosed clinically in people who have recently gone to altitude and it's almost a little bit like a hangover. It's diagnosed clinically with a headache plus one of the other symptoms of anorexia, nausea, dizziness, malaise, or sleep disturbance. And again this typically happens at about 2,500 meters and above, usually 6 to 12 hours following ascent. It lasts for a couple of days and it should not recur again at the same altitude. And a JAMA study looked at about a meta-analysis of that included 67,000 travelers and found a prevalence of 2,500 at 2,500 meters of 19% and 50% over 6,000 meters. But obviously there's great variability for this right because the faster you go the more at risk you're going to be. And for each 1,000 meters increase in altitude above 2,500 meters the prevalence increased 13%. Again on the more serious side of the spectrum is HACE. So again well less than 1% but potentially lethal. So this typically happens at a little bit higher altitudes, 3,000 to 3,500 meters. Occurs in people who already have signs of AMS. Also common in people who have high altitude pulmonary edema because those patients tend to be more hypoxic and that's what's driving this problem. The risks again are the same. The altitude you reach, how high you go, and individual susceptibility. But people present with encephalopathy, ataxia, progressive decline in mental function and consciousness, potentially leading to coma and death. You can essentially make a working diagnosis of HACE in a patient who's recently ascended to high altitude particularly 3,000 meters and more who are showing signs of encephalopathy. And if you have access to brain imaging it will show cerebral edema and an MRI shows typical T2 flare signal. So the pathophysiology of this is all driven by hypoxia. So if certain people might be a bit more at risk for this, so if you have a reduced hypoxic ventilatory response or increased metabolic demand or already pulmonary edema that's leading to hypoxia, the hypoxia will end up causing vasodilation in the brain. And even though there's also hypocapnia causing vasoconstriction, there's loss of autoregulation leading to increased cerebral blood flow, increased intravascular pressure. In people who are susceptible there's also mediators that end up causing vasogenic edema, leakage of the blood-brain barrier, cytotoxic edema, and ultimately increased ICP. And the mechanism of death is brain herniation. HAPE is the main cause of death from altitude illness. Again, two to five days after arriving at altitudes of 2,500 meters or more. Patients typically present earlier in the early stages of this with dyspnea on exertion, dry cough, and then this can progress to dyspnea with any exertion or even dyspnea at rest and development of pink frothy sputum. Patients are hypoxic, tachycardic, they may have fever, crackles, and imaging will show pulmonary edema. So the pathogenesis of HAPE is also again driven by hypoxia. So there's alveolar hypoxia and that leads to hypoxic vasoconstriction, but that hypoxic vasoconstriction is uneven so that there are some areas where more blood flow is going through the, you know, the generally unaffected vessel. So there's increased pressures in some of the capillaries and if you're exercising and your cardiac output is increased, if you already have a problem and you already have a restrictive vascular bed, this problem is made even more apparent. And this increased pressure in the capillaries ends up leading to ultra structural changes of the blood gas barrier and increased permeability and alveolar capillary stress factor, ultimately leading to the leakage of plasma and red cells into the alveolar spaces and high permeability pulmonary edema giving you the hypoxemia and pink frothy sputum that you can see clinically. So the most important thing for travelers and physicians as consultants to remember is that the best prevention is gradual ascent and there's the mantra climb high, sleep low. So it commonly suggested that you don't ascend more than 3,000 meters when you first reach altitude and that after that not more than 500 meters of sleeping altitude every next day and every three days or so take a rest day. So again gradual ascent is the most important thing to counsel people on. So in addition to gradual ascent other things to think about for prevention are pre acclimatization. So there is some data to say that if you go to altitudes of 2,000 meters or so for a couple of weeks you know high enough to start getting some of these compensatory responses but not high enough to start getting sick that people have an easier time and less incidence of altitude illness when they climb higher 4,000 meters and over. There's lots of different studies that look at hypobaric chambers simulating this but it's unclear how you know how high how long you know how long to get a benefit. Avoid sedatives, excess alcohol and again avoid vigorous exertion when you first arrive to altitude. There's different pharmacologic