Transcript
Speaker: Welcome to Critical Matters, a sound critical care podcast covering a broad range of topics related to the practice of intensive care medicine.
Speaker: And now, your host, Dr. Sergio Zanotti.
Speaker: Acute respiratory distress syndrome, ARDS, is a severe form of respiratory failure that affects approximately 200,000 patients each year in the United States, resulting in nearly 75,000 deaths annually.
Speaker: Over the last decades, tremendous efforts and research have advanced our understanding and improved our treatment of patients with ARDS.
Speaker: However, the mortality and morbidity of ARDS remains high.
Speaker: In today's episode of Critical Matters, our guest, Dr. R. Philip Dellinger, will share with us his thoughts on the current management of patients with ARDS.
Speaker: Dr. Philip Dellinger is Professor of Medicine and Distinguished Scholar at Cooper Medical School of Rowan University.
Speaker: He is Senior Critical Care Attending and Director of the Cooper Research Institute at Cooper University Health.
Speaker: Dr. Dellinger is a prolific author and researcher.
Speaker: He co-edited the second, third, and fourth edition of Critical Care Medicine, a major textbook published by Mosby, and co-edits the fifth edition to be published in early 2019.
Speaker: He is associate editor of Critical Care Medicine, the journal, and he has received multiple accolades for his contributions to Critical Care Medicine, including being inducted as a Master Fellow in the College of Critical Care Medicine in 2012,
Speaker: being a past president of the Society of Critical Care Medicine, and being the recipient of the Society of Critical Care Medicine Lifetime Achievement Award in 2015.
Speaker: Dr. Dellinger was the lead author of the 2004, 2008, and 2012 Surviving Sepsis Campaign International Guidelines on the Managed Severe Sepsis and Septic Shock, and a senior author on the most recent guidelines.
Speaker: He also has a long history of publishing research and editorial comments in research in ARDS.
Speaker: But most importantly, Dr. Dellinger has been a phenomenal teacher, a great mentor, and is a dear friend.
Speaker: Those who have grown under him in the world of critical care affectionately refer to him as Dr. D. Dr. D, welcome to Critical Matters.
Speaker: Thank you, Sergio.
Speaker: It's a pleasure to be here.
Speaker: So today the topic is ARDS, and I think that as many of the things that we preoccupy ourselves with in critical care, ARDS is a syndrome, and that has a
Speaker: presented its challenges in terms of definitions and making sure that we're recognizing the right patients.
Speaker: So why don't we start with definitions, a little bit maybe of historical perspective, and maybe talk about the most current definition or the Berlin definition.
Speaker: Certainly.
Speaker: The first consensus definitions for ARDS chose to differentiate
Speaker: lung infiltrates and hypoxemia due to left-sided heart barrier from infiltrates and hypoxemia due to acute lung injury and therefore required not having left-sided heart barrier infiltrates on both sides of the lung severe hypoxemia and acute
Speaker: The more recent Berlin definitions have attempted to offer some clarifications for benefit of the clinician, in particular, recognizing the fact that ARDS, or acute respiratory distress syndrome, can occur
Speaker: on top of some degree of left-sided heart barrier and therefore not having left-sided heart barrier as an exclusion factor.
Speaker: Furthermore, instead of dividing this non-cardiac lung injury into acute lung injury as it previously was defined as being between
Speaker: 200 and 300 and ARDS as being less than 200.
Speaker: It uses ARDS only and divides it into severe, moderate and mild.
Speaker: And in terms of the Berlin definition, can you comment also on the
Speaker: the timing issue.
Speaker: I think that that's very important, right, because there used to be some variations in what we consider acute.
Speaker: Any comments on that, Dr. Dellinger?
Speaker: Yeah, so the previous definition said acute, but didn't offer any parameters around the acute.
Speaker: The Berlin definitions defined acute as within seven days and with an identifiable trigger.
Speaker: There has to be some
Speaker: some evidence of some type of an acute event that could be a trigger.
Speaker: And I think that another aspect that is often not discussed with progress in terms of the Berlin definition is that they also evaluated other potential physiologic parameters, but ultimately used a cohort of patients to try to test these definitions out and see if there was any ability to discriminate at a higher level at the bedside.
Speaker: So that's also something that we've seen with new definitions for sepsis that seems to be a work in progress, although these definitions still obviously work.
Speaker: are not perfect.
Speaker: That is correct.
Speaker: So can we talk a little bit more, Dr. Dellinger, about the mild, moderate, and severe?
Speaker: Because I think that there's also implications in terms of treatment, prognosis, and just to make sure that our audience is very clear on that, you have classified mild as being a PaO2 over FiO2 between 200 millimeters of mercury and 300 millimeters of mercury, and that is with a PEEP or CPAP of fiber grader, correct?
