and a pleasure to be here I think we had some fantastic talks this morning I really enjoyed them I hope you did as well some of my discussion here will essentially perhaps maybe incorporate some of those earlier talks because I think they all made some very very good points this is a workshop so as we said this is very informal my goals are really to go over the settings for aprv instead of giving a lot of our research and our data we're going to just present how you actually set it so we're going to go over every every settings the physiologic rationale for these settings and hopefully that will encourage some some questions unfortunate is an hour and so we'll try to do the best we can and also it we're starting with the premise I think it's very important is that we we have evolved because we've used aprv for so long and our thinking I'm not sure if it's right or wrong but our evolution really has gone to prevention and prevention of acute lung injury a RDS but also what I would say prevention of ICU disease is I think we actually create a lot of our own problems that's my premise behind a lot of things and so this is where this motivation so first a little bit of background I think there's a pointer here aprv just very quickly most probably the easiest way to conceptualize quickly is that it's a CPAP type of breath so that means the patient can superimpose their breathing pattern any any time they want so that's the ideas the patient's actually breathing on CPAP the CPAP is released intermittently and so what that creates is the CPAP blocks if you will in fact if I were to color this area right here this would essentially be a straight line and the patient would be doing 100% of their minute ventilation using aprv and as you can see here Penny's doing this on the ventilator the patient can actually the patient was actually penny on a test lung who's actually breathing here the gray breaths represent the breathing so this is really again if this was a if I colored this completely blue it would seem just pure CPAP the releases really are there to aid in the metabolic loading that occurs in critically ill patients because they produce more carbon dioxide and so to some extent we're using pressure to create a more favorable point of inspiration a pressure volume point where the patient is above frc and below TLC so they're there at the compliant part of their pressure volume curve that's our goal and that's what we're trying to do is it decrease the elastic work of breathing with pressure decrease the metabolic work by intermittently releasing the the pressure and putting fresh gas in so that in essence is aprv here's the main settings and the names are you know we could call this PN span make it pressure control we could combine these two and call it a respiratory rate these are all the key elements and fundamentally I think what's important here because you can actually use this in a spectrum of diseases but you obviously will adjust it differently for different diseases which perhaps unlike conventional ventilation where we tend to sort of just focus on some very small points we might actually want to adjust these things based on the mechanics of the lung directly as we look at waveform graphics which are very important in aprv is to actually look at the waveform graphics so I'm going to go through each one of these settings and tell you some of the what we call important methodology for our what we've done in our patients and our clinicals our experimental data that shows that you can actually prevent lung edema a RDS and all the histopathology that comes along with it but one of the key things is actually to make it as much CPAP as you can in other words the patient is essentially on pure CPAP the time of the release when you add it up if you have a rate of 10 and 0.5 second release that's 2 minutes so the bulk of the time the patients in a CPAP phase of breathing so that's really critical and you can actually accomplish the entire ventilation that you need even in a non spontaneously breathing patient with this and again the key thing is to start the lung normal and keep it normal and that that's actually again the premise behind this a couple of key things that are different about aprv quickly is that we are trying to maintain an alveolar volume so if the alveoli are open then then when the heart returns blood it's going to dump the carbon dioxide into that space and hopefully what will happen is the gas will keep moving up to try to occupy areas where there's less carbon dioxide and hopefully what we can get is more diffusion and then of course once we do that we release the the gas full of carbon dioxide we put fresh gas in to continue this process so what we're trying to do is combine diffusive ventilation and convective ventilation and actually that's what happens in normal lungs you know just very quickly since we talked about volumetric co2 this morning I think it's important to just show you know very quickly here's volume here's your head title you see this little area right here of course represents the dead space gases the anatomic dead space here so we're flushing out on conventional ventilation but as soon as we switch over to aprv you see a straight line up because the gas has actually moved up into the bigger Airways and so we have a higher concentration of carbon dioxide so that the distance between these two increases the co2 per volume that you're removing so it's actually very efficient in carbon dioxide removal so that's just a rough overview now one of the things that is not necessarily essential but is definitely adds another element to aprv is that you're positioning a patient to start spontaneous breathing so to some extent in our unit what we try to do is get people breathing as soon as we can we actually try to get them to breathe within 24 hours of their admission regardless over their shock state any any of those factors and certainly there's some information about spontaneous breathing being bad for you but I just want to point out one thing which is really important it seems as though aprv is the only mode where you can spontaneously breathe and I would just tell you that that's absolutely not true unless you paralyze the respiratory system the muscles the brainstem will still want to will get feedback from the lungs from blood gases and drive breathing in fact you can remove the cerebral cortex and the patient will still breathe so it's really a something that cannot be sedated away when someone has a lot of stress but this is a low tide of I'm strapped a tient and what I want to just point out if you look carefully the patient is actually pulling their airway pressure down their peep level down and they're actually developing a lot of pleural pressure to suck this pressure waveform down so just because you're on you're not on aprv it doesn't mean you cannot breathe in fact I'll just show you that in an adult patient with a rigid thorax it's very very unusual to to have this happen unless you develop high plural pressure in other words this patient sternum is being sucked in word during inspiration and of course there's an intimate relationship between the thorax and the lungs the chest needs to expand as in order for the lungs to expand you can't have a shrinking thoracic cavity and expect good aeration so this type of desynchronize really unfavorable and can generate huge pleural pressures which aren't good for you now the thing is with aprv is that you're actually trying to silence