preventions. I'll look at that again on the next slide but particularly acetazolamide is prevention for acute mountain sickness and HACE and nifedipine for pulmonary edema and treatment for AMS if it's mild or moderate. A day of rest is typically okay. Again usually this dissipates in a day or two at altitude. You may use analgesics for a headache. You may give antiemetics for nausea. If it's more severe dexamethasone, potentially acetazolamide and if people remain ill the the next treatment is to descend. For HACE it's descent ASAP. So as soon as you recognize that someone is potentially having high altitude cerebral edema, any encephalopathy, the most important thing is to descend. Sometimes people are limited to being able to descend so the goal obviously is to increase oxygen. So supplemental oxygen people have portable hyperbaric chambers or gamma bags that can simulate a decrease in 2,000 meters so that's another option and dexamethasone as treatment. And for HAPE, again, descent, oxygen, hyperbaric chambers if necessary, rest, and nifedipine as well as treatment can be treated. So I touched on these, but again, this is just a list of medications for the prevention and treatment of altitude disease, acetazolamide for AMS and HACE. And again, that will end up causing more of a diuresis that ends up losing bicarbonate, causing metabolic acidosis and increased respiration. Dexamethasone as treatment for HACE and nifedipine for prevention and treatment of HAPE and potentially the PD inhibitors, tidalafil and silbenafil. So the last comment I'm going to make is that, you know, if you keep all this physiology in mind, you just want to make sure that you're identifying patients with comorbidities that put them at risk with flying or high altitude travel. So you want to identify those who are at risk at high altitude, so anyone who's at risk for severe hypoxemia or impaired oxygen delivery, right, your patients have COPD or heart failure, at risk for impaired ventilatory responses, neuromuscular disease, ILD, at risk for problems due to pulmonary vascular responses, so patients who already have pulmonary hypertension. Does hypoxia pose a risk of complications to the underlying medical condition? Do people have PFOs and when their, you know, PVR goes up, is that going to get worse? And then you're going to determine the need for further evaluation or counseling, which you're going to be hearing about in a little while. Thank you very much. I think in the interest of time, I'm not going to state all these bullet points, but this is a summary. All right. Okay. So we'll see if this loads. Yes. So happy to be here. Let's see. Is it that one? So I'm going to talk about scuba diving or diving physiology with, of course, some pulmonary applications. And I am originally a cardiologist, sorry, a radiologist from Sweden. And we moved to California about seven years ago. And I am a professor in hyperbaric medicine. I like the lungs. It's my favorite organ. There's something with some organs are just more interesting than others. It's a joke among radiologists. Among you, you're probably all interested in the lungs. I put a lot of extra information in the slides. So because this is taped, so if you need to go back and find the references or something, I'm going to go through some of the physiology, some of the problems we face. And I'm going to scoop over the basic stuff first. So asthma, what do we do with asthma? It's actually, the problem is if there is regional air trapping, could we have a bar trauma of ascent? And what we try to do is to look at exercise capacity and also look at the risk of having an acute asthma attack underwater. It's generally considered that asthmatics could do recreational diving if it's under well-controlled or very mild asthma. There is a link there. And Diver's Alert Network is an American organization, a nonprofit. It's all over the world, but they have some slides on their website where you can get a little bit more information. And you are probably the ones who are very well-suited to evaluate this. If you have somebody with asthma, you can look into how bad is it, treatment, and also exercise capacity. Another thing is, of course, COPD and pulmonary fibrosis. The current recommendation there is basically no diving. And there are a lot of people with COPD, and there are probably a lot of people with COPD that dives. And the whole thing of fibrosis and COPD, it's based on expert opinion. People like my predecessors who sat together with your predecessors and thought about this. And, I mean, there is no clinical trials made in this. So there is an ongoing question on how risky is this, and what do we do? There is an interesting paper on Bertholdt-Dubé, where they saw an increased risk of pneumothoraces in air flight and in diving. But the thing with the bull and the bleb, one of the theories of this bar trauma is that if you have these bullae, they would be more susceptible to a break. And somebody recently