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3: Mechanical Ventilation III: Management of Acute ...
3: Mechanical Ventilation III: Management of Acute Respiratory Failure (Robert C. Hyzy, MD, MCCM)
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This lecture is entitled Mechanical Ventilation III, Management of Acute Respiratory Failure, by Bob Heisey from the University of Michigan. Here are our learning objectives to recognize the causes of acute respiratory failure, describe evidence-based strategies for the management of ARDS via mechanical ventilation, and to list adjunct rescue modalities for severe refractory hypoxemia. At the outset of this lecture, I'd like to just briefly give you an overview of the classification of respiratory failure. Type 1 is hypoxemic due to VQ mismatch, shunt, or low venous admixture. Type 2 is hypercapnic due to increased head space or decreased vent ventilation. Type 3 is perioperative, and Type 4 is shock. Type 1 causes, of course, include pneumonia, cardiogenic edema, non-cardiogenic edema, which is also Type 4, PE, which is also Type 3, or phlebotic lung disease. Type 2 causes include neuromuscular disorders, such as kyphoscoliosis, myosinic crisis, Guillain-Barre syndrome, central hypoventilation, of course, COPD, asthma, and obesity hypoventilation. Type 3 and 4 causes you see there. I don't find this classification scheme to be particularly useful. I think most useful is to go to the bedside and say, what am I seeing? Am I seeing a lung failure in terms of hypoxemia? Am I seeing a bellows function failure of the diaphragm due to hypercapnia, mainly driving the respiratory failure, recognizing that you can have both. You can have a COPD patient become hypoxemic. You can have a patient with hypoxemic respiratory failure, fatigue, and develop hypercapnia. But I think the most useful strategy is to differentiate Type 1, hypoxemic, from Type 2, hypercapnic. Well, let's move on to talk about management of ARDS with invasive mechanical ventilation. Just a key point here with this x-ray, you must have bilateral alveolar airspace disease, a lobar pneumonia that's unilateral, doesn't cut it. That's not ARDS. It's difficult to tell cardiogenic from non-cardiogenic edema with an x-ray, but be that as it may, it must be bilateral. Let's press off into a case vignette. This is a 32-year-old female with ARDS who is COVID positive. The patient is intubated and begun on invasive mechanical ventilation. She is on remdesivir. She is on corticosteroids. Her bilo infiltrates. Ideal body weight is 66 hours later. The patient is tachypneic. Blood pressure, as you see, sat in 92. The patient is on assist control, 80% FiO2, PIPA 12. The tidal volume at this time is 360 cc with a peak pressure of 35, plateau pressure of 32 centimeters of water, blood gas 7.37, PCO2 38, PO2 64, 92% saturation. We now decide to, number one, decrease the tidal volume to 300 cc. Number two, increase the peak to 15 centimeters of water. Number three, add inhaled nitric oxide. Number four, initiate prone ventilation. The answer is to decrease the tidal volume to 300. The first principle of being lung protective is in order to try to get the plateau pressure down below 30. It was 32 in this instance, and the patient was not getting lung protective ventilation on the basis of ideal body weight. Let's talk a little bit about the physiology of ARDS. In ARDS, the lungs are diffusely involved, but gravity takes its toll by developing compressive atelectasis in the dependent lung zones. If you flip the patient on their belly, as you see here to the right, the dependent lung zones are anterior. If the patient is supine, they're posterior. But the issue there is, of course, that if you deliver tidal volume and it's too large, you'll only go to parvolungs, which is baby lungs, and you will not be lung protective. By giving a low tidal volume, you're acknowledging the fact that only parvolungs are ventilated, and you are not over-distending those lung zones. This, of course, came most notably from the ARDS ARMA trial, which was published over 20 years ago now, which demonstrated an 8.8% absolute mortality reduction and a 20% decrease in hospital mortality, as well as an increase in ventilator-free and organ failure-free days. The key point here, of course, is that tidal volume was managed based on ideal body weight, which is based on height, not absolute weight, in order to get the plateau pressure down below 30, usually at 6 cc per kilo, going down as low as 4 cc per kilo in an attempt to get the plateau down, but allowing up to 8, provided the plateau pressure remained below 30. Plateau pressure is felt mostly to be a continuous variable. Here is the data, or the data from the ARDSNet first-day plateau pressure. You see a little bit of a shoulder here around 30. In fact, the subsequent data set by Jesus Vier showed perhaps 30 is a threshold, but be that as it may, trying