All right. Good morning, everybody. So again, Robby Kamani, Children's Hospital Los Angeles. I'm going to kick things off here with respiratory land, a topic near and dear to my heart. We're going to talk about respiratory monitoring and mechanics. No disclosures that are really relevant for this talk. So when I was trained, actually, as a resident with Jerry in Seattle Children's, actually the pulmonologist taught us this conceptual model of respiratory physiology that's related to the compartment model, this idea that the respiratory system can be controlled by the CNS. There's the extra thoracic upper airway. There are the intrathoracic components, including the lower airway and the pulmonary parenchyma. Ooh, didn't like that. It disappeared. And then there is the, there we go. And then there's the extra thoracic component, as we might think about the chest wall and the respiratory muscles. And I think that this compartment-based approach actually has a lot of relevance as we think about acute respiratory failure in the intensive care unit. So I'm going to use this concept to go through the important principles that we might think about. Do you need to do something? Or no, keep going. OK. All right, so let's start first with the upper airway or the extra thoracic upper airway. So here are the board principles that they want you to know, thinking about the extra thoracic upper airway and upper airway obstruction in particular. Understand the location of the obstruction and how that location might affect the airway dynamics, including the glottis, the supraglottic, and the subglottic structures. Sorry, you guys might be having seizures here. Understand how the type of obstruction, whether it's fixed or variable, has relevance to the type of obstruction you may see. Flow pressure dynamics for flow limitation. Changes in airway caliber with spontaneous versus positive pressure ventilation. The rationale for therapies, such as gas, viscosity, and density. And then age-related airway dynamics. And let's start with that concept of the age-related airway dynamics. So what makes the pediatric patient more subject to upper airway obstruction? Well, there are a couple important anatomic considerations, right? They have a relatively larger tongue to an adult-sized patient, based on the size of their mouth. The larynx sits in a more rostral position. And the epiglottis, importantly, has this omega shape to it, as compared to the flatter shape that we see in the adult epiglottis there on the left, compared to the pediatric one on the right. And then what we've classically learned, of course, is that the shape of the larynx is different, right? The cylinder is what the adult larynx will be like, whereas it's more of a cone shape, right, in the pediatric airway. Although there's maybe a little bit of controversy about whether this is really the case anymore. But how this becomes relevant, of course, is that the total size of the pediatric upper airway is smaller. So if you have edema that develops, the same one millimeter of edema in a pediatric airway results in significant increases in airway resistance compared to that same one millimeter of edema in an adult airway. And this, of course, is given by Pousseau's law, where the resistance within the airway, or really within any structure, is proportional to one over that radius to the fourth power under laminar conditions, under turbulent conditions, and this is one over the radius to the fifth power. Now, what becomes relevant in respiratory physiology, and especially as we think about the extra-thoracic upper airway, is this concept of a transmural pressure, right? Transmural pressure is fundamental to both respiratory and cardiac physiology. The transmural pressure is the pressure inside a system minus the pressure outside the system, and it can be applied, really, to all of the different wall structures within the respiratory system. So as we think about the extra-thoracic upper airway, and if we think about during inspiration, what happens? We take a breath in, diaphragm contracts, right? Goes down. We generate a more negative pleural pressure. That negative pleural pressure gets transmitted to a slight reduction in the alveolar pressure relative to atmospheric pressure. The pressure in our airway is slightly negative relative to atmospheric pressure, and that's how we get airflow to come in, right? So on inspiration, under normal circumstances, the pressure in the airway is slightly negative relative to atmospheric pressure, just a small amount, assuming we don't have significant airway obstruction. What about exhalation? Reversed, right? Diaphragm relaxes, less negative pleural pressure, slightly positive alveolar pressure, slightly positive pressure in the extra-thoracic airway relative to atmospheric pressure, right? So then what happens in a circumstance where we have upper airway obstruction? So here's an example of a patient, for example, with croup. You have obstruction here in the upper