Hello again, as I present the second of my three presentations. This one on pulmonary waveform analysis, often called airway graphics. Terms of pulmonary waveform analysis, the vast majority of what we'll be looking at and focusing on is going to be patient ventilator dyssynchrony or asynchrony, two terms often used interchangeably. We can describe or measure many of the aspects of dyssynchrony objectively, but the truth is this is really pattern recognition. You need to know it when you see it. So this talk is largely going to be focused on examples of various abnormalities in the patient ventilator interaction. And then the last portion of the talk, I'll show you some examples of capnography, again, student recognitions. For patient ventilator dyssynchrony or asynchrony, we'll go through a series of examples so you can recognize it. Then we'll discuss why it is important to recognize, to diagnose dyssynchrony because of its clinical implications. And lastly, we'll go through various approaches to fix it. First we start off with airway scalars. These are normal scalars. On the top panel, we see airway pressure over time, middle panel flow versus time, and bottom panel tidal volume over time. When I look at airway scalars, I always start with the middle, the flow versus time, and I start with a simple basic question. Is this trace symmetric and pretty or asymmetric and ugly? If symmetric and pretty, more likely than not, there's normal patient ventilator interactions. If it's asymmetric and ugly, more likely than not, we have a problem with patient ventilator dyssynchrony. Once one assesses the flow time scalar, then we would move on to airway pressure and look at the relationship between flow and pressure. And lastly, much less helpful, is the tidal volume versus time scalar on the bottom. After assessing scalars, one then moves on to the airway loops. On the left side, we have the flow volume loop. On the right, the pressure volume loop. This is another example of normal. On the left, the flow volume loop is very symmetric, looks like an egg, the broad part of the egg on the top, the pointed part on the bottom, inspiration in yellow above the horizontal, blue exhalation below the horizontal. On the pressure volume curve, see nice upslope of the inspiratory limb in yellow. There's no evidence for either a lower or an upper inflection point. Nice hysteresis, as we say in this curve. Great examples here of normal. There are three different types of dyssynchrony. The first is trigger dyssynchrony, which may be an ineffective patient effort where the ventilator is not sensing. The patient, because the patient simply isn't providing the effort, often that can be addressed by increasing the sensitivity of the ventilator. Sometimes the issue is not the patient effort. It's actually an inappropriate setting on the ventilator, whether the trigger is set too sensitive or too insensitive. And lastly, there's double triggering, often viewed as a triggering phenomena. Many, many times, it is actually an inadequate inspiratory flow phenomena where the patient's actually trying to pull more inspiratory flow and thus double breeds despite having an adequate or appropriately set trigger. We can have flow dyssynchrony. And lastly, we can have cycle dyssynchrony, whether that be premature cycling or delayed cycling. Now we'll return to all of these entities with examples in the upcoming slides. Terms of dyssynchrony, there are various ways to quantify it, but it can be difficult, although I will show you an example in an upcoming slide. But again, the key here is pattern recognition. You must know it when you see it. In this relatively recent study of synchrony in mechanically ventilated patients, we see that synchrony occurred about 75% of the time. The 25, 27% of the time that there was dyssynchrony, the largest groupings there were trigger delay and delay in cycling off or cycling from inspiration to exhalation. Truth is the various percentages here really don't matter. The key is about 75% of the time. My experience is actually higher than that. If you have a well-trained RT staff, the presence of synchrony really does get into the 90-plus percent range. But for those patients who are dyssynchronous, you really need to look and assess the various causes of dyssynchrony, and we'll work through those one by one now so you'll be able to generate or develop the pattern recognition that I mentioned. What we see here is an example of a patient and their asynchrony index or the percent of time, percent of breaths per hour that the patient was exhibiting dyssynchrony or asynchrony. The horizontal axis is time in days for a duration of six days. We see a lot of variation throughout this time period, although it's not shown on the slide. The assumption could be that the higher asynchrony index periods were related to those parts of the day when the patient was more awake and more actively breathing, thus more likely to be dyssynchronous with the ventilator as opposed to those periods of time when she or he was sleeping. The purpose of this slide is to show that asynchrony or dyssynchrony is a dynamic process, and it really requires very careful assessment by the bedside team, our respiratory therapists, our clinicians, our clinical providers to really look for asynchrony. As I'll share with you in later slides, there are adverse effects to asynchrony, such that this entity really needs to be minimized or avoided. We'll start with a case. This is a five-month-old with chronic lung disease who's admitted with viral bronchiolitis. She's