So we're back and so now what we're going to do is take the principles that we talked about in our previous lectures and we're going to put those principles into practice. How do we use the things that we've talked about to really assess the effectiveness and safety of our mechanical ventilation strategies? So when we talk about it, what we want to think about is to ask ourselves three questions when we're rounding on patients who are ventilated. Are the settings that we have safe and effective? Is the patient synchronous with the ventilator? And if they're improved, is it appropriate for a spontaneous breathing trial or an SBT? So let's tackle the first question. The first question is, are the settings safe and effective? So what do we consider safe and what do we consider efficacious? And so when we're talking about ventilating patients, there are a couple things and we're going to talk about it in the context of ARDSnet recommendations, reducing acute lung injury. And we recognize that these ARDSnet safety protocols are not necessarily useful for everyone involved, but they at least serve as a guideline. And so what's effective settings? Effective settings are essentially arterial blood gases, ventilatory strategies that allow arterial blood gases to maintain decent PAO2s of about 55 to 80, and those are ARDSnet goals. And then to maintain ventilation so that our pHs are about 7.1, greater than 7.15 or so. And granted, we would ventilate someone without ARDS very differently than those with ARDS, but just some roundabout guidelines. And then we want to talk about safety. Are we using ventilatory strategies that will protect the lung? Are we using lung protective ventilatory settings? And let's go back to our previous lecture and just remind us of kind of what causes lung injury and particularly ventilator-induced lung injury so that when we're assessing our ventilatory strategies, we can make sure we're not contributing to lung injury or at least minimizing our contribution to lung injury. So remember before, we talked about stress and strain of the lung. The stress of the lung is the load that the entire lung feels, and it is measured by the transpulmonary pressure, reflected in the transpulmonary pressure, which if you recall is your airway opening pressure minus your esophageal, your pleural pressure dictated by measured by the esophageal pressure. And the strain is the alveolar stretch. And remember that stress of the system is universal, whereas strain can be regional depending on what's going on with the lung. So the three mechanisms by which the way we choose to set up the ventilator can potentially contribute to ventilator-induced lung injury is the collapse and reopen strain, so the opening and closing and atelectasis of the lung. The tidal stretch, which can be considered the dynamic stretch, alveolar stretch, particularly when we use tidal volumes greater than 8 cc per kilo. And then the maximal stretch, the static strain that the system sees, the transpulmonary pressures that are too great. So what is considered excessive in-inspiratory static strain? We talked about it before in our previous lecture, and we'll come back to it a little bit just as kind of a reminder before we move forward. So the in-inspiratory static strain reflects the volume associated with the in-inspiratory transpulmonary pressure. And remember, transpulmonary pressure is your plateau pressure minus your pleural pressure. So in normal subjects who have a normal total lung capacity, the transpulmonary pressure and the volume that's associated with the in-inspiratory transpulmonary pressure occurs at a transpulmonary pressure of about 25 to 30. So that's where we get kind of our upper limit of normal for transpulmonary pressure. When we think about excessive in-inspiratory transpulmonary pressure, we see that in a variety of ways. In normal lungs, so the global compliance is normal. If we have a high in-inspiratory transpulmonary pressure, we will see an increase in the in-inspiratory volume and the in-inspiratory static strain. And so in normal lung compliance, a transpulmonary pressure over 30 will cause increases again in both the in-inspiratory volume and the in-inspiratory static strain, which we want to avoid. In homogeneously stiff lungs, again, that is compliance that is globally reduced, even a high in-inspiratory transpulmonary pressure will not cause excessive static strain if the volume is not increased. And applying these same principles in a heterogeneously stiff lung, so there are areas that are compliant and there are areas that are less compliant. So the compliance is reduced only in sick regions, which is what we see in our ARDS patients. A high transpulmonary pressure will cause excessive regional static strain in regions where there's high regional compliance. Said a different way, in heterogeneously stiff lungs, if we have high transpulmonary pressures, we risk injuring the more normal lung units. So we want to keep that in mind as we are selecting our settings. Alright, so let us look a little bit more in detail about the impact of excessive dynamic strain or the impact of large tidal volumes that can produce lung injury, independent of the static strain or the pressure. And so this study was done in 1988, it was done in sheep and they did some things to have the sheep hyperventilate with tidal volumes of about 9 to 15 cc per kilo, with the control group of sheep being 7 cc per kilo. What they found is that in the sheep that received higher tidal volumes, they had increased transpulmonary pressures. And what they also