SCCM Resource Library-Perspectives: Esophageal Pressure for PEEP Titration

Video Transcription

Hi, my name is Dr. Jeremy Butler. Thank you so much for having me. I'm here to talk about a soft gel pressure guided peep titration.  So in terms of disclosures, I receive consulting fees for some work on clinical trials from Hamilton Medical and Sedona Medical, neither of which have anything to do  with the soft gel pressure peep titration.  Some of the work I'm presenting has also received NIH funding from the grants listed here. And I want to take a moment to acknowledge  the co-PIs on this trial, Danny Talmore and Stephen Loring, as well as all of the other EPVEN2 investigators who worked with us to get the EPVEN2 trial done,  from which I'll be presenting some new analyses.  So when you think about the pertinent extending pressure of the lung or lung stress, it's the transpulmonary pressure that's defined as the difference between  the airway pressure and the pleural pressure.  So the lung is an elastic structure, isn't just determined by the pressure that we measure on the ventilator, the airway pressure, but also the pressure outside the lung,  which generally in clinical practice is unobservable, the pleural pressure. A way around that is using an esophageal balloon catheter  to measure the pressure that is inside the chest, but outside the lungs. And so you see on this CAT scan here, where the esophageal balloon catheter would be positioned.  When you think about the location within the chest, it's roughly in the midpoint, both from an anterior posterior standpoint, as well as from a left to right standpoint.  So the esophagus as a floppy compliant structure,  as long as the patient's not swallowing, the pressure inside the esophagus is a reasonable measurement of the pressure, a reasonable estimate of the pressure  outside the esophagus or the pressure in the pleural space.  And so the pleural pressure can be estimated via esophageal manometry, at least the average pleural pressure in the mid thoracic cavity.  And so really the driving point behind a PEEP titration  using esophageal pressure is this question of whether adjusting PEEP to maintain a non-negative transpulmonary pressure might prevent adelect trauma.  And so sort of as a proof of concept, here's an N of one example of airway opening that occurs only with a non-negative transpulmonary pressure.  So the top wave form here represents airway pressure, the middle wave form, esophageal pressure, and the bottom wave form is changed in volume.  So you can see towards the left of the graph,  initially the values are relatively low for airway pressure and volume. And starting at about the middle third of the graph, airway pressure increases slowly.  And that was achieved here by connecting the patient to an ambu bag and slowly squeezing that manual ventilation bag to slowly raise airway pressure.  And you can see initially as airway pressure is rising, there's no change in volume. So pressure and suddenly the volume  going into the patient starts increasing. And so at the point beyond which airway pressure is greater than esophageal pressure  is the only point at which you observe airflow into the patient. And it's sort of a proof of concept of this idea behind adelect trauma that at negative transponder pressures,  there might be some airways collapse. Normally for adelect trauma, we think of small airways, but our observational data here supported by a recent Blue Journal article  from Laurent Bruchard's group indicate that even large airways collapse can occur in a subset of patients with ARDS.  So with this idea in mind that a non-negative transponder pressure might prevent adelect trauma, the EPVENT1 trial was conducted. And this was a trial that compared  esophageal pressure guided PEEP targeting a non-negative transponder pressure versus the ARDSNet low PEEP strategy. This was published in the New England Journal in 2008.  And one of the more exciting findings is that after adjusting for baseline differences in APACHE2 score, there was a significant mortality benefit  with esophageal pressure guided PEEP titration  for patients with at least mild ARDS with a P-to-F score, a P-to-F ratio of 300 or less. And the Kaplan-Meier curve was not quite statistically significant,  but obviously there was a compelling separation in survival curves to make people excited about this therapy. The trial has a number of limitations  that give pause to the excitement. I think perhaps the most obvious is it was a single center study and the study population was quite small. It included only 61 patients.  So obviously we're not going to change practice globally in a small single center trial.  Additionally, the comparator arm was the low PEEP strategy from the ARDSNet ARMA trial.  And one might argue that for more severity as patients perhaps a higher PEEP strategy is appropriate. And then lastly, the trial was actually stopped early.  The main endpoint was P-to-F ratio  and P-to-F ratio was significantly better in patients in the esophageal pressure guided PEEP strategy. That's not a clinically meaningful endpoint.  And so interpretations of mortality are really limited in the single center trial, although there was a compelling preliminary signal.  So with that in mind, we conducted the EPVEN2 trial, which compared esophageal pressure guided PEEP versus an empirical high PEEP strategy. So the comparator arm in this case  was a much more aggressive PEEP titration strategy and was using the original trial. What we found in this case was no significant difference  in the primary outcome of compositive mortality and days free from mechanical ventilation through day 28. So it's not confirmed the findings of the initial trial.  