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: Sound Critical Care provides comprehensive critical care programs to hospitals across the country.
Speaker: To learn more about our programs and career opportunities, visit www.soundphysicians.com.
Speaker: And now, your host, Dr. Sergio Zanotti.
Speaker: The COVID-19 pandemic continues to grow throughout the world.
Speaker: The United States has now become the epicenter of the pandemic with a rapidly growing number of cases and deaths.
Speaker: Today's episode will focus on our discussion on respiratory support and mechanical ventilation with COVID-19.
Speaker: Recognizing that we still don't know enough about this disease and still unclear what would be helpful and what would be harmful, we thought that a discussion on what we've learned so far and how to apply these thoughts at the bedside would be timely.
Speaker: Our guest is Dr. Luciano Gattinoni.
Speaker: a true thought leader in critical care.
Speaker: Dr. Gattinoni is Emeritus Professor of the University of Milan.
Speaker: He is currently working as a professor at the University of Göttingen in Germany.
Speaker: He introduced the concept of lung rest by extracorporeal CO2 removal and acute respiratory failure.
Speaker: He pioneered the use of thoracic CT and ARDS, which culminated in the baby lung, lung recruitability, and mechanical power concepts and theories.
Speaker: His research is focused on the pathophysiology and treatment of acute respiratory failure.
Speaker: including prone positioning, sepsis, and acid-base disorders.
Speaker: He has published more than 400 research articles and reviews in peer-reviewed journals.
Speaker: He has served as president of the European Society of Intensive Care Medicine, president of the World Federation of Societies of Intensive Care, Critical Care Medicine, and president of the Italian Society of Anesthesia, Analgesia, Reanimation, and Intensive Care.
Speaker: It's a true honor to have him as a guest.
Speaker: Luciano, welcome to Critical Matters.
Speaker: Hi, everybody.
Speaker: So I think that we are definitely living unprecedented times in terms of this COVID-19 pandemic really affecting every single country in the world and being, I think, in the forefront of our colleague intensivist day in and day out now.
Speaker: And I think that one of the things that I've noticed is that there's also been an explosion of information, an infodemic with good and bad information.
Speaker: But one of the reasons why I reached out
Speaker: was because I had seen in a lot of forums people posting thoughts and recommendations attributed to you that then when I finally was able to read an opinion piece that you had put in the blue journal, it didn't seem to represent exactly what you were saying and thinking.
Speaker: But I do think that there are some very important lessons to learn about what we know about the lung disease that COVID-19 is producing.
Speaker: So, Luciano, maybe we could start with just a basic review
Speaker: of our understanding of ventilator-induced lung injury and lung protective ventilation.
Speaker: And maybe you could just give us like a very basic overview on Vili and how you think about barotrauma, volume trauma, stress strain, and we can start there.
Speaker: Okay.
Speaker: Well, you know, the ventilator-induced lung injury, as it's called now, has been recognized just after the initiation of the ventilation in mechanical ventilation.
Speaker: and was called barotrauma.
Speaker: Why barotrauma?
Speaker: Because about 50%, 60% of the patient had pneumothorax, pneumobiliacinam and so on.
Speaker: So the pressure used was up to 100 centimeters of water.
Speaker: Then with Dreyfus, this concept shifted from barotrauma to volotrauma because Dreyfus said, okay, if I wrap the thorax
Speaker: with an unelastic substance, so I impede the dilatation of the thorax.
Speaker: I can use whatever pressure I want, there is no problem.
Speaker: It's the concept of the divers.
Speaker: You go down with a lot of atmosphere, you can go to 10 atmosphere and the land does not explode.
Speaker: Because you have 10 atmosphere outside.
Speaker: But the concept evolved to stress and strain, and basically to make short and long story,
Speaker: The strain, which I think is the fundamental part of the business, is when the lung structure is stretched over a certain degree over his resting position.
Speaker: Resting position is a function of the residual capacity.
Speaker: If I add the PIP, I already strain in part the lung.
Speaker: If I add the tidal volume, I strain even more.
Speaker: And what it appears quite consistent is that when the strain goes over the total lung capacity, not just for one breath, but for several breaths, and maybe for one day or several hours, the lung, you've got the ventilator-induced lung injury, which manifests with what?
Speaker: It manifests or with rupture, if you have a stress or strain or rupture,
Speaker: or with an inflammatory reaction, we cannot distinguish from the normal RDS, because you have inflammatory cells, edema, and so on.
Speaker: So, by the way, the last thing to remember is that the stress and strain are not distributed homogenous into the lung, but are particularly important in the lung region
Speaker: where the elasticity is different in these regions the stress and strain are concentrated because one ex one region or one structure expand more than the others this is called focused stress and is one of the problem of the non-homogeneity of the lung so basically the ventilator induced lung injury is
Speaker: A strain of the lung above is a physical capability, to which follows the rupture after days.
Speaker: But don't forget that within the lung there is one organ which is called heart.
Speaker: And we cannot speak about the lung if you do not consistently think to the immunodynamics.
Speaker: Because any time the lungs is hyperinflated or stressed, the heart,
Speaker: is compressed, disappear behind the vertebral column, the venous return decreases, the kidney starts to suffer, and so and so.
Speaker: So I think in the concept of VLE should be integrated also the concept of the immunodynamic involvement.
Speaker: So I think that to summarize,
Speaker: Yeah, to summarize for our listeners, Dr. Gattinoni, the stress really would be equivalent to the pressure, the transplural pressure, right?
Speaker: That's right.
Speaker: It's the transplural pressure which correspond to a given strain.
Speaker: You cannot strain the lung without applying a change in pressure.
Speaker: So these are two phases of the same medal.
Speaker: And the constant of proportionality between stress and strain is called specific elastance.
Speaker: So that means the transformatory pressure or stress is equal to K, which is specific elastance, times, let's see, tidal volume plus PIP volume divide the resting lung volume.
Speaker: This is the basic equation of stress and strain.