found is that in that group, there were more deaths. When there were 14 of the 16 sheep that were hyperventilated on review of the lung tissue, 14 of the 16 had evidence of lung injury, compared to the control group in which none of them died and on the pathology, there was no evidence of lung injury, the lung appeared normal. So again, that's just more evidence suggesting to us that tidal volume is important and not overextending the lung is important and preventing this dynamic strain to reduce lung injury, particularly during mechanical ventilation is important. And so what we've gathered from the NIH ARDS network studies is that we need to reduce both plateau pressures, so we need to reduce the stress of the system, but we also need to reduce tidal volumes and that is the strain of the system as we talked about. And so what the ARDSnet study showed us was that if we intubated people and ventilated them at low tidal volumes, defined as 6 cc's per kilo, compared to our standard 12 cc's per kilo, what we found was that the patients in the low tidal volume group had lower plateau pressures, less than 20, whereas patients in the high tidal volume group of 12 cc's per kilo had plateau pressures that were low to mid 30's. So you can kind of see some of our guidelines of aiming for low tidal volumes of 6 cc's per kilo and plateau pressures of less than 30 start to really come out in the data. What this particular graph is showing is that if you ventilated patients at 6 cc's per kilo, which correlated to plateau pressures that were on average in the mid 20's, you had less patients on breathing assistance at 28 days. So more of the patients were able to be freed from the ventilator compared to the patients who were receiving 12 cc's per kilo tidal volume. And just to remind us all, this study was actually terminated early because the mortality was statistically significant. The difference was statistically significant in the low tidal volume group. So if we put the ARDSNet data together in this nice little chart, we can see that it is not just the tidal volume, it is not just the plateau pressures, but it is both that impact mortality. We talked about it a little bit earlier. So what this graph is showing us is that if you use the best strategy, and that is keeping your plateau pressures low, which is less than 30, but additionally keeping your tidal volumes about 6 cc's per kilo, that is the best strategy to reduce mortality in ARDS. The worst strategy is to have really big tidal volumes, 12 cc's per kilo, and let your plateau pressures go above 30. And somewhere in between that, the mortality vacillates. But the take home points are both the plateau pressure and the tidal volume are important. The stress of the system and the dynamic strain is important. So let's talk about that a little bit more. Excessive dynamic strain is an independent cause of lung injury. Global dynamic strain is reflected by a normal tidal volume in normal lungs. But as critical care physicians, we don't often get to experience normal lungs. So there are some concepts that we have to remember. Excessive global dynamic strain occurs when global tidal volumes are excessive. All the tidal volumes, all the units of the lung are receiving tidal volumes that are too large. That makes sense. But what more commonly happens, and particularly in patients with ARDS, is we have this phenomenon of excessive regional dynamic strain, where there are areas of the lung that are being ventilated differently. And it is this excessive regional dynamic strain that can occur in the setting of even normal or low global tidal volumes if there is significant heterogeneity in the lung. And the tidal volumes will distribute to regions with the best mechanics. And so if you have areas of the lung that have better mechanics and you're using a higher tidal volume, you're going to potentially induce lung injury in those previously normal areas. So the idea that we're going to grapple with is, how do we decide what a good tidal volume is? And one of the things that I think that the literature is supporting is that we should move away from this idea of ideal lung size based on body weight. And we should start to adopt more what is a tidal volume based on the functional lung size. And how do we reflect the functional lung size? We can use the functional lung size, or the compliance, to kind of get assessment of where our individual patients are. And if you remember from our previous talk, we talked about the driving pressure, using that to make some decisions about the functional lung size of our patient, not the ideal lung size as is represented by their ideal body weight, but the functional lung size that is represented by their lung pathology. So I think we all are pretty convinced that low tidal volume ventilation is appropriate. I think we understand the impact of minimizing static and dynamic strain. And we also understand that there are some trade-offs that come with that. If you look at this study, and you're looking at the impact of low tidal volume on PDF ratios, what you see here is that if you ventilate at larger tidal volumes, and that is 12 cc's per kilo, you initially get improvement in your PDF ratio compared to your 60 cc's per kilo tidal volume. The larger tidal volumes, you theoretically get more lung recruitment. But by day 4, 3-4, that benefit goes away. And there's no difference. And what we believe is actually happening is that the benefit goes away because now in those areas that were previously recruited now may be injured from the high tidal volume