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Jeroen Molinger, MSc brings the research to the bedside. He ties together the importance of muscle maintenance, nutrition, and how to create survivors not victims.

 

Episode Transcription

Kali Dayton 0:01
Jeroen, thank you for being with us again. I know I’m taking a lot of your time. But I think we all really appreciate your expertise.

Last two episodes, we have talked about muscles, why they matter the role they play in multiorgan dysfunction. And then this last episode, we talked about nutrition and how metabolic needs change depending on the condition, the timing, so I kind of want to bring that to the bedside and what that all means and how we can apply that. You’ve mentioned different ways to measure metabolic needs.

Can you tell us more about what you and your team has developed as far as how to know exactly what a patient needs on that specific moment in their life?

Jeroen Molinger 1:51
Yeah, okay. Thank you again, for for having me. Good question. I think that’s still something we are kind of figuring out what kind of assessment we need to do.

Our current research is particularly focused on muscle metabolic changes over time, where the muscle itself is a kind of a big metabolic organ. So it’s easy for us to assess it in a way of course, the metabolic carts, which we already know, that can drive your metabolic needs, but also using body composition assessments. So bioimpedance, for instance, we have specific bioimpedance from Inbody, USA. Those are multifrequency bioimpedance devices that can measure very well your overall body composition, your total body water, the extracellular and intracellular water.

So you have to somehow combine that with the metabolic carts with the noninvasive hammer that I mix with the imaging, potentially from the CT scan, and also from the ultrasound on the bedside. And combine it also with both the computation for the impedance, and then also looking at your ABGs and combine all those datasets together, that drives your cardiopulmonary metabolic phenotype.

Are your patient being sedated? Yes or no. On the vent? Yes or no. And see what they need on a day by day basis. So it’s… you can imagine those…. this kind of an assessment suite right. So how can you use that and do this very easily? Right now, we have a kind of a assessment team, which does all the assessment separately also in our COVID patients before.

There is no one “silver bullet”. I think, in our research, the metabolic cart is kind of the the center. So to Vo2 and the VC02 and ventilation assessments is in the center and everyone is is kind of hooked to it. So we we combine the Vo2 with hemodynamics, we combine Vo2 with O2 differences in the arterial and venous side. So you can have far better insight in how is that specific patient being more inflamed, more hypermetabolic, or maybe potentially hypometabolic.

Because from a nutritional perspective, or even from an exercise perspective, overfeeding and underfeeding have significant effects. Honestly, you cannot afford mentioned that just the muscle protein synthesis goes down. So you will be having less muscle and we talked before about muscle mass itself and muscle quality in itself has for influence on their overall metabolic interorgan crosstalk with with all the systems. Also the the hyper- if you’re overfeeding patients, then you’ve given them a far higher load of carbon dioxide to breathe out, which is a larger and a higher load on the ventilator system – like the intercostal muscles and like the diaphragm, for instance.

And diaphragm is a kind of a, in that sense, kind of a weird muscle. Intercostal muscle is a muscle for the normal uses for when you’re having a kind of tress hold ventilation. So when you’re exercising so then the more intercostal muscles will come when you can use specific breathing, comparative intercostal and diaphragmatic function. The diaphragm itself is not a it’s kind of a weird muscle because it’s very thin. It is around two millimeters thick. And it can thicken about two or four millimeters depending on the size of the patient. But it has very strange kind of distribution of fibers.

So we know our fast fibers and our slow fibers. So our fast twitch and slow twitch. The slow twitch fibers are the fibers that you have in your muscle that are more normally made for long term endurance so that you can prolonged your exercising. The fastest fibers, the very thick fibers are your fibers you need for sprinting for very fast action, inspection. The whole metabolic need of the fibers are different. Normally have, it depends on the muscle you have around a specific distribution of fast versus slow. But in your diaphragm it is 50% fast and 50% slow. And that’s the only muscle in the body that has a specific distribution.

You can ask yourself, why is that? Is that kind of an evolutionary kind of point of view? -Because you can imagine that endurance, of course, makes sense because you have to endure your ventilation. And for my evolutionary biological perspective, ventilation is upmost importance because ventilation goes for oxygenation, oxygenation of the brain. So there’s kind of a veto in regard to everything else. Also is that the thresholds of fast twitch fibers is kind of weird. I think when you’re instantly provoking a muscle, giving them instant activation of always first gets you into the fast twitch fibers, and then you can recruit with the rest of the fibers.