Speaker: So I think that one, I have two questions.
Speaker: And the first question is that it is evident that no matter what we are doing with a patient or whatever syndrome they have, if they're on mechanical ventilation, considering ways to minimize the injury from stress and strain obviously is something that would help them clinically, right, as a basic concept.
Speaker: That's right.
Speaker: But, you know, I think that if you want to approach a rational mechanical ventilation,
Speaker: you have to know which are the lung condition we start with.
Speaker: The ventilable lung is very small, we call it baby lung.
Speaker: It's very small in one thing.
Speaker: If you have a lung with a very large volume, it's another completely different thing.
Speaker: But the concept of stress and strain applied in both conditions.
Speaker: In one, you will have less volume to cause
Speaker: let's call harmful strain in the other condition, will be a larger tether volume when we start with a larger resting volume.
Speaker: Unfortunately, nobody measure the volume and nobody measure how much volume is due to PEEP.
Speaker: The PEEP is a pressure and rise up the lung volume.
Speaker: So it's easier with the tether volume, higher is the PEEP, it's easier to reach
Speaker: the total line capacity, which is the limit.
Speaker: You know, the literature is full of a protective effect of PEEP.
Speaker: But this protective effect of PEEP are due because the PEEP is high or because the tidal volume has been reduced.
Speaker: Because you don't see any protection when you rise the PEEP at the same tidal volume.
Speaker: At that point, it may be a disaster.
Speaker: Matthew, that's an important point because
Speaker: A lot of people assume that high PEEP, independently of what else you're doing, might work or might not work.
Speaker: And I think that you're saying everything is really connected.
Speaker: That's right.
Speaker: To me, I repeat, I'm not the true in the pocket, but to me, this is a very severe mistake to consider that.
Speaker: The PEEP is for the rest.
Speaker: The second question Luciano I have regarding this whole concept of stress and strain and Vili is what about people who are not on mechanical ventilation?
Speaker: Is there potential for lung injury by increasing stress and strain in somebody who has respiratory failure and is spontaneously breathing?
Speaker: That's right.
Speaker: Okay.
Speaker: Let me consider it.
Speaker: What does the mechanical ventilation?
Speaker: The mechanical ventilation substitute the respiratory muscle, right?
Speaker: does not substitute the gas exchange, just substitute the respiratory muscle.
Speaker: So, if instead of the energy provided by the ventilator, I provide a similar energy from the muscles, the question of stress and strain are exactly the same.
Speaker: Change the hemodynamic, but the stress and strain are exactly the same.
Speaker: In Ted Kolbov, well, in the 38s, Barak proved that very clearly.
Speaker: In 1988, Mascherone and Kolbov, Kolbov was always 20 years ahead of the rest of the world, were injecting some acetyl acid in the cisterna mania of the ship, so the ship started to have a very big tidal volume.
Speaker: has to have a very big mechanical ventilation.
Speaker: In 24 hours, this lag had ARDS, perfectly in spontaneous breathing, with inner weight pressure zero.
Speaker: But the transpulmonary pressure was huge.
Speaker: And now this concept has been rediscovered, revised, and so on by Brochard, Perzentia, Slaski, when they describe the patient
Speaker: self-inducted lung injury which is extremely important overall in this codic 19 pneumonia i think but you know the same transformer repression if it's harmful maybe it's exactly hard from exactly helpful in mechanical ventilation and in spontaneous breathing the big difference between the two is the hemodynamics
Speaker: With the spontaneous breathing, you suck the blood into the central system.
Speaker: With the mechanical ventilation, you squeeze out the blood from the mechanical system.
Speaker: Yeah.
Speaker: And I think that those are important concepts, like you said, that we'll touch a little bit later when we talk specifically about COVID-19.
Speaker: But I think that to close this first segment, Dr. Gattinoni, when I hear people talk about lung protective ventilation,
Speaker: I think that most clinicians at the bedside think of two things.
Speaker: They think of small tidal volume and they think of a plateau pressure below 30.
Speaker: That's kind of in their mind.
Speaker: And some people might think high PEEP, some people might think low PEEP, but that's kind of what people think.
Speaker: But really from what I'm hearing you talk about, lung protective ventilation not only applies maybe to mechanical ventilation, but applies to any patient we're supporting and really is about utilizing the tools we have available to minimize
Speaker: damage on the lung from stress and strain.
Speaker: Would that be an appropriate way of thinking about it?
Speaker: Absolutely.
Speaker: I think what you have to think, the people is not accustomed to measure the pleural pressures, unfortunately.
Speaker: But what counts is the pleural, the transpulmonary pressure, so the difference between airway and the outside of the pressure, which is equal to the stress.
Speaker: And then the basic concept applied equally.
Speaker: And the tidal volume of enterase is protective.
Speaker: Well, we have the magic six milliliters per kilo, which is better than 12.
Speaker: Not necessarily, it's better than eight.
Speaker: Dependence and the compliance the patient starts with, you know?
Speaker: And the second concept, be careful with the hyper, how they call it, hyperprotective.
Speaker: Because the people say, if six is better than 12,
Speaker: five would be better than six four better than five three better than two minus ten better than zero is not like that because if you go at a hyper protective ventilation with the c4 of people the four of uh televolume you look at the co2 because you have a risk of hyperventilation and hyperventilation even if you use co2 remover is hyperventilation that means
Speaker: the gas which arrive at the alveolar level are not enough.
Speaker: The oxygen consumed is much more than the oxygen transferred from the air to the alveoli.
Speaker: That means after a while, this unit undergo in reabsorption at the lectasis.
Speaker: So this is the intrinsic risk of the very low so-called hyperprotective.
Speaker: I think we should protect some time the lung from the doctors.
Speaker: I agree.
Speaker: And I think that also what people, I think, fail when they don't understand, when we walk away from understanding the basic physiology, is that on average, if you took thousands of patients, because of what we've discussed, 6 mLs is probably safer in reducing the strain and associated with a lower stress than 12 mLs.