ventilation. Additionally, in this study, it showed that compliance was better in the high tidal volume ventilation. Compliance as a representation of alveolar recruitment. But if your compliance is better, but you cause significant injury, have you really done the best for the patient? So as we're thinking about this, I want us to go back to the three major mechanisms of ventilator-induced lung injury. Two, we've talked about it quite extensively. The first is the tidal stretch. I think we have the data. I believe we have the data that shows that tidal stretch resulting in dynamic strain when we ventilate over 8 cc per kilo of ideal body weight can be injurious. I think we have the data and are convinced of the data that maximum stretch or static strain can be injurious as well, extending pressures above 30. And then the last concept of ventilator induced lung injury that I want to make sure that we cover is this collapse reopen strain. And the collapse reopen strain is that the idea or the need to recruit alveoli, or another way to think about it is the ability to prevent derecruitment of alveoli so that you don't get the strain or the injury that comes with the opening and closing of various alveolar units. And so what we see on the left half of the graph is looking at transalveolar pressures. And we see that the transalveolar pressures go up with the inspiratory breath and they come down all the way to zero with expiration and in the absence of PEEP and you get opening of the alveoli and then complete closure of the alveoli. That's bad. That is injurious. What we want to aim for, what I believe we've all pretty much accepted as kind of standard of care, is to provide some level of PEEP or expiratory pressure to prevent that complete closing or atelectasis between breaths. We are trying to provide a level of PEEP that will prevent the transpulmonary pressure going less than zero because less than zero, as we talked about previously, basically is a situation in which we get alveolar derecruitment. But also, as we all know, PEEP is a two-edged sword. So PEEP is great. It helps with recruitment of alveoli. It can also cause ovarian distension and lung injury. It can also impact hemodynamics of our patient and have some deleterious effects on the hemodynamics of our patients. So we really need to find the best PEEP if there's ever such a thing. So there are many different ways that have been put out there to find the quote-unquote best PEEP. There are visual potentials to assess it, none of which I personally have used, but I understand the concepts. We could use CT. So we could adjust the PEEP and send the patient down for a CT imaging. And then adjust the PEEP again and send the patient down and see how much recruitment we have. We can use electrical impedance tomography, which is EIT. That is a process in which you can measure the electrical resistance of the thorax. And then you can look for the level or the plateau where all the recruitable alveoli have been recruited. And if you find that plateau, then you know you found your PEEP. You could also use our simple bedside ultrasound to assess for the presence of b-lines, to assess for the presence of consolidations thought to be due to atelectatic lung. You can adjust your PEEP and repeat your ultrasound and see if those have improved. There are mechanical ways in which we can assess our PEEP. We can look at our pressure volume curves on our ventilator. We can determine the best compliance for our patients. And then we can use our impaired tables, balancing our PAO2s with our plateau pressures and our FIO2s as we've done for quite some time with our ARDS-NED protocol recommendations, the high PEEP, lower FIO2, higher FIO2, lower PEEP protocols. So, in addition to PEEP having beneficial effects, but also potentially deleterious effects, we have to be careful of who we use high PEEP in. Our strategy should not be to use high PEEP in everyone, remembering that the ARDS-NED protocol was specifically looking at PEEP in ARDS and in hypoxemia not related to ARDS, high PEEP strategy is probably not the way to go. And this study that was published in JAMA in 2010 shows that if you look at the probability of patients leaving the hospital alive, if they had ARDS and underwent a high PEEP strategy, they had a higher probability of leaving the hospital alive than did patients who received high PEEP who did not have ARDS. And the concept behind this is that in patients with ARDS who have potentially more recruitable lung, they will benefit from the higher PEEP. But in patients who have other etiologies of hypoxemia that is not ARDS, and in that, they have a lesser likelihood of recruitable lung, the benefits of high PEEP are not there anymore. And so we really need to pay attention to and be careful with who we're applying high PEEP to. More along those lines, if you look at the relationship between oxygenation response and mortality, it really depends on whether there is a response to PEEP. What I mean by that is, if you take patients, when you increase their PEEP, and they have an increase in oxygenation from that, then that's associated with improvement of mortality, as we can see by that pinkish line. Whereas if you take patients and you don't have a change in oxygenation when you change the PEEP, there is no association of improvement with mortality. So there's a group of patients that we can fine tune this to potentially. It is our PEEP responders. If you don't respond to PEEP, we then have to start to weigh the risks and the benefits of using higher PEEP. So going back to our initial question