And if you look at the Kaplan-Meier curves, there's really no compelling separation between the two treatment groups whatsoever. So admittedly quite disappointing results  from what was intended to be a relatively confirmatory phase two trial.  So sort of going back into the mechanistic data from this trial,  there was no significant separation in PEEP between the two treatment groups. And I think that's an important finding here. If you look at day zero as baseline,  but day one through seven, the on-protocol values, there was no significant difference in terms of PEEP  with empirical high PEEP strategy versus a soft-shell pressure-guided PEEP strategy. And so in a skeptical interpretation of this data,  of these data might be that the trial compared high PEEP versus high PEEP  with no separation in treatment groups, there'd be no reason to expect a treatment effect, right? You achieve the same end result. So the nihilist might say,  well, soft-shell pressure-guided PEEP is not needed. If you believe in a high PEEP strategy, just go for it. At least for patients with moderate to severe ARDS.  And people with that sort of skeptical view of soft-shell manometry might point to this oft-cited meta-analysis published in JAMA almost over a decade ago now.  We looked at patients with moderate to severe ARDS and found that in those patients, a higher PEEP strategy, regardless of how you got there, was afforded a survival benefit  compared to a low PEEP strategy. Whereas in patients with mild or lung injury with a P to F, a 201 to 300,  if anything, perhaps the opposite was true, but there was certainly no signal for survival benefit. So people can point to this and just say, look, for a moderate to severe ARDS,  if you want high PEEP, go for it. You don't need a esophageal balloon catheter to tell you to do that.  However, that's not really a satisfying physiologic interpretation.  So we sought to reanalyze the EPVAN2 data  using a risk stratified and mechanistic analysis.  So first for the risk stratified analysis, one of the sort of standard things that's recommended in considering outcomes of clinical trials  is to evaluate whether the treatment effect observed on average across the trial applies equally to all patients. And usually the first analysis that's recommended for that  is to stratify by the baseline risk of your outcome. And so we reanalyzed the EPVAN2 data stratified by baseline risk of death as estimated with APACHE2.  So the first thing to do when you perform this sort of analysis is to confirm or demonstrate that randomization worked, that the risk of death  was similar between the two treatment groups. And so on the left here, if you look at APACHE score, indeed you see the APACHE score is evenly distributed and normally distributed.  And both the essential pressure guided PEEP strategy and the empirical high PEEP strategy. On the right, we used APACHE scores to calculate predictive risk of death.  And again, you see an even distribution between the two treatment groups. So randomization worked and risk of death by treatment group at baseline was similar.  So we then looked at baseline characteristics by APACHE score, splitting it about the median and pulmonary mechanics shown at the bottom here  were not significantly different between patients with a lower APACHE score versus higher APACHE score at baseline. However, a couple of things were significantly different.  One is one quite obviously vasopressors were used more commonly in patients with a higher APACHE as you would expect. What was interesting also was that body mass index  and body weight were significantly higher in patients with a lower APACHE score who were less sick.  So the lower APACHE patients tended to have a higher BMI.  So we then continuing with our heterogeneity of treatment effect analysis, we looked at whether the baseline risk of death helped explain differences in treatment effect  between the two groups. And showing first patients with a lower APACHE score, we found indeed that those patients with an APACHE less than the median  had a significant mortality benefit with esophageal pressure guided to PEEP compared to an empirical high PEEP strategy.  On the other hand, there was no significant benefit  with among patients with a high APACHE. And if anything, there's suggestion perhaps that the esophageal pressure guided PEEP strategy might be causing harm in those patients.  And sort of the proper statistical tests for heterogeneity of treatment effect of the interaction term was statistically significant here.  So in fact, there were sufficient data conclude that the effect of our PEEP strategy depended on APACHE score, depended on baseline risk of death with a mortality benefit  among patients with a lower APACHE.  Now, this sort of differential treatment effect was robust to model specification. So whether you looked at dichotomized APACHE as the Kaplan-Meier curve did,  you looked at APACHE as a continuous variable, you recalculated a modified APACHE removing the pulmonary component or used SOFA instead of APACHE.  The same story held for either Cox models or logistic regression models. So this signal seemed to be robust across analytical approaches,  suggesting that there was a mortality benefit in patients with lower APACHE or SOFA score.  