Speaker: But that's an average.
Speaker: This is absolutely true.
Speaker: But remember to look always to the pCO2 because the pCO2 tell you the degree of a very ventilation we are dealing with.
Speaker: So the gas exchange is mathematics, you know.
Speaker: You have to consider all the variables at play, not just to oxygen or just the CO2 or just the frequency or just the
Speaker: We tried to introduce the concept of mechanical power in terms of VIRIT, which is the product is a variable which takes together the pressures, the volume, and the frequency.
Speaker: And what we found, at least experimentally, for a given damage is reached when you give a given package of mechanical power.
Speaker: Sometimes with lower total volume but very high frequency,
Speaker: It's just as bad as higher tidal volume with far lower frequency.
Speaker: Frequency is always for God.
Speaker: But if I have a bad tidal volume, 10 per minute, 20 per minute, or 40 per minute, make a tremendous difference.
Speaker: But the people does not consider this one.
Speaker: I think the mechanical power will gain some popularity.
Speaker: Not now, because now the people is busy with other things.
Speaker: Yeah, it's hard to apply it to a thousand patients at once, right?
Speaker: Absolutely, absolutely.
Speaker: But I think it's important, I mean, no matter what's going on, to always try to learn from what we're seeing so that tomorrow we could do things a little bit better.
Speaker: Okay, but I don't know.
Speaker: I think the mechanical power will be implemented in the ventilator.
Speaker: So, sooner or later, we come out one number, joule per minute, and you know what is the energy we're putting in the system.
Speaker: Because all the data, all the numbers are available in whatever modern ventilator.
Speaker: And I think that also the interesting concept, I mean, that you said, like, frequency is always forgotten.
Speaker: But I think that also applies to clinical scenarios that I've seen, for example, people struggling with non-invasive, with a respiratory rate in the
Speaker: high 30s and they kind of puddle along and probably causing tremendous amount of injury to their lungs.
Speaker: And then when they finally get intubated, we kind of wonder why they have such a bad outcome, right?
Speaker: You know, what I found terrible in non-invasive ventilation is that theoretically, the only difference you have with the invasive ventilation is the tube.
Speaker: But with the non-invasive ventilation,
Speaker: you don't know anything or what you are doing.
Speaker: You don't know even how much is the tidal volume you are delivering.
Speaker: You do not have an idea of the transpulmonary pressure the patient is generating.
Speaker: To me, using the mechanical ventilation, without the esophageal pressure, they tell me how much are the swings of the pleural pressure of the patient, is asked to drive during the night, in a foggy night,
Speaker: without knowing where to go, maybe in a forest.
Speaker: Very dangerous.
Speaker: So let's talk a little bit about COVID-19 associated severe acute respiratory illness.
Speaker: And I think that one of the observations that you and your colleagues have made is that there might be things that appear to be similar to what we call ARDS, which is also a syndrome, like we all know.
Speaker: But there might be some things that
Speaker: appear to be different, and that might have implications in the way we should be thinking or approaching these patients.
Speaker: So maybe you could just start by giving us a summary of what we know so far, and then maybe talk about what is similar to ARDS, and more importantly, what is different to other forms of ARDS that we usually treat.
Speaker: Well, of course, I think I'm playing with ARDS since 40 years.
Speaker: But I never saw a classical ARDS, let's see, severe ARDS because this patient
Speaker: very often have a PF below 100, so they have an hypoxemia comparable with severe LDS.
Speaker: They have some ground less, so they have bilateral involvement of the lung, bilateral pneumonia, but the compliance is 60, 70, sometimes 80, in more than 50% of the patient when they do present.
Speaker: And I never saw something like that in never.
Speaker: Maybe it occurs one place, but really is extremely rare, I put it in this way, in a severe RDS.
Speaker: If you go to the Bellani, the SAFE study, you see that even the mild RDS, the compliance is always below 40.
Speaker: Goes from 40, 35, 30.
Speaker: Here we have a median and a mean greater than 50.
Speaker: So this is the fundamental basis to start with.
Speaker: We have to sit down and to say how this is possible.
Speaker: Then we have a lot of CT scan of the patients, which are done very rarely.
Speaker: And let me try to tell you
Speaker: The story, as I see the story which I collect, discuss with the nurses, with the colleagues from different hospitals in Nombardir and after studying and examining a lot of CT scan data coming from my colleagues.
Speaker: Have you five minutes of patience for that?
Speaker: Hello?
Speaker: Yes.
Speaker: Are you there?
Speaker: Okay.
Speaker: If we don't have the pathophysiology clear in mind, to speak about the treatment to me is nonsense.
Speaker: So, let's start in this way.
Speaker: The virus comes.
Speaker: What does the virus?
Speaker: While the bacteria affect mainly the alveolar size of the problem, we have consolidation capacity, the virus interferes primarily
Speaker: with the vessels and with the endothelial cells.
Speaker: So you have vasoplasia.
Speaker: Vasoplasia, what means?
Speaker: What means that the regulation of the blood through the lung is lost.
Speaker: If it's lost, where the blood tends to go, tends to go according to the gravity, which doesn't happen normally.
Speaker: We have quite homogenous distribution of blood.
Speaker: So we have, due to this vasoplasia, which may originate from endothelial stimulation and O and so on, for many, many reasons, possible reasons, you have a tremendous VAQ mismatch.
Speaker: VAQ mismatch is a rather complicated physiological concept, but very briefly means that if one part of the lung
Speaker: I have a lot of ventilation and very, very, very small perfusion.
Speaker: In the other part of the lung, I have a small ventilation and very, very high perfusion.
Speaker: What is the final result?
Speaker: If you play with the models, you may have tremendous hypoxemia, even with 60, 70, 80% of shunt.
Speaker: And this hypoxemia at the beginning is very sensitive to oxygen.