of are the settings safe and effective, how do we determine that? We first look at our ABG targets. Do we have effective oxygenation? Do we have effective ventilation as reflected in our pH? Have we minimized the lung strength? What is our in-inspiratory transpulmonary pressure? We want it to be less than 30. Have we minimized the dynamic strength? How do we do that? We use less than 8 cc per kilo tidal volume. If we are doing ARDSnet ventilation, we use 6 cc per kilo tidal volume. And then we have to kind of use all the strategies available to find the right balance between PEEP and FiO2. So we talked about a little bit before, and we'll talk about a little bit more now, but we'll discuss the fine-tuning of our safe settings. And what do we mean by the fine-tuning of our safe settings? This is where we bring back the concept of safe settings. And what do we mean by the fine-tuning of our safe settings? This is where we bring back the concept of driving pressure. We talked about using transpulmonary pressures and how it relates to chest wall compliance. And now we're going to talk about driving pressures as it relates to kind of PEEP and strength. Just reminding us, we define driving pressures as the pressure required to expand the lungs during tidal breath. And remember, it's assessed at a state of no flow, and so it's only determined by compliance. And we have to do this and make this calculation during our controlled breaths. We can't have patient effort because the patient effort will alter the results. The safe threshold for a driving pressure isn't really clear, but it's estimated of about a driving pressure of less than 20, and to be more specific, anywhere between 13 and 19. If your driving pressures are high when you go to make the calculations, you have two possibilities. You either have excessive regional tidal volume, even in the setting of normal global tidal volume. So that gets at this idea of heterogeneity of a lung, potentially. Or again, if you have this increased driving pressure, you may have inadequate or excessive PEEP. So when you see these high driving pressures, it has to cause us pause to cause us pause to kind of think about our ventilatory strategy and make changes as appropriate. So let's come back to our pressure-volume relationships, okay? And let's remember that we have a lower inflection point, which is the pressure at which, and we can think about it as PEEP, is the pressure in which we can prevent atelectasis. We can also think about our upper inflection point, and it's the pressure at which we can avoid hyperinflation, or the pressure if we go past it, we will get hyperinflation. And as we've talked about, we want to avoid injury, whether that's injury from hyperinflation or whether that's injury from the open-reopen phenomenon of atelectasis. Okay, so as we've discussed fine-tuning our settings, our safe settings, we're going to introduce the concept of stress index. And to introduce the concept of stress index, we must remember that pressure-volume relationships are occurring during tidal breath. And so if we understand that relationship, we can determine the stress index by analyzing the airway pressure profile during a controlled breath, and so it has to be a controlled breath, no patient effort, because it impacts the values, and during constant flow tidal volume. And we need constant flow tidal volume to eliminate the pressure effects of flow delivery. Okay, and if we want to evaluate the stress index, we are going to look for three patterns. Okay, the first pattern, and again, we're looking at our pressure curve under constant flow tidal volume. We're going to look at three patterns. The first pattern is our normal pattern, and our normal pattern, we're looking towards the end of inspiration. Normal pattern is going to be a straight diagonal line from inspiration to peak pressure. And a normal straight diagonal line is going to suggest that there's no more recruitment, and there's no over-distention, and that's what we're aiming for. That's a good stress index. The second pattern is a curve that starts steep, and then it flattens out. And that flattening of the curve suggests that additional recruitment is occurring, which is an indicator to us that additional peak is necessary. And then the third potential pattern is that the curve starts flat, and then it steepens. And so I've seen it described somewhat as the curve starts to bend towards the pressure axis. That is suggesting that over-distention is occurring, and if that is happening, we need to either reduce our PEEP or our tidal volume. So that's how we use stress index. To determine the safety of our settings. So here's an example. In A, we have a PEEP of 5, and we see in A that we initially have a nice steep curve, and then it starts to flatten out, which would suggest that we need additional PEEP. So we give additional PEEP as represented in B. So we increase the PEEP to 15, and in 15, you see a nice straight line. And that suggests that we don't have over-distention, and there's no further recruitment, which is the stress index that we're looking for. But let's say we got overzealous, and we increased the PEEP to 25. Now what you see in C is there's a steep curve, and then the curve starts to get steeper with the red line starting to point towards the pressure axis. That is an indication that we have over-distention, and if we were to see that, we would need to consider decreasing our PEEP or our tidal water. So back to our setting safe, we talked about our ABG targets. We talked about how to minimize our static strain