inspiratory muscle activity and what I mean by that it changes your way of breathing to focus on expert ory muscle use instead of inspiratory in other words expiration becomes active and inspiration becomes passive and let me just explain a little bit so if you look at the EMG s related to CPAP level because in again aprv is very similar to CPAP what's happening is the EMG output of both portions of the diaphragm the cost in the Kuril portion progressively go down obviously the position of the diaphragm is important but also when the brain is more satiated there's less desire to inhale in fact you actually switch over to your brain wanting to exhale your lung volume down and that's actually collectively termed defending your lung volume so I'll try to describe this a little bit better as we go along and I have some videos but what we're doing here is as you look at the diaphragmatic change this is change in pressure you can see that as you inflate the lung volume the progress the active portion of diaphragmatic contraction goes down but you still maintain total and similarly you can see here this is passive which is here and this is active and this is the lung volume is actually created by more passive expansion of the chest rather than active expansion of the chest and this is my final sort of technical slide on this but I just want to point out here's the diaphragm EMG so here's the signal so this line denotes when the actual EMG fires in other words you can detect the electrical signal but well before that you have a tidal volume you have flow of gas and you have a pressure drop in the airway and you can see that that occurs before actually the diaphragm is contracting and what's happening hopefully I can illustrate this is that let me just stop here for a second and explain the video but this is what you're going to see here is the patient will actually be squeezing their lung volume as you have your pressure high so during that CPAP phase the patient actually loads their expert ory muscles just slightly and then when as soon as they relax it's like a spring-loaded event and the CH and the chest starts to expand with air so it becomes very passive and hopefully you'll be able to see that here really is difficult to capture on video but hopefully what you'll see is the lot of activity with the belly there is a squeeze and then when he relaxes the chest should spring out a little bit but otherwise there's very little inspiratory movement in fact you should look for essentially that balance where they're not actively exhaling continuously because that's too much expert ory work and that maybe someone who's rejecting the lung volume you want sort of a balanced lung volume not too big not too high so that you're at the right portion this patient I don't know if it's any better you can sort of see their abdomen squeezed here a little bit you'll see just a and of course you can feel this and then they relax in the chest will spring up let me try one more patient maybe this is a little bit better this patient I want you to look since has a large abdomen it might be easier to see I just need to come around the side here okay we stripped over here okay let's come around the side and right here I want you to see the abdomen he's going to squeeze his abdomen down and then he's going to his chest is going to spring out I don't know if you're able to see that it's very subtle but as I said it's in real life it's much easier to see the other important thing is what pressure do we want to use and we'll talk a little bit about why we need pressure we need pressure to help the patient breathe here the idea is not to use the ventilator as a ventilator in fact the brainstem is a superior ventilator in my mind because that's the neural output that you want to use we don't need a clock and a ventilator or timer to go off we'd rather use something that the patient wants to use there the patient wants to to set their inherit rhythm of breathing so what we're trying to do is just position the patient in a part of their pressure volume curve where it's easy to breathe and that's where we breathe from we do not like breathing up here in fact we can't breathe up here our diaphragms are flat there's no way to actually move volume the only thing you do is pressurize the system when your lung is errorless below FRC it's equally hard to generate volume you just create pressure and nothing really happens so the nice thing about spontaneous breathing it's like taking a blanket off instead of doing fancy things you can just look at how the patient's breathing so for example this patient this patient is the COPD or who were feeding McDonald's daily for obesity no I'm kidding you know I don't know when we're going to be prescribing that but this patient actually is on thirty five of pressure now if I put any of you guys on thirty five of pressure I promise you and be very unhappy with me and you would not feel comfortable you would be a total lung capacity you wouldn't be able to do anything with your diaphragm divers probably inverted and so there's no way that you're going to be comfortable now this patient is taking huge tidal volumes the patient's breathing spontaneously at a rate of fourteen he's doing eight liters out of 12 as spontaneous so this is the spontaneous side of aprv this is the Machine side which is the Toth incorporates the total here you can see large rod if he was at his total capacity I promise you there's no way that he's going to do that and if he was below lung volume it would he would be very distressed into kipnuk so the thing I'm leaving out to you is this patient is in fact almost 300 kilograms with an open abdomen septic massively resuscitated and 35 is what gets him not to TLC but to a part of his pressure volume curve where he can breathe and again that's really important because I think as we talked about transpulmonary pressure is an important concept and we need to somehow factor that into the whole situation now one more thing about spontaneous breathing which I think was mentioned by Luigi earlier with E I T is that spontaneous breathing really has a better distribution of ventilation it's better to pull air into your lung then to push air into your lung as long as you are not developing high chloral pressure and this is just the difference between paralyzed ventilation and the huge diaphragm moved way up into the chest collapsed lung we have a lot of movement in the sternum you can see the chest wall enter just while moving quite a bit in CPAP breathing it's the abdomen that's moving the chest wall is actually pretty silent and you can see that there's more movement down here just much more favorable even distribution of ventilation which ultimately I believe is the way to protect the lung the need to protect the lung by maintaining a home more homogeneous lung as opposed to a lung that's collapsed over here overinflated over here this is where it becomes very difficult and our options become much much less so keeping the lung as healthy as possible which I think you can do is perhaps one of the advantages now remember that this is really a pleural pressure modification so is prone positioning so the spectrum is there's more than one way to modify plural pressure one is the patient can actually take a breath and pull some air into the basis for you because that's where it preferentially the gas comes it's it's when you force air into the passive system that it tends to go by them micro mechanics more of the system I'm just going