And you have if you have a lot of demand, then every single fiber will be recruited- slow or fast. But then comes the kicker somehow, going back to how ventilation goes is that this veto of perfusion of the muscle of the diaphragm is of the utmost importance of the body. So if there is anything that needs more perfusion than everything else will be facial constricted, even the legs so you can have a relative facial constriction or relative hypoxia in the legs from the skeletal muscles.

If there’s a high demand of the diaphragm, which it cannot deliver. So if you have a patient being sedated or being intubated, and it has to have a very high rate of ventilation, so there is from a brain perspective, a high need of oxygenation. So that muscle diaphragm will be working as hard as it can get. It will be kind of working like you normally do with exercises. Then the body will shift and the body will shift and making sure that the perfusion of that muscle was always there. And then it can give a shift in your Vo2 to over to 125%. So your all your perfusion of the of the of blood goes to the diaphragm instead of the rest of your system.

And in that specific framework, looking at fast and slow, you can see that even if you are…. there’s a big study done in with Divine, where they show the brains in patients who’s organs were being harvested, that they saw that the muscle biopsies in different parts of the diaphragm. They saw, even within four hours of mechanical ventilation, you already saw remodeling of your fast twitch muscle fibers in your diaphragm- when you’re just having a healthy guy who had an accident, died, he was brain dead and being harvested. Another guy who was already in ICU and had some other comorbidities that is even when you’re just young and healthy.

So there was an instant change in remodeling of the diaphragm not only looking at the less thickness, of course, it also happens you can have less thickness, but I think it’s more important that the quality of the diaphragm in regard to muscle distribution, muscle fiber distribution, and just the ability to to give power decreases significantly within hours after intubation. So yeah.

Kali Dayton 9:10
Then how does that impact their outcomes? You know, when I don’t think I don’t think at the bedside, that we really focus on the diaphragm, even nurses, respiratory therapists, it’s just not a huge part of our discussion like it is perfusing the kidneys and things like that. So why is the diaphragm so important in their outcomes? How does it impact being able to extubate, decreased reintubation rates, like what’s the big deal?

Jeroen Molinger 9:37
I think again, it makes sense that your inability to contract the diaphragm and that is measured. We can of course assess diaphragmatic function with the use of ultrasound. Ultrasound assessment, you can do very well you can measuring the inspiration, expiration. You can see the resting thickness versus the thickness doing the end of the inspiration, and that there’s a kind of a diaphragmatic thickening index. We know you should have around….. there’s a lot of studies done that show that if you have a lower than 40% thickening index- so you have an inability to thicken your muscle less than 40%- then you have diaphragmatic dysfunction. And then you have a high chance of having a being able to wean off the vent.

So if you’re going to do a breathing trial whatsoever, you will see there will be there will be issues afterwards. So you have to be intubated to work. And there’s so far more that we don’t know that potentially has influence on the diaphragm itself, just looking at pleural effusion. So imagine that you have a muscle that’s really laying in effusion. It’s is just soaking itself. It will be changing the connective tissue inside the pleural layer. So the virtual and visceral pleura will also change in morphology in how it thickens. If you have a pleural effusion on one side, and then the side is on the other side, then you have a double problem. And you have high pressure in a lower part of the abdominal part, abdominal region in KFD. And then also in the thoracic cavity. So you have a hyperfusion from lung, hypoperfusion from your abdominal cavity. So there is a high kind of a high pressure system over there where a muscle still needs to contract to move around.

Kali Dayton 11:21
Right. And if it doesn’t, it’s going to weaken even more.

Jeroen Molinger 11:25
And also have an inability to contract because you have a high pressure area in a cavity. So it should, there’s only contracting as also moving downwards and upwards. So there’s also a movement involved. And that movement only be done if there is a sliding possibility of the diaphragm coming around. And again, this is new research we’re doing right now. We see there’s a lot of issues with patients, potentially that you have a fast remodeling of the muscle, when there’s lots of effusion looking at ARDS patients, and of course, we saw a lot of our COVID patients have a huge amount of effusion, at the upper part of the diaphragm, which would potentially have huge effects on an diaphragmatic function.