And additionally, that interaction was also significant for models predicting ventilator and shock-free days. So it really seemed to be a convincing signal for a treatment effect.  Now, importantly, as I mentioned at baseline, there were differences in body mass index, but there was no evidence of an interaction between body mass index and treatment group.  So BMI was not associated with heterogeneity of treatment effect at all. So we don't think this is simply a matter of differences in body habitus at baseline.  So how do you explain this? How do you explain there being a mortality benefit in patients with lower APACHE score? And so I really think it has to do with thinking  about the relationship between illness severity and risk of death. So normally when we, I think about this relationship, it's a loaner association like this, right?  Or maybe a J-shaped association where higher illness severity means higher risk of death. However, for an ARDS trial, only a subset of that risk of death  is explained by ARDS itself. That would be what you would call your disease attributable risk.  The rest of the risk of death is explained by non-ARDS factors. You know, maybe it's the severity of the patient's sepsis or the severity of the patient's pancreatitis  or their baseline comorbidities. All the other things that go into patients' risk of death that might be captured in something like an APACHE score,  but don't really have anything directly to do with ARDS or at least with ongoing lung injury.  And so if you then think about the effect of APACHE, for patients with a lower APACHE,  their ARDS attributable risk of death is gonna be higher, right? For a given P to F ratio, if you have a low APACHE score, then the risk of death is gonna be driven  primarily by lung injury. Whereas patients with a very, very high APACHE who have extensive multi-organ failure and perhaps multipressor shock,  extent to which you titrate pre-PEEP precisely to attenuate VILI  is probably not gonna have that much of an effect on their mortality. You know, their risk of death is primarily driven by all the other factors  are related to their critical illness with only a relatively minor effect from ventilation-induced lung injury. And so there's certainly mechanistic plausibility,  if you will, on an epidemiologic view for why patients with lower APACHE might benefit more from a lung protective intervention.  However, that's not really satisfying from a mechanistic standpoint, right? And as I mentioned earlier,  one of the struggles with this is that there's no separation in PEEP between the two treatment groups on average over time, right?  So if there's no difference in your treatment effect, how can you just say, oh, well, APACHE explains it. And I think that goes back to  considering our mechanistic hypothesis  and so a lot of the focus is on PEEP saturation to prevent adalect trauma, right? And I think there's both animal data and some preliminary human data  that suggests that a negative transponder pressure may predispose to small airways closure and therefore, adalect trauma.  However, the other side of this is also very important, right? Having a more positive transponder pressure predisposes to overdistension lung injury.  And certainly if you have a PEEP that achieves a positive transponder pressure and then you totally ventilate on top of that, the risk of overdistension injury might be quite high.  So from a mechanistic standpoint, there's really reason to think that regardless of what the PEEP is, having a transponder pressure of somewhere around zero  might be maximally protective to both prevent adalect trauma and overdistension associated lung injury.  And so while there was no separation in PEEP between the two treatment groups in our trial, the more relevant thing to look at is the separation in transponder pressure  as shown on this graph here.  And so this is now displaying the differences in end-expiratory transponder pressure over time. And at first glance, again, if you look at the diamonds in the middle here,  there's really no signal for a difference in the mean transponder pressure over time, right? They're relatively similar. However, sort of on visual inspection  of the distribution of data here, while the means might be similar, clearly there is a difference in treatment, right? Does this really look the same?  What we see is that patients in the yellow boxes assigned to the esophageal pressure guide of PEEP strategy, in fact, have a much narrower range  of transponder pressures that they encounter, right? Pretty precise titration right around an expiratory transponder pressure of zero.  Whereas patients in the empirical PEEP strategy had quite a broad range of transponder pressures that they encountered. So while the mean values are the same,  for patients randomized to esophageal pressure guide of PEEP, the transponder pressure really was centered around zero, which was our mechanistic hypothesis  for where we think we would see the most benefit. And when you look then at outcomes based on what the end-expiratory transponder pressure is, what you find is that there is in fact  quite a significant association. Patients with a transponder pressure of right around zero, within plus minus two centimeters of water of zero tended to do the best in our trial,  whereas patients with either a more negative or a more positive transponder pressure had a decreased probability of survival.  We reanalyzed these data while this was done graphically using the absolute value of transponder pressure. And so you can think of that as the deviation from zero.  