to skip over some vit but in this one just very very quickly I just want to show this is maximum aeration this is on low tide of I'm strategy patients not breathing very well here but this the patient is starting to breathe here and you can see there's a shift more to the basal er part of the lung when you actually start spontaneous breathing I think we also need to consider something which is the diaphragm you know we believe that weaning should start as soon as you intubate or the concept of weaning in other words mechanical ventilation is fine but that's not our goal our goal is to get that patient off mechanical ventilation so I think we need to start thinking about how do you get this patient off ventilation as soon as you intubate them so what you don't want to do is the first 24-48 hours is create a problem for yourself later in other words we're just going to kick this problem down the road next thing you know we have a patient with diaphragm dysfunction and perhaps perhaps that might have some implication for delayed weaning and we spend a lot of time in weaning and this is where patients are very in my mind susceptible because they're not moving that fast we don't want to push them too hard to slow everything is fraught with danger because then what happens is we we expose the patients to more infections and complications okay so hopefully there's no questions so far okay and now we're going to talk specifically about the different parameters and I want to focus first on this P low of zero so again if you were to look at this well what's crazy about this is many things well first of all 28 going to zero looks bad I mean there's no question that looks bad it looks bad because we know from the only induced lung injury studies that you can take an animal and you go from 28 to zero and that's the most efficient way to actually destroy an animal's lungs and I've done it personally and that's very very rapid versus you know a more slow approach with a little bit of PEEP even low peep slows it down a little bit and secondly we may end up seeing that the volume that comes out is quite big so those are a bit contrary but I just want to explain a little bit further which is that we don't control end expiratory lung volume through pressure but we do in fact control it but we use time and the notion there is a time constants where the cluster of time constants is more in a narrower spectrum than the peeps spectrums that you might see in a patient's lungs so that's really the premise behind we specifically want to actually set it to a based on the peak expiratory flow now this peak expiratory flow is going to be dependent on many things the peak expiratory flow whether the patient has obstructive lung disease or the patient has an obstructive endotracheal tube the resistance of the endotracheal tube in other words the size of the endotracheal tube you can you can change the endotracheal tube and you'll change this flow pattern it doesn't change where you should truncate this but in essence the time factor will change because in fact we've changed the respiratory system which is essentially now including the whole circuit then the tracheal tube this is now part of the patient for practical purposes that this is what you're going to be dealt with until you get the patient off the mechanical ventilator so this is what we're trying to do and penny I don't know if you can show what happens you can see here it takes very little time incremental change and this is obviously a test lung but I can tell you in human beings it's very very small changes can result in dramatic potential for Dee recruitment so this is one of the most important things about a prvs we set this to this flow pattern as opposed to a number and we want this particular flow pattern so I think what she's done is increase the time low and you can see the point of this inflection point if you will or this point where the flow truncates and goes back up you've let more air out of the lung and where we're trying to do here is get some estimation of lung volume rather if you have a picture unlike peep where you just dial a number and we don't really know and we're using pressure but when we talk about the circulation we don't want pressure we want volume volume is something that we really care about what I care about is the lung volume what's the lung but I want to keep the lung volume stable I don't want to go from inflated to deflated and so we want some visual surrogate of that so that's why we use the flow pattern so the flow over time is a representation of volume this is time over here and this is flow so this area under this curve is exact the volume the expert or a volume so by truncating it and projecting where you go to baseline you can get some idea of your end expiratory lung volume and this should always be bigger than this in terms of area because then there's a problem the lung is closing down very very rapidly now I'll just show you a PR V set incorrectly this is what happens you get a lot of opening closing remember we're using zero pressure at some point if you extend the time out long enough you will in fact get zero pressure what we're trying to do is we're retaining this CPAP so when we drop the pressure the lung already has a certain amount of pressure we're trying to retain some of that we're not trying to let it all out we're trying to maintain it and then go back up because obviously in the lung you don't really have this this pattern it doesn't dipped quite down as much you can see that there is essentially a little peep level there but again that's not in the lung that's in the ventilator circuit on the north end of the endotracheal tube not the south end of the new trick too so if you set if you set it correctly and this is an injured lung model this is a tween and high tidal volume lung injury the lung is very stable once you go back to 75% this is acute lung injury that's not obstructive lung disease this is how you set it for acute lung injury or or a RDS or someone has the potential for that definitely go back to that previous slide actually what prompted this um inveigle microscopy was that I was reading an article that was titled a PRP had the highest worker breathing and you know of course I was like it's not what we see at all but indeed it most likely was and the reason was because the Telos were set so extraordinary early on and we're talking that's why I set this at one point two seconds we actually duplicated the study and this actually went to zero I mean it goes all the flow goes all the way to zero so they're actually the lung is collapsing so that's that's what actually prompted this it's not you know just just to show the difference it is how some people said so that was very important to see and this doctor Abacha will show you that we actually took that step further and did an abstract on so if you look at the lung grossly and this is our rat hemorrhagic model again we're going to zero here but actually there's very little movement so coming back to what you see on the ventilator twenty eight two zero the lung is actually moving very very little so there's very little movement in the water similarly just very quickly this is one of our pig lungs after 48 hours of septic shock and I think you just saw release they're very very brief movement and that little movement can actually take care of a lot of ventilation I think they'll be that there was another release there now again if you look at the intimacy between the chest