How exactly does the corona virus attack the lungs? How does it spiral out of control? What is a cytokine storm and how can a sick COVID patient survive the damage? Eric & Ken get deep into physiology and the threat of corona virus on installment 3 of Gut Check’s COVID File. Learn, like, and share… stay safe.

Unrefined Bakery  https://unrefinedbakery.com Use discount code “Gutcheck” for 20% percent off of your first online order!!!

KBMD Health https://kbmdhealth.com

Atrantil https://lovemytummy.com/kbmd
All right, gut check fans and everybody at KBMD health. Thank you all for joining us again for a third installment of the COVID file. Dr. Brown and I are here to talk a little bit about the physiology and kind of how people actually get sick. And Dr. Brown actually asked me to do a little role reversal. So can you want to explain a little bit what’s going on here?

Yeah, so this is COVID files number three, and we got a lot of feedback when Dr. Ackerman and I did 2.5 we’re all we did is talk about the gastrointestinal stuff. Then everybody else is in the news is talking about respiration, pulmonary stuff. And so we got a lot of questions about that. And I just happen to see that like, a world renowned infectious disease doctor, Dr. Peter Hotez was on Joe Rogan. And Joe was asking all these lung questions in detail, so I realized that you know, you’re an expert in this your training is a crna. This is right in your wheelhouse. So I thought that we could just do some of that. Even on some of these other shows, they’re interviewing virality and they’re interviewing epidemiologists and they go really, really into the science. What we know that calm is contagious. And we know that the more information you have that can actually calm you down. And that’s what we’re trying to do in this show. We’re trying to get people through this crisis. But I do believe that if you understand the physiology, then it makes sense why some people can get really sick and it makes sense why some people get better. And so you being an expert in this is just perfect. And we’re getting questions like this like from a Mike Logzen from Texas. Interesting. We have one of those working for us also.

Yeah I know, names like that. Just keep popping up there’s Mike Logzen one, Mike Logzen two I wonder if there’s a Mike Logzen three.

I know, so Mr. Mike Logzen and asked what are your thoughts on why younger people and healthcare workers are getting hit hard as this disease goes on? That’s a great question. And in fact very relevant. Newsweek just did an online publication that I received this morning, where it said the over 100 healthcare workers have died from COVID-19 So this is this is an important question. So really what we’re going to do with you today is talk about the pulmonary physiology and what happens and when people say, oh, this can affect you, and you get this rapid progression that can be very frightening and different things like that. But just understanding what’s going on, I think is the real important thing. So, I just want you to take it away. I’ll interrupt. I’m hopefully not too much, because I have a tendency to do that. And if I am just gonna wait I got a slide on that. We’ll get to that. So

A couple a couple of quick apologies that we learned in technology since we are all practicing social distancing and Dr. Brown or Ken is, is addressing his patients over in the Plano area I’m trying to help out over here in the in the Denton area. We actually are not together obviously, it’s while we’re recording like this, so I had to make some really bad drawing slides. Ken, you’re gonna love these they are they’re really, really artistic. And as I share them with you gonna pull our faces down from the screen. So bear with us, it’s not normal. But we’ll try to take some breaks in there, we’ve learned we can’t put them all up at the same time at least we’re not smart enough to do that. And Ken if I go too deep, if you feel like I’m losing votes just going back, hang with us though. The goal here is to show you how the disease itself is probably going to affect your lungs. And then to get to a point of showing you how we think we can work through it. I’m going to show you the tough parts, but at the same time, what it is that we’re hoping to do to really get people through it. So that’s

Really even if this is not relevant to you, I I do know where we’re going to go with this. And right now, the mayor of New York City is thinking about bringing in a doctor draft where basically they’re going to pull doctors out of retirement, they’re going to ask doctors in different specialties to try and help out with these pulmonary issues. So you can even forward this to your doctor if you have family or friends that are in the healthcare field. This is something you could forward to them. Because if I happen to get called in, I want to be informed on how to treat people with their pulmonary situation, not just their gastrointestinal. So this this could also be very relevant for healthcare workers, our frontline people.

I agree, I agree. And I’m hoping that we can make some make some light of not necessarily light but bring some information that gives some people some comfort. So you’ll see here my very first drawing right off the bat did not load the way I wanted it to. So that’s a little bit of humor there. And that’s about as good as these drawings are going to get. So I’m sorry, these are loans. That little green arrow is pointing up to a diaphragm, just a quick refresher, as a diaphragm contracts, it pulls down on the lungs, giving a negative pressure or pulling air into the lungs. And that’s important when you’re healthy. You’re pulling air in, you’re not necessarily having it pushed in some but what you need to recognize is that the lungs are made up of five different lobes the left lobe has two the right lobe has three and every single one of those lobes has tons, literally over 300 million alveoli per lung. So you a 70 kilogram average adult has around 600 million alveoli and that gives you tremendous surface area for oxygen and co2 exchange. That’s what keeps us alive and that’s what the oxygen keeps us alive in the co2, of course, is our waste gas that our body is pushing out. And if you were to spread it out flat, that equals to roughly a little bit larger than a tennis court, so Ken.

Wow, and so the analogy I always thought about this is a tree the main bronchus is the trunk, then you get split, and then it keeps going into smaller branches where the leaves could kind of represent the gas exchange or the alveoli. Do you visualize it like that?

Yeah, tree is exactly what they call it. It’s a tracheobronchial tree and it runs all the way out. There’s actually I believe, 23 generationss of tubes getting smaller and smaller and smaller until we get out to the alveolus itself. So alveoli is all of them. Alveolus is a singular one, don’t hold me to it, I often interchange them myself while talking about them. So one particular alveolus. I’ve just drawn an arrow, it’s in the lungs, it’s everywhere. But I’m making an arrow and a draw here, because this is what we’re really going to get started with on how it all functional I’m sorry, here’s the heart. We’ll we’ll talk about this a little bit later in positioning but know that the heart lies anterior towards the front of your body a little bit, and a little bit over to the left. So but that’s where the heart is located as it receives blood pushes it to the lungs receives the blood again and then pushes it out to your body. So let’s look at that alveolus. The alveolus right here, you’ll see inside the circle, that’s actually the external air that we’ve just breathed in. So that’s where our fresh air oxygen, oxygen rich air will come to, and it will be taken up by the capillary. The capillary is the blood supply that’s bringing up the gas that needs to pick up oxygen and let go of excessive co2 carbon dioxide, that’s the waste gas.