from the Netherlands, they did a check on 101 military divers that did chest CTs and they did X-rays. And the correlation, as we know, it's not very good. What we see on a chest X-ray is not always what we see on a CT. It went both ways. The other issue or problem is that they also did, some colleagues of them, they looked at forensic from something else, like road accidents or people who had no pulmonary disease but died. And about a third of those had pulmonary blebs and bullae. It's so common, so depending on the radiologist you have reading your scans, but we normally, at least in Sweden, we don't report if we see a small bullae or bleb unless it's sort of relevant or asked for. It depends also. I heard somebody make a study that said there are more bullae and blebs reported in elective CT than in acute CT, probably because if it's acute, you have more, less time. So you don't, you can skip over that not too important stuff. But the problem is if a third of people have these bullae, it used to be that you said, a bullae, you're off diving. And we had this interesting case some years ago. This was a woman who came for the five-year checkup of her colon cancer metastasis, and this turned out. And it turned out when we looked back that she actually had a similar CT five years earlier that looks just the same. She was over 70 years old. She's a marine biologist with over 3,000 dives. And to the best of my knowledge, it looks stationary. So we think it's a sporadic LAM, probably, and it's probably looked like that for years. So for some reason, if we're talking about communicating cysts and gas going in and out, I don't have a good explanation for that, but it is a bit of an ongoing question. Because what do we do? We used to do chest X-rays in military commercial divers to evaluate them. And that was probably, it's also for the submarine escape, people trying to escape from a submarine. You train and you get that risk of overexpansion. So the military did that. But if we switch it to do a low-dose CT, we see a lot more. Not to mention all the nodules we'll find, but we also see all these other structural anomalies. And I don't know what to do there. Maybe not look. Most recreational scuba divers in the world, you know, you go down to the beach, you show some money and you jump in the water and you get a course. It's very regulated on the instructor, how they train. But there is most places in the world, you have a form that you say, I'm healthy, I don't have asthma, I don't have any other issues, I can dive, fine, that's it. And then you dive. So the chest X-rays of today, that's mostly for military or some commercial divers. So I haven't, my theory, one theory I have is that this idea that a chest X-ray was good because you found if you have 18-year-olds going into the service, if you find something on a chest X-ray of an 18-year-old, there are probably some congenital issues or TB. So it's probably good to exclude those from diving. But what about this 40-year-old commercial diver who has been smoking and worked in the water for 20 years? They don't look as clean in their lungs, you know that. I also put in diving after COVID. We did have a bit of a scare there from what do we do with all these people that get COVID? And we came up with, there are two publications there. They're open access, so you can find them. If you just Google this on PubMed, you can download them. And they have those two tables which has been adopted by most of these organizations. And what we did was we based it on severity and then what you do as a physician when you have this. And then we added the 0.5 category when Omicron came around. Basically saying that if you have Omicron, it's more like a cold, it's upper respiratory. We don't really care about those if you recover. If we want to do the really quick short version of this, if you have somebody who's a diver, they get sick. If they want to get back in the water, if they're back to their normal exercise capacity, that's a good sign. You can always go by that. I mean, the normal exercise capacity of a person varies. Is it to be able to walk to the car and back or is it running six miles in 30 minutes? But it is a very good thing that we use, especially for the non-recreational divers. I mean, if this is your work, you should wait. And what you can do then, you can build on this. You can do a cardiopulmonary exercise test with a pulse ox, for example, if you find out. If they've had some severe lower respiratory disease, add a chest x-ray. I might go as, from my perspective, but I'm not licensed in the U.S. So, but I would say if you don't see anything on the chest x-ray, they are not sicker than anybody else, maybe. But a chest x-ray is a good sort of, based on that idea that if you have something that's severe enough to show up on the chest x-ray, history has shown us that maybe those shouldn't dive. But it is a question, what do we do with all these residual findings, all these ILAs or