Speaker: Correct.
Speaker: Moderate would be 100 millimeters of mercury to 200 millimeters of mercury with the same characteristics of the PaO2 over FiO2 ratio, and severe would be a PaO2 over FiO2 ratio that is equal or less to 100 with a PEEP of 5 or more.
Speaker: So is there a correlation between these three in terms of outcomes?
Speaker: Any comments on that, Dr. D.?
Speaker: You know, clearly, I don't have the table in front of me, but the PaO2-FiO2 ratio was clearly correlated with the increasing severity as the PaO2-FiO2 ratio got lower in these three classifications.
Speaker: So we have the benefits of technology.
Speaker: I'll bring up the table for you real quickly, but go ahead.
Speaker: Yeah, so, and when they added other things, it really didn't improve the performance of the predictor very much.
Speaker: So what they found when they published this was that the mortality for the large cohort with the mild definition was 27%.
Speaker: with a duration of mechanical ventilation on average of five days, for the moderate, 32%, with a duration of mechanical ventilation of seven days, and for the severe, for a mortality of 45%, with an average duration of mechanical ventilation of nine days.
Speaker: So like you stated, there was no added benefit in discriminating those different mortality groups if you added more complex aspects to the definition, right?
Speaker: That's correct.
Speaker: And I think that this is important for our audience because there is value in terms of making sure that you understand where your patient falls.
Speaker: And I think that we'll talk a little bit more further on.
Speaker: There might be implications of what are the type of therapies that you might be thinking of based on this mild, moderate, and severe classification.
Speaker: So these will be added to the show notes.
Speaker: Now, let me ask you, Dr. D., how do you...
Speaker: implement these definitions when you're seeing patients at the bedside.
Speaker: So I think that one of the problems is that we probably under-recognize ARDS or not calling it as such.
Speaker: We just talk about respiratory failure, but we might be missing patients that may be a little bit sicker if we actually thought about it in a more rigorous way.
Speaker: So how do you make this operational as a clinician?
Speaker: So I do it a little bit differently than I
Speaker: perhaps the textbook response would be, I tend to apply the ARDSnet therapeutic approach with the low tidal volume and PEEP setting and then see where my patient falls and make decision based on PAO2, FiO2 ratio
Speaker: for additional therapeutic intervention.
Speaker: I think it's very difficult to try to assess the PAO2-FIO2 ratio out front because a patient, you may be called to see a patient that's being totally inappropriately treated is on
Speaker: minimal or no therapeutic PEEP, has terrible oxygenation, is on various amounts of FiO2.
Speaker: So to me, it's more helpful to try to standardize my patients.
Speaker: So I think that if I'm hearing you correctly, a way to approach this at the bedside would be to think about
Speaker: When you're trying to make a diagnosis of ARDS, maybe think about the timing first.
Speaker: Has this occurred in the last seven days?
Speaker: Look at your chest imaging.
Speaker: Do you have bilateral infiltrates that are not fully explained by effusions, lung collapse, or nodules?
Speaker: Think of the origin of the edema, and that was an important point you made earlier, that it doesn't mean that you can't have some degree of heart-induced cardiogenic edema, but what you really are looking for is respiratory failure that's not fully explained by cardiac failure or fluid overload.
Speaker: Or I would even say that you think it's predominantly not related to cardiac, because if you think it's predominantly related to cardiac, then...
Speaker: the therapy should target the left-sided filling pressures.
Speaker: And I think that exactly, and I think that if those three are met, you then kind of optimize mechanical ventilation or step one, and then you make an evaluation of how severe the oxygenation problems are, and that gives you a mild, moderate, severe, which I think is a great way to think about it because at the end of the day, as we'll talk probably a little bit later, we can only help people by applying some of the basic evidence-based mechanical ventilation concepts to all these patients.
Speaker: Yeah, and can I give an example very quickly?
Speaker: If I come to the bedside of a patient that had a PaO2, FiO2 ratio of 80, but they haven't had any PEEP therapy applied, and when I exact the ARGNET initial ventilator setup strategy,
Speaker: and the PAO2, FiO2 ratio on 14 of PEEP goes to 210 versus 14 of PEEP, it's still in the toilet.
Speaker: You know, that's two very different patients that require two very different approaches.
Speaker: And I think that's a very, very important point.
Speaker: But I think that these definitions clearly can help our clinicians at the bedside think about these patients.
Speaker: But I think that the point of really making the final assessment of degree of severity and mild, moderate, severe should be after you have done some basic interventions that provide a baseline of what would be evidence-based.