and law chest wall and the long you'll just see this on your patient if they're not breathing this is one of my post-operative patients is just recovering from surgery you can see that very little movement of the thorax so even though the ventilator says they're going from 28 to zero the lung is actually moving very very little so it's actually a low amplitude ventilation versus a high amplitude ventilation just some quick T is a plateau of 31 here six ml 10 of P and you can see that we don't we don't retain the image on the screen here and then you add more peep of course you do but when you look at aprv you'll you'll notice that the aeration is maintained again even though you're using a pillow of zero so in other words we maintain the gas volume in the lung and in fact in our studies with injured long as it takes 24 peep to produce the same alveolar expert ory alveolar stability as it would with a kilo of zero set to 75 percent in an injured lung model so of course if you can save some pressure that means your total pressure may not be as high any questions so far this is the yes sir for example let's change your bottle foundation on your very to start your tea pot that's coming right up so just to finish the the Tilo P low portion of the setting and again setting P low of zero is easy because it's zero and then of course if you look at your flow pattern you can figure out you of course can freeze these things penny can you show what happens when you freeze the wave form you can freeze the wave form as soon as you freeze the wave form you get a scroll bar that you can take over and you can actually get your precise measurements if you will back to this one you can see we're going to zero here and again you can see how unstable the lung is at end expiration this is if you do 50% you still have some alveolar instability and 75% we have essentially a very stable lung compared in comparison to previously this is important because this may be a part of what causes more lung injury and in our lab when we produce alveolar instability this is what we see versus this is what we see with aprv and more homogeneity so this is looking at the percent in this area of alveoli that are inflated so the circles in case inflated alveoli and the red area that is not in case is the area of D recruited lung and you can see that we don't have very good crewman this is 16 of PEEP after lung injury and then we go to an exhalation and we lose a lot of our alveoli and also the alveoli are very different shapes they're actually not uniform and some are very big here we have much more uniformity in our alveoli and the histology just completely looks different and this is actually just six hours of instabilities small animal model and I do think personally that it's probably better to control end expiratory lung volume with time than pressure and one of the reasons besides the spectrum of people evel's that you might find is that peep good end expiratory lung volume we just increased the period of five but what you can see is all of a sudden is going to be lost of these recruited areas so pee pads this creep effect where the volume is actually redistributed out of the distal airspace and into actually the alveolar duct and we have some data on that I'll spare you that today but we do have some data that we're working on that the distribution and the terminal airway is actually different but there's still this creep effect if you will because we're just staying at that people just simply too long and if we just use time we may be able to capture just a more narrow spectrum and get the alveoli to behave perhaps a little bit better we still have this creep effect it really takes us 20 24 centimeters that we found is really what it takes to stabilize an injured lung and this model is tween with high tidal volume to produce alveolar instability so now the p hi back to your question so why do we want to use a P hi well we said firstly we want to create enough pressure so the patient's on a stable part of their pressure bottom curve just like we are I mean we're breathing at a point where gas exchange or mechanics are efficient because your lung your your breathing the act of breathing should cost the least amount of money let's say which is carbon dioxide and oxygen so we will always want to ventilate with the least amount of energy and so in order to do that well the chest has to overcome a lot of things in our in our patients because we are not just ventilating a pair of lungs and as dr. Grasso pointed out we have the elastance of the chest-wall I would like to just take one a sort of additional piece of information there which is that you need to think of this almost in four dimensions you know we look at x-rays we look at think at scans but this is moving and one of the things that's important is that the chest wall is actually an elastic structure just like the lungs are and the chest wall actually creeps and in fact if you look carefully plural pressure as you hold pressure in the lung we of it and the chest wall the chest wall is a slow compartment and after a while you get progressive creeping and the plural pressure actually drops so if you look carefully we may also be affecting the pleural pressure by actually changing the the thoracic compliance similarly if you look at stair-stepping recruitment maneuvers they're generally tolerated better as dr. Grasso pointed out that the hemodynamics as long as you're sending the energy to expand the thoracic cavity rather than towards the mediastinal structure you're going to have better thoracic but the lung inflates faster than the chest wall does so the creep effect may be something we need to consider important but also the abdomen and of course now we know that the abdomen is a huge part of this and this causes a lot of dysfunction this is just one of my patients who've actually received lots of gunshot wounds for I don't know what he was doing but now you can see that when you resolve his Ilyas he's able to inflate as long so there's obviously an importance of this boundary the abdomen so of course when we look at what we're doing to a patient so a patient comes in they don't have a RDS or acute lung injury but we're going to resuscitate them and I do believe a lot of our diseases are a byproduct of resuscitation what's going to happen with resuscitation we have permeability we have inflammation we're going to produce edema we're going to lose extra vascular plasma water and it's going to go into spaces where ideally they wouldn't go to but they're going to so we're going to worsen respiratory mechanics to some extent the P high is to change to go in concert with the changing and worsening of the whole respiratory system compliance because if you counter that then you can maintain lung volume instead of the extra thoracic component shrinking long volume down you're going to counter that with that continuous pressure I would say that this is probably in my opinion one of the things that's kind of disappointing with recruitment maneuvers I've never been able to reconcile the fact that recruitment maneuvers are very transient but you're swollen a patient is not transient they stay like that for days and days and days so how can we expect a maneuver that pops the lung open for a few hours and then all the things that want to collapse the lung again are still present so we actually incorporate a diuretic approach but I would tell you it's not diary Singh the lung it's actually diary Singh the abdomen because