fibrous bands? And we are probably on a case-by-case basis there. It depends, of course, also is this a person, it's their life, it's their livelihood. I mean, or is it, oh, I kind of like to dive and climb mountains and, oh, yeah, I can skip the diving. I mean, it's a, I think it's on that level, too. So, another thing that happens when we go in the water is immersion pulmonary edema. And the shift of blood going into the chest causes this, which is generally considered cardiogenic edema. And if you add exercise, that increases the risk. It happens in triathlons, surface swimmers. It happens also in military trainees. We have these, in San Diego, we have these tryouts for the Navy SEALs, where people are going through sort of horrendous physical tasks, and they also get it. One important thing with pulmonary edema of immersion is not to confound it with pneumonia. Some radiologists might read it as pneumonia if you just see a chest x-ray with changes on. These are, the edema goes away usually in 24 hours, and there is no infection if it's a SIPE. So, these are, maybe they don't show up, but you can see the curly B lines in the middle there, and you see the patchy alveolar infiltrates. And SIPE has these very typical images. One is the interstitial edema. It looks like a classic heart failure, left ventricular heart failure. But, and when it gets worse, you get these patchy alveolar capacities. We found something very interesting by, sort of by chance. A colleague of mine, Dr. Cebreros, he started doing respiratory panels on these candidates because of COVID. And these, we didn't have those with COVID, but it was interesting that 80% of them who suffered SIPE, or at least suffered SIPE enough so they had to be medically evaluated, had a pathological respiratory panel. That study is very interesting. It was published in CHESS, but we don't have a proper control group. But 80% is still an indication, or maybe there is a risk factor, maybe indication that infection is a risk factor, which is not unlikely. Other risk factor for SIPE is hypertension, cold water, heavy exercise, actually being female. In these triathlete swims, about 80% to 90% of cases are female. They have a high risk of suffering this, which could be due to anatomy, but we don't know. Or I, if we continue, if you dive deep, these days very few dive with hard hats. But you could fall underwater, and if you have one of those hard hats, and you don't feel gas, you could actually be sucked up into this metal thing. There was a few cases in the past. But what happens is when you, if you hold your breath, and you dive, your lungs are compressed. It's Boyle's Law. Air is compressed. And you also feel, of course, the ears. You can have sinus squeezes. But if we stay to the lungs. Oh. Can we lower the volume somehow? I don't know if I can scroll in this, actually. It's not too loud? All right, better now. So there is a sport where you free dive. Of course, it starts, but somebody wanted to see how deep can I dive. And it comes from spear fishing, which is a way of harvesting food. This specific technique here is, of course, if your anchor from your sailboat gets stuck under a coral or a rock, you need to pull yourself down, dislodge that thing, and get up. It's also used, of course, before we had scuba tanks for various kinds of harvesting of food on the bottom. The pearl divers in Japan. But we are inclined to compete. So some people wanted to compete and see how deep can you go. And there are different disciplines. This one is where you pull yourself down and up. Most ones you swim with your fins. You can see he has a lanyard. He has a line attached to the rope. Because if you go down 100 meters, you want to know the shortest way up. And it also has a safety feature to it. So this rope goes down to a platform. And then it goes over the boat or the surface platform. And then there's a big weight. So if something happens down there, they pull that weight over board and the whole thing sort of flips up. So they suck the guy up or the girl. Yes. And so what happens when you dive? Of course, you need to survive on your oxygen stores. I'm not going to talk much about oxygen hypoxia. You can lose consciousness from that. We will see that later. Yes, a little spoiler alert. This guy is still alive. I met him in July. So not a spoiler alert. But what happens is when you start, you weigh yourself so you're floating on the first 10, 20 meters. Because if you regularly do these dives, you want to, you know, if you get tired, you want to be buoyant at the end. That's where the risk is. It's like if you go down 100 meters and up, you're not going to, you're most likely going to have problems at the surface because you probably did 99 meters the day before. He pulls something at the bottom and then he starts ascending. So, but the weight is that he was just falling because when the lungs are compressed, you get heavier. So the buoyancy goes down. So then you need to pull yourself up. And