airway. What is the patient gonna do to try to overcome that obstruction, right? Well, they're gonna have to generate more pressure to try to get that same airflow to come in, right? So they generate a more negative pleural pressure. The alveolar pressure also becomes more negative, and the pressure in the airway at this point distal to the obstruction can become very negative, right? So if I think about the transmural pressure, it might be minus 25 in this portion here of the extra-thoracic airway relative to the atmospheric pressure on the outside of zero and we get dynamic collapse during inspiration, right? And this is why if you look at the sort of classic finding of extra-thoracic airway obstruction from a lesion like croup, let's say, or even a superglottic location, something like obstructive sleep apnea, compared to more of a fixed airway obstruction like we might see with subglottic stenosis, the predominant pathology is on inspiration. So here's a classic flow volume loop, inspiration down below, exhalation down above, and you see this flattening of the inspiratory portion here where there's no augmentation in flow, right? With the relatively normal expiratory portion of the loop where you go up to a peak flow and there's a passive exhalation here. This is in contrast to a fixed type of obstruction that you might see, for example, with subglottic stenosis, where you have the disease both on inspiration and exhalation with flow limitation. Now you can diagnose flow limitation with a flow volume loop, but in fact, a better way to diagnose it would be if you had a flow pressure loop, where the pressure reflects the pressure that the patient is trying to pull, i.e. the negative pressure they're pulling, an estimate of their pleural pressure. And here you can use something like esophageal manometry to estimate their pleural pressure and couple it with flow. And this is a classic example of an extra thoracic upper airway obstruction. Flow is on this axis, pressure is on this axis. The patient tries to take their breath in, they achieve a certain flow and they cannot augment their flow anymore, i.e. flow is not going up despite continued effort. So there's this flattening of the inspiratory portion of the flow pressure loop. Now this circumstance, this is an example of an extra thoracic superglottic obstruction. How do I know that? Because when we do an airway maneuver, a jaw thrust, a chin lift, it goes away. So if you're able to manipulate this with an airway maneuver, by definition, the obstruction is in the superglottic space because you can change it. You let go of the airway maneuver and now that flow limitation comes back. All right, so there's your upper airway obstruction model. This is the Cliff Notes version of the course. There's a lot more to it, but these are the most important concepts, I think. So let's move into the interthoracic space and lower airways, okay? Board principles of lower airways, understand airway and lung tissue resistance to airflow, airway resistance and the effect of the pressure-volume relationship in the lung, understand lung volumes in both health and disease, flow-volume relationships during tidal breathing and forced exhalation, and gas flow limitation and its applicability to PFT. So I'll cover some of these concepts. So why is it, right, that we see younger patients or patients less than three that have problems with significant lower airway obstruction? Well, it has to do with anatomical considerations of the central versus the peripheral airways, right? So what this graph is showing is conductance. Physiology, we like to use the same word in opposite ways. So conductance, remember, is one over the resistance, right? So what we see is the peripheral airways and then the central airways. So there's not a significant relationship of the central airways as a function of age of resistance, right, the resistance is relatively constant as a function of age. But we see this marked change in peripheral airway resistance that will drop or the conductance will increase as patients get older, right, in particular once they get over the ages of four or five. And if we look at animal models of this, what's the rationale for it? The rationale for this is the growth of the airways, not in terms of the caliber or size of the airways, but we develop more peripheral airways, right, in parallel as patients get older. So if we look at the infant model compared to the adult model, there are many more of these peripheral airways in parallel that have a net effect of dropping that total airway resistance. And so this is why our youngest pediatric patients, you know, for example, are more prone to lower airway obstruction from conditions like bronchiolitis, you know, as an example. But as we go back to the concept of transmural pressures, we're talking about the upper airway, right? This was the extra thoracic upper airway. Now I wanna go into the chest and think about the lower airways. And when we think about lower