Speaker: So I think that would be a great
Speaker: segue into talking about mechanical ventilation and ARDS.
Speaker: And I think that, how would you define in broad terms, Dr. D, the goals here?
Speaker: Well, I think the goal is to minimize overinflation and minimize collapse of lung at end expiration of
Speaker: due to inadequate PEEP settings.
Speaker: And that is what we traditionally have referred to as ventilator-induced lung injury, volutrauma, atelectotrauma, and I guess that's where this whole concept of protective lung strategy comes from.
Speaker: Correct.
Speaker: How would you do that?
Speaker: So how would you implement a protective lung strategy?
Speaker: What does the evidence tell us that we should be doing all these patients?
Speaker: So I think step one is to go as quickly as possible to six mLs per kilogram predicted body weight.
Speaker: If someone is on 12, for example, when you begin ventilator strategy, you would not go from 12 to six because you want to make sure it's tolerated.
Speaker: So you would decrease 12, 10, 8 with the goal of getting to six.
Speaker: But as you go down, you'll need to make decisions about tolerance by the patient.
Speaker: But I think you take your patient to six mLs per kg and then you PEEP set.
Speaker: And you look for the PEEP setting that gives you, with that fixed tidal volume, the PEEP setting
Speaker: that gives you the optimum balance of overinflation and not having excessive atelactasis at end expiration.
Speaker: So as you go up on PEEP,
Speaker: you're going to induce some overinflation in some areas of the lung that have relatively normal compliance, but you're also going to open up lung that was previously closed and also create better compliance in lung units as you increase the volume in the alveolus.
Speaker: So you're looking for that sweet spot with your PEEP
Speaker: that gives you the best balance of minimizing adalecta trauma or lung collapse at end expiration and avoiding overinflation.
Speaker: So we spoke about using the low tidal volume and you said how you would get there.
Speaker: For example, somebody was at a higher tidal volume when you first saw them.
Speaker: What if you happen to intubate the patient?
Speaker: Do you usually start around eight and then go down?
Speaker: Do you start at six and see if they tolerate it?
Speaker: If this is a newly intubated patient that you suspect has ARDS?
Speaker: Yeah.
Speaker: So it depends on, you know, how severe the hypoxemia is.
Speaker: If
Speaker: If the patient looks like they're trying to die on me from hypoxemia, I'll have a mental image of the chest X-ray and how bad it looks.
Speaker: I'll know what the oxygenation was on high-frequency nasal cannula oxygen.
Speaker: And then I'll say, I don't have time to be ginger with my PEEP application, so I'm just going to start
Speaker: at 12, and ideally, in the best possible worlds, you would like to start low and use incremental recruitment by going up slowly on peak
Speaker: in order to make that decision on where's my sweet spot for PEEP.
Speaker: If you have a patient that's now getting six mls per kg predicted body weight title volume, and you go from a PEEP of eight to a PEEP of 10 to a PEEP of 12 to a PEEP of 14 to a PEEP of 16 to a PEEP of 18, and as you go, there's, there's,
Speaker: a variable called driving pressure, which is the difference between the PEEP and the plateau pressure measured with an inspiratory hold, where at the end of inspiration, instead of opening the expiratory valve and closing the inspiratory valve, you
Speaker: you close the inspiratory valve and you don't open the expiratory valve and that gives you an end inspiratory pause pressure, which is an estimate of the alveolar pressure at end inspiration.
Speaker: And the difference between the total PEEP, which is typically the set PEEP, in the plateau pressure is driving pressure and that represents compliance.
Speaker: with a fixed tidal volume, and in the absence, with a fixed tidal volume, the driving pressure represents compliance, and the lower the driving pressure, the better the compliance.
Speaker: So if you look for the PEEP that gives you the lowest driving pressure, that would tell you that you're in that sweet spot
Speaker: for opening up lung on one hand and overinflation on the other.
Speaker: And as a point of reference, I mean, the value that people talk about for driving pressure is usually to have it below 15, like 13 to 15.
Speaker: It would be a good target, correct?
Speaker: Correct.
Speaker: I think that, you know, there's database data looking at
Speaker: you know, what driving pressures give better outcomes, and that is a range of driving pressures that you would like to reach.
Speaker: In actuality, as long as you can improve by decreasing driving pressure, by definition, you know, you are improving compliance.
Speaker: Now, someone might say you're improving compliance, but some
Speaker: at some expense of more overinflation by definition,
Speaker: So maybe you just leave good enough alone if you get it to 13 to 15.
Speaker: And I think that the other measurement that we didn't touch on, which I think is part of this conversation, is just looking at your plateau pressures.
Speaker: And can you talk a little bit about the airway plateau pressure, what it means?