intubated shortly after admission for a pending respiratory failure, ventilated with SIMV pressure-controlled breast support mode of ventilation with a set respiratory rate of 28, peak pressure 28 sonomas of water, PEEP of 7, and a pressure support of 12. The patient's sedated with infusions of fentanyl and Procidex, and this infant experiences an acute episode of tachypnea, subcostal retractions, and agitation. Here's the graphical display of the patient's ventilator. On the bottom, airway flow over time, and on the top, airway pressure over time. I'll give you a moment to look at this before I advance to the next slide, which will be a question. This is the same graphics on the insert here, and the question is, the patient's acute clinical change in clinical status is most consistent with what? Worsening bronchospasm, pain, flow asynchrony, trigger insensitivity, or air trapping? Well, the answer here is trigger insensitivity. What we see on the bottom, flow versus time, these first three breaths are not associated with any significant change in airway pressure, such that the patient is trying to breathe, is moving flow in the system, but the ventilator is not sensing the patient's effort and thus not responding. Here in breath four, you see a start of an inspiratory breath. When the patient wants to exhale, the ventilator that's blind to the patient fires a breath on the patient's what should be a spontaneous exhalatory phase, and chaos ensued. And this is the period in which the patient's agitated, desaturated, increased in intel, CO2, et cetera. So the underlying problem here is trigger insensitivity. Now, the boards may not ask a question as straightforward as I just did. Question that may follow is that optimizing which of the following ventilator parameters would be most likely to decrease oxygen consumption in such a patient. And in this case, you would have to know that the problem was trigger insensitivity, such that one would then adjust the trigger sensitivity or choice four. By improving or adjusting or correcting the trigger sensitivity, the oxygen consumption of this patient who's greatly agitated due to patient ventilator to synchrony would decrease and thus the correct answer to the question, trigger sensitivity. Here's another example of trigger insensitivity. Here's another example of trigger. Asynchrony or dyssynchrony is shown by the arrows. The patient is trying to generate a breath. You see a deflection in inspiratory flow at each of those arrows. But in each case, there's not a corresponding change in airway pressure. So this example is a little less dramatic, a little less obvious than the one I showed previously, but represents the same entity. Here's another example of trigger desensitivity. This one, even more subtle. You see where the laser pointer is, deflection in airway flow here and here with only a very minimal change in airway pressure and no measurable change in tidal volume. Much more of a subtle example, and I've shown you that trigger desensitivity really based on the patient's inspiratory effort and agitation at the baseline situation can be reflected with either clinically significant effects of trigger desynchrony versus less obviously clinically significant effects. One general entity which is unlikely to be the case on this schematic because of the rate, but one also needs to consider when you see deflections in inspiratory flow without changes in pressure, could it be cardiac oscillation, cardiac artifact? Always possible, but if that were the case in this particular slide, the patient obviously would have had a profound sinus bradycardia. When looking at airway graphics, most of the clinically pertinent findings are the airway flow and airway pressure scalers. Tidal volume over time is less helpful, although in this case it shows a significant air leak. And one of the teaching points is if you ever see a perfectly vertical, as you see here, or perfectly horizontal line, one has to think about artifact because the airway graphics packages are always going to connect the dots. So in this case, the end of exhalation has occurred and the ventilator doesn't see the last portion of breath. And at the start of the inspiration of the following breath, the line comes back to zero and the straight vertical line indicates the air leak. And one can measure the air leak by the difference between this horizontal blue line and baseline. Of course, that's more easily determined looking at the digital displays of inspiratory and exhalatory tidal volumes, but from a pictorial perspective, this shows air leak. One can also see air leak on the flow volume loops on the left. Exhalation here in blue, tailing off, ending at this point, and then the red continuing to the start of the next breath. Now in this situation, we know from the scalers that this is in fact air leak. If looking at just the loops, this tailing off of exhalation could in fact be profound increased airways resistance, small airways disease, such that flow is being exhaled at such a slow rate that the sensor is not noting it and correlating it or showing it as an air leak as opposed to the slower rate that is being exhaled. Thus, sometimes it's a little difficult on the leaks to determine the difference between an air leak and profound increased airways resistance. But the answer to that is most often seen on the airway scalers, and I'll show you some examples later in this presentation. The other extreme of trigger insensitivity is a trigger that's too sensitive, also known as auto triggering, where the