airway obstruction, the transmural pressure becomes highly relevant more during exhalation as compared to during inspiration with the extra thoracic upper airway. So again, think about the transmural pressure in the intrathoracic airways now during exhalation. So again, I take my breath out, right? Take my breath out, pleural pressure becomes slightly less negative. Alveolar pressure, slightly positive. Pressure in these lower airways, slightly positive relative to what's the pressure outside? It's the pleural pressure, right? So the pressure inside is my alveolar pressure, my airway pressure, the pressure outside is the pleural pressure. So the relative difference of pressures here that are important in the intrathoracic space, right? Inside alveolar pressure or airway pressure, outside pleural pressure or a surrogate of intrathoracic pressure, okay, is the way you can think about that. So under normal exhalation, it's slightly positive. So then what happens when I develop a lower airway obstruction, right? What's happening with lower airway obstruction? So lower airway obstruction, most classically think about a condition like bronchiolitis, think about a condition like asthma, right? The area of obstruction here is in the distal, small or medium-sized airways. And it's characterized by the patient by air trapping, right, it's hard for that air to get out. What does the patient do as a consequence of that if they can't get that air out, right? They generate a very positive pleural pressure and have forced exhalation, right? So the pleural pressure now is much more positive. Your pleural pressure is positive. So then what's happening at this point, proximal, so to speak, of the obstruction, right? Just before this obstruction. Now my airway pressure here is slightly positive still at plus two, but the pleural pressure or the interthoracic pressure is much, much higher, right? So then I can have dynamic collapse on exhalation that you see with lower airway obstruction compared to the extra thoracic upper airway where we have dynamic collapse on inspiration. Okay, now what has to happen, right, for this to occur is that you have to have this point of obstruction, right? Because we can generate a very positive pleural pressure when we exercise, but we don't have airway obstruction that occurs, why? Because as I generate that very positive pressure during exercise, right, a large pleural pressure, if there's no restriction to the airflow, right, then that pressure is also gonna stay positive within the airways, right? And there's no gradient. There's no transmural pressure gradient, so to speak. But if I've got this equal pressure point or this point of obstruction, right, then at this point here, the pressure is much lower than the point across the outside and you get more of that dynamic collapse. So this is why, for example, when they do pulmonary function testing, right, you do a forced maneuver. You have a maximal effort maneuver because you may not detect subtle amounts of airway obstruction under tidal breathing conditions. It's only when you generate that very high pressure in the interthoracic space that you might be able to see that that patient, in fact, has an area of obstruction, which is why PFTs do forced expiratory maneuvers. On spirometry, what do we see? Well, the classic finding for expiratory disease, right, here we look at exhalation up above. This is a spontaneously breathing patient. Inspiration down below, expiration or exhalation up above. And what we see is a few important findings. First, this flow is less than what we would see normally, i.e. what's this flow? This is the peak flow, right? So we see a reduction in their peak expiratory flow. And then the most classic finding here is that there is the scooped out appearance of the expiratory portion of the flow volume loop with a long amount of time for it to return to normal. Now, this is a patient with asthma. They get a bronchodilator. What do we see? We see improvement both in tidal volume on inspiration, but a reduction of that scooped out pattern that we see in the expiratory portion of the flow volume loop, as well as an improvement in the peak flow, although it might not get back to what we would see under normal conditions if the patient did not have evidence of lower airway obstruction. Important relevant concept as we think about lower airway obstruction is the time constant, right? So what is the time constant? The time constant is the resistance times the compliance, okay, so anything that is gonna increase your resistance is gonna increase the time constant. Anything that conceptually is gonna decrease the compliance, right, is gonna decrease the time constant. The time constant is the amount of time it takes that alveolar airway unit to fill, right, to 2 3rds of its capacity or to empty. So classically, we think of somewhere between three and five time constants as what is required to fill the alveoli to its normal capacity. So that concept becomes relevant