and our dynamic strain. We talked about our P to F ratio balance, and we've just talked about another way to fine-tune that by using the stress index or the driving pressure. And that fine-tuning can relate to either the PEEP or finding the right tidal volume to reduce lung strain. So the first question we asked ourselves are, are settings safe and effective? And we've gone through a series of ways to evaluate that. The second question or assessment that we should make with every patient around on a regular basis is, is the patient synchronous with the ventilator? Patient synchrony is important for many reasons. And so what we know, what Dr. Tobin has shown, is that when we have a breath, there are places in which synchrony, dyssynchrony can occur. It can happen at the trigger point when the breath starts. It can happen during the flow component of it, and it can happen during the cycle component of it. And a lot has to do with our settings, a lot has to do with patient effort, triggering of muscles, et cetera, and we'll talk about that in more detail. So when we talk about asynchrony, we wanna think of it in three different groups. The first group is a group of dyssynchrony at the onset of the breath. That's either delay triggering, missed triggering, auto-triggering, or reverse triggering. That's at the onset of the breath. The second group occurs during the breath, and that's flow asynchrony. And then the last group occurs at the cycle, and that's either double triggering, premature cycling, or delayed cycling. And we'll talk about some of these in more detail. So let's first understand how to recognize asynchrony. The clinical signs of asynchrony are excessive breathing effort during the trigger or flow delivery phase, and inspiratory or expiratory efforts during the cycle phase. The simple way to say it is it just doesn't look like a nice waveform. When you see that, you wanna pause and wanna look more closely to see what's going on with the waveform. The waveform looks off, the patient doesn't look comfortable, what's happening? The way to recognize asynchrony from a graphical standpoint, you can look at triggering loads in the airway tracings or the esophageal pressure tracings. You can look at the airway pressures and see that they're being pulled down. Or you can look at the airway pressures and note that they aren't at baseline during cycling or during turning off. Things haven't stopped despite we're at the cycle phase of turning off. So one form of asynchrony is intrinsic PEEP triggering load. And essentially, we can see this in patients with obstructive lung diseases, specifically in patients with COPD, who have some intrinsic auto PEEP. And what the intrinsic auto PEEP does is it makes the work, it increases the work that the patient needs to trigger the ventilator. And so there's some common things that we can do to relieve the auto PEEP and reduce the work required by the patient to trigger the ventilator, which could include prolonging our expiratory time, which would potentially mean decreasing our set inspiratory time or decreasing our tidal volumes. And there is a possibility that you can add a little bit of PEEP as well, as we see in this situation where the first example is no PEEP, and then you add a little bit of PEEP to reduce the auto PEEP and reduce the effort and the work that's required to trigger the breath. The next cause of the synchrony is reverse triggering. And reverse triggering occurs when a patient's inspiratory muscle effort results from reflex mechanisms triggered by the mechanical insufflation with the ventilator controlled breath. Okay, stop. The next form of asynchrony that we will talk about is flow asynchrony, and you can have typically two types of flow asynchrony. You can have insufficient inspiratory flow, where the patient wants more than is being delivered, or you can have excessive inspiratory flow, where it's just too much for the patient to handle. When you have flow asynchrony from insufficient flow, the flow that the patient is receiving is lower than his or her demand. This typically occurs when we as physicians set the flow too low, and in modes in which the patient can't change the flow by increasing the spontaneous efforts, we will get some form of flow asynchrony. To fix flow asynchrony, we need to either increase the flows or consider other modes of ventilation that will allow the patient to find flows that meet their ventilatory demand. So we could either reduce their ventilatory demand, so if they are febrile or anxious or in pain or acidotic, we can do things to correct those and reduce the ventilatory demand, or we can simply increase the flow, making sure that with increases in flow, we are not adversely impacting airway pressures that could be detrimental. Additionally, if the patient is in a volume control mode in which we really do determine the flows, we can consider switching the patient to a pressure control mode or a pressure support mode in which the patient can alter their inspiratory efforts to meet their own ventilatory demands. So let's take that concept and apply it. We have a patient, and you have the current tracing on the left, and you can see that there's some desynchrony there if you look at the pressure curve. And you have the curve on the right in which you have made some adjustments. And the question is, the patient has the ventilator changed from the left to the right panel to address the discomfort. What was the change, and did it help? So if you picked B, you noticed that we took the patient to a pressure support mode. In that pressure