ventilator is triggering itself. Sometimes it's hard to determine whether this is auto triggering or patient being perfectly synchronous. Some of the clues here that this in fact is auto triggering, it's again, we see this perfectly vertical yellow line showing an air leak. And when you see here on the flow versus scaler trace that each breath occurs exactly as expiratory flow hits zero in the face or at the same time of a major air leak, significant air leak, one speculates that in fact the ventilator is triggering itself, known as auto triggering. Auto triggering may occur in the absence of an air leak as shown here. How can one tell whether this is in fact auto triggering or not? One of the ways to determine this would be to change the trigger sensitivity and make the ventilator a little less sensitive. Although it's not an ideal thing or approach for patients is to, quote, lock them out. For just a few breaths, if you increase the trigger sensitivity, you can then tell whether the patient is spontaneously breathing or not. Others take the patient off the ventilator and look at the patient's respiratory rate to get a sense of what the patient's breathing without the ventilator. Of course, that creates a ventilator disconnect and the risk for loss of lung volume. So rather just titrate the trigger sensitivity to try to get a sense of whether or not the ventilator is auto triggering or in fact it is a patient who is being tachypneic and just so happens to be starting an inspiratory effort exactly at the time that the prior exhalation has concluded. The other way to help determine auto triggering is if you have an esophageal catheter in looking at diaphragmatic activity. You can see whether or not there is a diaphragmatic contraction at the point of inspiration. And in this case, there's not. Again, suggestive auto triggering where we see a change in flow in the circuit without diaphragmatic activity. Now let's move on to a second case. This case you'll see is essentially the exact same scenario. I kept it simple by duplicating the scenario. But of course, I'm going to show on the next slide a different tracing and then ask you similarly the question of what is causing the patient ventilator to synchrony. So here are your airway scalers, flow versus time on the bottom. Airway pressure versus time on the top. I'll give you a moment to look at this and to think through what is occurring. Of course, the arrows are drawing your attention to an abnormality, asking whether this is a pretty symmetric or an ugly asymmetric trace. It is symmetric. Each of those breaths are the same. But there's that ugly jaggedness at the top of inspiration that one needs to consider and further assess and address. So the question associated with this tracing is that the patient's acute clinical change is most consistent with an increase in airways resistance, inadequate tidal volume, flow dyssynchrony, agitation, or airway trapping. And the answer is flow dyssynchrony. Each of the arrows that I highlighted previously shows an area in which flow that should be constant. This is square wave constant flow. That should be a plateau. It's being sculpted downward. I call that the M sign, where a patient is trying to take in air. And that's because if a patient is being flow starved, to be able to generate a new breath, one has to slightly exhale to inhale again. It's a typical pattern to create that double breath, that breath stack. And that's what we're going to be looking at today. So let's take a look at that. Now, having said that, some ventilators do allow for an augmentation of inspiratory flow, even in a constant flow mode, in which case you'd see a decrease in airway resistance. And that's because the patient is trying to create a new breath. And that's what we're going to be looking at today. So let's take a look at that. Now, having said that, some ventilators do allow for an augmentation of inspiratory flow, even in a constant flow mode, in which case you'd see the second half of the hump, the second half of the M, slightly higher than the first half. I just don't have an example in my teaching files to share. But this is flow dyssynchrony. And this is what you see in square wave constant flow waveform, where a patient's inspiratory demand or the inspiratory flow a patient wants exceeds that set by the clinician. As I mentioned earlier, the differences between double triggering and flow dyssynchrony sometimes is more one of semantics. In this case, we see on the left side double triggering. The reason that it's more likely to be double triggering, as you see on the top here in the label, this is pressure control or variable decelerating waveform. So the patient can get the inspiratory flow that she or he wants. In this situation, if the patient's not flow limited and you see this double breathing, it's more likely than not a double triggering, a problem with triggering of the breath than it is flow. Whereas if you have a patient who's in square wave constant flow and you see this double breathing, this double breath on top of breath, this is more likely to be a flow dyssynchrony because the flow is capped at that square wave constant flow as determined by the clinician. A little bit of a nuance, often it's hard to distinguish the difference, but it really does depend on whether the patient's in an inspiratory flow pattern that's variable decelerating or an inspiratory flow pattern that's square wave constant. And then just another example here of double triggering, this double breath, breath on top of breath, and you see it right