And that was also significantly associated with mortality. The closer to zero you were, the better the patient did.  But importantly, just entering transponder pressure as a linear covariate, just saying, okay, is more positive better, is higher PEEP better?  That was not associated with mortality at all. So it really seems to be a U-shaped relationship  with greatest likelihood of survival around a transponder pressure of approximately zero centimeters of water.  So looking at a stratified analysis by Apache, since that's what sort of led us down this path initially, for patients with a lower Apache,  there's indeed that mortality benefit seen again. For patients with higher Apache, while the same type of relationship is there, it was not statistically significant.  So perhaps this explains the heterogeneity treatment effect by Apache. The patients with the greatest disease attributable risk of death, that is those  with the less extra pulmonary organ failure, lower Apache score, tended to see this benefit with an expiratory transponder pressure titrated right around zero, whereas that benefit  was not significant in patients with higher Apache.  The tidal volume is 300, doesn't tell you something about lung strain. So if you think about PFTs here and how they relate to transponder pressures, normal tidal  breathing is represented in the middle there. When you do an inspiratory capacity maneuver, when you go up to total lung capacity, that  typically occurs at a transponder pressure of around 20 to 25 centimeters of water in healthy normals, whereas the transponder pressure of around 10 is normal and inspiratory  stress and a transponder pressure of around zero occurs at physiologic functional residual capacity. It's what you normally see in healthy normals around FRC.  And so these same numbers extrapolate to the baby lung in patients with ARDS. And so if you're thinking about how to use esophageal manometry to understand the competing  effects of PEEP titration, we'll envision the following scenario. So you have a patient where you're trying to both prevent adelectrauma, which would  be focusing on the end-expiratory transponder pressures, as well as preventing excessive overdistension, which might focus on the inspiratory transponder pressures.  And so you start out with your tidal volume of 60 cc per kilo and a relatively high driving pressure, right? So you're not fully preventing adelectrauma.  You're not fully preventing overdistension injury, but you're at least trying to minimize them both.  So now you could just say, okay, well, 60 cc per kilo, and let's titrate PEEP to achieve a transponder pressure of zero at end expiration.  Doing so would exacerbate overdistension, right? So you're going to put the patient's end-inspiratory lung volumes closer to total lung capacity  of the baby lung, maximal stress and strain.  And so that of course will cause more lung injury and the benefit of PEEP will not be observed.  Now you could say, okay, what we want to do is we want to minimize end-inspiratory lung injury, overdistension lung injury. And so you could just drop PEEP.  And that's probably more protective, right? I think the preponderance of data suggests that overdistension injury is more harmful than adelectrauma. So this would be reasonable.  Let's use a low PEEP strategy in a patient that has this terrible signal for overdistension with higher PEEP.  And that's something that a couple of trials have indirectly done, but hasn't been explicitly targeted.  But I think really, if you wanted to maximize lung protection, you would try to do both, right?  You would try to titrate your end-expiratory transponder pressure to prevent adelectrauma, and you would try to adjust the height of volume to prevent overdistension.  So really what we're talking about here is if you're in a scenario where you're going to be raising PEEP, and that predisposes to overdistension injury, then you should  also simultaneously lower titra volume. And simply, it's something that hasn't been tested in clinical trials, right?  The titra volume is set at 60 cc per kilo, and it's generally left there unless you're hitting some upper limit of plateau pressure, upper limit of transponder pressure.  And that's probably not the optimally lung protective ventilation strategy, at least in patients with severe ARDS.  And so I think really, what we're left saying is that the ideal PEEP strategy is not a higher PEEP strategy. It's not a lower PEEP strategy.  It's a precise PEEP strategy that might try to minimize stress in a way to account for  the competing effects of mitigating adelectrauma and exacerbating overdistension when you increase PEEP.  And so really, an ideal PEEP strategy might titrate to achieve a transponder pressure  near zero at end expiration, and then simultaneously lower titra volume to minimize overdistension.  So in conclusion, remember, esophageal pressure is a diagnostic tool to understand pulmonary mechanics. It's not itself a treatment.  It's just giving you additional information to think in a more sophisticated way about how you might manage the patient.  The data that we presented today suggests that targeting PEEP to approximately equal the pleural pressure, offset the pleural pressure, might improve survival in patients with ARDS,  particularly when the risk of death attributable to lung injury is high. That is when patients don't have extensive multi-organ failure.  These are obviously promising preliminary data, but I think they in themselves are not yet sufficient to warrant broad adoption of a esophageal pressure-guided PEEP strategy.  