Speaker: And you talked about how you measure it already, but what numbers should we be targeting in patients with ARDS?
Speaker: Yeah, so you'd like to have a plateau pressure
Speaker: no higher than 30 the general feeling is that the lower the plateau pressure the better but the plateau pressure is going to be determined by your peep or total peep and your tidal volume if if your plateau pressure certainly if it's higher than 30
Speaker: you would want to further decrease your tidal volume.
Speaker: You can see that there's interaction between decreasing the tidal volume to decreasing plateau pressure and driving pressure.
Speaker: So you can decrease driving pressure by decreasing tidal volume.
Speaker: But the beauty of the driving pressure is you want to have a fixed tidal volume and see what the best driving pressure is at that fixed tidal volume.
Speaker: And I think that you mentioned compliance as well, Dr. Dellinger, and just to review for our audience, static compliance is usually the tidal volume divided by the difference between your plateau pressure and your total PEEP.
Speaker: So what you're saying is that really from a practical standpoint, if your tidal volume is fixed,
Speaker: all you should be looking at or what you can be using at the bedside is the plateau pressure minus the total PEEP, which is your driving pressure.
Speaker: Is that correct?
Speaker: Correct.
Speaker: You don't have to actually calculate static compliance because you've already decided what tidal volume that you want to use.
Speaker: And therefore, without calculating the
Speaker: mLs per centimeter of water, you know that when driving pressure is going down, that compliance is improving, and when driving pressure is going up, compliance is worsening because you have a fixed tidal volume.
Speaker: Excellent.
Speaker: So I think to cap this part, clearly every patient with ARDS should receive a protective lung ventilation.
Speaker: And so far, what we talked about is three very important parameters that we should follow at the bedside.
Speaker: One is your tidal volume in mls per kg of predicted body weight, which, as our audience might recall, is not the same as ideal body weight, and it's calculated from your height.
Speaker: Number two is a plateau pressure of 30 or below, understanding that if it's above 30, we should probably do something to decrease it.
Speaker: And number three is to keep an eye on this driving pressure, which is the plateau pressure minus the total PEEP, to try to figure out what is the sweet spot for the ideal amount of PEEP in terms of
Speaker: preventing derecruitment of collapsed lung units, but also preventing overdistension of those lung units that are already open.
Speaker: Now, Dr. D, how would you incorporate or add to this your ABG?
Speaker: What are the targets that you're looking at in your ABG in terms of for your ventilation and oxygenation?
Speaker: Yeah.
Speaker: Sergio, could I, I think it's, we need to make one other real important point that
Speaker: when you just did that very nice recap, I realized the plateau pressure of 30 or less with even lower being making you feel better is that that is based on normal body habitus and that if you have a very morbidly obese or obese patient or a very anisarka-laden patient,
Speaker: then that plateau pressure is not only pushing out lung, but it's pushing out the chest wall and the abdomen.
Speaker: And you can allow higher plateau pressures in those circumstances.
Speaker: You have to sort of eyeball it unless you are measuring esophageal pressure, which would give you a little better handle.
Speaker: That's not routinely done.
Speaker: I can tell you, I don't routinely monitor esophageal pressure.
Speaker: But I just say, you know, in this morbidly obese patient, that plateau pressure of 34 is just fine, and I'm going to leave it alone.
Speaker: Okay.
Speaker: I think that's a great point.
Speaker: And I think that with obesity, just recognizing that the size of your lungs might not change.
Speaker: That's a function of height.
Speaker: But the compliance and the effect of the chest wall and everything we're measuring can be dramatic.
Speaker: taking that into account like a dunges you mentioned is very important.
Speaker: So what would you say for the ABG?
Speaker: What are your goals or your parameters that you're looking at?
Speaker: What should be the targets to complement that with the measurements that we're doing at the vent side?
Speaker: So you anticipate in the more severe ARDS patients
Speaker: that you're gonna be using this low tidal volume in all of them and maybe even lower in some, you can decrease it all the way to four mLs per kg predicted body weight to get that plateau pressure down.
Speaker: But that's gonna decrease your minute ventilation and that's gonna decrease your alveolar ventilation and that's going to decrease
Speaker: your ph so we're going to go into permissive hypercapnia you can increase the ventilator rate to compensate for some of that low tidal volume but you may need to accept ph's i feel comfortable with 725 or more sergio with some exceptions you don't want a high pa co2
Speaker: with increase intracranial pressure or perhaps even severe pulmonary hypertension.
Speaker: But you should anticipate in most patients willingness to accept a 72573 or less.