support mode, as you can see in the flow diagram up at the top, the patient was able to adjust their own flow rate, improving synchrony. And so our graphs look better, and we don't have that desynchrony that we see in the pressure curve at the bottom on the left. The next vent asynchrony example that we'll talk about is the double triggering from premature cycling. When we talk about double triggering, what we're saying is that the ventilator is delivering two consecutive breaths in response to the patient respiratory muscle effort. And premature cycling resulting in double triggering typically occurs when the ventilator ends the injection or ends the inspiratory flow sooner than desired by the patient. Said another way, the ventilator inspiratory time is shorter than the patient's neural inspiratory time. So the patient wants a longer inspiratory time, and we haven't given it to the patient. So the patient takes another effort to try to get in a bigger breath. If you encounter this and you're in volume control or pressure control mode, you can attempt to correct it by prolonging your inspiratory time. And these are things that we commonly look for and wanna make sure that we adjust. Why do we need to pay attention to and correct asynchrony? Because the consequences of asynchrony are significant. If the patient fights the ventilator and is uncomfortable on the ventilator, that leads to increased sedation, and we understand the impact of increased sedation resulting in prolonged intubation and delayed weaning. Vent asynchrony can increase the patient's work of breathing resulting in tiring out of the patient, which will again potentially present in delayed or prolonged weaning. Can lead to dynamic hyperinflation, which is we've spent a lot of time talking about, can lead to ventilator-induced lung injury, can also lead to muscle damage, which all of these things can lead to delayed or prolonged weaning, which then can lead to longer ICU hospital stays and higher costs for the patient. So this is just a table looking at the frequency and consequences of asynchrony. And the point of this chart is to say, this is something that actually happens a bit and we need to pay attention to it. And it is something that potentially has a negative impact on our patients' clinical outcomes. If we look at the bottom, we see that patients who have a high asynchrony index have prolonged mechanical ventilation days. They have more referrals for tracheostomy and they actually have a trend towards higher mortality, although it is not statistically significant. So we've asked a question about, are our settings safe and effective? And we talked about how to fine tune them. We've talked about, our settings are relatively safe and effective from a strain and stress standpoint, but we still have to make sure that we have appropriate settings to avoid vent desynchrony. And we hope that with that effective, safe strategy that causes the most patient synchrony, we can get our patients better to the point that we need to consider doing spontaneous breathing trials to wean them from the ventilator. And so that's what we'll spend the next several minutes talking about. So what are our criteria for vent discontinuation? When we're thinking about our patients and we should be asking ourselves these questions every day, we're looking for stability or reversal of their respiratory failure. We are looking for pretty decent oxygenation defined as a PDF P to F ratio greater than 150 to 200. We want a PEEP of ideally less than five, but we can consider it less than eight. And we want a FIO2 less than 40%. And some data says less than 50% will be acceptable. But we wanna know that we can provide enough supplemental oxygen support to maintain appropriate oxygenation once we wean from the ventilator. And we want appropriate pH. We want evidence of appropriate ventilation as well. We also want evidence of hemodynamic stability. And so some school of thought is they should be completely hemodynamically stable with no suppressors and no inotropes. Others would say, we don't need complete hemodynamic stability in the sense of a little bit of levo, one microgram per minute levo. Probably shouldn't preclude you from an SBT, but obviously two or three pressors should. And then the patient should be able to take reliable inspiratory efforts. So if there's some intracranial process or there's too much sedation on board that the patient cannot take reliable inspiratory efforts, they are not candidates for vent discontinuation and we should reevaluate why that is. Once we determine that a patient is a candidate for vent discontinuation, we need to do a spontaneous breathing trial or an SBT. And the SBT is our most effective way of assessing successful removal of the ventilator. So for SBT, we can do two forms. One is a pressure support trial of five over five. So a pressure support of five and a PEEP of five or the T-piece trial. The T-piece is closest to mimicking extubation. You completely take the patient away from the ventilator, have them breathe through the endotracheal tube, which creates a little bit more resistance so we're really making the patient work. The pressure support trial is actually the more updated recommendation and supported by the literature. And then we need to make an integrated assessment of how our patient is doing on the spontaneous breathing trial. What is their ventilatory pattern? Are there any changes? Is it sustainable? What does their gas exchange look like on this spontaneous breathing trial? Hemodynamically, what do they look like? And the