So that’s the exchange, the oxygen goes in carbon dioxide goes into the little alveoli, then we breathe that out.

That’s exactly right. And you’ll notice, even though my drawings are poor, you’ll notice you’ll see the capillary here in a moment is going to start to kind of pull away in distance and that just makes it harder for that gas exchange. Inside the alveolus there are two specific cells that we have in there pneumocytes. So site means cells, pneumocyte one offer gas exchange pneumocyte two are there for surfactant, they make surfactant. Now, granted, the there are more pneumocyte twos than there are pneumocyte ones, but the pneumocyte ones actually take up far more real estate for gas exchange but the pneumocyte twos make that very important surfactant which allows the alveoli to expand without collapsing. And that becomes a problem for us as we as we move along. What we’ve returned to you here in this particular drawing, I’ve only drawn a pneumocyte two because that’s where the infection occurs with the current virus that we’re addressing the coronavirus.

We’ll just say Remember, a lot of people were talking about the ACE two receptor, this is what they’re talking about on the news, the these type two pneumocytes have a lot of these h2 receptors. So that’s the target.

That’s correct. I didn’t throw that on there. But that’s, that’s a definite point. H2 receptors are located right there on that type two pneumocyte. The little blue dot at the top is going to represent a Coronavirus. And it’s going to attach to this type two pneumocyte. So next what happens we’re just going to be reminded here that surfactant is important. It breaks the surface tension. Without it, the alveolus will collapse. Very important. I’m going to remind you a few times about that. So now, the little blue dots inside of the type two pneumocytes represent the replication or basically the the increasing number of viruses that have just now been transcripted. They’re they’re multiplying, and now it’s infected the cell.

So just to go back to our very first COVID episode, the virus gets into the cell hijacks, it gets the cell to produce more of the virus. That’s why they’re growing inside the cell itself.

They definitely are. And then this is not what the cell is programmed to do. So unfortunately, the cell is going to rupture and die, and the virus is going to escape to the alveolus. Now I’m going to stop real quick and remind everyone. Remember, I said that there are type two pneumocytes actually out number the type one. So the problem is it’s not just one type two pneumocyte in this particular alveolus is is infected, probably most, if not all of them in this alveolus certain thing. And so this is happening all over this alveolus. Well, not only is new virus going to escape. These little red dots I just added in there represent inflammatory mediators, and they carry a message. They are searching for help. And not only that we now have a ruptured and dying and dead cell. So you’ll notice I’ve drawn in here, Ken, what would be inside an alveolus like this? What are these things called? You remember?

Yeah, I believe you’re going to talk about macrophages now.

Yeah, macrophages. Exactly. They are the janitors of the immune system. And he’s there to just generally clean up regular debris and cellular debris and then take it in and then basically, it usually gets ushered out or absorbed by left, etc. But what we have now is a crisis situation because it’s not just happening at this time to new massage. It’s happening probably to most of them. They all begin to be picked up these inflammatory mediators are picked up by the macrophage itself, and that’s going to activate it. It now knows it needs to release some messengers of its own to call for help. And right here is the beginning of something they’ve been talking a lot about in the news, especially for young people. And that’s the cytokine storm. Because these interleukin one, interleukin six, and tumor necrotic, factor alpha are all cytokines. And they are going to be released and picked up by the blood supply the capillary right down here, and they are going to have some immediate local action. And as this is happening, remember I said there are up to 600 million alveoli throughout the throughout your lungs is this begins to happen in this section. Imagine all of the interleukin one, six and TNF alpha that will be picked up by the blood supply and now begin to spread throughout the body. So you can see now they’ve made their way into the capillary bed, and a few things are going to happen right off the bat. Once they first enter the capillary bed. The capillary itself is going to dilate. That’s going to lower the blood pressure, but it’s going to increase the blood flow. This happens with injury all over the body we we have an injury, you have swelling, it’s very, very normal because you’re bringing in other things to help repair. But when this happens over and over again kind of an uncontrollable situation like we’re going to talk about, that’s why we know that we need to manage this particular situation. The permeability of the capillary itself is going to increase that’s going to allow for some fluid to escape the capillary bed, and then begin to infiltrate the alveolus itself. So fluid, also known as blood plasma escapes to the interstitial space, which is the space between the capillary and tissues, and then also goes into the alveolus.

So, the permeability or now we’ve got a leaky capillary bed. Permeability is not necessarily something that is in response to it it is because the capillary basal dilation is stretching it too much, are you aware of how the leaky capillary happens?

In a, in a really microbiology term, I think what happens is that those cytokine, if I’m recalling correctly, the cytokine mediators activate endothelial cells, which are the cells inside of the capillary. It actually caused them individually to constrict which makes holes. So if you can think of two large men and suddenly they become skinny men without moving their feet, there’s now space between them. Does that make sense?

Yes.

That’s kind of that’s kind of how I remember it anyway. But that allows the blood plasma which is normally contained in the capillary bed to then escape go into the interstitial space migrates into the alveolus. And this is not what we want. I’m going to reiterate that surfactant is important. It breaks the surface tension of liquid. Without it, the alveolus will collapse. Well, we just had those type two pneumocytes that were producing surfactant. But now they are beginning to be damaged and not produced surfactant at all. And when they were producing it, they were producing the correct ratio, which meant that for the fluid that was there, remember, when we breathe in it’s 100% humidity in the alveoli. Once we don’t have surfactant, now we don’t have enough in the ratio to help keep it open. So losing cells that produce surfactant, and then we dilute the existing surfactant that is going to increase our surface tension. And the potential of collapse of the alveolus is inevitable.