to get the plateau pressure under 30 is where basic lung-protective relation resides. And we do have an issue with regard to COVID-19. We're all still working through our patients in the pandemic. Early on, it was felt that these patients represent a qualitatively different group of patients who have low elastance or high compliance. But this data actually, from the Blue Journal last year, looked at pre-COVID ARDS and found that even then you could tease out a subgroup that had high compliance, which is over here. So perhaps it's a matter of degree with more of these COVID patients fitting to that high compliance group, low elastance, but clearly this can also be seen in ARDS. And I have another lecture that will go a little more in depth into this whole COVID-19 issue. But what's true is that even though lung-protective inhalation with low tidal volumes has been around for many years, the uptick has been inadequate. This is data from LungSafe. It came out five years ago now. If you can see to the right, all the dots should be here. Everyone should be below at least eight and apply it to 130, and a lot of dots are not. And this was an international data collection of institutions that cared about ARDS. And even then, recognition of ARDS was inadequate and lung compliance with lung-protective inhalation, rather, was inadequate. We do have an issue of cyclic atelectasis. I mentioned from the earlier pictures I shared with you, the ventilation goes to the baby lungs. Depressive atelectasis is in the pentalung zones. You do have an area that open and closes with each breath. It's called cyclic atelectasis. And the question is, and the next question asked by the ARDSnet was, if you open the lung, if you apply PEEP to mitigate this degree of opening and closing and recruit more of the lung, is that beneficial, i.e., is a high PEEP approach beneficial to ARDS patients? And this was looked at in the alveoli trial, and this was looked at in the two-year trials called EXPRESS and a Canadian trial called LOVES. And none of them showed a mortality benefit except when you took them all together into a meta-analysis. The meta-analysis now is 11 years old. The question there was, does a high PEEP approach versus the conventional low PEEP algorithm utilized in the ARMA trial, does a high PEEP approach additionally, incrementally benefit mortality beyond that which might be achieved with a low tidal volume ventilation approach alone? The answer is only true by meta-analysis. Later at that, at least Kaplan-Meier's, it was only true in patients who had a PDF ratio under 200 by the old definition of ARDS pre-Berlin. It wasn't true for people who had a PDF higher than that. And other meta-analysis have shown really a challenging issue whether or not just merely using a high PEEP protocol can benefit mortality. We had multiple studies and still did not, it certainly harm did not occur and you had the option of going with a high PEEP, but taking a one-size-fits-all approach to giving a high PEEP algorithm compared to the low PEEP algorithm of the ARMA trial was not really a compelling argument. You wouldn't hurt them, but the question is, would you help? And added to that, of course, is the ability to look at a transponder pressure with esophageal balloon, thinking that that might make us smarter by examining transponder pressure and it did not show benefit in the second epithet trial that Danny Taylor did. If you look at just the ability to recruit the lung, and this is a high PEEP table from the LUVS trial, the Canadian trial, it does appear if you look at CT scanning of the lungs that perhaps this approach is the best trade-off between recruitability and not over-descending a lung when you compare it to other ways to give a high PEEP titration, which would include the EXPRESS trial done in Europe, where high PEEP was titrated to plateau pressure, stress index, which I won't go into, not a lot of trials on that, or Danny Taylor's esophageal pressure. So for my money, if I'm going to choose a high PEEP approach, I consider using this table from the LUVS protocol. I have a tendency to want to use high PEEP, but more on the issue of recruitability in just a minute, I use a high PEEP in patients who are recruitable, more on driving pressure in just a minute, I use driving pressure to help me decide who's recruitable. So we looked at LUVS and EXPRESS, those two negative trials, which were only positive when you threw it together with the ARDSnet alveoli trial, and if you teased out recruitable patients, you say taking a one-size-fits-all approach and giving everyone a high PEEP really didn't benefit in each individual trial, but if you looked at the recruitable patients, high PEEP clearly had a mortality signal, which begs the question of heterogeneity. The issue with regard to ARDS is heterogeneity of recruitability. And we think, too, this is a Blue Journal article actually from last year, that