here in flow versus time, pressure versus time. And if you look carefully, there's this double, this sculpting, this double hump here in the diaphragmatic activity. So flow synchrony is the ideal matching of inspiratory flow of event breath to inspiratory demand during either assisted or supported ventilation. Dyssynchrony is the inadequate flow at any point during inspiration, causing an increased or irregular patient effort. It leads to increased worker breathing and quote, a patient fighting the ventilator. You can see flow dyssynchrony on the airway loops as well. On the left here, we have a pressure volume loop, and we see here an inspiration, this inward sculpting, this leftward downward deflection and pressure showing the patient trying to pull more flow or having flow dyssynchrony. We see it here in the pressure, sorry, in the flow volume loop. In this case, this is an older trace. The loop is going clockwise, but inspiration is below the horizontal. And we see here this inward sculpting, this inward deflection of flow with the patient trying to take a double breath. So you can see flow dyssynchrony on both the airway scalers as well as the airway loops. So can flow asynchrony occur in pressure control ventilation or PRVC, those modes that have variable decelerating inspiratory flow? And the answer is yes. If this were a dynamic curve, what we would see here is a figure eight. We would see a figure eight here with this great leftward sculpting of the inspiratory limb. How does inspiratory cross expiratory? This is just a pictorial display. It's the fact that the inspiratory limb is being pulled so far leftward, it has no relationship to the expiratory limb, that we see what graphically appears to be a figure eight. This is a situation that occurs when a patient is pushing the inspiratory flow limits despite variable flow. And we see this with an infant who's at the upper limits of the infant settings on the ventilator and should be placed in the pediatric setting or a patient who's on the upper limits of a pediatric setting who needs to be in an adult setting such that the ventilator will release additional inspiratory flow. Do not see it often, but you will again see that in those patients that the larger size of the windows for neonates and pediatric modalities are often in those patients with huge high inspiratory demands. Okay, let's move on to cycle dyssynchrony. So this is the failure to appropriately cycle the breath. And what we see here in exhalation, we see a prolonged expiratory phase and then a delayed or inadequate emptying of exhalation before the next breath, often known as air trapping or intrinsic peep. Stated in words, cycle dyssynchrony is the failure of airway pressure, volume, and expiratory flow to return to baseline prior to the next ventilator-assisted breath. It is related to an inadequate inspiratory to exhalation ratio, also termed premature termination of exhalation, intrinsic peep, dynamic hyperinflation, or gas trapping. All of these are synonymous terms, and it's a failure of exhalation to complete before the initiation of the next ventilator or spontaneous breath. In the situation of intrinsic peep here, often one sees increased work of breathing, often associated with an increase in mean interthoracic pressure, which may or may not be clinically significant. If clinically significant, this can lead to a decrease in cardiac output, as I'll talk about later in the cardiorespiratory interactions talk, and also could lead to decreased trigger sensitivity to make it more difficult for the ventilator to sense a patient inspiratory effort, especially if the ventilator is set to be a pressure-triggered approach. So now let's discuss why recognition of patient-ventilator dyssynchrony is important before we move on to, quote, fixing it. These are three now classic publications that show the importance of optimizing patient-ventilator synchrony. In adults, Art Slutsky, back now 30 years ago, showed that optimal patient-ventilator synchrony allows for more optimal use of nutritional support. In neonates, optimal patient-ventilator synchrony has been shown to decrease ventilator-induced lung injury. And across all patient populations, patient-ventilator synchrony improves patient comfort and reduces work of breathing. On the other side of the equation, dyssynchrony has multiple adverse effects or adverse outcomes on patients. First, ultrastructural injury to respiratory muscles can occur due to the excessive work of breathing. Dyssynchrony can worsen respiratory mechanics, as we previously discussed, by increasing intrinsic PEEP. It may alter gas exchange because of the ineffective movement of gas in and out of the lungs. It wastes respiratory work. Stated differently, it wastes the caloric intake. This is especially true of some of our smaller, weaker babies, those babies that you see that are, quote, breathing hard on the ventilator and failing to grow. Those patients are dyssynchronous or, in fact, wasting the calories given to that infant. And often, in those situations, optimizing the patient-ventilator interaction leads to steady and gradual growth. It can confound lung-protective strategies. Breath stacking can lead to incremental increases in PEEP, inspiratory pressure. The patient discomfort can lead to sleep fragmentation. Often, these patients are given excessive and presumed unnecessary sedation, which in turn leads to increased length of ventilation and potentially withdrawal syndromes. At some points, it simply confuses clinicians, which delays necessary weaning