What I would like to havem is if you want to do a breathing trial, combine that with assessments of diaphragmatic function, can you routinely somehow see- does that diaphragm really take over? So if you have less assistance in your breathing? Do you see that the diaphragm will thicken better and will move around better without being being assisted? If that’s not the case, I think then you already have a discussion because you can see that the body is unable to to ventilate, to function.

Kali Dayton 12:41
…independently breathe. And I think with the breathing trials, I think there’s there’s a lot going so that you have heavily sedated a patient for a while, when you wean off that sedation, they’re likely to be hypoactive delirium. That obviously impacts their ability to ventilate. But I don’t think the diaphragm ever comes up in those discussions. And I think… some of our ICUs end up taking most patients that are on the ventilator for more than a week. And it’s just assumed…it’s par for the course you… if you get intubated… if you’re certain level of acuity, you’re gonna be “trach’d, peg’d and sent to LTACH.”

But I think the assumption is that because it’s because they’re “so sick”, or because their “lungs are so sick”. But this makes me wonder- how much of it is because the diaphragm is impaired? Because the ventilator settings can be fairly low by the time that they’re trach’d. They have to be to be able to be trach’d. And so if they had functional diaphragms, could they prevent tracheostomies? In the “Awake and Walking ICU”, I can think of maybe five to seven patients that I’ve ever seen throughout the multiple years I’ve worked there- cases in which we’ve had to give people tracheostomies- and they’re very unique cases like muscular dystrophy, and very specific to that. Never because of ARDS or very high acuity, respiratory failure. And so what role do you surmise, does early mobility or walking on the ventilator play in preserving those muscles?

Jeroen Molinger 14:15
I think I think is vital, just from a biomechanical point of view. Again, it’s kind of where but nobody really thinks about biomechanics in the ICU. And it’s kind of weird, because there is literally biomechanical movement going around. So if you just look at the facial layers, so it’s looking at the facial fibers of the diaphragm, and if you follow it up from the whole dome, kind of form shape it has goes down the way it really goes down all the way to your upper leg to your facia- to your muscle to your psoas us muscle.

So even the psoas muscle itself is connected by connective tissue with facia to your diaphragm. So your position and your angulation of your hip can have significant effects on your diaphragm itself. So what we are we did was it’s kind of some kind of preliminary data set. But imagine- I think this kind of my introduction, where I think it’s so important to, to walk with a vent, is that if you have a patient who has has an inability to thicken the diaphragm. What we did was, if you put someone vented on their side, and you’re looking at his right side, there have an issue with thickening of the muscle.

If you’re putting a hip more to extension, you literally giving more more…. literally stretch out the fiber. So there’s more to the fiber length, and the ability to give power for the diaphragm was changed significantly. So it will be easier for a diaphragm to thicken, because it cannot take and in a very loose way, it has to have some kind of tension. So if you pre-tension the diaphragm already, then it has the ability to thicken far more clearly. And that’s be done if you’re laying down. But if you don’t just walk when you have extension of your hip, then you have your specific biomechanical strain on those muscle fibers and those facia and that tissue, then you have a far better function of your diaphragm, because you’re literally using it in a functional way in a functional biomechanical way, how it should be.

Kali Dayton 16:29
And that makes so much sense because that was my question throughout this process is- the ventilator is almost doing the work for the diaphragm…

Jeroen Molinger 16:39
Yeah,

Kali Dayton 16:39
So why do patients in the “Awake and Walking ICU” have so much stronger diaphragmatic function, if they’re on the ventilator just as much as any other patient. …. but walking ignites the, the diaphragm and preserves its function mass. And all the connections!

Jeroen Molinger 17:01
There’s a lot stuff done right now. I don’t know which group is the worst, but you have potentially also to simulate the abdominal muscles, which also give them more pretension to the diaphragm, which also helps you and during this breathing trial and have a less, again, it’s all about intraorgan crosstalk with muscles and how they somehow correlate to each other from a metabolic perspective, but also for biomechanical facia perspective.

There was a study done I know, again, I think it was in Florida because they knew, even if you’re not in the ICU, but during doing surgery. They saw that also doing surgery and you have a long term thoracic if you had to ask surgery, when you have a very long time, are you being sedated and being being ventilated, that also people have huge issues with their with their diaphragmatic function afterwards.