So the surfactant the way I’ve always kind of thought about it when you don’t have surfactant, the alveolus they will stick to each other they cannot slide and open up and so it becomes a very in the dumbed down terms like it like a stuck balloon that’s that can’t expand.

That’s correct. Now written consolidation up here, it may be a little premature at this point. But we will return to it. This is the method of how consolidation occurs. Like I said, forgive me for my drawings, I just did these and snapped them and loaded in the computer. I knew, I knew I couldn’t draw and talk at the same time very well. But regardless, you’ll see that fluid’s beginning to build up. Little red dots in there represent cellular debris. Also, some virus is still trapped in there. Some proteins which are broken ours are still stuck in there. But remember, I warned you earlier, the capillary beds beginning to pull away, right, the interstitial space is also continuing to fill up along with the alveolus. That pressure outside the alveolus and in the water on the inside of the fluid on the inside, will basically make this alveolus you have the potential to collapse it will not expand nor contract with each breath. It basically just kind of floats as a membrane would between two liquids. I’ve also drawn oxygen up here at the top and co2 still in the capillary bed. The sheer distance for the diffusion is going to render This alveolus is incapable of gas exchange. That’s that…

So in this picture, just to clarify the oxygen that you breathe in hits this fluid, because the alveoli is filling up, and it’s not getting to the other side where it needs to go.

That’s correct. It cannot just really won’t diffuse that even though macroscopically may look like a short distance. It’s it’s still far too far for efficient gas exchange for oxygen and co2. So remember, this is what it should look like the oxygen will come in you right next to the alveolus to the capillary co2 goes, goes out O2 comes in. No big deal. That’s just not what’s happening right now. The next step that happens and takes us to full consolidation is going to be the summoning of these neutrophils another part of our immune system, they normally would come in, and in a healthy IV alveolus would more or less be able to target viruses and other pathogens that could be found within the lung. But in this particular situation, especially with the amount of fluids taken on, they actually become a little bit indiscriminate. And they use two agents primarily: the reactive oxygenation species and various proteases. And instead of a targeted attack, with the dilution here, inside the alveolus it actually just becomes kind of a, a wide away, wide array spray of attack. And not only do they grab ahold of some of the proteins that don’t belong there and some of the cellular debris that needs to go. They’ll also end up attacking indiscriminately against healthy lung tissue, healthy pneumocyte ones and pneumocyte twos.

So when people talk about a bacterial pneumonia, this is the beginning of having a super infection in addition to the damage that the virus has already caused.

It is it is and again, Brown and I are not telling you any of this stuff so that you become panicked. But really it’s the opposite. knowing what’s happening may help you understand number one, what it is that your health care provider needs to do to keep you and your family safe if you happen to find yourself in this situation. And number two, I think here in a moment, as we wrap up some of this, this discussion, you’ll see maybe some things you could do at home to outrun some of this.

Yeah. So what we’re doing, what you’re doing is you’re setting the stage work that you if you understand the physiology and the pathophysiology, then you can start doing some modifications to try and improve. And that’s where we’re headed here.

Definitely. And again, this is called consolidation at this point. This just basically establishes it’s just a word that says that this side has been consolidated, it’s not functioning, air will not be exchanged here, we will not have oxygen pick up nor co2 blown out by this alveolus. Now you kind of have to picture not just this alveolus but the entire portion of the affected lung is now experiencing a portion of consolidation. So let’s talk about what’s happened so far. We’ve lost type one and type two pneumocytes: one is how we breathe or the gas exchange two makes the surfactant to keep the alveoli open. Our gas exchange, of course is going down. Our surface area, our tennis court size of surface area for us to pick up oxygen is being decreased. And our diffusion distance at the alveolar level is increasing, even for those that haven’t been consolidated, right. So we have a decrease in gas exchange. You’ll see this little abbreviation I’ve debated on whether or not to put it up there, they’ll PaO2. That simply just represents the pressure of oxygen in the artery. Big P means pressure little a means artery. O2. So that’s just a cool shorthand that medical workers use to identify the partial pressure of the oxygen in a particular location. Inevitably, it just means that we have low oxygen and that gives us a word called hypoxemia.

Low oxygen.

Yeah, low oxygen.

Can you just on that note right there because we use pulse oximeters all the time, and even get them at Walgreens, can you explain the difference between the number on the pulse oximeter and the PaO2?

That’s a, that’s a great thing. So on a pulse oximeter that really is only reading the percentage of the red blood cells that are fully saturated. So there are actually four binding sites on a normal red blood cell for an oxygen molecule to bind on to an iron molecule. If all four of the sites are occupied before the red blood cell has delivered it to a tissue, and it will be counted as one that’s saturated. So if you have 98% saturation, that means 98% of your red blood cells have all four sites occupied before they deposit one. This is a little bit different. This is actually the carrying capacity of, of the red blood cells and how much of the oxygen is actually present to make a difference. So SPO2 talks about how well the red blood cells are actually picking up the oxygen to take it somewhere. But let’s talk a little bit about this. Ken you said that your son went to play in in I believe was in Mexico?

Yeah it was Mexico, very high altitude. He was there for four weeks, I think. Yeah, very high altitude. So essentially it was high altitude training in several tournaments.

We can use that kind of an example, when he was up there, do you think for one second that his oxygen saturation was ever at risk? Probably not.

No.

He was saturating them just fine. But what he didn’t have was a high enough oxygen pressure. So his body sensed that sensed the decrease in oxygen pressure and begin to produce more mature red blood cells to become more of the bus carriers to pick up more oxygen and take it out. So we probably remained at 99% saturation the entire time, but he actually just needed more oxygen molecules themselves to sustain it because there’s just less atmospheric pressure at 7,000 feet.

Yeah, and that’s what we had to come to that conclusion because when it came back, we he got to work up by his pediatrician. And we were all a little bit alarmed to see that his hemoglobin and hematocrit had jumped way up. And it was in response to being in high altitude. So it was the body’s adaption to it.