the benefits of low tidal volume are actually greatest in patients with stiff lungs, which stands to reason. In other words, even the ARDSnet ARMA trial in 2000 allowed you to go to eight per kilo provided your lungs are compliant, but this suggests that lung protect ventilation is best considered not only on the basis of low tidal volume on an ideal body weight basis, but also with some rendering or some consideration of driving pressure. So what is driving pressure? The driving pressure is the plateau pressure minus PEEP. And this is a retrospective analysis of some of those trials I just mentioned, alveoli, ARMA, LOVES and EXPRESS. So this is not a prospective study, but a retrospective data mining, if you will, which demonstrated the mortality benefit with driving pressure was even greater than that which was seen tracking out plateau pressure. These are mathematically coupled variables. The ability to do a prospective trial is quite challenging, but there is something to be said for incorporating driving pressure into your approach to a patient, particularly when it comes to PEEP titration and determining recruitability. This is the same paper by Jesus Villar that in this case looked at kind of a threshold of driving pressure saying around 19, others would say 15. Driving pressure can be used to help manage the ARDS patient when you go up on PEEP to see what happens to driving pressure. You want to keep the plateau under 30, driving pressure under 15. And we have other additional papers. This was just out of the White Journal earlier this year. And the idea here is that the change in driving pressure with PEEP titration will help you determine whether or not you are benefiting the patient. So, if you are cracking up the PEEP and driving pressure goes down and PO2 goes up, I think you've got a recruitable patient on your hands. If you go up on PEEP and driving pressure doesn't go down and plateau pressure goes up, well, maybe that patient is best served by a more conventional low PEEP titration table such as that used in the original ARMA trial in 2000. So, here's some conventional ventilator strategy from a review six years old now. And this says low tidal volumination, six per kilo, recognizing you go up to eight or down as low as four, keep plateau pressure under 30. Recruitment maneuvers more will go on to that in just a minute, but there's different ways to do that. And driving pressure here, it says 20, I would argue. Most recent studies that have looked at this issue, a post hoc in terms of data analysis would say 15 centimeters of water. We do have something called the R trial, which I'm taking on with you separately. So, people believe that opening along with PEEP is a good idea. I went through some of the big trials, and that didn't satisfy investigators who believed sort of in a one size fits all approach that high PEEPs would benefit people. The R trial came out now four years ago in JAMA. And this was an unusual trial in a number of respects. Some of those earlier high PEEP protocols involve PEEP tables going up progressively on PEEP. This was doing something quite different. This is what was called an aggressive recruitment maneuver where the patient was given high pressures and held for up to five minutes, and then decreased the PEEP from that recruitment breath down. Control group was a low PEEP protocol such as ARMA, the classic, which is the table I produced with you here. And what was unusual about this approach was it truly opened the lung. It really did open the lung. They didn't consider subgroups, but they used an aggressive recruitment maneuver and then titrated PEEP down rather than more conventional LUVs, alveoli, express starting low PEEP and going up. And the reason I took this study on separately is it had a higher mortality. Here's the aggressive recruitment maneuver. They actually had to modify these recruitment maneuvers to not be as aggressive halfway through the protocol because they found they were having some early cardiac arrests and barotrauma. And as I said a few moments ago, there's different kinds of recruitment maneuvers. These aggressive recruitment maneuvers should not be performed. Unless the ARC trial is showing increased mortality, you shouldn't do this particular approach. Now, there's other kinds of recruitment maneuvers, and even the LUVs trial used one. A 30 centimeters of water hold for 30 seconds is a different ballgame for something that goes on for minutes and minutes like this. So here again, the results, increased mortality. And so this is a bit of a one-off. In other words, a truly open lung approach with the aggressive recruitment maneuver and decremental PEEP titration should not be performed. A high PEEP approach alone with a table such as LUVs can be performed and provided, in my judgment, you pay attention to whether or not recruitability is taking place, and I would use the change in driving pressure