and extubation because a patient is perceived inaccurately or inappropriately to not be ready to move forward towards spontaneous respiratory breathing. More objectively, dyssynchrony has been shown to have adverse outcomes on patients. What we see here on the left in the first column is a series of patients that have an ineffective effort index greater than 10% and the right column less than 10%. And what we see is significant differences in duration of mechanical ventilation, 28-day ventilator-free days, ICU stay, as well as hospital stay, all improved in those patients that have a lower index of patient ventilator dyssynchrony, stated differently, improved outcomes in those patients that are more synchronous with the ventilator. Having said that, those improvements did not correlate to any changes in mortality. So the patient's overall mortality was the same, although how quickly they got better, how quickly they extubated, how quickly they left the ICU and hospital all improved with better patient ventilator synchrony. So patient ventilator dyssynchrony can result in an agitated patient with increased work of breathing and increased O2 consumption. Minimizing patient ventilator dyssynchrony will decrease O2 consumption and likely improve cardiorespiratory interaction. In the Papazian study of neuromuscular blockade for early ARDS management in those adults, what we see here is a speculation that the neuromuscular blockade may have improved lung protective ventilation by improving patient ventilator synchrony speculation, but it is a plausible approach to improve the outcomes in those studies that showed just that with a neuromuscular blockade. All right, now we need to discuss how to fix patient ventilator dyssynchrony and to correct the abnormalities at hand. So one option is pharmacologic sedation, it works. If you sedate a patient, that patient is more likely to become synchronous with the ventilator. However, doing so is more likely to increase length of ventilation and potentially length of ICU stay. So one should optimize patient ventilator synchrony by assessing the patient ventilator interface before administering sedation. It is shown in this early PALISI study that increased sedation use in the first 24 hours of weaning increased length of ventilation in pediatric patients with acute lung injury. Key here is hands-on prevention. The careful assessment of airway graphics and respiratory mechanics is essential. Dyssynchrony can usually be avoided by vigilant adjustments by the clinician. One should assess airway graphics and adjust ventilator settings before increasing sedation. Terms of correcting dyssynchrony, the hands-on approach, assess the patient and the patient's airway graphics. Assess for trigger dyssynchrony, assess for auto triggers, flow dyssynchrony, cycle dyssynchrony. Assess for auto trigger versus tachypnea, then assess for air leak and adjust the trigger if indicated. Assess the overall ventilator support, adjust the inspiratory flow generally increase if a patient has flow dyssynchrony, change to variable inspiratory flow if the patient is on square wave constant flow. Assess for intrinsic PEEP and adjust the inspiratory time accordingly. Consider a change to flow cycle modes of ventilation, i.e., pressure support ventilation to allow the patient to more adequately assess or adjust his or her own inspiratory times. Another approach advocated by some to optimize patient ventilator synchrony is to use the electrical activity of the diaphragm by placing an electrode as part of a nasal gastric tube down through the nose into the, sitting at the lower part of the esophagus at the level of the diaphragm. And what you then are able to do is to assess the relationship between changes in pressure over time here on the top, flow over time with diaphragmatic activity. And you can see when the patient's diaphragm is contracting not so much the diaphragm contractility but the electrical impulse leading the diaphragm to contract and the relationship of that electrical impulse to the changes in flow and subsequently pressure. One such mode that allows the clinician to adjust ventilatory support using the electrical activity of the diaphragm is NAVA, Neurally Adjusted Ventilatory Support. We see here on the left side, press sport ventilation, on the right side, NAVA. In the lower panel, we see diaphragmatic activity. On the upper panel, we see changes in pressure over time. What one will note, on the left side here using the diaphragmatic electrical impulse as a monitor only, we can see breaths that are not adequately being conveyed with changes in pressure up here in the press sport tracing. However, in NAVA, which allowing not only the diaphragm to be monitored, but to use the diaphragm to trigger the ventilator, we see improved synchrony here with NAVA. This is another example of the same finding with improved synchrony with NAVA versus in this case, pressure control ventilation, NAVA on the right, pressure control on the left. So I'll show you with some data in upcoming slides, the general take-home message here is that there are studies that have shown that NAVA does lead to improved patient-ventilator synchrony. However, there's lack of data that shows that any of these improvements seen in patient-ventilator synchrony correlates with changes or improvements in clinical outcomes, i.e. mortality or other more gross markers of outcome. And this is one of the studies that demonstrates changes in synchrony between the quote, best pressure support and NAVA. And what we'll see here is that