of the ascites and that's how we think sometimes that helps because clearly if you come back to EIT as you increase pressure in the abdomen and this is done with installation of co2 you can see that you're essentially making the lung airless and it's only until you actually use some countermeasure in this case peep that you're going to have some reagent and then you take it away which is the green bar here and you go right back to where you were so this transient approach may not be appropriate so one way to think of the P high and sometimes I say this is a continuous recruitment maneuver that you can ventilate through because essentially you're trying to somehow match against the forces that are trying to collapse the lung and that's simply a bunch of these things we know that the lung gets heavier because there's permeability and along the hearts there the abdomen and of course overall as dr. Gould pointed out this may not be a normal position and most of the time when the patients say wait a minute this is not a normal position we tie them down to make sure they stay in that position so this is why we have a hand in a lot of this and I'll just show you quickly some of our patients you can see how tight his abdomen is massive resuscitation here this is actually a very unfortunate this is when we were doing ECMO this is actually 1998 and I've to tell you a story this is the first patient that we could not oxygenate we couldn't do anything he's on his lungs are this big on the x-ray huge huge you know hundreds of units of blood cells I can't tell you how much I can't even remember quite high this is the small intestines and so we're trying to figure out a way to to ventilate him and so I of course suggested proning I don't think penny like that none of the nurses liked that idea at all then they of course gave me a nice little hand gesture and so we decided instead to stand the patient up and as soon as we stood this patient up he will finally hit a hundred percent saturation so we got him and he eventually died I mean he had half his liver was missing bad shock this patient actually had a transection through his aorta and vena cava so both were completely wide open and just hemorrhaging to death I don't know how many times he arrested you know to be honest with you it's amazing he actually lived for three days but nonetheless this is just to illustrate how important the abdomen is in the respiratory system you have to push the app in a way to make the thoracic cavity larger to actually accommodate the lung and this is a from our lab you can see that the pigs look nice before their septic shock and then you know we're about to make their incision this is after 57 liters of fluid and you can see that they're very very swollen very very tight and this is what our pigs look like but obviously we need to counter this is a force this is actually a force that's going to transmit to the thoracic cavity and it's going to transmit that pressure so of course we can't just use pressure we have to sustain that pressure because these forces are in fact sustained and even if you just look at lung recruitment we know that if you hold the right pressure it takes a while for the lung to sort of wiggle itself stagger itself to more normal inflation so it's really difficult to imagine how we will ever actually do that by not focusing on lung volume and you know just very briefly we think a lot about the airway pressures and all these numbers here but what's really happening in along with the end game here is what's happening in the distal airspace that's the business end of the lung that's the functioning end alone if you look at alveolar pressure you can't really achieve it until you have a significant amount of time so the lung is just opening and then we take the pressure away so I don't know if we can actually recruit with with that strategy whereas you need a certain amount of time in order to do that in fact this is what happens this is 24 of PEEP within an injured model and we're going to transition to aprv and you're going to see that with just a little because of the time change because our time is essentially prolonged here if you will you're going to see additional recruitment and this is of course the idea is not to go up on pressure for recruitment but to go this way for recruitment so pressure is important and we all think about pressure but remember the recipe includes time that's why recruitment maneuvers are done over a period of time the problem is they're transient and we may need more so is in essence that's the idea of the P hi now just as a very quick clinical scenario most of our patients when you use this on normal lungs post-operative lungs people were you know maybe just been resuscitated most of our patients are between 20 and 30 with the majority being 20 to 25 somewhere around that as a pressure in the old days when we use this for rescue we were well into the 40s and 45s now the caveats there are of course if you have a patient who you suspect their transpulmonary pressure as the patient I describe to you that's this big massively recessed a huge abdomen it may be that their alveolar pressure is going to be significantly safe at a forty forty-five and that's where we were before these patients now I do want to talk about patient comfort and just quickly transition into weaning and you can see what we try to do is get our patients up and walking I will tell you that we use a lot of decks med etomidate and this allows us to do things like this I think we would we we used to do this but it was really a much harder struggle so I wouldn't say that we could not do it at all without decks mohammadi but it just makes it easier it's my less of a hassle to actually get these people walking and moving and I'll just jump over to this patient all of these patients at the time when we're actually walking them they're still by airway pressure still pretty up high up there this patients airway pressure would you believe this guy's mean airway pressures 27 and look he's taking nice spontaneous breaths there he's not distressed at all this is after walking his total minute ventilation or spontaneous no the cameraman was well actually it was me let's see if we can go back to that quickly but but his mean airway pressure is 27 and again he had massive resuscitation he had lost his arm on a forklift and had really bad shock and was bleeding and a lot of tissue injury and what we call sterile sepsis and so I won't bore you with that but we obviously are able to walk a lot of our patients and they're quite comfortable this is one of our chronic ECMO patients who was in the hospital for a long long time he had a massive BP fistula after essentially having bilateral lower lobe receptions a complete resection so he just has upper lobe and actually a partial upper lobe at that point and finally got him off ECMO massive bilateral Bronco pleural fistula eventually became closed on their own but he's going to take his first step here after a hundred and some days of being in the hospital and I think I'm going to take a picture of his feet here there you go what's amazing to me is that the next day they just look so much stronger I mean I have sequential videos of our patients walking and so what I would tell you is don't get discouraged if you want to do this even if you just stand and pivot for three seconds the next day they'll do five seconds then they'll take a step and that's how you start this process and I think you know we're always trying