what happens, of course, is you have a supply of oxygen from your blood and the stores that are in your lungs. And that is what you have. And there are some risks with pressure changes. There are some risks with how to sort of overextend your capacity. This dive I'm going to show you because it was a very good rescue and it's a very good footage. Normally they don't do as bad as this guy did. Normally they pass out just, if they go overboard, they have an issue when they're fairly close to the surface. So what happens then, when you start getting hypoxic, your brain, it's not there yet. So anyway, so what happens when you squeeze the lungs, imagine when the gas is compressed so much that the lungs are completely collapsed almost. And then you get a sub-pressure. The pressure is going to be lower in the airways and you have athleticis, and that also creates this fluid shift. And the freedivers call it squeeze when they sometimes come up and they bleed or they spit up blood. And whether it's a form of this sipe, immersion pulmonary edema, or if it's something else, that's up to figure out. Now you're going to assume, you're going to see he's going to get in problems. You see he's trying to swim with his legs. He's getting tired and you see he's getting uncoordinated. So he's losing consciousness here. And so the safety divers, they have safety divers, and what they do is they put a hand over the mouth so you don't get aspiration, and then they swim up. They prefer to do it by freediving because a scuba diver is not as good at swimming. You have the pressure changes and the risk with that, but it's also all that gear to handle. So there are quite a few people that can swim to 60 meters or 200 feet and swim around there a little bit looking for fish. For them to go down and be safe is not an issue. And this is a good way of seeing... Oh, if you look at his... You can see white foam coming from his mouth. Now you're getting all of it, okay? Keep aiming, keep him off his back. I can turn off the volume. So he passed out, which is hypoxia, but he also had this kind of squeeze incident where he got a pulmonary edema. He got basically a flash pulmonary edema of some kind, and this is a very organized competition. They had good safety, and you're going to see he's going to sit up very soon here. The difference of passing out from a hypoxic incident in this case is, of course, the heart is still beating. It's not a cardiac arrest. So they don't really need CPR. You need to give them some air. It's why there are these happy moments where people have looked at, you know, TV or Baywatch or something, and they saved somebody at the beach. They have pulled them up, and they blew a little in their face, and they wake up because it's not like a damaged heart. Now he's sitting up, and I have another picture. This is not from him. It's from a woman. That came into the hospital. Normally we don't do CTs on those. They're very rare occasions, and she had a saturation of 75. She had been diving to 75 meters and you can see the patchiness of a typical, severe immersion pulmonary edema in that. And I have about one half minute left. This is North Shore. If you have some time, you can go there and swim with turtles. This was a few years ago though. Last one. If you do a barotrauma of ascent, you have too much pressure. You get arterial, the lungs can rupture, you get gas bubbles that goes to the brain. And it's an acute indication and we want to treat that with putting people in a hyperbaric chamber, compress them and give them oxygen. If you don't have access to a hyperbaric chamber, give them 100% oxygen. Not a little nose thing, real 100% oxygen. So we don't know how to do that. Which could be of interest. This is also something that can happen when you are doing a CT guided lung biopsies. There are sometimes cases where you get arterial gas embolism from barotrauma and those are preferably treated with hyperbaric oxygen. They usually recover much better if we do that. But it is a problem that the chambers in the US are actually disappearing in the hospital base. We only have 67 chambers we know about that are 24-7 at this time because the reimbursement is better for having these small chambers out in an office building next to it than having these 24-7. It doesn't pay as well. That's where the hyperbaric field is at least. But if you have access to a chamber and you have this, you should give them proper pressure. There's also a whole market in the sort of alternative medicine where you buy one of those sleeping bag pressure chambers and they're not as good. It's not the same thing. So anyway, that was what I had for you. Thank you. You want the sound back? Just push the button here. So I'm the third guy and I've got the... With all that that means, I've got to keep you in your seats until 4 o'clock. So we're going to try to make this worthwhile. So I'm from Baystate Health where I direct the NTM and bronchiectasis clinic and these are my