So by donating a very small group was they did a control group and a basic group. So the patient was on the table. And they they inserted electrodes bases on the diaphragm with a very small kind of pacing. So it is I think, two or three contractions a minute, just slow pacing of that muscle diaphragm during the surgery on one side, and the other side, they didn’t do anything. And they compared afterwards. And you’re they saw that the the nonpacing side already showed remodeling, and the pacing side showed no remodeling at all.

So you are able, if you just somehow stimulate that muscle, and again, it doesn’t have to be kind of same. What I bet I said before in our first podcast is just, you always have the issue with recovery. So you have to make sure that your architecture of the muscle stays stays good, it doesn’t change. So you’re gonna have the tissue, the rigidness of the muscle has to stay there. If it changes over time based on a fusion or just being sedated and reducing it, then you have significant issues, just basing it somehow. And one of the stuff potentially be not through a invasive way of putting electrodes on the diaphragm, which I think people still do. There’s a potential and also basic diaphragm directly, potentially. But if you’re just doing it from the abdominal muscle itself, it’s the same way doesn’t have to have a very aggressive contraction. It just has to move. It just has to move.

Kali Dayton 19:24
Maybe that’s why even the studies showing that dangling at the bedside or sitting in a chair….

Jeroen Molinger 19:31
Exactly.

Kali Dayton 19:31
Vastly improve outcomes. Of course walking is always going to be better but even that alone, we don’t think about the abdominal muscles either, or the intercostal muscles or….

Jeroen Molinger 19:40
again, when you when you see people walk, of course, they’re not running on the ICU with the vent, it’s all very slow pace and that’s fine. Even a slow pace always give rise to the specific recruitment of those abdominal muscles and also in giving rise to prominence of the diaphragm. Yeah,

Kali Dayton 19:56
So in your ideal world, how would we structure this as far as protocolize,preserving the muscles from the moment a patient has been intubated or admitted to the ICU? Let’s say admitted to the ICU because I have concerns about high flow nasal cannula maintenance, and lots of things. We talk a lot about ventilation on a ventilator. But I think this applies to any patient in the hospital period. In your dream world with all the resources, all the technology available, how would we improve mortality through this?

Jeroen Molinger 20:29
Good question, I think some of the stuff that we’re working on here at Duke, with both Dr. Paul Wischmeyer and I trying to see if we can put off a formal clinical metabolic nutritional service. Of course, in the ICU, but also outside the ICU, even on the floor. Also following our patients being discharged from the ICU, because that’s the biggest issue we come to and are still having. And then I have also referred therapists, physical therapists, extra physiologist, and dietitians, being involved in the kind of specific task force, who are able to do hands-on, those specific assessments on a day by day basis.

Even have, and that’s what we were trying to get into a specific rounding for that task force all over the of the hospital to have specific tailoring needs for nutritional and exercise on those patients. And I think it’s not that far away, because of course, it takes a little bit time to do so. But you have patients who you can have very small, because they’re doing fine, you have patients that has had any more assessments done.

So you can do the muscle style assessment, for instance, where you can drive muscle size, but there’s more muscle quality can easily be done early in the morning. There’s a specific team going around, it takes you two to five minutes for for for just the muscle ultrasoun done for. It may be interesting to, to mention, I think I mentioned that before. Currently, we’re seeing that there is a specific change in other muscle groups that are of interest. Not only the the most straightforward ones are of course the ones that the diaphragm, but also of course, the leg. But right now we’re looking at different muscles as potential looking at the swallow muscle, so your tongue muscle.

So sort of dysfunctional, we’re seeing also after getting ventilation is a very significant proportion of the people we’re seeing that I think within that group, you have two people those are that we’re having direct issues with the ventilator tube, and that’s they reason why they got sort of this dyfunction of the muscle of the tongue. And potentially, that’s the people we’re looking into is that I think there were already people being prone for swallow dysfunction because most of the tongue itself are very specific in regard to their histology. And the whole muscles in the head have a specific in histology. Not only this part of the tongue, but also your temporalis muscle.

We know already, I think in the dietitian world, we have temporal wasting. So if you’re looking at patient, you see very significant wasting of the temporal region so you have a more concave kind of a skull. But that only talks about the size. And what we saw was that the muscle in the head itself are far more sensitive, and overall changes than the muscle of the leg. So we see that the brows muscle change over time rapidly, than we see the leg does. And now I’m trying to figure out how this is the correlation between the temporalis muscle, the muscle of the tongue, and the muscle of the leg and then potentially at diaphragm move in the intercostal muscle.