Speaker: Now, when this patient is going to the hospital, we have several patients, and this is consistent observation throughout the world, that come with 60, 65 of oxygen saturation, that means 35 of PO2, and do not accuse anything else.
Speaker: but some fever are not disnoic.
Speaker: Why?
Speaker: Because when you have this kind of hypoxemia, which is due to the vasoplegia, the brain, our center reactor, activating, trying to increase the tidal volume, so increase the minute ventilation.
Speaker: Now, if you have a good compliance, if you increase the tidal volume, you don't have any Dysnear.
Speaker: Because you make an effort and you find that the air coming into the land is exactly what we expect for this kind of effort.
Speaker: Is this clear, this concept?
Speaker: Yes.
Speaker: This may happen when you have some effort.
Speaker: I expect some amount of air and I receive less.
Speaker: Now, let's see, I have a patient that comes three days later into the hospital.
Speaker: and he stays at home with these big breaths.
Speaker: Big breaths, what does that mean?
Speaker: It means a big shift of pleural pressure, big negative pressure.
Speaker: And so we are back to tidal volume and to self-inductive lung injury.
Speaker: If I have this, I start to have more blood, return blood into the lung,
Speaker: I have to filter more plasma and the lung becomes more heavy and so become more edematous.
Speaker: And the picture starts to resemble to RDS because the compliance goes down.
Speaker: And from 70 goes maybe to 50.
Speaker: Three days later is at 35.
Speaker: At this point, you are perfect picture of RDS.
Speaker: And you see this perfectly well, following the CT scan with these patients.
Speaker: You see exactly the transition from what we call L light status, that means low VQ, low elastance, low longwave, low edema, to the high status or high type, which is high elastance, which means low compliance, high volume, high
Speaker: lung weight etc etc so at this point i have some patient coming in the hospital which breathes normally without this name some patient coming this night some patient coming severely this night what they do have in common they are all hypoxemic because the hypoxemia is due to this tremendous vacuum mismatch
Speaker: At this point, if I have a lung which is full of gas, or a lung which is without a very small amount of gas and a lot of edema, would you use the same therapy?
Speaker: Or in a lung full of gas, can you explain to me why to use 15 of PIP with a mask?
Speaker: One, look at the PO2.
Speaker: If I apply
Speaker: the PIP 502 table, you end up with 20 of PIP.
Speaker: With 20 of PIP, you kill this patient, not all, but a good amount.
Speaker: Just to tell you something that me impressed a lot.
Speaker: I was called a couple of days ago from an hospital in Switzerland.
Speaker: They had 40 patients with COVID.
Speaker: And they were applying.
Speaker: As soon as the chef went to see the inspiratory effort, that means the negative pressure of the CILI, he was taking immediately the patient in intensive care because they had a space for that.
Speaker: And he was putting in paralysis and mechanical ventilation.
Speaker: So reducing this tremendous possibility of VILI.
Speaker: 40% of the patients all survived.
Speaker: In a hospital, 20 kilometres close to there, they were applying similar amount of patients.
Speaker: They were applying the suggested guideline.
Speaker: So, IPIP and then maybe delayed intubation and so on.
Speaker: The mortality was greater than 50%.
Speaker: In Athens,
Speaker: They told me the mortality was about 90%, applying the forms of ventilation that you apply in LDS.
Speaker: Then you tell me the patients were different, the ones were older, the comorbidities were different.
Speaker: But when you go from 0 to 50 to 90, I think we should, with extreme honest
Speaker: intellectual honesty, ask ourselves, are we doing something dramatically wrong?
Speaker: This is the first question.
Speaker: Before to say, no, this patient is different from mine because... Having said that, I think if I take a patient with 70 on compliance and I give a mask of non-invasive ventilation with 50, well, I have two possibilities.
Speaker: The idea would be to measure the inspiratory effort.
Speaker: But you can, okay, you don't have an esophageal balloon, you don't know how to use, okay.
Speaker: But look carefully.
Speaker: For one hour or two, what is the effort that the patient makes?
Speaker: If he start to use some respiratory accessory muscle, if he have some...
Speaker: ribs inflow, if you have a change in abdominal movement.
Speaker: If the patient is like this, you mean that it's continuing to induce a very big damage in his lung.
Speaker: At this point, I would suggest an immediate ventilation and paralysis.
Speaker: If the patient, very few, can support that, maybe you
Speaker: cut the visceral cycle because if the patient continues, it will get edema.
Speaker: If he got edema, he will have greater inspiratory effort to keep the tidal volume.
Speaker: And so you have a tremendous picture.
Speaker: So I think if the patient needs inspiratory effort associated with low oxygenation that does not respond to 5, 10, 15 or oxygen therapy,
Speaker: I think for what we know now to suggest immediate intubation and without any spontaneous movement of the patient.
Speaker: So, or deep sedation or paralysis.
Speaker: Of course, the patient will improve the PO2.
Speaker: What do you do when you start to see the PO2, which is good in the LDS?
Speaker: You start to win.
Speaker: If you do that with this patient after two days, you lose what you ever gave because this disease, disease not syndrome, requires time.
Speaker: And until the virus has not been eliminated by our antibodies or some miracle, you cannot win the patient.
Speaker: You just, the patient, start to breathe as hell
Speaker: and to have again dysmnea and then again edema and so on.
Speaker: So this depends to me, the therapy to be introduced depends on the phase that you see the patient and at what is the stage at the end.
Speaker: Although I do not have the ideal therapy, I know what is wrong.
Speaker: In this condition, it is easier to
Speaker: do mistake doing something then don't doing nothing you know sometimes i wonder if the patient comes perfectly okay with 70 of saturation and 14 of hemoglobin it's not different for the patient with neither saturation 95 a 10 of hemoglobin which is are used in intensive care i should put a very strange thing or just to be patient and to observe
Speaker: and to think at the physiology and to try to measure whatever is possible to measure i know that in front line is difficult but you don't have to lose the entire paradigm and i think that a couple of things i want to dive deeper in dr gatti noni number one is i think that something that that we're seeing across the country and in our group i mean we have cared for
Speaker: probably over 500 COVID critical care patients around the country.