Speaker: And for the PAO2, we typically use saturation targets of
Speaker: 88% are higher in more severe ARDS and less severe ARDS where you can build in a little safety cushion for mucus plugging.
Speaker: You might want to run it more in the 94, 96 if you can do that with reasonable oxygen FiO2.
Speaker: So I think those are very important parameters.
Speaker: And I think that, like you said, you mentioned esophageal and pressure monitoring, but that is not commonly done, might be something that in some situations might be useful.
Speaker: But for most of our providers practicing in the community, by following the
Speaker: plateau pressure, making sure that they have the right tidal volume based on predictive body weight, following the driving pressure, and then following the gas, you can really, I mean, target your mechanical ventilation very adequately, and I think that that's what we should be doing in every patient.
Speaker: Let me ask you a little bit.
Speaker: We talked about people a little bit, Dr. Dellinger.
Speaker: You talked about that incremental increase by a factor of two, trying to find the sweet spot with the driving pressure.
Speaker: What about recruitment maneuvers?
Speaker: Where do we stand today with recruitment maneuvers?
Speaker: Yeah.
Speaker: So I think, you know, I was a, I'm a big fan of ESPN 30 for 30.
Speaker: And I must admit, for years, I was a big fan of the 40 for 40 recruitment maneuver, which was applying 40 centimeters of water CPAP
Speaker: for 40 seconds to try to open up atelectatic lung and then find the PEEP that holds that.
Speaker: There was a study published in 2017 that used much more exaggerated recruitment pressures and times repeatedly that produced worse outcome when PEEP was set with recruitment
Speaker: maneuvers, but these were really dramatic, sustained, high pressures.
Speaker: I think when you take the approach of, I'm going to go with my fixed low tidal volume, I'm going to go to eight a peep and leave it there for three to five minutes if you can.
Speaker: and then I'm going to look at driving pressure, and then I'm going to go to 10 for three to five minutes and look at driving pressure and oxygenation, and then 12 and then 14.
Speaker: You know, that is allowing the incremental increase in PEEP to do your recruitment for you.
Speaker: And I also, you mentioned that, you know, we're really,
Speaker: Figuring the bedside practitioner that maybe doesn't treat a lot of ARDS will be listening to this podcast.
Speaker: And if you say, you know, all this driving pressure stuff is just too darn confusing for me, is there an alternative that's simpler?
Speaker: And the alternative would be just to use the ARSnet PEEP table and look at where your
Speaker: your PAO2 is and where your FiO2 is and see if you're in a box.
Speaker: And if you're not in a box, then you're either too high or too low and you just look for, you adjust PEEP to get your FiO2 down.
Speaker: And that's been done in some of the ARGNET trials.
Speaker: So there's certainly nothing wrong with that approach.
Speaker: There are two PEEP tables, one for patients that have the moderate or severe ARDS, that's called the higher PEEP table, and a PEEP table for the mild ARDS, that's called the standard PEEP table.
Speaker: But you can just find whether you're on the right PEEP by finding yourself in these tables.
Speaker: So I think that we will add those tables to the show notes, but I think that...
Speaker: It's a great point that you talked about the ART trial that was published last year that really showed significant increase in mortality with these very aggressive and very prolonged recruitment maneuvers, which is really not what most people are doing in the clinical setting today.
Speaker: But it seems that as of now, your preference, Dr. D, and what the literature would support is either an incremental raise and peep
Speaker: using driving pressure and other parameters to find the sweet spot, or simply recurring to the ARDS net PEEP table and just making sure that for the given PAO2, FiO2, you have the right PEEP.
Speaker: Is that correct?
Speaker: That is correct.
Speaker: And the old logic was that there's probably some lung that you can only open up
Speaker: with much higher pressures than you're going to get to with the incremental recruitment where PEEP is the recruitment.
Speaker: When I trained, there was no recruitment maneuver.
Speaker: No one talked about recruitment maneuver, but we were recruiting just by increasing the PEEP with fixed title volume.
Speaker: You continue to raise your end inspiratory pressure
Speaker: through the raising the end expiratory pressure with fixed tidal volume.
Speaker: And is there still a place for some patients in whom you would do the 40 of CPAP for 40 seconds?
Speaker: Or that's really something that you have walked away from?
Speaker: No, I'll still do it.
Speaker: I'll do it when I get a fresh ARDS patient that's trying to die from hypoxemia.
Speaker: You know, I'll just go straight to a
Speaker: 40 for 40 recruitment maneuver or in a patient that's already has high plateau pressures, I would even be willing to do 50 for 40.
Speaker: Just for when I feel like I've got just so much boggy atelectatic lung that's trying to take my patient down and I just want to do something to open it up and then go to a higher peak than I would typically
Speaker: use with the incremental PEEP recruitment.