Well, that’s I completely agree with that. And that’s actually you guys, that’s actually a normal thing to have happen. You have a higher red blood cell count at a higher altitude.

So now you’re going to talk about the thing that’s, that’s the hard part, which is the work of breathing goes up.

It definitely definitely work of breathing goes up fighting this tougher distance of diffusion losing a portion of your lung capacity to move gas is going to increase the work of breathing and then throughout this theme Ken, you’re going to see the word work pop up because it works in the complete opposite direction of what’s happening in the lungs for someone to more or less recover on their own. So cough is going to set in if it hasn’t already, that’s going to increase the work of breathing. And don’t forget these viruses are pretty smart. That’s actually going to help spread the virus. So that’s a, that’s no good either. Work by the body requires more oxygen again, that’s why I’m going to highlight that and just kind of think about that for a moment. If I’m decreasing my availability to get oxygen, but the work and the demand is going up. I’ve got an intersection of a problem here. And if not recognized soon enough, it could just get worse. So let’s talk about why the why hurting your lung and recovering from an injury is probably more important than just hurting your ankle now. This is Mike Logzen’s number three. This is his ankle.

Yeah, he sent us a picture. He said you can use my ankle as an example. Thank you.

Yes. So Mike number three thank you for sending in this photo. And Mike is into jujitsu and he showed me after one of his injuries that he has that ankle twisted, and he said ouch. But the good thing about hurting your ankle, okay? You do get edema just like what we’re having up here, the fluid buildup in the lungs, you could get edema have a swollen ankle. But the good thing is I don’t have to breathe through my ankle, there is no mouth there, I’m not going to have to draw any air at my ankles, so I can just lay up and rest. The problem with having adema or fluid buildup in the lungs is we’re compromising our ability to simply recover. And so that’s why it’s such an urgent situation. And I didn’t I don’t think we mentioned this before we moved on here Ken. What we’re describing here is a acute respiratory distress syndrome. And so that’s ARDS. You may hear people in the news reference, acute respiratory distress syndrome or ARDS. This is kind of more or less getting to the point where we’re spiraling a little out of control as far as the lungs are specifically. So let’s look systemically or all over the body. Remember interleukin one and interleukin six. Well…

Those were the the initial inflammatory mediators set off when the virus attacked the type two pneumocyte, then the response of that is to release these inflammatory mediators.

That’s correct. And they were picked up by the capillary beds. And now remember, they’re not just working locally. If we have a large portion of the lungs, releasing these same mediators, they’re going to eventually make their way to the central nervous system or the brain and spinal cord. They’re going to trigger the hypothalamus, which will then release prostaglandins, that raises your body temperature. And guess what, that’s what we end up turning into a fever. And unfortunately, fever is just going to be more work. It requires more metabolic work for your body. So we are still yet increasing the demand for oxygen. We as we referenced earlier, PaO2 remembers just a simple shorthand for the pressure of Oxygen or the number of oxygen molecules in the artery. It’s low. So this is hypoxemia. Now the trigger that Lucas had whenever he ended up producing red blood cells was they his chemo receptors, noticed that they were a little bit low on oxygen carrier, so they produced more red blood cells. The chemo receptors here are going to try that. But in the interim, they’re also going to trigger the sympathetic nervous system. And when they do that, that’s going to set off anxiety, getting people a little bit worked up, but it’s also going to be don’t forget the sympathetic nervous system is your fight or flight response is going to increase your heart rate, it’s going to increase your respiratory rate. That is just more work. The demand for this oxygen just keeps going up.

And all of that just on that last slide there, Eric, remember that the heart rate is that that’s compensatory, because it says we’re not getting enough oxygen. So if I pump faster, we’ll at least get more oxygen around if I breathe in, quickly I’m hoping to bring in more oxygen in the heart tries to pump it fast. And that just becomes a bit of a slippery slope. And that’s where you’re going to get into right now.

You’re right. And think of healthy lung at this point. If we were simply just had healthy lung at just this point and these are the triggers that high heart rate and a high respiratory rate would basically put everything at ease because hypoxemia would be solved. That’s not what we’re dealing with at the moment. So this is obviously a progressive disease, we have this increase in cytokines, interleukin one, six, TNF alpha, you can have what they call SIRS for short or systemic inflammatory response syndrome. Then this is kind of interchangeably been used with cytokine storm, but essentially, this is what’s happening. These cytokines are triggering all levels and manners of other problems throughout the body. And what we have because of the dilation everywhere, is we have a decrease in peripheral vascular resistance, that’s just the resistance that we have at the edges of our of our water, right, we have an increase in permeable capillaries that Dr. Brown described earlier just means that they become more porous. That’s where we’re leaking that blood plasma, the fluid when we leave that fluid that decreases our blood volume. And we have this systemic all over the body vasodilation, so all of the vessels have lost this resistance. And it’s because all of the vessels are trying to get more of the blood flow, that basically we’re running out of that amount of blood.

When I did Critical Care Medicine, the way to think of that when the body’s when the body’s trying to compensate by trying to get more blood to everything. If you open up the arteries, or if they vasodilate, and you can keep up with it. Then you get more blood flow where it needs to go. But if you can’t keep up with it, imagine a hose. You know the hose that has a little nozzle on it. You can run water and that the smaller the hose, the higher the pressure it goes through. If you keep putting on bigger hoses, then it just comes out as like a little trickle. And that’s what’s going on and that’s what creates this hypotension or severely low blood pressure.

Now it’s a it’s an excellent visual. Yeah, it’s a high pressure with a garden hose. Same amount of water through fire hose. Not so much pressure.

Exactly. Yeah.

So just like Dr. Brown just described, we now are hypotensive. We don’t have that pressure everywhere. So now we’re systematically hypotensive. That comes with its own consequences. It’s going to retrigger the SNS as if we didn’t need more agitation.

SNS-sympathetic system: fight or flight.