as we now need to manage our patients with lower airway obstruction when they're on the mechanical ventilator, right? And so if we take an example of a patient we just maybe just have intubated with asthma or even severe bronchiolitis, right, that is under neuromuscular blockade. Most important, one of the most important concepts is that we allow enough time, right, for exhalation because that patient is now passive. If they were allowed to still be active, they could augment, right, with forced exhalation. Now they're passive, so they're dependent upon the mechanics of the lung or the alveoli and the airway together. So one of the most important concepts, of course, is as we look at this flow versus time loop that we provide them with enough time for exhalation, i.e. flow returns back to baseline before the next breath is started. If not, then we have the situation of auto-PEEP and air trapping, right? So more and more and more of that air gets trapped in that alveoli and they get significant dynamic hyperinflation. Now that's the important concept when the patient is under neuromuscular blockade. What about a patient that's spontaneously breathing, right? Well, what do we often do to the asthmatic patient that's spontaneously breathing? We put them on CPAP, right, or we put them on BiPAP. How's that working, right? How is that helping? Well, conceptually, this comes back to this idea of matching their intrinsic PEEP, right? So this patient is air trapped here, has high amount of pressure in the alveoli at end expiration, right? So if we think about what that patient needs to trigger a breath when they're breathing spontaneously, right, they have to lower their alveolar pressure substantially, right, to generate airflow. So from 15, they have to go to, they have to pull 16 centimeters of water, right, to have an alveolar pressure less than atmospheric pressure. If I apply CPAP to that patient and I match their alveolar, their airway pressure here with their alveolar pressure and I stay below their intrinsic PEEP, now they simply have to pull this just a small amount. If they make this 14, right, now they'll get airflow to come. So the use of EPAP or CPAP, right, with a patient with lower airway obstruction is to match their intrinsic PEEP and help them get that breath in. That's the main concept that you're trying to get at there. Okay, so I got the three-minute warning, so I gotta go faster. So let's go to, don't I get more time? We started early, right? So now we go to the pulmonary parenchymal disease, right, the restrictive physiology. And here, the concept, this is a curve that you should all have ingrained in your memory, right? This is the relationship between an expiratory lung volume, which is what you see on the x-axis, and pulmonary compliance, which is what's in black on the y-axis, or pulmonary vascular resistance. And you see the magic point, right, at FRC. At functional residual capacity, pulmonary compliance is best, pulmonary vascular resistance is lowest, and so an optimal FRC is our target, right? Like all other components we were talking about, right, this is, even as we think about the pulmonary parenchyma, it's about differences in transmural pressure, right? So there are three important transmural pressures that are relevant. One is the pressure across the respiratory system, where the pressure inside is the alveolar pressure, the pressure on the outside is atmospheric pressure. But that's composed of two components, right? The pressure across the chest wall, which is the difference between the pleural pressure and the atmospheric pressure, and the transpulmonary pressure, right, which is the difference between the alveolar pressure and the pleural pressure. And in fact, this transpulmonary pressure is the pressure that we probably should be most concerned about, especially as we think about the risk of lung injury that may occur. Any, like any system, according to Boyle's law, right, as we increase the transmural pressure across it, right, that's how we can increase the volume. The pressure times volume in one system is equal to the pressure times volume in another system. So we think about what happens with patients with parenchymal disease, right? They have worsening pulmonary compliance, right? How does that manifest? That manifests with a higher pressure that is necessary to generate a tidal, a given volume, right? So we see the slope of this pressure-volume curve shifted down and to the right, right? Now, when we have a disease condition that's heterogeneous like ARDS, we in fact, if we do the total lung inflation from the very low lung volume to total lung capacity, we may see these inflection points that develop in that pressure-volume curve. Where the compliance is poor, we get above some certain point, the compliance increases. We go above another point and the compliance starts to decrease again, right? So this is conceptually the point of low lung volume here where we wanna apply enough PEEP, right? To