Speaker: So I might do 40 for 40, get a big bang boost in my oxygenation and just throw a PEEP of 12 or 14 in to see if I can hold it.
Speaker: And I think that it's probably good advice also for our audience to realize that this has potential complications.
Speaker: You want to talk a little bit about the dangers of high PEEP, of a high recruitment maneuver, Dr. D?
Speaker: Yeah, so we've always realized that PEEP is a huge offender for increasing intrathoracic pressure because we spend most of our respiratory cycle in expiration.
Speaker: So when you raise expiratory pressure, has a major effect on intrathoracic pressure.
Speaker: So as you increase intrathoracic pressure, you increase the right atrial pressure
Speaker: because of pleural pressure.
Speaker: So it goes, intrathoracic pressure, pressure goes to pleural space, pleural space wraps around the mediastinum.
Speaker: That raises the right atrial pressure because it's thin walled.
Speaker: And therefore your downstream pressure for right heart filling is decreased.
Speaker: So you decrease venous return to the right heart by increasing intrathoracic pressure with PEEP.
Speaker: Luckily, in ARDS, lungs are poorly compliant, so you don't get as much of that intrathoracic pressure transferred to the right atrium because the ARDS actually protects the transmission to the pleural space.
Speaker: But you certainly get some, and often you're dealing with septic shock and you're dealing with bad ARDS.
Speaker: And as you crank up the PEEP, you anticipate you're going to need to compensate for that by increasing the pressure in the large veins outside the thorax, which is the upstream pressure for blood return to the right heart by giving fluid.
Speaker: So it may be PEEP increased fluid, PEEP increased fluid, PEEP increased fluid.
Speaker: Inseptic shock.
Speaker: Now, if the patient's not in septic shock, you don't need to be as vigilant, but you would need to recognize that if the blood pressure goes down, not only do you need to think of pneumothorax, but you also need to think of decreased blood return to the heart and how fluid might be the next step.
Speaker: So what about... And recruitment... Go ahead.
Speaker: Recruitment is just...
Speaker: is a really big increase.
Speaker: When PEEP increases intrathoracic pressure, adding a high end inspiratory pressure just further increases intrathoracic pressure, and you worry about a recruitment maneuver being even a bigger insult than would incremental increases in PEEP.
Speaker: and you worry about pneumothorax with the hyperinflation.
Speaker: So I think that we covered, Dr. D, a lot of territory in terms of what we believe every patient with ARDS should receive in terms of initial mechanical ventilation.
Speaker: We talked about some of the parameters that the clinician should be following at the bedside, the things that we should be worried about.
Speaker: But refractory hypoxemia will be the
Speaker: The topic of a future episode, because I think we could talk about that for another hour.
Speaker: But I do want to just ask you, in terms of those patients, that we maximize the low tidal ventilation, we optimize PEEP.
Speaker: We have them on the ARDS network protocol and are still either having severe hypoxemia, high plateau pressures, or persistent respiratory acidosis.
Speaker: What are the next steps that you would consider in terms of step two and three based on evidence right now?
Speaker: Yeah.
Speaker: So two things.
Speaker: Yeah.
Speaker: One is I follow the, not surprisingly, I follow the surviving sepsis campaign guidelines.
Speaker: So I use neuromuscular blockers in all patients with a PaO2, FiO2 ratio of less than 150 or maybe 150 or less.
Speaker: And I do that to take the patient's inspiratory effort away to avoid overinflation, which is the potential proposed mechanism for why two days of neuromuscular blockers in one large study did improve outcome.
Speaker: So until there's contrasting evidence, I will use
Speaker: neuromuscular blockers for two days.
Speaker: And I use prone positioning in that same patient group with the PAO2-FIO2 ratio of 150 or less.
Speaker: And do you do the prone positioning, Dr. D, after you do the neuromuscular blockers?
Speaker: I would.
Speaker: And how long would you prone somebody?
Speaker: I would.
Speaker: You know, first time, typically 16 hours, 16, 18 hours.
Speaker: And then by 16 to 18 hours, you would anticipate that there would be sustained improvement.
Speaker: Well, the first thing is, if I prone the patient, I'll only leave them prone if it improves oxygenation.
Speaker: And certainly, if it worsens oxygenation, as can't happen, I flip them back in a hurry.
Speaker: But assuming it improves oxygenation, I'll leave them 16, 18 hours and then put them back supine.
Speaker: You know, sometimes just one proning session, they fly.
Speaker: But if they slowly deteriorate again, then they're headed back for another 16 to 18 hour proning session.