Thank you for batting clean-up there. Sympathetic nervous system, there poor profusion of organs. This is where things begin to really kind of spiral out of control if we didn’t get there soon enough. Okay. So we we have the lungs that’s that’s a set of organs right? But we’ve got brain, heart, liver, kidney, also very, very important. If we have poor perfusion we risk getting multi system organ failure or msof. So kidneys liver and heart. Here’s here’s the the reason why I’m highlighting these is these are the ones and almost in this order which will begin to throw off markers that we can we can sample for with laboratory with laboratory work and see the status of a patient. As kidneys begin to lose perfusion, they will increase our blood, our blood, blood urea nitrogen will begin to increase as well as the creatinine and it’s simply because the pressure is not great enough for to be cleared by the kidneys. And the problem is is those are toxic at high levels. We don’t we don’t need those circulating like that. The liver itself will begin to sustain some acute damage because it’s not being perfused and the wastes aren’t being carried away. So we have an increase in AST increase ALT and an increase in bilirubin We also may end up detecting later as we progress an increase in C reactive protein. More interleukin six, just in case we didn’t have enough of that circulating around your, your liver guy here is going through us and interleukin six as well as possibly some fibrinogen. And then if we get to this point and the heart begins to not be able to perfuse, the myocardium or the heart muscle, the heart could begin to throw off some chaperonin or CKMB markers, very similar to what we would test for for somebody who’s had a heart attack. Or they may also, unfortunately be at the point that could suffer uh…

Looking at this looking at multi system organ failure. When I was a resident or when I was a medical student, you’d show up and you have to do rounds. And so you’d have your patient the attending would show up. You’d go 24 hours, what’s gone on the last 24 hours you tell them you’re like okay, well we’ve got blood pressure has consistently been dropping, we either try and keep it up or we keep an eye on it. BUN has gone up creatinines gone up. We’ve got a slight bump in the liver test. So far troponin is normal. And that’s almost how you would say it because you’re like, we’re heading there. We have to stop it before. Because once that heart once you start having a heart attack, that’s your last. That’s that’s the thing that’s going to really give up, so…

No joke. There’s there’s a, and let’s reiterate, before we get to this point, this is why we want you to know what’s happening. We don’t want to get to this point. We’re going to reiterate what we want to steer away from.

This is why whenever they talk about the healthcare resources, why it’s so important, because one thing that I want to get out there right now, because we’re learning data about COVID19. And now it looks like we’re getting close to 30%. I’ve seen some studies when you’re looking at the data of young people getting it not dying, but needing hospital facilities to stop them from going into multi-organ failure. So it is no longer just very old and sick people, they just have, they already walk in before all this starts happening with some other underlying problem. We believe that’s why they go into multi-organ failure quickly. So this is relevant for everybody, that this is why we need to make sure that we continue to practice social distancing so that we do not overwhelm the health care system 100%.

That’s, that’s what we’re trying to work against, for certain. So let’s look at this patient right quick. We’ve had a decrease in oxygen. Remember, our lungs are damaged. And I’ve kind of just made a summation of the workload, these are the demands, we’ve increased the work on the work of breathing, the fever, the heart rate, respiratory rate, the anxiety, not to mention, the organs are starved for it. We’ve got hypotension everywhere. We’re in a little bit of trouble here. So come in, whenever, certainly when it’s appropriate, and you have the right signs and symptoms which we’ve addressed in in the COVID files one and two and two and a half. But what will happen if you end up getting managed in this particular situation, first, they’re going to try to find out how much fluids that can give you to resuscitate some of that blood volume. And it’s not just as easy just giving you what’s missing because remember, we have permeable capillaries, giving too much of fluids. This is a delicate balancing act, giving too much of the fluids could actually exacerbate or make the problem worse with some of the interstitial fluid bonds. So we’ll be using some medicines as well. Some medicines that will help what we call pressors to bring your pressure up some diuretics to help pull off some of the excessive fluid. So there’s there’s a significant balance there, but

It just shows why people like you get subspecialty training and ICU doctors and pulmonologists that anybody that works in a critical care unit. That’s why it’s so important. They’re really good at this and there’s an art to it, and it requires definite increase learning not just this is what’s a little bit scary. If they ask a gastroenterologist like me to come in and say, hey, look, we’re losing people, we need your help in the ICU. One of the reasons why we’re doing this is because as a health care worker, I feel like I need to refresh myself on things that I’ve not done in a long time.

That’s a really good point, because a lot of what you do is a long term solution as you take care of the patient and a lot of what I do both in anesthesia and then whenever we were doing critical care is, it’s very acute. It’s very short term. Most of the medicines we use are, I mean, they’re they’re instant, they’re in and they’re gone, right? So it’s very much like that. So what happens after this is fluids and medicines aren’t going to do it. Well we need to ventilate, which is how we breathe, duh. But if you can’t do it on your own, we’re going to look at mechanical ventilation. That essentially means that we’re going to have to insert an endotracheal tube to control the airway now. Ken at a later time or if we have enough time today, we can talk about some of the alternatives between just breathing room air to this but for this particular episode not to get too far, let’s just go straight to ventilation if that’s okay.

Absolutely, yeah.

Okay.

Because that’s that that’s what everybody’s been hearing on the news also is just we’re gonna run out of ventilators.

Well, yeah. Very, very good point. So some of the other stop gaps in between the cpap, the bipap and in high flow in the tents over the head. Those are all great if they work. I mean, goodness gracious, high flow nasal cannulas absolutely but there’s there’s peculiarities with each one of them. The critical part here is we just don’t have enough ventilators if anybody gets pushed to this area. So we’re going to have to connect that endotracheal tube to the ventilator. And you’re gonna love this drawing. I mean, anybody would obviously recognize this anywhere that’s that’s definitely a ventilator, or a flux capacitor.