to help guide that. But as you see in the ARC trial, issues with regard to ventilator-free days and pneumothoraces, barotrauma were all of concern. Six-month mortality was higher, 28-day mortality was higher. So this approach has been abandoned, and rightly so. Let's go back to our patient vignette here. Remember, we dialed down the tidal volume 12 hours later. The patient's febrile, blood pressure, as you see, on cyst control, 18 breaths per minute. On 100%, FiO2 with PEEP at 12, tidal volume is 300. PEEP is 32, plateaus now under 30 at 29. Blood gas, as you see, though, includes a PO2 of 59 and only 89% saturation. So the best evidence at this juncture suggests you should now, number one, administer a neuromuscular blockading agent, number two, institute ECMO, number three, start high-frequency oscillation, number four, prone the patient, number five, increase PEEP. It's a little bit tricky here, for those who truly believe. We just got through talking about high PEEP, but I think the single best answer is prone positioning the patient. Let's talk about rescue modalities. I think you can probably move prone ventilation out of rescue into routine at this point, but here's some of the things to consider. We talked a little bit about recruitment maneuvers before, differentiating that aggressive step, stair-step approach from a more square-wave approach. I'm for the second kind at times, but against the ARG approach, vasodilators, high-frequency, and ECMO. Let's take these on in turn, but here's a survey from a few years ago about the things that were being used at the bedside for refractory hypoxemia, and you see the neuromuscular blockade was very popular, whereas prone positioning, much less so. Now, I happen to believe that there's a lot of bad things that happened in the pandemic, but one good thing I think is that prone ventilation, which had been underutilized prior to the pandemic, really had a significant increase in use as a result of the pandemic. And I think that is one of the few good things to emerge from the pandemic. Let's talk about neuromuscular blockade, here you see train-of-force stimulator. And the accuracy article came out some years ago now, which seemed to suggest a benefit to early neuromuscular blockade. Now, no one's gonna argue that some patients need neuromuscular blockade at times. And in fact, even though perhaps my colleague, Ivor Douglas at Denver General can prone a patient who's not neuromuscular blockaded, most patients do end up paralyzed when they're receiving prone ventilation. That's why I chose to tell you about this issue of NMV first, but this is for early use for 48 hours in patients P to F under 150. And the early indication in our France was this was beneficial, that was criticized for various regions such as you see, but we in the Pedal Network did a subsequent trial. And here you see the curves here and we found no mortality benefit. This is for early neuromuscular blockade, P to F under 150 on at least eight a peep, which isn't to say you can't use it at some point for some people, but you don't routinely use it for people who have Berlin moderate to severe ARDS. So let's talk about prone ventilation. When I show this slide to my old friend, Kathy Volman, and I say, what's wrong with this picture? And what's wrong with this picture is you got one person proning somebody. And I think the reason that, one of the reasons anyway, that the uptake of this modality had been slow is it's a pretty challenging effort in the pandemic getting four people that have done PPE, get in the room to flip them prone is a challenge, but it got done. And the big article here is ProSeva. I'm gonna sort of cut to the chase here. ProSeva now is eight years old, but there were a number of proning articles earlier that were negative. But when you look at these survival curves, you can't help but be impressed that the prone group had a lower mortality quite significantly so. There's been different views on this, but if you look over time and you say that maybe they finally got it right. Instead of using old fashioned, not lung protective ventilation, using lung protective ventilation with low tidal volume, you see a proven mortality. And over time they learned flipping people for at least 16 hours a day using lung protective ventilation seemed to be the key variable here to perform benefit. What's important to recognize about ProSeva is that again, it took three to four patients and it was on 16 hours a day, but if you look at the enrollment criteria, and this goes back to that Q&A I gave you a few moments ago. Sure, once you're intubated, they try to make you better. I mean, if you were better right away and LungSafe showed us none of these 21% of patients after 24 hours no longer meet ARDS criteria. But if you still met criteria and your PDF was under 150 with a PEEP of at least five, you were proned. So there's nothing wrong with proning