you see a decreased or improvements in auto-triggering in effective efforts, double-triggering, late cycling and premature cycling with NAVA compared to the best pressure support. One can argue that some of those differences seem negligible and probably clinically insignificant, but if taken in composite and we look at an asynchrony index, percent of breaths that are asynchronous, we see a notably and likely clinically significant reduction in patient-ventilator asynchrony with the use of NAVA, that electrical diaphragmatic activity to trigger the ventilator, than the patient's change in flow in the system. So now you need to know it when you see it. Here, we're gonna go through a series of pattern recognitions and a series of examples to really bring home some of these important points. First, overdistension, an increase in airway pressure at the end of inspiration without a significant increase in the delivered tidal volume. It's beaking at the end of inspiration as shown here as I'm highlighting in the, with the laser pointer. So a common question, how is overdistension objectively defined? Is it objectively defined as the beaking? Of course not, because this is much more subjective than objective. But using formulas, is it the C20 or the compliance of the last 20% of the breath over C total, greater than one, less than one, a difference between dynamic and static compliance? Or a static compliance less than 0.5 ml per centimeter of water per kilo? Give you a moment to think about that. And the answer here is that if we take the compliance of the last 20% of the breath and we compare that to total compliance, we see that at that upper inflection point, compliance flattens or worsens as the lung becomes over distended, the lung at this point is changed, its compliance has changed. And thus the ratio of compliance of the last 20% of the breath, if that's less than total compliance, I'm sorry, if that over total compliance is less than one, showing a reduction in compliance after the upper inflection point is an objective marker of beaking. Stated differently, overdistension, beaking, overdistension, beaking at the end of inspiration is defined as C20, compliance of the last 20% of the breath over C total, total compliance being less than one. All right, next case. Six month old infant with chronic lung disease has been in your ICU after respiratory arrest on the wards. The infant awakens and experiences an acute episode of agitation, tachycardia, and hypercarbia per entitled CO2 monitoring. This is the airway graphics display. If we look in the middle, flow versus time, we see a trace that symmetric breath to breath, but clearly something that has ugly deflections and it's something that's not typically seen. So you know automatically that we've got some problem with patient ventilator synchrony. Give you a moment to look at this and think about it, and then we'll come to a question. So this patient's clinical change is most consistent with one, worsening bronchospasm, two, tracheal malacia, three, water in the circuit, four, mucous plugging, or five, pneumothorax. Again, a moment to consider this. And the answer here is severe tracheal bronchial malacia. Inspiratory flow is hitting an obstruction The ventilator knows that it has not completed the breath. It has not reached either the set tidal volume or set peak inspiratory pressure for the duration, inspiratory time as determined by the clinician. And thus the ventilator, as flow decays, because it hits, the inspiratory flow decays, as it hits an obstruction, the ventilator ramps out more flow, decays and ramps out more flow until the breath terminates. This oscillation in inspiratory flow is a servomechanism between the ventilator and the patient. And in this case is reflective of tracheal malacia. You can ask some of the other questions about why not secretions and why not water in the circuit? And I'll explain those with examples coming up. And here's the exact same situation, same patient, same time, just looking at the flow volume loops. And you can see the same oscillation in the flow pattern. One of the points I neglected to mention on the prior slide, which is important to determine this is tracheobronchial malacia, is that's a fixed obstruction. And as you noted on the prior slide, each one of those breaths looks identical to each, every other breath. Now, this is a trust me slide. This is the exact same patient, seconds later with all parameters being the same except going from variable decelerating flow to a constant flow waveform. And miraculously, the obstruction seems to disappear. Of course it hasn't. This is to stress the point that you only see those changes in the inspiratory flow if the patient is in a variable inspiratory flow mode such that the ventilator responds accordingly. In this situation, that flow is going in at a set rate regardless of the obstruction, and you don't see the bounce back phenomena. If we were to do a head-to-head comparison, you would see a higher peak pressure here in this variable, I'm sorry, in the square wave constant flow as flow is being pushed in past the obstruction. And to make that point, this is the same patient with the same problem. To make that point, this is the same patient at the point in which the flow is changed from that square wave constant flow back to variable decelerating flow. And you can see the obstruction is still there. In fact, in the expiratory flow waveform here, you can start seeing an obstruction to expiratory flow as well. Looked at this prolonged period of time it takes for