Yeah, I was gonna say it looks more like a flux capacitor than a ventilator but…

The blue represents the endotracheal tube that goes down through the trachea there, but I want to call your attention to one small thing, that little bitty red circle represents a balloon. We…after we put a tube into someone’s trachea, we actually inflate this little balloon, and it secures the tube in place. And it gives a true closed circuit meaning air is not breathed around it, we can now control the ventilation. And in this particular case, with such a contagious virus, we can prevent the spread of the virus from coming out of the lungs and through the mouth of nose because it’s closed.

That was the that was the big argument in the very beginning. Is this just droplets or can this be aerosolized and in the beginning, it felt that possibly if you don’t have a closed circuit, then you’re allowing somebody to aerosolize it in a room. And now we’re putting healthcare workers in a room with higher amounts of virus and so the likelihood of getting infected without proper protective equipment. I think that’s why health care workers are our frontline people and they’re putting themselves they’re heroes because people taking care of these patients especially in the beginning, that’s why so many Chinese doctors died when they didn’t realize what they were dealing with.

Yeah, it’s it’s a pretty hairy topic all around and the intermediary steps to getting someone from, you know, being able to walk around to the event, where do you stop and is there enough…is there enough PPE for the others outside of this little bitty ballooned cuff to handle that? Some things that we’re going to do with and I don’t want to get too deep here, but some things that someone would do when they when they put somebody on a ventilator is they would have to look at small measurements, one called tidal volume, that’s just the amount of air that you’re breathing in and out with each breath. If the if, for instance, the average 70 kilogram person takes in around 500 to 550 milliliters or cc’s of air, which with each breath and blows it out at rest,

So that that’s just your normal breathing. So everybody that’s listening to this, their breathing normal, that is your tidal volume. That’s what you normally do.

Correct. And the amount of times that you breathe in a minute is just a respiration rate. At rest, relatively healthy people, adults about 12 to 14 times a minute. So you can see something here though the bottom two minute volume and PEEP, those are those are our calculations and and therapies that are specific to a ventilator and minute volume is simply the respiration rate times the tidal volume. So if somebody breathes in and out 500 cc’s, and they do it 12 times a minute, their minute volume would be six, six liters. Does that make sense?

It does. And I think the key here is the PEEP because this now the physiology that you taught in the beginning, pathophysiology. This is where the PEEP becomes really interesting.

Yeah. So let’s, I’m so glad you said that. So everybody remember PEEP, we’re going to address it. This is what the vent can do for us, and that we can’t do with without it, okay. So just just looking at what we would do with someone who happens to be sick and dealing with an ARDS situation acute respiratory distress syndrome, we’ve lost some of the lung availability, so we can’t put in the same volumes as normal. So we’re gonna have to turn it down. But we want to maintain a relatively close minute volume. So we’re going to increase the respiration rate to make that equation somewhat balance out. Now, that’s just to get us started. Granted, we will be able to check what we call arterial blood gases and make certain that we’re doing it the right way. And we can check our therapy but at the same time to get someone set up. These are some of the calculations that we would make, but what we’re going to do is begin to apply PEEP, okay, and I’m going to break that down here in just a moment. But first, you may wonder why am I seeing people on TV or why do I see someone that I know who’s being treated for ARDS or specifically COVID ARDS in this prone position. Prone means face down spine to the sky laying on their abdomen or stomach, and getting respiratory therapy. If you recall, I drew the heart earlier in one of the earlier slides, and I showed that the heart is located a little anterior, so towards the front, and a little bit over to the left. But essentially, when you lay on your back, that gravity is still pulling down on the heart, you’re you’re kind of occluding a good portion of the lungs that lay along the back part of your body. Does that make sense?

It does and I think that this is something that we need to get through because this may be early intervention. We’re seeing a little bit more of this, and here’s why.

Yeah, so that’s exactly right. And something you can actually do at home, even if you’re not feeling great. Recruitment I’ve written on here, increasing recruitment, recruitment just simply means I can make use of these alveoli all those allow the alveoli everywhere else. If I can use them, I’m recruiting them to be a part, right. So if the heart is more anterior and I’m getting more exposure to more lung tissue that’s still healthy, I’m increasing my recruit. So we’re going to have to monitor for status after we get onto a ventilator. Like I said before, we’re going to look at arterial blood gases. These are just figures that we look at. I’m going to show you the numbers but you don’t have to memorize them of course.

You make it seem like it’s a test.

I know, I know, I want everybody to write in email. If you can recall this you can recall this slide. Normal pH which is how we measure our acidity or bass or alkalinity is 735 to 745. CO2 is 35 to 45. That’s that’s what we breathe out. HCO3 is bicarbonate. Okay, that’s what our kidneys are doing to help give us balance. But remember, they’re not being perfused so they’re not really making it like they need to in our PaO2 we’ve referenced it several times, but that’s the pressure of oxygen in the arteries. It’s normally for a healthy person. 80 to 100. Well, this is what it looks like when we run the first ABG, we’re going to be acidic, because we’re not getting rid of waste gas, and we’re not producing enough bicarb. Okay. And so our oxygen is really what we’re going to have to get control of first. And then we’re going to work towards a better acid base balance as we as we treat the patient.

So for non healthcare workers. This is an arterial blood gas. This is a measure when somebody is in the ICU. And these numbers tell a story, depending on what’s happening, they say if you’re getting slightly better, slightly worse. And by the time what’s really cool, as I’m looking at all of this, usually there’s involvement of multiple specialties, helping out which is why one ICU person can occupy possibly a critical care doctor, possibly infectious disease, possibly a nephrologist-a kidney doctor, and they all look at these numbers and make decisions and tweaks on the patient. This is just shows how complex a patient in the ICU really is.

Without question. Positive end-expiratory pressure.

This is our PEEP.