Speaker: And I think that that whole point that you made about patients is very important also as we're trying to extubate these patients.
Speaker: I think people are finding that if they extubate them too quickly, they often will get re-intubated.
Speaker: And I think it just applies to a very basic concept that I think I learned as a medical student.
Speaker: If it takes you eight days to get sick, it doesn't take you two days to get better, right?
Speaker: Absolutely.
Speaker: I mean, this pneumonia lasts at least 15 days.
Speaker: If you pretend to wait after five days, it's a disaster.
Speaker: Not only you have to wait to wait to the patient, but you have lost maybe 30% of the benefit you had before.
Speaker: And I know that to be patient, to do nothing is difficult in intensive care.
Speaker: Because in testic cancer, people are accustomed to, I turn it off, I see the result, I'm fast, quick, and rational.
Speaker: But in this case, to be rational, you have to be slow and quiet.
Speaker: Yeah.
Speaker: And I think it applies also to other therapies, and it's something I worry about.
Speaker: We've all been taught in medicine, first to no harm, primum non nocere.
Speaker: And I think that when you are dealing with thousands of patients,
Speaker: anything that potentially could be harmful gets magnified at such a level that I think it's extremely dangerous.
Speaker: And I think that people are very anxious.
Speaker: And like you said, they feel that doing something is always better than not doing something.
Speaker: And I think that not only in our discussion with mechanical ventilation, but with all these drugs that are experimental, there's no proof that they work.
Speaker: I also fear the same consequences.
Speaker: Let me lead to two words about the drugs.
Speaker: Now, unfortunately, this patient,
Speaker: and overall in emergency, go through infectivologists, pneumologists, or somebody that never saw one ventilator and acute respiratory failure, and they were given whatever, with one result, antivirus, chloroquine, anti-LA6, anti-L1, whatever.
Speaker: Okay, cortisone, yes, cortisone, no.
Speaker: The result with the antivirus,
Speaker: that you kill the liver and you don't kill the virus.
Speaker: And I'm not aware of any drug which is effective.
Speaker: I think that these people, we have to wait for them.
Speaker: We have to do the research and some studies, okay, this work or not.
Speaker: At the moment, I think the only thing that we can do is to provide nutrition, to keep the patient alive as more gentle as possible and pay, I forgot this,
Speaker: as this is a vessel endothelial disease, is probably one of the most pro-thrombotic situations you can observe in intensive care.
Speaker: That means the microtrombosis may be absolutely frequent and also some macrothrombosis as a pulmonary embolism or a brain damage with that.
Speaker: So I suggest, and look at the didymer.
Speaker: When the didymer is greater than 2000, we start with the prophylaxis as double as normal, and we start with the anticoagulation when the tendency of the didymer goes up.
Speaker: Believe me, this is an extremely important.
Speaker: I lost my friend, one friend of mine, 10 days ago, he was recovering from pneumonia and he got a stroke.
Speaker: And all the patients, all the people who did the autopsy, they did at least a report of 50 autopsies in Malaysia.
Speaker: They had endothelial cells flowing in the blood and a lot of micro thrombosis at the histological examination.
Speaker: And I think that obviously that goes into also the whole idea of the VQ mismatch that we started the discussion with and what happens in this early phase.
Speaker: Two more questions, Dr. Gattinoni.
Speaker: So these phenotypes of L and H, the low and high, some people have presented that as two distinct diseases.
Speaker: From what I understand, you're really thinking that is one, it's a progression, right?
Speaker: That's right.
Speaker: the one is the progression to the other.
Speaker: Sometimes the progression stops naturally, okay?
Speaker: And some patients stopped after the status L. Some patient progresses to the status H. I think that some therapy helped to progress from L to H because a wrong therapy would force the patient to have
Speaker: Too many effort compare what is allowed in this condition.
Speaker: But I think that the picture I put in this, I don't remember if in the editorial or in ECM editorial, is the same patient, seven days apart.
Speaker: And the seven days were CPAP, a lot of inspiratory effort, and very badly tolerated
Speaker: non-invasive ventilation.
Speaker: Yeah.
Speaker: And I think that we can go a little bit deeper into some of the treatments, but I think that early on, obviously, people have recognized that these patients are hypoxic, so the immediate reaction is you give them oxygen.
Speaker: And like you said, in many patients, that's enough, and the majority of patients do better.
Speaker: Now, as the oxygen requirements keeps going up, the next step in our usual approach to these patients is to escalate there and either use high-flow nasal cannula, high-flow oxygen,
Speaker: or in some people they would use non-invasive.
Speaker: And I think that people have been focusing on the non-invasive mostly as something to avoid because they're worried that that can increase the aerosolization of droplets and increase their risk of infection.
Speaker: But really I think that the point here is that there's potential for more injury, there's potential for worse outcomes, and that has been suggested in some of the series.
Speaker: when you're making these pathophysiological observations, that makes sense.
Speaker: So it's not that you cannot use non-invasive, but if you use it within an hour, either it's better or it's a problem and you have to move to intubation.
Speaker: Is that the way to interpret?
Speaker: My suggestion is you can try, but limit the time, and please be extremely careful to the minimal sign of inspiratory effort the patient is made.
Speaker: The idea would be to put an esophageal pressure, but nobody put esophageal pressure in the peacetime.
Speaker: You can imagine the wartime.
Speaker: It's not practical.
Speaker: Okay, but you know, sometimes the people with a helicopter is more practical to put esophageal pressure inside.
Speaker: Anyway, to me, what we can do in terms of not harm is to
Speaker: avoid the patient in patient inflicted self-inflicted lung injury silly this way okay which is a real story so up whatever side that this patient may generate silly you have to intubate paralysis and keep for the time sufficient to heal
Speaker: What about high flow oxygen, Dr. Gattinoni, and the concept of dead space in these patients?