disclosures. I think Meredith and Peter, they've adequately covered the first two points. And so we're going to do the third, which is to review the guidelines for clearance for patients with additional focus on those recovered from COVID-19. So first let's go high. We're going to run quickly through some basic physiology just as a recap because Meredith did that wonderfully. And then we're going to move on quickly to obstructive diseases with COPD being an exemplar and then restrictive diseases and then post-COVID. So here's our guy, a 72-year-old guy who likes to go to Florida. He's on oxygen. He has not traveled since the pandemic. He no longer has to wear an N95. He's got his first, second, third, fourth, fifth, sixth COVID vaccine and he's ready to go. Can he fly? How do we decide if he's able to fly? What preparations should we make for flying and what considerations are there at the other end? So this is a quick run on the physiology. You can see that in harmony with Dalton's law, as you ascend the ambient pressure decreases and because we're in the troposphere, the relative concentration of the gases are fixed. And so the partial pressure of each gas will decrease as you go up. Now you would think that this would altogether, the partial pressure of oxygen would altogether track the decrease in the atmospheric pressure, but remember that that's diluted by carbon dioxide and water vapor. And so you can see that the alveolar pressure decreases somewhat more rapidly than that of the ambient pressure. Of course, there are other considerations, right? Ambient temperature, increased UV light, decreased humidity. And these are all things that we take into consideration with our patients who are going to high altitude. Now again, Meredith had put up this cartoon and I just want to focus on the ventilator response. Note that early on within minutes, the patient will have hyperventilation due to an increase in respiratory rate and tidal volume, the short-term potentiation, and then there's short-term decrease. And then subsequently within days to weeks, patient starts hyperventilating again. And this is due to increased sensitivity of the peripheral chemoreceptors as well as increased gain at the central level. And so the patient begins to hyperventilate again. Now remember that most of our patients with COPD, they've got dynamic airway hyperinflation. They will have increase in the end-expiry lung volume, increase in thoracic gas volume, and therefore increase intrathoracic pressure. Remember that the heart is like a box within a box. And so the increased intrathoracic pressure will decrease transmural pressure, particularly on the right atrium, decrease venous return, may also increase pulmonary pressure. The patients, as a part of their hypoxic response, will increase heart rate and increase cardiac output. And therefore, the transit time within the lungs, as we've discussed previously, will decrease. And so these things combined in patients who are ready at the limits of their physiologic reserve with COPD will serve to unmask serious disease and can cause clinical problems. Interstitial lung disease, again, the patients are unable to adequately increase the ventilatory volume. And there's already impaired gas diffusion across the blood barrier. And now the diffusion gradient is somewhat that more shallow. The pressures, the diffusion pressures are decreased. Pulmonary hypertension, hypoxic vasoconstriction is exaggerated in some patients who've got already baseline pulmonary hypertension. And some of this is genetic. And of course, we can all figure out the effects on the heart. Patients with coronary artery disease will have a significantly increased cardiac work. They won't be able to mount their cardiac output. And it will unmask ischemia. Therefore, who needs pre-flight evaluation? So this comes from the British Thoracic Society. And the Europeans, there's an excellent review in the cited article. Patients with severe COPD or asthma, severe restrictive lung disease. If you look at the British Thoracic Society, it suggests that patients with an FEV1 less than 50%. In this European review, they suggest FEV1 less than 30%. So there is some give in terms of which patients we'd be doing a pre-flight evaluation on. And clearly, as the other speakers have pointed out, a lot of this needs to be personalized. Cystic fibrosis, patients with previous air travel intolerance, and patients with cardiac disease, they need to be considered closely, as well as the others that you can see there. What about the high altitude climbing? This comes from the Wilderness Medicine Society. It suggests avoiding high altitude travel for patients with severe COPD. And you can see what qualifies. And then assess need for supplemental oxygen in patients with an FEV1 between 1 and 1 and

panel discussion

Hawaii

deep diving

high altitude exposure

physiological responses

hypoxia

high altitude illnesses

scuba diving

pulmonary edema

patient clearance