This is PEEP. So we drew attention to the few slides back. And if I’ve done a little bit better job of putting them in the correct order, we would’ve hopped straight to this. A healthy person when we bring them into, to the OR, and we end up having to use intubation or something like that. Super healthy, you may not have to give PEEP at all. Generally, people end up having, you know, two, three, and all the way up to five. A healthy person can have up to five centimeters of water of pressure and just represents pressure, but just look at the five. And what that does is that holds open the alveolus after you’ve expired gas. Now this is kind of important in that when we breathe and you’re healthy, remember at the very beginning so your diaphragm pulls down, you’re pulling air in your chest wall, is expanding out. It’s literally pulling an external force outward to create a negative pressure to pull air in. Well, that doesn’t happen with a ventilator, we’re having to force air in. So we use people and healthy people, just so that we can keep recruitment up of healthy alveoli already. Well remember, right now we’re not only fighting the fact that we’re pushing air in, we’re actually fighting the fact that we’ve got fluid trying to leak into our healthy alveoli. And if we lose an alveolus to consolidation, it’s 99% chance that we are not going to reareate or re-recruit that alveolus we end up just losing it. So somebody who is already in ARDS, we’re going to start start at 10 to 12 centimeters of water pressure for P and that’s a healthy dose of P and does a few things for us for certain it keeps the alveolus open. It allows us not to give too long of a period of time of high flow oxygen which is 100% oxygen and that’s a whole that’s a whole ‘nother issue. But it really will allow us to save good good parts of the lung. And I should say here Ken, there are possibilities of applying PEEP, where you’re not necessarily intubated somebody with a cpap or bipap mask on this solely secure. You can still experience PEEP in that particular situation or even I think some high flow nasal cannulas are credited with some some portions of PEEP.

So yeah, so just the whole PEEP thing was always confusing to me when I was studying it, but the way the way that you’re describing it, we know that when these alveoli start to go through that whole process that you talked about in the beginning, capillaries start dilating. Well, these, it starts to put pressure on the alveoli. And by the PEEP, you can actually force that alveoli to try and maintain at least some gas exchange so that the leakiness and the fluid creeping in doesn’t win. It doesn’t completely close off the alveoli.

100%. It’s this, the PEEP is…you’re exactly right. The peak is literally there, not only to keep the alveolus open, but in this particular situation on an ARDS patient, we’ve increased it because we need that extra help to help keep that fluid at bay in the capillary bed. We’re not we’ve already lost the part of the lung right now during this disease state that we can’t re recruit while it has fluid in it and is going through its consolidation phase. We need to maintain what we still have. So I wrote right here, increase area recruitment, maybe. It’s a really, really, really slight, maybe. We’re doing that but by proning and turning down. We’re doing that by oh, and Ken you’ve seen these beds before, there are beds that actually are are specific for ARDS patients where you lay them in prone, but they actually turn them from side to side and move them around. And that’s literally to increase and maintain the area of recruitment,

And those are very high level high specialty beds, specifically only for this type of patient. And there’s if we are, we have few ventilators, we got even fewer of those real specialty beds.

That’s exactly what I was thinking. But we our main job here with PEEP, our main job here with the ventilation is to preserve the area of recruitment. And of course with the PEEP like as I mentioned earlier, we want to decrease the need for 100% O2. Some people have even even to ask why. Why would you want to do that? The here’s the danger of the fine line here working through mechanical ventilation. Yeah, so to higher pressure. So we want to be able to dial in and give someone enough of the air that they need to ventilate. We’ve lost part of the lungs, so that’s going to increase the pressure if we don’t dial back the volumes etc, etc. Just remember, if we are apply too much pressure, we can actually spread ARDS because we’re causing damage to healthy tissue. If we give 100% oxygen for too, for too long, we can actually spread ARDS because it leaves reactive oxygenation species, which is exactly what the neutrophils were using to destroy what remained of the virus and unfortunately, healthy tissue.

I know this is not ventilators are not like the way I treat a microwave which is just on high every time and just turn it on and let it roll. Ventilators…it’s such a it’s such a nuanced art. And, you know, and nobody’s discussing that on the news where they’re like, you know, we’re going to run out of vents Well, we’re also going to run out of people like you that know how to run these vents. So, you know, and I, this was not to scare anybody, this is not to get too sciency. You and I talked about this. I feel that here on gut check project COVID files, we see that there are going to be some doctors. And when I was watching the Joe Rogan show, they were they were talking about how doctors are stepping up, they’re switching and trying to help out in this area. And I know that there are probably some doctors like me that are like, okay, I want to help out. There’s going to be or if we get recruited to get in there, then I better do a refresher course. And all I have are a bunch of, you know, really old textbooks that will take a long time to get through. This is just the beginning of something so that they can at least go talk to a family member maybe so that maybe other people will go oh, I understand why my grandpa’s on a ventilator now, not necessarily to COVID. This is just what happens. So I really appreciate you taking the time to do that. I think this is the opportunity to teach a lot more people about this kind of thing. And hopefully this will spread with some healthcare workers. So it will make them feel more comfortable.

And when I told you that was a a because you only asked me a couple days ago if I could, if I would consider, you know, kind of throwing these together and, and I threw something by you. I said what, what would you think if somebody kind of had an idea on something they could implement that actually would be positioning, but not necessarily related to ventilation? And then you threw out the idea of what how did you say if you feel like you’re getting sick, and you’re not feeling well get ahead of the curve, lay down down on your stomach…why you kind of talk about…

Well, it was just one of those things. So an ER doc did an observation. And he he published something where he showed that he actually published it on Twitter, of a patient on there in the prone position on their phone, kind of said when she was on her back, she was struggling. So when when she rolled over, she could breathe easier. I think one of the problems is when we feel real sick, and we’re just laying in the same position the whole time by rolling around and at least laying on your stomach for a bit…then you could switch to your side and back to your stomach. This is the same thing you’re talking about this could actually help recruit. And in the early stages might be able to buy a little time. And maybe ER doctors watching this would understand, okay, if somebody comes in, put them on their belly, then we can do some of these other things like high flow nasal cannula, or this this particular guy was looking at it and he was trying to give a whole flow gram of what he’s been doing, and preventing people from going on ventilators. So it’s a it’s a really cool concept. And by understanding the pathophysiology that you explained…now that makes sense, why that could be a way to help people out.

