Before we go into ARDS, I wanted to deal with two principles from the other lecture, so that we can carry that over into ARDS. The first is transpluminary pressure. Remember transpluminary pressures are what actually inflates the lung, OK? And so when we're ventilating, and particularly when we're ventilating in very noncompliant lungs, we have to keep that into consideration. The equation for transpluminary pressure is alveolar pressure minus pleural pressure, right? And so in spontaneously breathing folks like ourselves, we generate a transpluminary pressure by dropping our pleural pressure, which will increase our transpluminary pressure and we'll get a volume. The stronger we, the more negative force we create, the larger our tidal volume is going to be, OK? It is the opposite in positive pressure ventilation. In positive pressure ventilation, we are, in fact, applying pressure to increase the alveolar pressure, and that's how we increase the transpluminary pressure, and that's how we get a volume, OK? And so your volumes in mechanical ventilation have everything to do with your transpluminary pressures. When it really comes into play with chest wall abnormalities and obesity, you have to keep in mind the impact of chest wall restriction, et cetera, on your ability to generate appropriate volumes based on your transpluminary pressures, OK? The second concept I want us to remember is the driving pressure, OK? The driving pressure, it's kind of, I like to think of, so in the, in the slides you'll see that, like, you can think of transpluminary pressure as the stress of the system, OK? It is an equal pressure kind of across the system. The strain of the system, and where we're going to get into a little bit of trouble depending on how we ventilate, is actually the driving pressure, OK? And the strain can be different depending on where in the lung this pressure is actually applied. And so the driving pressure is your plateau pressure minus your PEEP, OK? And our goal driving pressures, anybody remember what the goal is? Less than 14, less than 15, OK? So when we're talking about ARDS and trying to make sure we're doing safe ventilatory strategies, some of that is we have to keep in mind our driving pressures. So those are actually the only two big concepts that we didn't get to in the last session, So with that, we'll talk about acute respiratory failure and ARDS. So reminder that we have four types of respiratory failure. We have type 1, which is our hypoxemic respiratory failure. We have type 2, which is our hypercapnic respiratory failure, which I would say between those two is probably 90% of the respiratory failure that we all see. And then we have type 3, where that perioperative respiratory failure, whether it's from atelectasis or you had a surgery and your abdominal wall is not as compliant, so you get into respiratory failure. And type 4 is that high demand respiratory failure that we see in like septic shock, cardiogenic shock. They just, because of the demand, it's hard to keep up, OK? So we're going to use a lovely COVID case to kind of walk through the principles of ARDS, OK? So the case is that we have a 34-year-old woman who has COVID who now has ARDS, OK? She comes in. She has bilateral alveolar infiltrates. We are stabilizing her. We put her on ACVC. We are starting at FIO2 of 80% with the PEEP of 12. And our tidal volumes are 360, which is our goal of 60 CCs per kilo ideal body weight based on our ARDSnet protocol. Her peak pressures on these settings are 35 with plateau pressures being 32. We're barely making it right now. You do an ABG, her pH is 737, PCO2 of 38. Her PAO2 is 64, which gives you a P to F ratio of PAO2 to FIO2 ratio. Can somebody pull out the calculator because I am not going to be able to do the math, but it would be 64 over 0.8. It's going to be real low. So a normal P to F ratio, a normal P to F ratio is like 400. Our P to F ratio is less, for simplicity's sake, say it's 64, 80, it's real bad still. So the question is, what do you want to do now? Do you want to decrease our tidal volume? Do you want to increase our PEEP? Do you want to start some inhaled NO? Or do you want a proner? Prone. We want a proner. Why do we want a proner? So there are two basic physiologies of hypoxemia and ARDS. It is VQ mismatching and it is shunt physiology. So proning is going to help with which part? The VQ mismatching. The PEEP, the really high PEEP that we're using is helping theoretically with our shunt physiology. We need help with our VQ. And so what proning does is it actually changes the dynamics of the chest wall so that you get redistribution and then you can improve your VQ mismatching. It is actually not the changes in blood flow from posterior to anterior. They did all these like physics studies and they show that it's literally a change in distribution of lung tissue that then improves the VQ mismatch. So how do we manage it? We have two basic things that we know improves ARDS and that is low tidal volume ventilation, which is 6 cc, 