Speaker: Well, you know, dead space, anytime you have a VAQ, the mass distribution, you have, of course, if you have low ventilation in one part, and high perfusion in the other part, I have high ventilation and low perfusion, which is read as dead space.
Speaker: Plus,
Speaker: There is also the possibility of microthrombosis.
Speaker: But remember, this patient at the beginning, I don't think they do have in general microthrombosis because they come with a PCO2 25, 30, 35.
Speaker: When the PCO2 goes up, that means that the structure of the lung starts to modify.
Speaker: I am far more afraid from the rise of PCO2 than from decrease of oxygen.
Speaker: because the PCO2 change reflects the structural change of the lung.
Speaker: Yeah.
Speaker: And I think that's also something analogous to what we've seen in ARDS.
Speaker: Patients can tolerate hypoxemia.
Speaker: I mean, you can go to the top of Everest and have a PO2 that's very low and come back down.
Speaker: You're not critically ill.
Speaker: But still, even in critically ill patients, we've seen that.
Speaker: But when you can't ventilate somebody, like you said, it reflects that there's been a change in the lung, and that's usually a very bad sign for that patient.
Speaker: Yes.
Speaker: Yes.
Speaker: So let's talk a little bit about how you would approach them once they get intubated.
Speaker: You talked early on, especially in this low phase, early on that you would obviously, deep sedation if possible, paralysis, make sure that you're looking at.
Speaker: In a patient which manifests some effort, okay?
Speaker: Because if the patient does not manifest any effort, maybe may tolerate easily.
Speaker: but this patient has to be observed carefully.
Speaker: The worst is that for reason of lack of beds, or for a lack of attention from the doctors and nurses, the patient stays two, three days having a big inspiratory effort in a spontaneous breathing or even in an invasive mechanical ventilation.
Speaker: This is the point.
Speaker: The motor is...
Speaker: the behavior of the pleural pressure swings that you don't see, but you have to imagine that do exist.
Speaker: Yeah, and I think that that's a good point that we have traditionally not really applied or thought about.
Speaker: And I think in terms of current recommendations, Dr. Gattinoni, I think that you could still fit these into a way, a rational way of approaching this.
Speaker: And I think that people recommend that we use
Speaker: lower tidal volumes in general four to eight doesn't mean that everybody should be six so for example if somebody has a good compliance maybe eight it's a perfectly you know for this patient if you have a compliance of eight in the patient who did a big start to big effort you have intubated the compliance is 65 i do use eight or you six look at the pco2
Speaker: if the pco2 go to 60 with 6 use 8 or even 9. look at the plateau pressure will be far from b30 the plateau pressure will be 22 23 with the people 7 8 because you don't require any big people to correct a little bit the distribution of the blood remember you don't have any recruitability in the health patient
Speaker: and you have some recruitability not tremendous in age patient.
Speaker: You know what it seems to me?
Speaker: I don't have patient enough, but in a patient which look in the sequence in the CT, maybe they start L, they become H. When they start to recover from H status, you see that the big consolidation in the dependent region decrease, and you see back still,
Speaker: the ground glass.
Speaker: So you see the virus behind that.
Speaker: It's very interesting, you know.
Speaker: Not laser.
Speaker: Yeah, yeah.
Speaker: It's tough because of the numbers, but like you said, I mean, there's always an opportunity to learn and understand also that people want dogma and want an answer.
Speaker: Give me a formula that I can apply to everybody and they'll be saved.
Speaker: And I think that that type of magical thinking is very dangerous.
Speaker: Yes.
Speaker: I'm afraid it's very dangerous.
Speaker: I mean, tell me why do I need a doctor if I have to do medicine in that way?
Speaker: And tell me why I should use a standard therapy, let's see, for an unstandard situation.
Speaker: Why I have to use gasoline for a car which goes with diesel?
Speaker: I'm afraid of the car.
Speaker: Dr. Gattinoni, so I think that in terms of, I think the tidal volume, like you said, look at the compliance, look at the effort, very important, look at the plateau pressure, all those things I think people have recognized.
Speaker: What about the PEEP?
Speaker: Would you think that the way to really, the way I've always thought about PEEP is use the least amount of PEEP that you need.
Speaker: Is that still true?
Speaker: Stay in that line, which is perfect.
Speaker: The minimal amount of PEEP that you need.
Speaker: In this patient, in a patient, I think you can run easily with seven, eight of people without any problem.
Speaker: Because when I told you the compliance we measure, all the compliance, 78, were measured at five of people.
Speaker: So in standard condition when we measure that.
Speaker: Interesting.
Speaker: So I don't see any reason to have
Speaker: 15 of people, and I know that this may be a disaster.
Speaker: And any time you play with people, and I know that very few do that, look at the heart function or look at the echo where you increase people, look at the right heart with the echo and see what's happened immediately.
Speaker: Or take a venous blood and look at VO2.
Speaker: Or look at how goes the plateau pressure.
Speaker: Increase PEEP, keeping the tidal volume.
Speaker: The pressure rise as I rise the PEEP, rise more or rise less?
Speaker: Can you have an idea what's going on?
Speaker: And then set the minimum.
Speaker: And I think that that's an important concept.
Speaker: You're not saying don't use PEEP, you're saying use the minimum amount of PEEP because as you go to the H phase and you might have more recruitability and more like an ARDS picture, you might need a little bit, you might need higher PEEP, right?
Speaker: You may need a higher PIP.
Speaker: And the best thing is to make a test and to measure.
Speaker: Because also in this one, you don't have it.
Speaker: We never observed so far spectacular recruitability.
Speaker: I say recruitability, not spectacular increase of oxygen.
Speaker: Because it is an oxygen is another thing than the recruitability.
Speaker: The oxygen may increase without any recruitability.
Speaker: as in air patient.
Speaker: The option is increasing proposition or with some people and so on, not because of the accountability, but because of a flow diversion.