flow to return to zero baseline. And in terms of inspiratory flow, not a dramatic increase, but you can see that the peak pressure is higher here in square wave constant flow than in variable decelerating flow. Now, what I previously showed was an exaggerated and really probably the most impressive example of fixed airway obstruction that I had seen in airway graphics. This is a much more common example with a double camel hump instead of the triple showing inspiratory flow again, hitting obstruction, ramping up, and then the breath terminating. And lastly, in this series, you'll see the same thing as the prior slide here in the flow volume loop with a single camel hump here as flow hits the obstruction and then ramps back up to complete the breath. Another example of tracheobronchial malacia. Next case is a two-year-old girl ventilated for acute lung injury secondary to viral pneumonia where entire CO2 increases from mid 40s to upper 50s over about 10 minutes. The respiratory rate in this patient also increases from 20s to 30s, but there's no significant change in saturation heart rate or blood pressure. Here's the patient's airway scale. Here's the patient's airway scalars in the middle where we'll start flow versus time on the top pressure over time, and again, volume over time on the bottom. I'll give you a moment to look at this series of tracings, think about it, and then follow up with a question. So this patient's clinical change is most consistent with what? Worsening bronchospasm, tracheal malacia, water in the circuit, mucus plugging, or pneumothorax. So similar question, similar scenario, different tracing, again, similar answer choices. So in this case, the answer is airway obstruction due to secretions. We see the same phenomena we did in the prior example here. Hits an obstruction, flow increases again until the breath terminates. Same thing here. Well, what's the difference in this situation versus the prior one? The difference here is that every breath is the same. So wherever this obstruction is, it's variable. So also you see the bounce occurring here in exhalation in this situation. So what would cause this variable obstruction in the airways? It's gonna be mucus plugging or secretions, and if this patient were to be suctioned, then the secretions would disappear, correct? Of course, correct. But in this case, what we do see is not so much suctioning. We see this change from a variable flow pattern, again, to a square wave constant flow pattern, and the obstruction secretions appear to disappear simply because of change in flow pattern. We do see the obstruction, the bounce here still on exhalation. So the solution to this situation is not to go to square wave constant flow, but rather to suction the patient and the situation will resolve. So as we go through these answers one by one, it's not worsening bronchospasm because the key component of this abnormality is inspiration although we do see it exhalation as well. Tracheomalacia, as we talked about in the prior example, would be constant breath to breath. Water in the circuit, I'll show you in the next slide, tends to be much more of a fine sawtooth pattern. Mucus plugging is the answer, and pneumothorax would simply not look this way. A different ventilator display here, but this is water in the circuit. This really fine tooth, sawtooth pattern that's occurring throughout inspiration and exhalation is water in the circuit. Usually easily assessed by looking at the circuit and easily fixed by draining the circuit. If we now move to the exhalatory side of the cycle, we're gonna look at the lung volume prior to inspiration or the end-exhalatory lung volume, FRC, and we're also gonna look at total PEEP and total lung compliance. The key here in the pressure volume curve is to avoid a zone of derecruitment and adalectasis, and as I showed previously, to avoid this zone of over-distention and to ventilate in this quote safe window. So in a pressure volume curve, right here we see this recruitment interval, this lower inflection point. This is a period of time in which, or portion of the breath in which pressure is increasing, but there's no associated increase in volume delivery. This is the lung that has collapsed and is taking pressure to pop the lung back open. The other way of describing the situation is simply inadequate PEEP to maintain the lung open at end-exhalation. The solution here is more PEEP. If we look at increased expiratory resistance, we see that here in flow versus time, this tail of exhalation, probably the example I showed you earlier where it really tailed off until the next breath may have been a better example. It's hard to quantify this. This is something you just need to see, pattern recognition, to look at that tailing off of exhalation as to what we should generally see in a normal situation is a rapid return to baseline. If the end-expiratory lung volume's too low, lung compliance is gonna be low, TATA volumes are gonna fall, and the patient is gonna become tachypneic. This may then result in premature termination of exhalation and intrinsic PEEP and its associated adverse effects, and also the increased opening pressure that I showed in the prior pressure-volume curve may result in increasing opening pressures, increased risk of barotrauma, increased risk, more accurately, of adelectotrauma. If the end-expiratory lung volume is too high, we can have risks of pulmonary overdistension and associated volume trauma. So the increased expiratory resistance or this obstruction to exhalation may be caused by airway