somebody early who meet this criteria. In fact, the ProSeva study use an old fashioned low PEEP table such as ARMA as I shared with you moments ago in all patients. And in fact, prone studies are all low PEEP algorithms. The other thing I want to point out is there's a tendency to want to stop proning because it is challenging for our personnel, but they really only stopped it when the PF ratio had improved and the patient was on NFI2 of no more than 60% with a PEEP of no more than 10. Now, when we examine what the best way forward is, and one reason to advocate more for prone ventilation was a paper that came out in Blue Journal this year, it's called a network meta-analysis. And this is post hoc data analysis. What a network meta-analysis seeks to do is to make comparisons even when such comparisons have not been made in a randomized trial. So for example, there is no randomized trial comparing a low tidal volume, high PEEP approach such as alveoli, loves or express against a low tidal volume prone population. But if you try to, through the way that network meta-analysis is done, make that comparison, you see that low tidal volume prone comes out ahead compared to low tidal volume, high PEEP. And you see other comparisons here, but the key point here is that it is never wrong to prone a patient with a low PEEP protocol who has persistent ARDS and is hypoxemic 12 to 24 hours after with a ZPF ratio under 150 and at least five of PEEP. That comparison has not been made of a direct, but when you try to make it, that's what the results show. There's other rescue modalities in ARDS. So here's a question for you. Which of these modalities has been shown to decrease mortality? Number one, airway pressure release ventilation. Number two, ECMO. Number three, high frequency. Number four, recruitment maneuvers. Number five, inhaled nitrate. Well, the answer is ECMO with a little bit of an asterisk attached to it, but it has been shown on an evidence basis. We know recruitment maneuvers, our studies are few and far between. I commented already my heartfelt bias, which is to say those aggressive maneuvers should not be performed. And in fact, when the ARD trial came out, we decided to not allow for those, but in old fashion, 30 for 30, if you will, or 40 for 40 can be done. Inhaled nitrate has been studied for many, many years. The PDF ratio indeed goes up, but there's no mortality benefit. High frequency had two major RCTs, probably the best symbols ever for studies I've ever seen. Oscillate done in Canada and Oscar done in the UK. The key thing that happened here was, it's one thing to say there's non-inferiority, but in Canada, there was higher mortality with high frequency, which is why now the oscillators tend to be on the shelf collecting dust, even though there was some post hoc analysis that suggested the very severe patients with PDFs under 100 may in fact benefit. And perhaps another trial might occur ultimately, but for right now, collecting dust as it should. And then we have the EOLIA. And again, I mentioned that this is evidence-based to show an improvement in mortality with an asterisk. And what's the asterisk? Well, in fact, they had very aggressive powering of this trial and it met stopping rules for futility. So even though there was a trend towards lower mortality in ECMO, the study actually technically was a negative trial. However, when you look at a tentative treat basis, tentative treat basis, survival or treatment failure, you see a clear mortality benefit. So I'm fond of saying this is the most positive negative trial ever. And when you look at a Bayesian analysis now, which is a complex way of looking at your priors, if it's called, with regard to what your expectations are, you see a mortality benefit. So I'm willing to accept that in the severest of the severe, ECMO should be performed, even though on a technical basis, the EOLIA trial was negative. So this is now pre EOLIA. This is pre-Rose study, but Eddie Fan was the lead author on the guidelines for mechanical ventilation ARDS. And so at least what did we learn from that? We learned that lung protect ventilation has got a strong recommendation of moderate quality evidence which is to say, keep the plateau under 30 and keep the tidal volume four to eight in order to do so. Prone ventilation on the basis of PROSEPA had a strong recommendation of at least moderate quality evidence. High frequency had a strong recommendation of moderate quality to not do it because it caused harm in the Canadian trial. Opal lung ventilation, conditional moderate against this pre-ART. Recruit maneuvers, conditional low. ECMO had a no recommendation that was pre EOLIA and things that were not commented on because for one thing, they're not ways of giving ventilation were inhaled nitric. But again, PO2 improves but not mortality. Neuromuscular blockade or mortality benefit early on with accuracies. But the Rose trial says no