But I think the when I started off with the systemic mitochondrial dysfunction, where the muscle is one of the kind of a cool proxy to measure it is also very real in regardless to swallow dysfunction. So you’re going to have people who in the ICU who are, maybe, for my direct functional perspective, not had a swallow dysfunction yet, but the muscle itself is already prone to be dysfunctional if there is a high metabolic or high oxidative stress moment, Which of course happens when you have intubation. And when you have ARDS, or or sepsis, or COVID.

Kali Dayton 24:15
…and does that apply as well to patients on a high flow nasal cannula?

Jeroen Molinger 24:19
Yes, absolutely.

Kali Dayton 24:19
… Still having a high hypermetabolic state likely and high respiratory rate work of breathing. I put a little survey because I one of my concerns with high flow nasal cannula is of course swallowing. Yeah, a lot of patients are not safe to swallow. But as I did, I worked in telemedicine and I noticed that a lot of… almost every patient on high flow nasal cannula was still eating without even a swallow evaluation from speech pathology. And so that concerned me. Are we not thinking about slowing that they look like they can swallow, then they are swallowing well. I don’t think that’s true.

And then I asked the followers on instagram, kind of what they what they’ve been doing and they said that as far as enteral feeds that high flow nasal cannula only…41% of responders said that they give their patients of high level cannula and enteral feeds 0 to 30% of the time. And then only 19% said that 80-100% of the time do they give their patients a high flow nasal cannula, enteral feeds, which was really shocking to me.

I’m thinking of these COVID patients that are on high flow nasal cannula for sometimes weeks.

Jeroen Molinger 25:34
Yeah.

Kali Dayton 25:35
So if we have these units that are not allowing their patients to get out of bed if they’re on high flow nasal cannula, and then we are not feeding them, you know, they they’ve got their tray in front of them, they’re taking a few bites, “they’re probably getting enough, they’re fine. They’re not moving anyways”…

Jeroen Molinger 25:48
oh, that’s definitely a huge group who has a very high risk of malnourishment. And that’s only the acute phase, imagine what they’re going to have, or going to get, for my mobility point of view when it can home. Because there is so much stuff we just don’t know. And even you can you can we can assess those patients the same also with a medical cart, right? Yeah, it needs more kind of specific terminology. But we can even do or use patients with a…. let’s put it this way. We can use metabolic carts, even with a mask, which I mean a high Fv02. We can do also assessments for patients with the metabolic cart with a with supplemental oxygen, so being able to drive their metabolic needs.

Kali Dayton 26:35
How would that impact the intubation rights? If patients were being nourished and preserved their diaphragmatic function? Would we prevent intubations, if they weren’t deconditioning to the point of not being able to keep up with the pulmonary fibrotic process?

Jeroen Molinger 26:50
Yeah, because if those functions are optimized and increased, and also your ability to operate will be higher. So in the end, though, definitely, again, I think it’s not science yet, because it’s a very hard thing to some companies will make sense that there’ll be those people who will be less at risk of getting intubated. Yep.

Kali Dayton 27:14
And I’m sure dietitians are aware of this. And I asked the listeners, if dietitians….

Jeroen Molinger 27:21
It’s a big struggle for them. Right now. I’m not a magician itself. But I’m also my my kind of funny slogan is, “I think nutrition is still sexy”-, because nutrition is not supposed to be sexy somehow. Nutrition, from my point of view, how we are seeing it, it is a very complex science. It’s not just giving people a amount of of food, you have to have more in depth knowledge about physiology and about metabolic carts and about potential imaging stuff.

So that’s right, and also the dietitians I work with here in Duke, everyone needs to be trained that way. So we have the new dietitian running in right now will be completely different than than those who were running in ICUs before, because they have the possibility to have more knowledge about this space, and also have the ability to use these devices, new use this technology. But of which my assessment, I think it’s a kind of a kind of a cool kind of citation. He says that “The ultrasound probe should be kind of the stethoscope of the of the dietitians”- that’s their way of assessing patients. And I think that makes sense. And, of course, making also the case that the dietitians and physical therapist, those have to be a team. So they have to work together.