Speaker: The flow goes in areas in which the VAQ is more favorable.
Speaker: That's it.
Speaker: So let me ask you, since you mentioned about propositioning, that's been, I think, recommended and a lot of people who have done it, including myself, have seen it.
Speaker: Basically, you have a response, but it's not as the response requires proning for longer periods of times, which goes along with two observations you've made.
Speaker: One is that this is a slow process in improving, and two, that perhaps the benefits of prone positioning are related to redistribution of blood.
Speaker: So obviously, when you put them back, that redistribution changes again, and you have to prone them again.
Speaker: But you think that prone positioning, I mean, because of that mechanism, if it works, I mean, might be something to think about.
Speaker: Well, I think as a rescue maneuver you can use.
Speaker: You don't have anyway big damages with prone position.
Speaker: Even it lacks in health patient the prerequisite to really be effective, which are the better distribution of stress strain.
Speaker: But consider also that you have a lot of patients.
Speaker: Having 20 patients, 25 patients in prone position may stress the nurses
Speaker: at a degree which you may avoid.
Speaker: Why?
Speaker: In patient, in the age patient, I think the proposition is absolutely correct.
Speaker: Because proposition basically makes less dangerous whatever thing you do to the lung.
Speaker: So, is there some form of protection, the proposition?
Speaker: I would use it as a therapy in
Speaker: in age patients, I would use as a rescue also to save the nurses in the L patients.
Speaker: And what about people have proposed, and I've seen in some patients with ABGs, non-intubated patients who, I mean, can self-prone or cooperative proning, and just telling them, sleep on your belly, I mean, when you can.
Speaker: and checking the gases and seeing amino change.
Speaker: Obviously, it has to do probably with redistribution of the blood.
Speaker: But any thoughts on that?
Speaker: Well, no, we have some of my colleagues who have studied this problem, put it dirty and so on.
Speaker: So somebody will come out.
Speaker: My suggestion, ask the patient.
Speaker: Ask the patient, do you feel better in this position or in that position?
Speaker: It's very simple.
Speaker: It's not intubated, it's conscious, and it can tell you perfectly.
Speaker: Some colleague of mine told me that the patient said, oh, okay, I'm much better in this position.
Speaker: Some other patients say, no, I prefer the semi-requimbing position to the supine.
Speaker: Some patients increase in the supine position the PO2.
Speaker: The problem is that when you lose our regulation of blood,
Speaker: The blood follows the gravity, I don't know what, but it depends how the lung is compromised.
Speaker: And the blood goes to the gravity.
Speaker: But it's an interesting thing to study.
Speaker: Anyway, in prone position, usually the oxygenation goes up, at least for the first four or five days.
Speaker: Then the response for oxygenation becomes lower.
Speaker: In a patient non-intubated,
Speaker: I would put in proposition if the patient are very hypoxemic and maybe even overall have dyspnoacality or start with some dysnare waiting for the bed and the intubation, I would ask the patient because the patient is the better judge of his condition, I think, in this situation.
Speaker: He breathes better or not.
Speaker: Yeah.
Speaker: And in terms of steroids, I think that clearly for the L phase, I mean, probably the data would say don't use it in everybody.
Speaker: But now I think that some people have concerns with the effect it might have on viral pneumonias with prolonged viral shedding and replication.
Speaker: What are your thoughts, Dr. Catinoni?
Speaker: Let's see.
Speaker: I don't want to give you the impression that from LH is just due to the doctors and so on.
Speaker: You may go from LH probably, even with what we call, what you think is the best treatment, because of the aggressivity of the virus and the host response.
Speaker: As everything starts with a reaction in the endothelial
Speaker: and with some cytokine storm.
Speaker: I have several colonists who start to measure the cytokine.
Speaker: All the inflammatory cytokine goes up.
Speaker: The anti-inflammatory cytokine in some patients are close to zero, in some patients are activated.
Speaker: But I think if the logic of steroids and so on is to decrease the progress, the over-inflammation, I would use at the beginning more than at the end.
Speaker: I would use in L phase to prevent a possible transit to the H phase.
Speaker: But I don't have any, really any answer because in my life I saw the steroids coming in and coming out so many times in 40 years that I stopped to believe to them.
Speaker: Yeah.
Speaker: So I think that theoretically, I mean, that would be the argument, but like you said, I mean,
Speaker: So far, we have not been able to show that really we should or shouldn't.
Speaker: I have an adult response.
Speaker: If you see the patient, I think with 80 milligrams of prednisone, you didn't carry the body.
Speaker: Okay.
Speaker: And so I think in some situation, I would not hesitate to try.
Speaker: So we don't have to be so dogmatic because there is some rationale.
Speaker: I think if the patient is six to six,
Speaker: mechanical ventilation with 35 of peak 60 pco2 etc etc you may give the steroids but it's just for you not for the patient exactly and the last thing i wanted to ask you about treatment and then we'll wrap up and i'm very thankful for your time and generosity with all your your thoughts it relates to uh obviously concerns about um lack of ventilators or potential
Speaker: shortfalls in the numbers of ventilators.
Speaker: I mean, I know that there was a lot of talk about that in Italy.
Speaker: Now it's occurring in New York and in the United States.
Speaker: And I don't want to get into the ethical aspect.
Speaker: I think that's a conversation for a whole episode.
Speaker: But what about the thoughts of having more than one patient on one ventilator?
Speaker: It just seems that with a lot of things that we discussed and the potential for harm, that could be a very bad idea.
Speaker: Well, I think that if one ventilator lets see,
Speaker: you have the chance to kill one patient 50%.
Speaker: With two ventilators, I think the chance to kill two patients are 70%.
Speaker: Because all you know the physiology and the mechanical engineer so good that you use just the force of the ventilator for that.
Speaker: And you perfectly regulate the resistances, the diameter, the calibre.
Speaker: You choose the patient with a perfect, similar compliance characteristic.
Speaker: But during the war, this does not work, I think.