However, planning is ongoing for a confirmatory phase three trial that might be able to lend  more definitive evidence into how to incorporate esophageal pressure-guided ventilation into normal clinical care. Thank you for your time.  How are you gentlemen? Nice to see you. Hello, Dr. Beatlow. Hello. I know that the technical issues surrounding today did not subtract at all from the quality of your talk.  This was very, very good. And there was a large number of attendees. My question is, as I played with, and I can only say play, with esophageal pressure monitoring,  our nurses had required quite an amount of in-service. So are your nurses comfortable with the systems, or does respiratory provide the work, or do  your fellows actually provide more of the work? That's a, thank you for that excellent question.  I think it's, if there's a decision made to introduce this more widely into clinical practice,  I do think, to your point, that it will need to be individualized to each site's specific expertise and programs.  And so, for instance, where I trained at Beth Israel Deaconess in Boston, the respiratory therapist did this as part of their routine practice.  You know, there wasn't a question if a patient had ARDS, they would get esophageal balloon, the RTs would put it in themselves.  They would interpret the values, they would print out the screen, and they would show you what it was.  And that was a very advanced level after having done it as an institution for probably close to two decades, that they had that sort of approach.  In my current institution, it's entirely reliant on the physician implementing, or placing the balloons and interpreting the values when it comes up.  And I can imagine putting it in a hospital, relative expertise and comfort of nurses and respiratory therapists and physicians with a ventilator and with placing the catheters  and patients would require a specific intervention plan. That they had that sort of approach.  In my current institution, it's entirely reliant on the physician at Beth Israel Deaconess and implementing the values and interpreting the values when it comes up.  And I can imagine putting it in a hospital, relative expertise and comfort of nurses and respiratory therapists and physicians with a ventilator and with placing the catheters  and patients would require a specific intervention plan. That they had that sort of approach.  In my current institution, it's entirely reliant on the physician at Beth Israel Deaconess and implementing the values and interpreting the values when it comes up.  And I can imagine putting it in a hospital, relative expertise and comfort of nurses and respiratory therapists and physicians with a ventilator and with placing the catheters  and patients would require a specific intervention plan.  All right, can you guys hear me? Yes, and that's without an echo, so that's wonderful, Javier. Great, I apologize for the technical difficulties  on what's going on, but hopefully it's taken care of. Going back to the questions, Dr. Beitler, I was wondering when monitoring esophageal pressures  and dealing with mechanical ventilation,  is there any mode of ventilation that works best for esophageal pressures, meaning you have volume control versus pressure control? Yes. If the patient is not adequately sedated,  you know that higher volumes and flow rates are valuable in pressure control because of the technical difficulties. Does it matter at all when you use the ventilation?  That's a excellent question.  So in my mind, at least one of the strengths of thinking about respiratory system mechanics in terms of transpulmonary pressures and focusing specifically on lung mechanics  as opposed to the lung and chest wall combined is the interpretation of the values I think is arguably more straightforward,  even though obtaining those values is a little more tedious.  So regardless of not only ventilator mode, but patient effort, the transpulmonary pressure is the transpulmonary pressure. So if you do an airway occlusion  and are trying to measure, let's say a plateau pressure, the only way you get a true plateau pressure is if the patient is passive on the ventilator.  If they're pushing against a closed valve, which they often will do, then that number is meaningless. For the transpulmonary pressure,  when you occlude the airway with that breath hold and the patient makes an effort, the volume in the chest is constant and so is the transpulmonary pressure.  So you'll see on wave forms that the esophageal and airway pressure rise by the same amount if the balloon's in the correct place. So in that case, I think you get data  that is much more interpretable than you would otherwise get. But with respect to particular ventilator modes and one being more advantageous than the other,  I personally at least am a big believer that it's less about the ventilator and more about the person using it. And so I think the expertise of yourself and Dr. Patrick  and people at the bedside is far more important and relevant than choosing one particular ventilator mode over another or one particular ventilator manufacturer  over another for that matter.  Thank you so much for that.  Dr. Patrick, do you have anything to add?  