for all comers and then driving pressure, just no prospective data. Everything I share with you about driving pressure as much as I think it's important variable to consider is all post hoc analysis of earlier trials. So let's delve a little bit into these. I know that APRV has got its heartfelt believers. I've had some discussions with those. There really was only one RCT that was a Chinese study that had a baseline imbalance in acuity with randomization. A PEED study that had a higher mortality, a Utah study that showed they were giving large tidal volume breaths. So I know that airway pressure release has got its believers but the data is lagging behind. And of course, the true believers say that the reason is that these trials did it wrong, that you must personalize airway pressure release ventilation setting the lower pressure based on changes in low mechanics. So these earlier trials were not sufficiently subtle if you will, to do it right. And which may well be true, but I await an RCT that shows me that this will incrementally benefit patients compared to what we conventionally do, which is what I've described for you today. So in the boards, at least internal medicine boards, mechanical relation takes about 6%. A lot of what I told you about ARDS, I do want to comment about a few other topics that are non-ARDS related, just as we close out this lecture. And of course, one is the ABCDF bundle, which I believe others will go into great detail, but this is a bundle that revolves around the invasively mechanically ventilated patient involves sedation holidays, spontaneous breathing trials. The liberation guidelines that came out four years ago now, and again, the problem with guidelines is they're frequently not living guidelines, but they made a strong recommendation for non-invasive isolation for patients who are high risk. It's been subsequently showed by the Spanish group that for the high risk patient population, which included a subset of COPD patients, that heated high flow was just as good, but they recommended augmented spontaneous breathing trial, recommended protocolized sedation, mobility, a liberation protocol, a cuff leak test, and corticosteroids for failed cuff leak tests. And again, if you look at these, you see a lot of Cs, conditional, or moderate or low quality of evidence for a lot of this. So a lot of these recommendations were based on not a lot of evidence. The strongest was the non-invasive one, but again, this is before subsequent data examined the issue of heated high flow. Heated high flow was just emerging by the time that this guideline went to press. You do think about wean, resting, and liberated patient earlier, trial now from four years ago, said, look, if you can wean a patient and then don't poop them out after the SVT, and then try to extubate them more rapidly after they rest for a bit, you might get away with a lower reintubation rate. Other new data said how it's the best way to do an SVT. The guidelines recommended using some degree of pressure support. You can decide how much is appropriate for you. This is a study in JAMA from two years ago now that compared a PSV as eight for only 30 minutes to a non-augmented trial, which is to say good old-fashioned T-piece times two hours, and found that really PSV of eight times 30 minutes was enough. I'm still kind of a two-hour person, but it does give you proof of concept for being a little more aggressive to extubate people. I'm not here also to tell you the best way to do a spontaneous breathing trial. Karen Burns out of Toronto were participating in a trial to re-examine the issue of T-piece, but the point of the matter is there's a lot of ways to do a spontaneous breathing trial to understand that for most patients, most of the time weaning is readiness testing, and then we've changed the terminology, but then we liberate the patient once readiness has been ascertained, providing things like a cuff leak are present. So let's go back here now to our patient who's unfortunately still on the vent after 10 more days. She's weak and is on 40% with a PIPA-5, so has improved significantly in terms of gas exchange, but is still stuck on the vent and has failed spontaneous breathing trials quickly, 25 minutes after a couple of attempts with rapid shallow breathing. You would now decide to continue to optimize medical management and attempt an SBT daily in advance of liberation, two, proceed with tracheostomy and daily face mask trials, three, proceed with tracheostomy and PSV CPAP trials, or four, excavate heated high flow. Well, I don't have an answer for you because the issue of when exactly to perform tracheostomy is not completely determined. I will say that there was a study that showed that early extubation when you failed to wean was not advantageous, more on how to wean a patient once they are trached, but if you thought the patient's getting close, it wouldn't be wrong, but I