It’s interesting that you say in that in those terms, too. And what it is he’s doing with the flow gram because it reminds me back when I first started helping manage some, some ARDS patients. We were told that it’s just not common to have to get into this. It’s not commonplace to have to always do ARDS patients. It’s usually your larger hospitals that really kind of encounter those right?

Yeah.

So being reminded of that, I will say that the one takeaway I had from well over a decade ago is whenever somebody is in ARDS, they can’t be proned fast enough. They they cannot be proned fast enough, nobody will say that’s too early, you know, actually getting ahead of the curve. Recognizing that you’re having a loss of gas exchange real estate built, get some for yourself lay down on your stomach begin to breathe. It doesn’t matter if you look a little funny. So what saves your life. But if you began to feel sick or have shortness of breath while you’re waiting for someone to go and seek help for you, get yourself in that position so I mean, ER, home, waiting to get a ride,, whatever it takes.

Because well, yeah, I mean, so if this actually pans out, this may make a big difference, especially if what what he discovered. So we have a lot more cpap machines available and bipap machines, which are just the same thing that many people have obstructive sleep apnea. If what he’s suggesting is that he’s seen people he’ll put prone put them on a bipap or a cpap machine, increase the PEEP. Basically that’s what they’re doing is increasing the PEEP, put them on a prone position and saving them from going on a vent. There’s a lot of people with cpap machines next to their bed including this guy right here talking. I’ve got apnea, and I wear a little nasal pillow. I know I’m not alone because Chang Raun did a social media post about how people if you have sleep apnea, then you’re going to be at risk for developing something, also. So make sure you wear your CPAP machine if it’s dusty in the closet.

Yeah, that article. I found that really interesting how, how well he described being able to do some of the intermediary steps to cpaps the high flow nasal cannula. I don’t disagree with the thing that he’s saying the and he even addresses it in there. If you could just simply answer the question of the danger of the aerosolization of the disease versus preventing someone from having to get some mechanical ventilation, but the one thing he uses that several people still do is the rocks equation know the threat. But essentially you’re taking some status measurements to see…okay, are we beyond any of these intermediary steps, do we need to move to a ventilation? But I think I think that his piece is…it preserves equipment, it still requires people that don’t feel well, they feel like that they’re beginning to lose their breath to go seek help now.

Yeah, that’s, that’s, that’s the key people are like, well, when should I go in? And, you know, the ERs are trying to say, well, if you’ve got a mild fever and see if you can ride it out if you can do this, but the second any shortness of breath starts happening, I think you got to get in and get some of this equipment on you to prevent you from going into ARDS. It’s almost like you have an obligation to get there before because it’s becoming a slippery slope, then.

Hey, you know, Mike wrote that question over to you and I and he was asking specifically about the healthcare worker, and younger people, you and I kind of have similar takes on what we think and maybe maybe slightly different. Did you have an idea on what you thought could possibly total theory but just could possibly be lending itself to younger people or healthcare workers?

Yeah, I mean, my my view on the healthcare worker is just repeated exposure and repeated exposure and repeated exposure. You took a little different take on it on the workload. So tell, go ahead and tell me your take on that one.

I mean, I number one, I completely agree with repeated exposure. I think that somebody who’s healthy and they’re a healthcare worker, they probably can fend off a couple of small assaults, right. But if it’s continuing to attack other healthy pneumocytes, kind of what we laid out today that you’re going to initiate a cytokine storm, unfortunately for somebody else who had they just small, you know, had a small encounter probably wouldn’t even notice that they have been contaminated. But yes, the workload, ultimately, that’s, that’s the sign of failure for really any organ system is their workload, and there’s just not enough supply whatever that supply happens to be for any one of our organs. So when the lungs just simply cannot produce and share enough oxygen for the rest of the body, but the rest of the body is churning and it’s programmed responses to basically kind of amp up. It’s a tough scenario to work out on one’s own without some medical intervention for sure.

Mm hmm. And that’s it. So that’s a really good point that maybe the healthcare workers themselves number one, repeated exposure, but number two, are still yeah, they’re still running around still, you know, busting their butt and, you know, maybe subtle changes in that tidal volume like you’re talking about is really what what starts the downhill, slippery slope. So, but it’s so you know, the whole point is to educate on this and hopefully, if a healthcare worker gets something out of it, that’s why we’re doing this one. Normally, I think you and I try to be a little bit more lighthearted and jokey but I asked you as a favor to me to refresh my memory. So thank you very much for doing that. I’ve I’m dusting the cobwebs off, but I think that…

If you have any specific questions and if I can answer them, shoot, I don’t mind answering questions about vents or any of that kind of stuff. So any questions about any of the episodes you know, you can always email us at kbmdhealth.com go to contact us and let us know or gutcheckproject.com same thing. Well, probably…

You know what, I mean I think that’s thing once we get on Instagram, I have a I would like if anybody is a healthcare worker, a respiratory tech or an ICU doctor and ICU nurse and we got something wrong let us know because…

Oh, yeah.

This is this is not you know. My specialty is a gastroenterologist so this is a learning curve for me on this one, but yeah, I think we did. We’re right at about right at about 55 minutes or so. So we try to keep this around an hour we you know, and see what we can do and you covered a lot of material in an hour, so that’s awesome. That is absolutely awesome.

Hey, man, my dry erase board is worn out.

Yeah. Oh, Yeah, because you would have to erase…oh, you only had one.

Man it was it was it was draw, take a picture and then wipe it away. Yeah and unfortunately I didn’t have I didn’t have Gauge or Mac available to help me kind of sketch those out because those are really really rough Picassos I just threw together.

Yeah and you know what it looks like your drawing skills were just starting to improve if you would have done a little bit started looking like real lungs.

If only you knew how long it took me just to print the words I used.

Well, that’s awesome. All right, well, I’m gonna call this our COVID-19 file number three in the books. Share it with somebody if you think that they could benefit from this information. So great job, Eric.

We’ll see y’all next time. Thank you.

Take care.