Speaker: And I think it's important for the audience to also understand that both of these interventions that you have referred as being things you utilize in patients who are moderate to severe ARDS with low PAO2, 502 ratios have been shown in large randomized trials to improve mortality.
Speaker: Right.
Speaker: So these are evidence-based interventions that as far as we know from literature that has looked at this are not probably applied to the full extent of what they could.
Speaker: So I think the penetration is still suboptimal.
Speaker: And I think a lot of clinicians are jumping to less proven therapies before they go through these steps, which I think is an important take-home message.
Speaker: That's correct.
Speaker: I agree totally, Sergio.
Speaker: We'd like to also get your thoughts on adjunctive therapies for ARDS and what are some other things that we should be considering in these patients.
Speaker: Obviously, steroids, very similar to the story with steroids and septic shock and sepsis, seems to be a pendulum that goes back and forth with every couple of years.
Speaker: But where do you stand today on steroids in ARDS?
Speaker: What do you recommend based on the literature?
Speaker: Yeah.
Speaker: It's controversial.
Speaker: You know, it's still a good pro-con at a national meeting.
Speaker: I personally do not use steroids empirically in ARDS.
Speaker: There are some people that do.
Speaker: I think the evidence is somewhat conflicting from physiologic improvement.
Speaker: It's been shown to worsen outcome in influenza ARDS.
Speaker: I think it makes me, if I don't know what's causing my ARDS, I certainly would be very vigilant to look for steroid-responsive causes of ARDS.
Speaker: And if I have something to suggest a steroid-responsive cause, like
Speaker: eosinophilic pneumonia or some type of vasculitis or something.
Speaker: But I don't just give it for severe hypoxemic ARDS.
Speaker: And I think that you mentioned specific populations where it's been shown to actually worse outcomes, and one of those is viral influenza or viral pneumonias.
Speaker: Also, there seems to be some concern about rapid tapering being a problem.
Speaker: Any comments on that, Dr. Dellinger?
Speaker: Well, I think the Lazarus trial, which was when steroids were given for late ARDS,
Speaker: and shown not to benefit.
Speaker: Some people believe the reason that trial did not show benefit was the rapid taper of steroids, because a lot of those patients came off the ventilator faster, but then went back on the ventilator and ended up having bad outcomes.
Speaker: So, you know, if I do use steroids and ARDS, which I don't, but if I started tomorrow,
Speaker: I would be very cautious about how rapidly I tapered.
Speaker: You've also had a lot of experience research-wise and obviously clinically with inhaled nitric oxide and vasodilators.
Speaker: Any role for that today in ARDS?
Speaker: Yeah, I guess I'm historically prominent in showing that empiric use of
Speaker: inhaled nitric oxide does not improve outcome in ARDS.
Speaker: Therefore, relegating it to patients that are dying from hypoxemia despite everything else you're doing.
Speaker: And I have used it for that on
Speaker: quite a few occasions when you just, they're just dying from hypoxemia, you've done everything else.
Speaker: You should have proned them by then.
Speaker: They should be on neuromuscular blockers, should be on ARSnet protocol.
Speaker: You should have looked for the sweet spot PEEP, but if you still can't get the PAO2 up, then a selective inhaled vasodilator, either inhaled nitric oxide or epoprostenol,
Speaker: epoprostenol i think is the choice for many institutions because it's cheaper but that's what uh that's circumstances where i would use an inhaled uh selective pulmonary vasodilator it makes sense i mean you're you're sending something that'll dilate the blood vessels in the area where you're ventilating so you
Speaker: You send it down to the alveolites that are open and it diffuses across and attracts the blood flow as a vasodilator.
Speaker: One thing that does bother me is I see a lot of patients that I pick up that have been shotgunned when they first
Speaker: came to the ICU trying to die from ARDS, they got everything, and they got it sort of in a cocktail and their own selective inhaled pulmonary vasodilator.
Speaker: And I find one of the first things I do is make sure it's making a difference.
Speaker: And then I just titrate that down as an isolated variable.
Speaker: And often I find that it's not producing
Speaker: significant effect, probably 40% of the time I'd say.
Speaker: Yeah, and I think in an era, and obviously we definitely in our practice are very conscious of providing value, so improved outcomes at lower cost, using costly therapies that provide no value is probably not a good idea.
Speaker: I agree totally Sergio.
Speaker: Well, finally in terms of adjunctive therapies for ARDS, any comments on fluid management?
Speaker: Yeah, I think it's, there's reasonable evidence that a fluid conservative, fluid restrictive approach in patients that aren't in shock and don't have tissue hypoperfusion improves clinical outcomes such as getting patients off the ventilator quicker, getting them out of the ICU quicker, and it makes
Speaker: As we were just talking, it makes economical sense to do it.