to get ahead of things and the reason of course is the ICU is full of complications in fact what I tell my fellows I've renamed the ICU to the intensive complication unit because that's what we're good at we're good at creating more complications so that the first thing is to get out of our way of what we do to patients now I want to talk about weaning quickly for the sake of time here weaning is actually fairly easy what we're trying to do is increase the CPAP blocks and we're trying to actually transfer the minute ventilation over to the patient so what we do is increase the CPAP block and that forces the minute ventilation to move over here and then we assess whether the patient is capable of maintaining their work of breathing within a normal range we don't want to excessive worker breathing but we don't want someone not breathing at all so we're always trying to look at that we also look at the morphology of the waveform and you know this total work of breathing and we have an index that we look at to tell us whether someone's exceeded their work of breathing before this we do something called a stretch test which penny maybe you can describe so what we do is here's my patient just admitted not breathing we could be over ventilating the patient or the patient could be too sedate so what we will do is increase the t hi we stay in the room we increase the T hi and we look at their minute ventilation their baseline minute ventilation and after several minutes depending on you know where their pco2 is and where their rate of rise is we determine whether they pass or fail this stretch test and what that tells us is the patient cannot breathe so their minute ventilation just drops and you know sometimes that happens it kicks into apnea ventilation but that's what ends up happening and so we don't leave that patient we put them back then we discuss with the nursing staff we renegotiate their pain sedation approach because we don't want to compromise on either and we want to make sure that our patient is breathe so we actually are quite successful doing that in 24 hours sometimes it takes us a little bit longer but the vast majority we can get these patients breathing once you get them breathing it really is just comes down to Ken can you handle more work I'm going to give you more stuff to hold and every time we do that we just asked what their work of breathing is and they tell us because they don't lie about that the rate goes up and the tidal volumes go down it's pretty predictive so that's what we end up doing and next thing you know when you reach a certain pressure you will actually find yourself essentially on straight CPAP and then when we get down to a certain level typically we excavate our patients from 15 of CPAP successfully as long as they need other parameters we use the rapid shallow breathing index a modified version of it and that's how we actually wean the patient so you can see hopefully this is the screens we try to set up so we want to know they're minute ventilation total how much what percent and you can see on the now we have this so this patients doing 60 percent of their minute ventilation so they're essentially 60 percent and I'll tell you another thing is that when the patient is still being resuscitated and swollen we actually do not route the pressure so in that case we don't lower the pressure we actually just extend the time and so weaning is not just pressure reduction weaning is still actually incorporating the patient to do more breathing so we look at weaning not just as weaning is only a pressure reduction in the system and we reserve pressure reduction when the system is less indominus when the compliance of the whole thing becomes less adem minutes and that's I think more integrated rather than focusing on the lung like we sometimes do as the only thing there that it's just sitting there and that's the only thing we're doing it has a lot of interactions with the rest of the body and which which state the patient is in which phase of their illness are there and certainly there's another phase where you're able to reclaim that edema fluid we're able to diurese patients to me it makes more sense to reduce pressure when the whole system compliance is improving because your diary seing the patient and they're putting out lots of fluid so we actually reserve the pressure reduction to later we call that more of a staggered pressure reduction so you don't see a lot of pressure reduction and all of a sudden we're able to move very very fast the advantage of that from my perspective is that we've maintained lung volume whereas if you just go by weaning pressure what you'll if you notice your lung will slowly start collapsing and so we're setting up our patients for extubation failure I think because their lung keeps shrinking and then we're going to take the tube out and it's going to shrink even more and then we're going to say go ahead and breathe on your own and when they struggle then we have to do other things so let's see if there's more questions yes sir so do we we can do that you know we typically increase the time high to 30 seconds and in fact we try to have this rule where you have to be a thirty seconds if you're if you're pea highs down to 20 in other words we want to see that you're almost a CPAP before we switch you to CPAP because a tee high of 30 seconds is essentially two releases per minute that's almost CPAP and again we look at indices of of your ability to breathe so we do that little test if you pass that test we move you down to CPAP because we need some they go over to ASE or so your mind escapes they would typically try this take them off a therapy they look good let's just go in a pressure support right ASV is that what you're yeah we don't do that we go straight to CPAP and again the idea here is two more CPAP with release to pure CPAP without release or whatever you want to call it so the idea is to just lose the lose the black stuff or the blue stuff here and gain the grey stuff we're trying to slowly spread the Machine apart and have the patient put more of their breathing in there until they're actually doing the bulk of the work and they're comfortable because that's what you need at some point when they're on CPAP they're just like you and I except you're breathing on a platform of zero and your lungs are pressure independent and what we're trying to find out there is where can we make your how do we get your lungs pressure independent maintain your lung vine because lung volume is what keeps us comfortably breathing I mean no question there's a lot of other volumes that are in the lung tidal volume but I don't think we can just pick out one volume in the lung and say that's the most important I think we have to think of lung volume as a whole in general also because a lot of that is connected dr. Bacchi room light turned it drop and stretch and it's it's a way to actually reduce the mean airway pressure very slowly because if you drop the pressure without increasing time you're going to really take a big hit with your mean airway pressure yeah that's a bit typically when your patient when you'll see they'll start getting to kipnuk they're not as comfortable because they've had a bigger loss of mean airway pressure whereas if you take it from pressure but give it to time can you show that on the ventilator penny so what she's talking about is the area under the pressure curve is that mean airway pressure go through to a key high of 24 down to 22 but I wouldn't