Kali Dayton 28:38
And like salivating just thinking of this kind of process. How different would that be? And I think if teams, it sounds like a lot of teams don’t have dietitians as part of their rounds. And sometimes I think it happens, like you say, “what feeds do you want? What’s the rate? Okay, great.” And that’s it. But if they were really integrated in the discussion, how could How much could they impact our outcomes?

Jeroen Molinger 29:01
No, absolutely.

Kali Dayton 29:02
Yeah, I think it comes down to our culture, our priorities, again, the mindset.

Jeroen Molinger 29:05
Absolutely. I think the more I’m seeing over here, technology wise, and device wise and all the stuff that’s not that’s, of course, hard, but that’s not the hardest. The hardest is just changing mindsets and changing paradigms. And I think we have we have a good start here. I do. I think we have a cool team. We are very passionate people over here. We’re willing to go all the way and I think we are hopefully getting there. We’re again, my dream will be and eventually we will get there. I’m pretty convinced about it. Yeah.

Kali Dayton 29:06
Okay, I’m going to take it back to one little question. Someone asked about how to manage stress induced hyperglycemia. And I saw an article just now that that one week of bed rest leads to substantial muscle atrophy and induces whole body insulin resistance and the absence of skeletal muscle lipid accumulation. And in this study, it was healthy young males. Again, not critically ill, but they were just in bed for a week and they had About a 1.4 kilogram lean muscle loss after one week, and you touched on this throughout the other episodes. So would our hyperglycemia rates be improved if we didn’t have such severe muscle loss, in addition to the high propofol use?

Jeroen Molinger 30:15
Exactly? Yeah, I think I think we’re kind of running in a circle right now. Because right now we one of the ones is using the resistance another way, trying to get rid of it in in giving them insulin. And it is mainly muscle movement, insulin resistance, which you can which you can potentially change by alter optimizing the muscle quality itself.

So the whole glute stretch locations at the muscle, you can change, the climate change by the use of electro stimulation can be changed for mobilization even sitting up already. If it’s just any activation of the muscle that give rise. We know that the mainly the fastest fibers are muscles to be trained to be more insulin sensitive. So that’s that’s the kind of kind of the nitty gritty.

I think it’s it’s it makes sense that you have to have a very and again, that that’s one of the stuff I saying already, at the early mobilization starts off upon admission. And then of course, define earlier, I think any mobilization has to start upon admission. Because that makes sense. There is no way we should stop it. There is any mobilization that can even be passive motivation whatsoever, but there has to be done. Because there could be no discussion that you’re saying right now. We cannot do it.

Kali Dayton 31:33
…and it can be dose dependent. With we adjust all sorts of things for patients status, capacity, function, wherever they’re at as far as medications and different treatments. Exercise can be the same thing. But it has to be something has to be right away. And in the ICU world, the big word is “rehabilitation”, which I completely appreciate. I think any patient, no matter how optimal their care outcomes, were are still going to need some rehabilitation. Yet what if we focused equally or even more so on preservation?

Jeroen Molinger 32:03
Yeah, yeah. Preservation optimization. I think we are creating already people who is who are in need of rehabilitation, because we did not a good job in the sense of good, we have a bad done a better job, if we did already before.

Kali Dayton 32:20
Absolutely. And thanks to your work, we’re hopefully going to change our culture and our practices. Anything else you would share the ICU community?

Jeroen Molinger 32:27
No, no, I think I hopeful that I can be some kind…. of a people try to see my point of view a little bit and to see what I can do on that. Also, for my nurse perspective, and a dietitian perspective, and I from a physiologist perspective, I think there has to be in far better understanding and forbidden discussion about how the organ systems all somehow interact with each other.

And also maybe kind of, advocating for myself, that I think there is also a a very significant position as an exercise physiologist resources in the ICU. It’s kind of weird, but I think it’s there. We can be helpful in regard to our specific skill set and knowledge about how those frameworks of exercise in a clinical space and even in a critical illness space can work out. And again, it’s all it’s all teamwork. No one is doing it on their own. You can only get this done if we if we work together.

Kali Dayton 33:20
Absolutely. And I think you’ve demonstrated the value that you can bring to critical care. I think you’re gonna be our go to guru. We’ll probably be circling back to you in the future with lots of questions.

Jeroen Molinger 33:29
Yes, sure. Sure.

Kali Dayton 33:31
Thank you so much.

Transcribed by https://otter.ai

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