obstruction, potentially an endotracheal tube occlusion, bronchospasm, a blocked expiratory valve of the ventilator, often overlooked. The prolonged expiratory phase can cause, quote, grass trapping, increased work of breathing, a reduction in trigger sensitivity, and as we started this talk with, potentially trigger insensitivity and a worsening of patient ventilator dyssynchrony. Here's an example of extreme increased airways resistance, expiratory resistance. As you see here, expiratory flow just continues without any trend up towards the zero baseline, and the next in-story effort occurs well below zero. Profound example of increased expiratory resistance. Same patient, same situation here shown on the left in the flow volume loop, exhalation here in blue, and then just tails off. Now, as I acknowledged much earlier in the flow volume loops it's very, very difficult to assess the difference between extreme increases in expiratory resistance and air leak, so I would not try to distinguish those differences. This is a very, very simple example of the differences, this pattern that this flow loop as shown here could be either, but when you correlate it as I did on the prior slide with the airway scalars, the answer becomes pretty straightforward whether it's an example of increased expiratory resistance or air leak. So I'm gonna summarize this portion of the presentation before I move on to just a few examples of capnography graphics. With that, I just wanna stress that it's important to optimize patient-ventilator interactions, need to optimize both inspiratory and expiratory synchrony, it's important to choose the appropriate inspiratory flow, and from a synchrony perspective, that's most commonly, most often variable decelerating flow. Also need to be sure to set the trigger sensitivity and the cycle time appropriately. It's important to optimize lung volume to minimize ventilator-induced lung injury, somewhat beyond the scope of this talk, capnography can be used to assess dead space ventilation as another form of respiratory mechanics monitoring. And lastly, just gotta keep in mind that bedside respiratory monitors provide tremendous information that must be integrated into routine ventilatory management. And in the last couple of minutes, I'll share some examples of capnography, particularly for the purposes of pattern recognition. This first example is one of esophageal intubation, where you do see some CO2 present for the first three, maybe four breaths before they extinguish. This is an example of a patient who had prolonged bagging prior to intubation, such that CO2 was entrained into the esophagus and stomach. And once an ET tube was placed inappropriately, some of that CO2 was detected before being washed out. The important, real important clinical teaching point here, this is why the color change devices, the colorimetric devices lead to false positives and can be inaccurate and generally, in my opinion, shouldn't be used is because of this phenomena. With intubation is much more accurate to be using a CO2 capnogram as shown here to be able to quickly see an esophageal intubation, despite a few breaths early on that do show carbon dioxide elimination. Mainstem intubation, and I do acknowledge this is more of a teaching phenomena than real life, have not seen this often despite mainstem intubations, but for the purposes of teaching, I will offer that here. And what you see if you do place the endotracheal tube into the right mainstem or left mainstem, if you're good enough to get it in that direction, you will see the camel humping, the smoothing off of the pleth tracing such that you get this rounded appearance compared to a normal entitled CO2 trace as shown in the shaded gray. Okay, normal entitled CO2 trace here, and now we see one consistent with bronchospasm where the obstructed airways take longer to empty and contain higher CO2 concentrations, thus producing a slower increase in exhaled CO2 concentration and the sloping plateau phase. So this shark fin approach is very typical of significant bronchospasm. In the case of bronchospasm, whether the entitled CO2 accurately reflects a true entitled CO2 value in breath B or does not in breath A, depends on whether or not the patient fully exhales. In the situation of A, there's breath stacking, incomplete termination of exhalation, and the patient never fully reaches a true entitled CO2 state. Well, generally better diagnosed through the airway graphics we previously discussed. Here we see patient ventilator dyssynchrony with inspiratory efforts as shown by the arrows during the expiratory phase of two breaths. And lastly, trigger insensitivity. A patient is trying to take a breath here as shown by the arrow, and the ventilator is not sensing the inspiratory effort and remains in an exhalatory phase. So I'm hopeful this presentation helped overview and provide some useful information both clinically and for the boards in terms of patient ventilator dyssynchrony, how to recognize various abnormalities in airway graphics through pattern recognition, and similarly through some examples of capnography. And again, please feel free to reach out if I can answer any questions prior to the interactive sessions that we'll have in late August and September. Thank you for your attention, and I wish we could do this in person in a future year. Thank you so much.

pulmonary waveform analysis

patient-ventilator dyssynchrony

airway scalars

airway loops

trigger dyssynchrony

flow dyssynchrony

cycle dyssynchrony

ventilator settings adjustment

capnography