just drop the pressure now I'm going to take the time I and I'm going to take it out for five and a half seconds out to six and a half seconds so my mean airway pressure is relatively stable it really hasn't changed much because even though I brought it from here from pressure I gave it over here to over period of time yeah eventually of course the pressure is going to be reduced are we still okay on time baby can you sauce a little bit late something bread say another five minutes of Sun and if you're cheap I issue my friend came over he called me the noticed entity 30 seconds we don't do it in one move so we progressively in ya bridge adversely affects Turkey Earth you know we clinically we don't see that in our in our lab data doesn't support that either in fact they're actually more humid inherently stable even with their septic shock and I think the property problem is you know again matching the right pressure and where your patient is on that pressure-volume curve so clearly the right heart does not like high lung volume it doesn't like low lung volume either so if you look at pulmonary vascular resistance very high at the extremes the lowest point of pulmonary vascular resistance at least from the right heart perspective is FRC so FRC is the ideal position for your patient and we of course I don't know that at the bedside I don't I don't measure that I think it's tedious I think it's difficult there's error what I simply do is just default to the patient's brain stem and I look at the patient's neural interaction and I know that the brain stem is getting all kinds of feedback back to the brain from the system it's looking at stretch receptors and it's telling the respiratory muscles what to do so by uncovering that you can see a little bit of what's happening as long as the patient takes these nice breasts that they're not having a lot of distress then somehow their brain stem is satiated to the point where they must be on a better part of the pressure-volume curve then I'm going to guess at and so I look for those kinds of things so it does require you to understand some of those things which are not you know difficult to understand yes sir you advocate using this impatiens work entertaining emoji entity economics we do we do actually you know actually there's some there's some very small data but I can tell you we've done that for years so the key thing I think is the sooner you do it and someone like that the better the reason is that you know if you do have collapsed lung if you're trying to recruit them you need you need that long T high and so you lose diffusive ventilation by having low surface area it may come back as you recruit the lung but that may take 1224 hours and generally you can't tolerate high cps for that period of time so that's sort of the caveat there so but if you do it early and actually aprv is associate with better survival blood flow better spinal flow better gut flow and especially if you do this with spontaneous breathing so and again in our head injured patients we're actually using more decks better tama dean than before trying to minimize the propofol we use a very high doses of propofol we've minimized that a little bit we sometimes use them both together to spare we use it as a propofol sparing device in and what you find is that you can get these patients to breathe most head injured patients actually breathe too much not at all not that they don't breathe at all so you don't have to do that you don't have to get them breathing but that always helps lower central pressures and so on it comes back to where are you in the pressure-volume relationship a normal person there ICPs could go up if their lung volume becomes too high and the pressure in the thoracic cavity goes up but if you're using you know if you're going from a low long volume to make medium lung volume then you don't see these adverse effects it's really when you overdo it for that patient or under do it for that patient the apricot yeah is a problem you need especially a CPAP with release and how often it of course how you manage this yeah so you know typically in an adult patient at T high of three to five seconds to three to six seconds and we usually start at five T hi oh this is for an adult and that almost always gives you a low slightly low pco2 so we actually have low pco2 so the rate in aprv is usually under twenty it's closer to ten twelve the total rate and it doesn't like high rates at some point if you try to increase the rate with aprv you're actually making it more bulk ventilation than diffusion the longer time you have the more diffusion you get but for diffusion to occur you need surface area so that's why you're really going to rarely find a co2 problem when you do this from the very beginning when the lung is actually fairly healthy you know we always use it I mean years ago we had a arbitrary P low of five to something like that but we later found out that that was not necessarily and that's where you actually see hypercarbia if you want to have a harder time clearing co2 just dial in a small pillow you're going to see a lot more hypercarbia so here we actually are able to improve the co2 clearance by reducing that that pressure low I think that's actually a very common thing the literature just doesn't support that hyper copy that co2 removal is actually more efficient in aprv we please oxidation is always up just before we got the cellphone specialist let's say you do have the copier let's see can you guide us through your thought process how you troubleshoot them sure absolutely the first thing is that we we don't want to alter the time low for hypercarbia I think if you try to do that and actually that was one of my earliest mistakes 20 years ago we thought well just increase the T low and what happens in that situation is the pco2 gets better for 30 minutes 60 minutes yeah so what you're doing is actually making along more unstable and what you'll find is the po2 goes down and now the pco2 is actually higher than what prompted you to make that change in the first place so really that that controller is to maintain end expiratory lung volume and we can it would take a long discussion to tell you how we arrived at 75% of the peak expiratory flow but I'm happy to do that for anyone who's interested and might get bored in the stories but that's really the balance point between keeping the lung stable at end expiration so that's not where you go to fix it so where you go to fix it is really your pea high and your tea high so the first choice would be to make sure that you actually have enough pressure that you have optimal alveolar volume now again it's easy to say that up here in reality of course we're trying to look at things and title I mean we can maybe I can show a very interesting slide with n title you can use capnography and things like that to give you an idea where you are with recruit ability you can do little tests to see if someone's recruitable and that's what you want to first do is is this P high adequate and of course you can always look at the patient look at the patient feel their stomach feel their belly if it's a big tight abdomen and your P high is 25 there may be a good chance that you need to get closer to 30 on that patient so those are some you know critical things the other thing is the combination of pressure and time might improve recruitment and co2 will go down even though the bulk rate has gone down a little counterintuitive but if you increase diffusion you actually