stay above that lower inflection point. And this is the upper inflection point where we wanna limit tidal volume or inspiratory pressure, right, to avoid overdistension that may occur. And under normal circumstances, right? The relationship between the closing volume of the alveoli, right, and functional residual capacity is such that the closing volume lies between FRC and residual volume. That is, the alveoli will not close if you're living at normal functional residual capacity, right? But unfortunately, there's an age dependence to this, right? And so as we think about the relationship between FRC minus the closing volume of an alveoli, right? At our 20s, when we were all in our best, right? We had this optimal difference between FRC and the closing volume. But as we get older, or in fact, as we get younger, right? Now there might even be points at which the closing volume is higher than the functional residual capacity. What does that mean? So we think about our babies. Many of them may have closed alveoli even where they are breathing with their tidal breath at functional residual capacity, which is why babies grunt, right? To try to maintain that end-expiratory lung volume. Okay. The other important concept briefly that I'll get to is this idea of work of breathing, right? And work of breathing functionally can be computed as you think about the pressure volume curve. It's the shape of this curve, and it's the area under this, within this sort of football shape that helps determine the work of breathing. So if I've got a poorly compliant lung, what happens? This poorly compliant lung now has to pull more pressure, right, to achieve the same tidal volume. This area has now increased. If I've got increased airway resistance, you have this expiratory component that also starts to happen, where the patient has to generate expiratory work, and you see that the pressure, in fact, becomes less negative. The pleural pressure becomes less negative on exhalation. And again, the area under that curve gets increased with flow-resistive or expiratory work. The other important concept to differentiate lower airway-based work and parenchymal work is the difference between static versus dynamic conditions, right? So under static conditions, that's what's giving me a reflection of what the lung is seeing, i.e., the alveolar pressure. Static compliance is calculated as our tidal volume divided by our driving pressure, where the driving pressure is the plateau pressure minus the PEEP. So this is what the lung is seeing, okay? Not truly the lung. This is the respiratory system because the chest wall is still considered in the driving pressure calculations. As compared to dynamic conditions, right, which includes the work that has to be done for airflow. And so this is where the peak pressure is used, right? And you may see this difference between peak pressure and plateau pressure, dynamic versus static conditions, right? And where the dynamic compliance is the tidal volume over the peak divided by the peak inspiratory pressure minus the PEEP, okay? The last concept is what I was alluding to, differentiation between the total mechanics of the respiratory system versus what's happening at the alveoli and happening at the chest wall. And you think about a baby that looks like this, right? When I apply a pressure, the lung may not see all of that pressure because a lot of that is being used to dissipate what's happening at the chest wall or the abdomen. So here the transpulmonary pressure is what's relevant, where the transpulmonary pressure is the alveolar pressure on the inside minus the pleural pressure measured under static conditions, i.e. we have to do an inspiratory hold at the end of inspiration and then an expiratory hold. And if I have an example of a five-year-old girl that's very obese here and I apply this inspiratory pressure of 26 to a plateau pressure is 23. So the total driving pressure in the system is 15 centimeters of water. If I have a same patient that's skinny and I have a driving pressure of 15 centimeters of water, are the lungs seeing the same thing? No, because some of that pressure that we apply to the respiratory system is dissipated to move the chest wall out of the way. And in fact, you can see that here on an esophageal catheter where you see this positive deflection in this girl who's passive, where about four centimeters of water of the pressure that we applied at the airway actually is being used to move the chest wall out of the way so that net total transpulmonary pressure for this obese child is much less than what it would be with a skinny child when given the same driving pressure. So the driving pressure alone is not the only marker of lung stress. The more important marker is that transpulmonary pressure, the alveolar pressure minus the pleural pressure. Okay, and that's it. Thank you. Yeah.

respiratory monitoring

airway obstructions

pulmonary compliance

transmural pressure

respiratory physiology

lung mechanics