Okay, we have a couple of more questions from Dr. Diaz Gomez. It says, Dr. Biler, would you advise to have quantitative echo monitoring for esophageal pressure monitoring  if you're pursuing higher PEEP levels? If so, which echo parameters? If you're talking specifically with respect to echocardiography, so one of the potential appeals, again,  looking at the data that are out there where they've assessed with echocardiogram the effects of different transponder pressures,  it seems that maximal cardiac output actually happens when your index pituitary transponder pressure is around 50 to 60. It happens when your index pituitary transponder pressure  is around zero.  And if you are either below that or above that, then you tend to see a decrease in cardiac output. And that goes all the way back to the idea  that was advanced in respiratory failure with Peter Suter's classic 1975 New England Journal paper of PEEP titration and respiratory system compliance where he showed the same thing  that with the lowest driving pressure, when you titrate a PEEP to achieve the lowest driving pressure, that's when you had the highest cardiac output.  And so I do think it's not unreasonable to be concerned, or of course it's reasonable to be concerned about when you're increasing PEEP  potentially having adverse hemodynamic consequences. And perhaps that was in part a signal we saw in the trial which targeted transponder pressures well above zero  in the intervention arm.  But I think if you're doing what I believe is probably the safest approach based on the data and targeting a transponder pressure of around zero,  I think the risk of adverse hemodynamic effects in that setting seems to be less and supported by the echocardiographic data when those values have been targeted.  Thank you so much, Dr. Beiler. And we also have another question right now from Lauren Nelson.  She says, we routinely use esophageal monitoring in patients on high PEEP, usually more than 20 centimeters of water pressure to help guide cardiovascular support  and fluid management in the 80s and 90s. Do you find value of this when interpreting vascular pressures?  That's an excellent question. I think it's something that really honestly is under investigated. So if you think about the sort of story that I told and everyone's familiar with  about using esophageal pressure to interpret pleural pressures, if you think about the venous system, that is again, is another very compliant system  that's within the chest cavity and outside the lungs. And so I think part of sort of the dirty literature on how to interpret things like central venous pressure  is plagued by the fact that the venous system is compliant. And we know from respiratory failure research that pressures in the pleural space  can be all over the map in critically ill patients. And so while I think there are, to my knowledge, there are not strong data to tell us how to use  those types of measurements, I do think considering a transvascular pressure, at least on the venous side in the same way that you would think about  transplantary pressure on the pulmonary side  would make a potential physiologic sense.  Now, how you use that to guide fluid management or hemodynamic management, I personally have no idea. A lot of people spend a lot of time,  a lot of space in journals opining about that, but I do think part of the issue with that literature historically has been exactly to the point of the question  that we haven't really incorporated our basic understanding of the physiology that the venous system is a compliant structure where pressures outside the veins unquestionably  will impact the measurements you get with the central venous catheter.  Now, how you use that to guide fluid management or hemodynamic management, I personally have no idea. A lot of people spend a lot of time, a lot of space in journals,  but I do think part of the issue.  Historically has been exactly to the point of the question that we haven't really incorporated our basic.  we're so left.  One last question, Dr. Byler.  When would you decide to put an esophageal balloon catheter into a patient? If we're trying to optimize PEEP on a patient and we can easily do so by driving pressures,  what would make you take that extra step? Is it based on a patient that has a high BMI? Is it on patients that just have mild to severe ARDS?  What would make you choose esophageal pressures versus other modes for optimizing PEEP on a patient?  That's an excellent question.  I think it's,  candidly, I think we still don't have a definitive idea of what exactly to do with the measurements. I think that the first step that the community has made  is recognizing that there is some sort of  physiological value or meaning to these measurements.  But as I made the point at the end of my talk, how we translate that into interventions that are gonna benefit patients is unclear.  I think as you suggested and as one of the other questions raised, at least for my practice, certainly when we start to reach higher levels of PEEP in the high teens and the 20s,  I feel much more comfortable having transpulmonary pressure measurements just to make sure that I'm not exacerbating over-distention in those patients.  I think that BMI example is another good one where there's often this assumption that patients with higher BMIs have higher pleural pressures and still it varies. I'm clear.  I think as you suggested and as one of the other questions raised. Well, thank you very much, Dr. Byler. It looks like we just ran out of time. I wanna thank all of you, Dr. Byler,  Dr. Herbert Patrick, for being with us and all of you for joining us on the Society of Critical Care Congress. And we hope to see you next year  at the 51st Society of Critical Care Congress in Puerto Rico. So thank you so much and please continue to submit your questions.  ♪♪♪