Speaker: Of all the evidence-based literature, I think it's the least currently practiced in our ICUs, maybe even less than prone positioning, which is to try to minimize fluids, even to the point of giving Lasix.
Speaker: You know, now we don't have as many CBPs in our ICU patients, but getting the CBP down to values of very low, four or less, as long as the BUN creatinine tolerates it and urine output and blood pressure gets patients off the ventilators.
Speaker: And a lot of these people got a lot of fluid early.
Speaker: It's sort of a de-resuscitation.
Speaker: Sergio, I remember once,
Speaker: I had a patient that we were talking withdrawal of support on Friday afternoon.
Speaker: You came in on Saturday morning, started giving a bunch of Lasix to my patients, and I think you dried out their brain, and all of a sudden their neurologic exam perked up.
Speaker: Yeah.
Speaker: Like they say, rather be lucky than good, right?
Speaker: Sometimes those things work.
Speaker: But I think that these are all very valid points.
Speaker: And what's very interesting from my perspective is that everybody in critical care is always very interested and concerned with the next thing that's coming down the road.
Speaker: Yet there is
Speaker: ample opportunity to implement more effectively all the things we talked about that are proven to make a difference as of the current evidence that we have today.
Speaker: Studies have shown that the penetration of low tidal volume in recognized ARDS patients is still
Speaker: So a third of patients don't get low tidal volumes and plateau pressures at below 30.
Speaker: So I think that all these things that we talked about today should be our first and foremost concern in making sure that we provide what really works first.
Speaker: And I think that, Dr. D, that we will have another opportunity to talk more about refractory hypoxemia and things that are maybe more experimental in the future.
Speaker: But this has been, I think, a wonderful conversation.
Speaker: And one of the things that we like to do at Critical Matters is also tap into the wisdom of our guest and really ask them a couple of questions that are outside of the confines of the specific topic we're discussing.
Speaker: Would that be okay?
Speaker: That would be fine.
Speaker: So the first question relates to books.
Speaker: And I would like to know what book or books have influenced you the most or what book have you gifted most often to others?
Speaker: I think the book that I remain impressed with to this day, because I so much enjoyed reading it and the message was the last book in the Douglas Adams Hitchhiker's Guide to the Galaxy, the book So Long and Thanks for All the Fish, which is what the dolphins said to Earth as they blasted off in a spaceship as the true
Speaker: supremely intelligent beings on earth realizing that the humans had sent the world to hell in a handbasket.
Speaker: So I like that one.
Speaker: Well, that's a great book.
Speaker: And I think that it also, this is a question that we've asked several guests.
Speaker: And I think that what it really always reminds me is that we learn from stories.
Speaker: And some of those stories are fictional stories and others are non-fictional, but there's still a tremendous amount to be learned from fictional stories as they apply to life.
Speaker: So we'll include a link to the book in the show notes.
Speaker: The second question, Dr. D., is,
Speaker: What do you believe to be true in medicine or in life that most other people don't believe?
Speaker: That if you show compassion as a physician, that it will do as much for you as it does for the patient and their family.
Speaker: And I think that that's an important, important lesson that sometimes in this burnout critical care environment, people tend to forget.
Speaker: No, it can make your day.
Speaker: The last question is, what would you want every intensivist that's listening to this podcast to know?
Speaker: Could be a quote or a fact.
Speaker: Yeah.
Speaker: So I, you alerted me to this one in advance and
Speaker: You know, there's a thousand.
Speaker: And it's easier for me just to go to something that I would want every person in the world to think about, and particularly professionals and particularly physicians that get a chance to make a difference in so many different areas.
Speaker: I'm a huge fan of Martin Luther King, as you know, and Gandhi.
Speaker: And Martin Luther King said, the ultimate test of a man or woman is not where he stands in moments of comfort and moments of convenience, but where he or she stands in moments of challenge and controversy.
Speaker: And I think that those are wonderful words.
Speaker: And like you said, I mean, definitely apply to a lot of what we do in the ICU, but to life in general.
Speaker: And I think that this would be a perfect place to stop.
Speaker: Dr. D, I would be remiss if I didn't thank you first for all you have done for my career, for my learning and critical care, and for many others.
Speaker: So first of all, thanks for being such a wonderful mentor and teacher for so many critical care providers, including myself.
Speaker: And second, thank you for the time and the willingness to share your knowledge with our audience.
Speaker: And we hope to have you back on Critical Matters soon.
Speaker: Thank you, Sergio.
Speaker: It was indeed my pleasure.
Speaker: Thanks again for listening to Critical Matters.
Speaker: Make sure to subscribe to this podcast on iTunes or Google Play.