4 to 8. We typically land at 6 cc per kilo ideal body weight. That is height, not width, okay? You probably all have had experience, you know, even if you're a little bit heavier, if you're shorter, we need to, for safety sake, for lung injury protective strategies, we need to do it based on your ideal body weight, which is governed by your height. Okay? All my fellows during COVID were carrying around this ridiculous like ideal body weight chart. MD Calc has it, something, just make sure it's ideal body weight. Never trust the ventilator. I don't know where the respiratory therapists get the ideal body weight from. That's no knock at them. That is just never trust the ventilator, okay? If you like the math, you can calculate it yourself, but MD Calc has a good calculator. What'd you say? Yeah, exactly. Why do we do that? That is the only thing up until a couple of years ago that showed improved mortality and that was low tidal volume lung protective ventilation, which was six cc's per kilo. Okay? Why do we do that? Because in this very heterogeneous lung, there's a lot of different physiology, right? And so we want to minimize additional injury and stress in the lung. And so we want to minimize over distention of some parts. We want to minimize the opening and closing of the alveoli, which creates additional strain and injury. And so we practice a higher PEEP phenomenon to kind of help with the shun and prevent the opening and closing, but we also want lower tidal volumes to prevent overstretching and further injury. Okay? This is just more data. We don't have to go through it, but, you know, there are resources there so that you can see that there is... Every time we repeat a study in ARDS, it shows us that low tidal volume is beneficial and it also shows us that if we use PEEP to recruit alveoli, there is improvement in mortality with that as well. Okay? Oops. All right. The driving pressure, right? The driving pressure you can consider to be the strain on the system. We want to reduce the strain so that we can reduce further injury. And so it is that driving pressure, that plateau minus the PEEP, that studies are showing we should pay more attention to than the actual tidal volume. Okay? And so... And there is mortality benefit in some studies to suggest that it is the driving pressure that we should be paying more attention to. So the plateau pressure minus your PEEP is actually a good measure of is this a safer ventilatory strategy in a non-compliant, non-stretchy cytokine-driven lung. Okay? And again, remember plateau pressures, we try to keep them less than about 14. Okay? And like all things in medicine and all things in ARDS, we try to do what we can, but ultimately we want to keep the patient alive as well. Again, alveolar recruitment is important. And so that's why the higher levels of PEEP continue to be the main, one of the mainstays of therapy for ARDS. You want to keep those alveoli stented open. We want to recruit alveoli. We want to prevent the opening and closing of alveoli. So we need to keep them stented so that we reduce further lung injury. So the higher PEEP serve as multiple things. We're helping with the shunt, but we're also, it's a recruitment maneuver as well to kind of make sure that we keep the lungs open or the alveoli open, minimize injury and improve the shunt physiology. Okay? So there is some mortality benefit associated with using higher levels of PEEP. Okay. Questions about that? Okay. So that part is, although the answer was prone, we haven't gotten there yet, but low tidal volume ventilation and higher levels of PEEP for the very low PEDF ratio. Okay? So 12 hours later, your patient is febrile. Her blood pressure is 130 over 80. Her SATs are 92%. She is on a hundred percent FiO2 with the PEEP of 12. Her tidal volume now is down to 300. And why did we potentially do the tidal volume down to 300? Her plateau pressures in the previous one were 32. Our global plateau pressures are 30. And so maybe trying to make some benefit there. Okay. Her peak pressures are 32. Her plateau pressures, you got them in a better situation. Okay. And her ABG as such, she now has a PEDF ratio of 59. Okay. Let me correct something I said before. That first question was asking us to bring our tidal volume down to 360. I mean from 360 to 300 because the plateau pressure was 32. This question is asking, now that your plateau pressure is down to 32, what do you want to do? Proner. Okay. Proner. Okay. So we're reaching our goals of plateau pressures, 60 Cs per kilo. Now we're going to proner. Okay. So what works? What doesn't work? Okay. I think that the evidence suggests that neuromuscular blockade does not impact mortality. Sometimes it's useful. We'll talk about the PROSIVA study. The PROSIVA study does not require neuromuscular blockade to actually enter into the protocol. Prone ventilation is the only other thing up here that has shown mortality benefit in ARDS patients. And we'll talk about that a little bit more. Recruitment maneuvers, they are