question that we're always asking ourselves does the patient look comfortable on it? If the patient looks horribly uncomfortable on the spontaneous breathing trial, it might not be the best time. We need to figure out what's driving the discomfort and try to work with that and try again. We typically recommend doing spontaneous breathing trials for about 30 minutes. Some of the literature, particularly on the T-piece trial can go up to 120 minutes. The first five minutes or so need to be closely monitored. And at any point, the vitals change, the patient changes, then we stop the spontaneous breathing trial, figure out what's the driving force behind those changes, make some improvements and try again the next day. Let's say our patient passes the spontaneous breathing trial. The next question we have to ask ourselves before we actually remove the ET tube is can the patient protect his or her airway? Having a good cough is essential. Having low suction frequency is very important as well. Less important is the gag, less important is the gag, the cough reflex. We know that that can be a little tricky, but I maintain we should still at least get that information and at least discuss it before we make a decision about removing the ET tube and alertness. So a patient who's not quite a RAS of zero may still do well with extubation. If they're a RAS of minus one, perhaps even minus two, probably more minus one. If they're a minus five, they're not gonna do well. And we have to accept and know the data that says that we should expect extubation failures of about 10 to 15%, but that shouldn't stop us from attempting extubation in patients who otherwise meet criteria. If we proceed with an SBT and the patient fails, we return the patient to their last comfortable full vent setting and we try again tomorrow. The data does not support weaning of the ventilatory setting from day to day. The data doesn't support trying again later on in the day. The data supports figuring out the potential causes of the SBT failure, working on those and being prepared to try again the following day. And so as we approach SBTs, we should be thinking about this, we should be acknowledging that we have potential failure. Let's kind of go back to our three questions. Our first question was, are our settings safe and effective? We talked about appropriate PAO2s and appropriate pHs to suggest that we have appropriate ventilation. We talked about appropriate assessment of our stress and strain of our system. We talked about utilization of transpulmonary pressures and aiming for transpulmonary pressures less than 30. We talked about and looked at the data to support using low tidal volume ventilation, which is tidal volumes less than 8 cc per kilo. And definitely in patients with ARDS, the data suggests that 6 cc per kilo would be appropriate. And we talked about using PEEP to FiO2 tables, but we got into some nuances of that. And using distending pressure calculations and stress indices to determine if we have the appropriate settings, and particularly the appropriate PEEP settings. The next thing we talked about is, is the patient synchronous with the ventilator? We want the patient to be as comfortable as possible on the ventilator. We talked about common causes of vent desynchrony, which are premature triggers, flows, cycle issues. And we need to pay attention to our graphics to make determinations about what's causing the patient's desynchrony. And then the last thing we talked about is, is an SBT indicated in our patients? And the SBTs, we should be thinking about it every day. Is the patient on low ventilatory support? Is the patient triggering spontaneous breaths? Is the patient hemodynamically stable? And can the patient protect his or her airway? And so the last piece of information I want to talk about and bring more recent data to us is, what should we wean to? We decide to take the ventilator away. What should we wean our patients to? As a prophylactic measure, we recommend weaning to high flow oxygen therapy via nasal cannula after cardiothoracic surgery. That's a grade two plus recommendation with strong agreement. Again, as a prophylactic measure, saying we're going to do something preemptively to avoid some reactionary problems, we suggest use of high flow oxygen therapy via nasal cannula after extubation in the ICU for hypoxemic patients and those at low risk of reintubation. And thirdly, as a prophylactic measure, we suggest the use of noninvasive ventilation after extubation in the ICU for those at high risk of reintubation, especially hypercapnic patients. So to put these recommendations in simple terms, if you are in the cardiothoracic surgery unit or you were intubated for hypoxemic respiratory failure and you have lower risks for reintubation, you should be extubated to high flow nasal cannula, typically for about 24 hours, and then weaned down as appropriate. And if you are intubated and you are at high risk for reintubation, you're hypercapnic, you have neuromuscular weakness, high risk for intubation, we should extubate you directly to BiPAP. We should not go to high flow and then try to salvage using BiPAP. We should intubate you directly to BiPAP, give you some time on the BiPAP, see how you do, again, about 24 hours, and then start to reduce support. So that's all I have for you, and thank you for listening.

assessing effectiveness

mechanical ventilation strategies

ventilated patients

settings safety

patient synchrony

spontaneous breathing trial

ventilator-induced lung injury

low tidal volume ventilation

plateau pressures