don't need as many frequencies and then of course you do have the option to reduce the t low sorry the t line penny-can you're on standby so if you reduce that you will increase the bulk ventilation rate and the way I think of it is that we we go down to in some extreme cases we go down to 80% of the pressure cycle to be the CPAP phase we might lose something there in terms of alveolar stability or recruitment and so on but you still will gain it eventually so you can actually shorten your T high to give you the final piece to co2 control which is that you're relying on bulk ventilation I think you would do that after if you have tried it the other way and your diffusive components ever each day yes but you oh absolutely I think my P high is ina so I have enough alveolar volume and maybe mighty high or trying to take it out to six seconds seven seconds that's too much so instead I'm going to go back and both ventilate more but be careful of one thing which is that the mean airway pressure can go way down by sure if you take a tea high of six seconds and now make it three seconds you've lost a lot of mean airway pressure so you have to make it up by putting it on top so typically when you bring the tea low but I keep saying TiVo sorry when you bring in the tea high you will have to sort of raise the pressure and as in yeah as a general rule that's what you generally have to do also you can skip over that step entirely by just thinking about your patient if someone has pulmonary fibrosis and they're on the transplant list you're not going to get diffusion don't waste your time you know stretching them out to to gain surface area you're not going to recruit that long if the lung has the potential to recruit then you can do that you have to decide do I want a blood gas it's horrible the first hour slightly better the second hour eventually better the sixth hour you have to decide whether you're treating a lung or a blood gas so recruitment always has potentially a little bit of pain while you're trying to get somewhere sorry to say we play having that dr. Bacchi and I think the good way to start learning how to use it is in being patient I think that's a time when you want the passion for anything and it's a good way to become familiar with the strategies in the technique and understand the nuances as a classical switch I may be a stupid can you I think the audience is usually can you just explain why you're sort of forwards the very large tidal volume that you often see on the pressure relief which is sometimes way about six months of chemo isn't the problem that trick question yeah I don't I don't know for sure that it's not a problem of course we have data to show despite these tidal volumes it's very long protective in fact it stops lung injury I think the important thing is to decide whether there's a connection between the micro and the macro ventilation and I think that's really an important concept because when we're talking about six ml's the whole idea is to prevent alveolar / distension and in fact that's the mechanistic answer that you will get when you say what is the mechanistic reason for benefit at the alveolar level or from low tide of I'm strategy of course I can't find the slide I'm looking for but maybe you guys can recall the the difference out here we go finally excuse me so the idea is that at the alveolar level and I say this sometimes and people think I'm crazy so I'll just say it again I think aprv might be a better low tidal volume strategy and the paradox there is the paradox that we've gone through with the macro ventilatory parameters you see the tidal volume is huge we know that's injurious low no peep setting that's injurious big amplitude injurious yet the data shows completely the opposite so the disconnect could be that there's non-linearity between what we see on the outside of the ventilator and what's happening in the lung and I in an editorial in critical care medicine that's coming out soon I make that point using human dynamics or macro circulatory shock resuscitation versus micro circulatory shock and the two are not linear so I think if we want to broaden our perspective a little bit about mechanical ventilation we need to look more at the at the alveolar level and just very very quickly what we find is that this LV list has a greater change and this is some of the new data we're trying to put together so what's happening is you have less alveoli contributing to the total tidal volume that's going to ultimately come out but they're actually bigger and scattered in size as you can see here this is low tidal volumes strategy between the two after lung injury and in aprv we have smaller more uniform alveoli and they change very little but then you get a huge volume because every single one of them just had to give up a little bit so there could be that paradox of course I can't prove that yet but we have some preliminary data to suggest that that may be something that's really important to investigate and understand better because maybe we do want to use low tidal on strata we just maybe haven't figured it out you know what seems intuitive on the surface may not really translate to what we want at this level and the counter being the truth about you eating Evan downs basically 5 out of 15 well typically once there P high is 20 then we skip over to you know 19 of CPAP because the mean airway pressure you know goes up a little bit if you go to 20 to 20 so this C mean airway pressure is a little higher so we go to 19 this is just part of our protocol 19 and then we take two more steps so typically we reduce by two once you're in CPAP we look at your rapid shallow breathing index and then we just keep going because remember this is spontaneous breathing so we use work index to work of breathing indices to help us figure out how much load the patient has you mean got about 15 and then we extubate if they pass they're what we call monitored breathing trial this is something else we do that's I'm sure unusual but we leave them on the ventilator for their trach collar trials or when we do a spontaneous breathing trial we're able to see all these parameters instead of guessing at them instead looking at rate especially when we're doing trade collar trials because you know it's a guess and we use saturation to tell us the patient's finish their trial when in reality we just fatigued that patient and wipe them out or let their lungs collapse or do something wrong and it's the last thing to go we're very good at reacting to the SAP monitor but way in advance so what we look for is how well they're breathing so we basically turn them to zero and then we just use the ventilator not as a ventilator but as a monitor so something we we do and we find that it gives us a lot more information and the nurses are clued in to what to look for and so it's just much easier for them to know that the patient is in distress before that occurs key and lock key applies to sue well the CPAP to zero yeah or the P hi to zero whatever you want yeah but that's for the most important trait called a fire yeah but but if you're intubated and shakily we'll put you to zero and typically we do 30 more than 30 minutes less than 60 that's sort of our approach I don't know if that's exactly perfect but then we if you maintain your rapid shallow breathing index within a range we extubate you may see the show not go go to use I'm sorry no no we usually go straight to you know air solid mass or nasal kenya or is nothing at all so thank you