helpful. They do not, they improve oxygenation. There's no data to suggest that they impact mortality. Okay. Inhaled NO. I mean, if we need a little extra room for oxygenation, fine, but it doesn't impact mortality at all. Okay. And then some of the other, what do you call it? Other like high frequency ventilation and stuff, again, no significant impact. Okay. This study was looking at neuromuscular blockade and the ultimate endpoint, which was a difference in mortality at 90 days, did not show mortality difference. If you adjust it for some things, there was maybe a mortality difference, but the initial primary endpoint did not, which was 90 day mortality, did not show any benefit with the use of neuromuscular blockade. Okay. PROSIVA. I think we got to go, we got to know ARMA, ARDSNet, we got to know PROSIVA. PROSIVA came out and PROSIVA was like, we have to be a little bit more intentional about the people that we choose to prompt. Okay. And what PROSIVA said is that we need to optimize our patient the way we are instructed to do per the ARDSNet guidelines, which is why that first question was bring her tidal volume from 360 to 300 to get her plateau pressure less than 30. And if you still have a PDF ratio of what, what was PROSIVA's ratio? PROSIVA said, if you do all of that, low tidal volume ventilation, get your plateau pressure safe and the PDF ratio is less than 150 and there are no contraindications, flip those folks over. Okay. Anybody know or remember the PROSIVA protocol for proning? Like how long the patient's prone? 16 hours. 16 hours is a long time prone. 16 hours in a prone position, see what the oxygenation does, flip them back over for eight hours. If there was improvement with proning and you lose that improvement in the back in the supine position, you can consider reproning if that PDF ratio is still less than 150. You can continue to do that until it either does not get you the benefit that you're looking for or somehow there's some contraindications. Okay. That PROSIVA was the other, the only other thing that we've talked about that has literally shown mortality benefit in ARDS patients. Okay. Okay. ECMO. ECMO is a, I like to think of it and I think the data supports it as like kind of a rescue therapy. You should consider ECMO, but it needs to be in patients where there is a bridge to something else. Okay. And I'm not dealing with the ethics of ECMO and the bridges, but when you put somebody on ECMO, I truly believe that given no significant mortality benefit, you have to be thinking forward about once I put this person on ECMO, what is the next step? What is the way out of ECMO? If there is no way out of ECMO for whatever reasons are decided at that point in time, I would strongly suggest you reconsider ECMO because then all the ethical issues then start to pop up. So it is a bridge to something. Whether you think the lungs are recoverable or like a Northwestern, you'll transplant anybody from with this new set of lungs. But it has to be a bridge. Okay. So what works? Low lung protective ventilation, keeping those plateau pressures less than 30, doing about six cc's per kilo, but there's a range of about four to eight. When I always look at the literature, the studies compared it to 10 to 12 cc's per kilo. I've never ventilated anybody at 10 to 12 cc's per kilo in my life. However, we're going to roll with it and we're going to just say, let's keep it at six cc's per kilo. Okay. And then we're going to prone people who we've done all of the other stuff per ARJNET and we still have a PDF ratio less than 150. Okay. Remember Berlin criteria used PDF ratio to actually assess severity of ARDS. So if you have ARDS and have a PAO2 to FIO2 ratio of 200 to 300, you have mild ARDS, 100 to 200, you have moderate ARDS and a PDF less than 100 is severe ARDS. So it's those moderate and severe ARDS folks who benefit from proning. If your PDF ratio is greater than 150, the mortality benefit to prone is not there. And Proceva says, just keep doing what we know works, which is low tidal volume ventilation and lung protective strategies. Okay. Again, APRV continues to make its way into ARDS strategies. Many of you have said you use it. I think it's based on kind of where you are. The idea being it's a really potentially really good mechanism or a mode to recruit because that's that sustained positive pressure over time, a quick drop down to zero pressure to kind of release the gases and then come back up. Okay. But it's one of those things that it doesn't impact mortality, but I do believe in if something's not working and there are other potential options to try, it's worth a try, but it doesn't necessarily impact mortality, and it should not get you away from what we do know impacts mortality, which is low tidal volume ventilation, higher PEEPs, and proning. Okay. I know Dr. Cuppey is going to talk about liberation, so I'm not going to cover that part, and I'm going to keep us on time.

ARDS

mechanical ventilation

transpluminary pressure

driving pressure

ECMO