do think the issue of tracheostomy needs to be considered at that juncture. So tracheostomy. When we look at timing of tracheostomy, the literature is a little bit unusual in that the definitions of early versus late vary per study. There's no uniform consensus. Here, six to eight days was compared to what's late at 13 to 15 days and found no decrease in ventricular associated pneumonia by doing it early, no real differences in hospital length of stay, one year survival. So why do it six to eight? Well, I think most people would agree that six to eight is probably a little too early for most patients most of the time. Internationally, a survey some years ago showed the median of about 11 days. Certainly, if you're on the vent beyond a week, beginning to think about a trach as I shared with you in the patient vignette is important. This is a study called TrachMap where they actually, if you can believe it, trached a patient at four days versus more than 10. Clearly, a lot of patients got unnecessary trachs traching at four days. So no one's gonna argue an early trach of four days when you think you might get the patient better. So I don't have an answer for the timing of trach. That's why I left the question somewhat ambiguous for you. But I do have an answer with regard to once you are trach, what the best way to wean someone is. And this is Martin Tobin's work from a few years ago now. And the issue of augmented spontaneous breathing trials with PSV and CPAP, I think can have a value in the patient with an ET tube, but it would appear that that is not as quick a way to wean a patient once they have a tracheostomy. That using a trach collar without augmentation via the ventilator is a way to get patient off the ventilator permanently sooner. And I would advocate for that. Yes, that's a little more work for your respiratory therapist who prefer the patient hooked to the ventilator because they can get the ventilator alarms. So last slide here, what have I told you? I told you the difference between types of respiratory failure, type one being hypoxic, hypoxemic, type two being hypercapnic. I told you that the basic fundamental ARMA, ARDS 2000 lung protective ventilation was getting the plantar pressure under 30 with a tidal volume, generally six, but going as low as four in order to achieve it, but going up to eight if compliance permits. High PEEP ventilation can be considered, but no wrong recruitment process. I would argue that consideration ought to be given to recruitability and looking at driving pressure and changes thereof as one goes up on PEEP as a guide. Prone ventilation has got a strong recommendation and at least I think the use of it has increased since the pandemic began. Looking at network meta-analysis, low tidal volume plus prone ventilation seem to be advantageous to low tidal volume high PEEP, which is my old algorithm. In terms of using ECMO, a negative trial, but as I said, the most positive negative trial ever. I think using nitric or high frequency are not recommended. Same thing goes for APRV until we get more data. A protocolizing sedation weaning is the best way to get the patient off. Early trach, certainly less than a week or eight days was really no advantage. What to say beyond that is a subject of opinion, but the 10, 11 days internationally. And then trach mass trials are better than pressure support ventilation trials for getting the trach patient off the vent sooner.
Video Summary
In this lecture, the speaker discusses the management of acute respiratory failure, particularly in patients with acute respiratory distress syndrome (ARDS). The speaker defines the types of respiratory failure, with type 1 being hypoxemic and type 2 being hypercapnic. They emphasize the importance of using lung-protective ventilation strategies, such as keeping the plateau pressure below 30 and using low tidal volumes (around 6 cc per kilo) to avoid over-distension of the lungs. The speaker also discusses the role of prone ventilation in improving oxygenation and reducing mortality in ARDS patients. They mention the use of recruitment maneuvers to open up collapsed alveoli and the importance of considering driving pressure when determining whether a patient is recruitable. The speaker briefly discusses other rescue modalities, such as neuromuscular blockade, ECMO, and high-frequency oscillation, but notes that the evidence for their efficacy is limited. They also touch on the timing of tracheostomy and the use of tracheostomy collar trials for weaning tracheostomized patients from mechanical ventilation. Overall, the speaker emphasizes the importance of individualizing management strategies based on the patient's condition and response to treatment.
Keywords
acute respiratory failure
acute respiratory distress syndrome
ARDS
lung-protective ventilation
prone ventilation
recruitment maneuvers
tracheostomy
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