Video Summary

Dr. Jeremy Butler presented a talk on esophageal pressure-guided positive end-expiratory pressure (PEP) titration for patients with acute respiratory distress syndrome (ARDS). He discussed the role of transpulmonary pressure in determining lung stress and the use of esophageal balloon catheters to measure pleural pressure. The EPVENT1 trial compared esophageal pressure-guided PEEP titration with the ARDSNet low PEEP strategy and found a significant mortality benefit in patients with mild ARDS. However, follow-up analysis with the EPVENT2 trial did not confirm these findings. Dr. Butler then analyzed the EPVENT2 data further and found that the treatment effect of esophageal pressure-guided PEEP titration depended on the baseline risk of death. Patients with lower APACHE scores had a mortality benefit, while those with higher scores did not. He proposed that an ideal PEEP strategy would aim for a transpulmonary pressure near zero at end expiration and simultaneously lower tidal volume to minimize overdistension. Ultimately, Dr. Butler acknowledged that further research is needed to fully understand the benefits and implementation of esophageal pressure-guided PEEP titration.

Asset Subtitle

Pulmonary, Procedures, 2021

Asset Caption

The Society of Critical Care Medicine's Critical Care Congress features internationally renowned faculty and content sessions highlighting the most up-to-date, evidence-based developments in critical care medicine. This is a presentation from the 2021 Critical Care Congress held virtually from January 31-February 12, 2021.

Learning Objectives

Define the setup for measuring esophageal pressure on different ventilators
Recognize the physiology of esophageal pressure monitoring on gas exchange and lung injury
Determine which patients will benefit from esophageal pressure monitoring and which will not

Pros and Cons of Esophageal Pressure in PEEP Titration
Jeremy R. Beitler

Meta Tag

Content Type Presentation

Knowledge Area Pulmonary

Knowledge Area Procedures

Knowledge Level Intermediate

Knowledge Level Advanced

Membership Level Select

Tag Positive End Expiratory Pressure PEEP

Tag Mechanical Ventilation

Year 2021

Keywords

esophageal pressure-guided PEEP titration

ARDS

transpulmonary pressure

EPVENT2 trial

mortality benefit

baseline risk of death

APACHE scores

ideal PEEP strategy

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