Speaker: So I think the double ventilator was, I think, patented 20 years ago in the States.
Speaker: But I think really is not medicine to me.
Speaker: Altura, that Kamar, Brody, so very distinguished.
Speaker: And very, very dear colleagues, they say, no, if you do the good protocol, good.
Speaker: But try to imagine how to win the patient in double ventilation.
Speaker: Until you put the patient and keep paralyzed, you are just sitting, and you do like this, okay, maybe you can survive.
Speaker: But when you have to follow all the course of the disease, it's very complicated.
Speaker: I think that's important because, like I said, I think with the anxiety that people have, everything that's new and different sounds like that's what we should be doing.
Speaker: And I think that people obviously are not thinking, what are the things that we understand?
Speaker: What are the things that we can apply and how can we first avoid doing more harm?
Speaker: But you know, by the way, it's not really so complicated.
Speaker: Because let's see, once we have decided to put a patient that's late, you put a sedation.
Speaker: Paralyzed.
Speaker: They avoid spontaneous breathing.
Speaker: Put eight to 10 people after checking the hemodynamics and don't do absolutely nothing for 10 days.
Speaker: But the usual, of course, the usual care.
Speaker: There is nothing to do.
Speaker: This sometimes is the problem.
Speaker: Nothing to do.
Speaker: Please don't go, oh, I have to win.
Speaker: Ballooning, you don't have to win anybody at the moment.
Speaker: because you make a disaster.
Speaker: I have to change the FiO2 and the change.
Speaker: No, don't do it.
Speaker: Leave the patient in peace until the body wins the virus.
Speaker: What you do may be more dangerous than what you don't do.
Speaker: And when you multiply that by the numbers that we're seeing, obviously the potential for harm raises exponentially, which is some of the things that I always worry about.
Speaker: Yes, yes.
Speaker: Well, Dr. Gattinoni, go ahead.
Speaker: No, no.
Speaker: Just one consideration that I already did with another one.
Speaker: I think it's very irritating somebody to hear somebody that's saying, as I do now, do this, do that, suggest that, sitting in the office, relax with some water to drink, have a good time outside.
Speaker: But believe me,
Speaker: You are in front line.
Speaker: In front line, sometimes it's very difficult to see the course of all the battles, which is easier when you collect a lot of information from different sources to make a story.
Speaker: So the story I told you is not just from one or two people.
Speaker: It is collected from several colleagues.
Speaker: And I didn't find anybody until today that told me, no, the patients described are completely different from what we have seen.
Speaker: Everybody sees exactly the same patient.
Speaker: Depends the difference sometimes at the timing at which you see them.
Speaker: Therefore, it's fundamental to have an idea of the timing of the course of this damn disease.
Speaker: which is under the umbrella of RDS, but to me, well, to call it RDS is difficult.
Speaker: But let's call it as you want.
Speaker: There's no problem.
Speaker: Yep.
Speaker: I think that's important.
Speaker: And like I said, I really appreciate your time.
Speaker: We traditionally close the podcast with a couple of questions that are unrelated to the topic that I think that what I found is that even in those, these very difficult times where people are very focused on
Speaker: a lot of what has not happened yet and trying to figure out how to deal with things.
Speaker: Routine, I think, is always a good anchor to kind of bring us back to center.
Speaker: So would that be okay, Dr. Gattinoni?
Speaker: Okay.
Speaker: So the first question relates to books.
Speaker: And is there a book or books that have influenced you the most or that you have gifted most often to others?
Speaker: Well, a good question.
Speaker: Well, there are several, I'm afraid.
Speaker: But the first that will occur in my mind is Siddhartha,
Speaker: by Herman Hesse and The Prince from Machiavelli, which is an unbelievably great book.
Speaker: If you want to be a chief, read The Prince.
Speaker: And I think that one of them really focused on finding yourself and the other one on dealing with others.
Speaker: But I think it's a very nice combination, so we'll definitely put those in the show notes.
Speaker: The second question relates to what do you believe to be true in medicine
Speaker: or in life that most other people don't believe?
Speaker: And I think that the whole conversation has really centered around one of those things, but I'll let you answer it anyway.
Speaker: That's right.
Speaker: I think that what is true in medicine is pathophysiology and physiology.
Speaker: And a lot of people do not, it's not that they do not believe, but they do not know, which is even worse.
Speaker: Yeah.
Speaker: I think that that is something true that we see, I mean, a lot of colleagues in terms of how they apply not only these concepts but also, unfortunately, how they interpret what's published, right?
Speaker: It's not evidence-based, it's just reference-based and anything that's published in social media seems to have the same weight as a peer review article in a high-impact journal.
Speaker: What would you want every intensive is to know?
Speaker: Oh my God.
Speaker: I think I would suggest to read three books, which are books of mono-autors.
Speaker: One is Respiratory Applied Physiology by NUN.
Speaker: The second is The Pathway for Oxygen, Viable, Function and Anatomy.
Speaker: The third one is Acid-based and Electrolyzed Equilibrium
Speaker: by rose all mono author all the view of the same brain in a big problem i don't like the books which are the collection of several authors i prefer to read the soul of one single author in a single issue these make my life different these three books in terms of profession
Speaker: So we will definitely link those to the show notes.
Speaker: Dr. Gattinoni, thank you so much for your time and for sharing with us your thoughts.
Speaker: I think that definitely a lot of wisdom and a lot of actionable things here for our audience.
Speaker: I hope you stay safe and that we have a chance to talk again soon and hopefully maybe even see you next year, maybe in a conference in Mexico City.
Speaker: You be careful because at the moment are you more exposed to the problem.
Speaker: but remember that the people we end up with age status are probably one over 500 of over 1 000. so the chances are are very low but you have to know it okay absolutely thank you very much
Speaker: Thank you for listening to Critical Matters, a Sound Critical Care podcast.
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Speaker: Sound Critical Care is transforming the way critical care is provided in hospitals across the country.
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