All right, with that, disclosure is nothing relevant to this topic. Here we go. All the different modes of ventilation. So we're going to talk about mechanical ventilation, and if I can squeeze in a few minutes at the end, we'll talk a little bit about cardiorespiratory interactions, because we don't have a session on that here. So in terms of all the modes, simple thing is, for the most part, forget about all of them. We're not going to ask questions about specific nuanced modes, specific types of ventilators. The things that might show up, if anything, you may see something on APRV, fast forward, you will see a question on that later. Maybe something on the oscillator. Maybe something NAVA. I don't think so, because it's so proprietary. But other than that, they can ask you concepts. So don't worry about specific modes. Just forget about them for the boards. Real life mention, for yourself in real life, the approach really varies on the technology you have in your unit. All of us have different ventilators. We have different modes. Know what you have. Use what you have. Don't worry about all the others. And keep in mind that there is no outcome data that ever has shown that any mode of ventilation is better than any other mode of ventilation for pediatrics. A little different in neonates, but in PEDs, all the modes are equivalent. It's how you use them. And in general, there may be a preferred approach based on pathophysiology, and that's what we'll talk about. And that's really what you need to focus on, is the pathophysiology. For the boards, what you need to know is what defines the modes. What is intrinsic to all of these modes? And with that, what we're going to talk about is how the ventilator takes a flow of gas, sculpts it to get the desired breath. What we have here is the type of breath, the mode type. Come back to that. Cyst control, spontaneous breathing, SIMV. The quantity of gas flow, which is the limit, pressure, or volume. What triggers the breath and triggers the start of flow to the patient. What ends inspiratory flow, and that's one of the points that a lot of folks don't realize. So cycle. When you hear about cycle, that's the cycle of inspiration to exhalation. Trigger is exhalation to inspiration. What triggers the breath and what cycles the breath to exhalation. And lastly, we'll talk a little bit about the type of inspiratory flow or the flow pattern. I've taught all my fellows this for all the years. If you ever get a question about mechanical ventilation and have no clue what's being asked, the answer relates to flow. Because all a ventilator does is take a flow of gas and sculpt it. So just say flow. And I asked my fellows that first year, second year, by third year, they finally figured it out. So you're all fellow grads, so it's flow. Mode types. Control modes, same thing as cyst control modes. Terms are interchangeable. Definition. A mechanical breath in a cyst control mode is defined by a fixed inspiratory time period. That's the difference between a mechanical breath and a spontaneous breath, a supported breath, an assisted breath, a pressed support breath. That is defined by a variable inspiratory time. That's the difference is whether inspiratory time is set by the clinician or the RT, or the inspiratory time is set by the patient. Cyst control versus a spontaneous breath. SIMV, mixed modes, a little bit of both. Okay? All right, we'll go through these pretty quickly. What limits a breath? It's the size of the breath. Pressure or volume. You're not going to get asked a question of pressure versus volume. That's pro cons at Congress. If there's something that you're seeing in Congress as a debate, they're not going to ask you the question because there's no absolute answer. Okay? And these, of course, are clinician determined. Trigger. What initiates the breath? What signals the ventilator to start a breath? Generally it's flow. It can be pressure. That's more of the older ventilators. We don't do much of that anymore. Or time. If your patient is heavily sedated or paralyzed, it's time for the next breath. So the start of the breath, flow, pressure, or time, and you determine that as the clinician how you set it. Cycle. Cycle from inspiration to exhalation. What cycles a breath? I've already gone through it in terms of the mode types. If it's a full mechanical breath, flow. If it's a spontaneous pressure-supported breath or volume-supported. If we look at this, if you have a set inspiratory time, the cycle is time. That is determined by the respiratory therapist. At the end of the inspiratory time of .x seconds, the ventilator's expiratory valve opens and the breath cycles from inspiration to exhalation. Straightforward. Everyone knows that. How does flow cycling work? So in a respiratory breath, what happens? What happens here is the peak inspiratory flow rate is whatever the ventilator determines it to be. Let's just pretend it's 10 liters per minute in a baby. When that flow decays to a preset level, some ventilators allow you to set it. The percent level, most ventilators, it's fixed at about 25%. So when flow is still going into the patient and it's 25% of peak flow, so my example of when inspiratory flow drops to 2.5 liters per minute, 25%, the expiratory valve opens anticipating exhalation. So flow cycling is a decrease in the peak inspiratory flow to a percent as determined generally by the ventilator, sometimes by the clinician. Flow patterns. Okay. Two flow patterns. Square wave, constant flow. Flow increases to a preset clinician-determined level. Decays there throughout inspiration and then decays into exhalation. Traditional standard volume control ventilation, rarely used today in pediatrics. Variable decelerating flow. Flow increases to a peak level as determined by the interaction between patient and ventilator, not clinician set, and decays at a variable rate as determined by the ventilator until exhalation starts. And sometimes you'll see, if they went into the physiology here, the physics of gas flow, how does flow relate to airway pressure? If flow is square wave constant flow, so flow is constant, the rate of rise of airway pressure is linear or constant, and what you see here is a linear increase in airway pressure. For decelerating flow, the rapid increase in flow at the start of inspiration correlates to a rapid increase in a change in pressure and then a decreasing in that increased rate or a curvilinear change in airway pressure. So these are the relationships for the two flow types between flow and airway pressure. What's often asked or can be asked is the relative differences here in terms of the relationship in flow to airway pressures, and I'll show this on the next slide a little bit better. But for square wave constant flow with a linear increase in airway pressure, the peak pressure tends to be higher in square wave constant flow than variable decelerating flow, assuming tidal volume and inspiratory time are the same. The rapid increase here in airway flow relating to the increase in airway pressure tends to lead to a broader base, and so mean airway pressure tends to be higher in variable decelerating flow. If you look at that in words, what we see here is that a variable decelerating flow provides the same tidal volume, same inspiratory time, as square wave constant flow ventilation but with a lower peak pressure, presumably leading to a less risk of ventilator-induced lung injury, and a higher mean pressure leading to potentially improved oxygenation. So variable decelerating flow ventilation tends to be better for those patients with ARDS because of the lower peak pressure and higher mean pressure, thus trying to match the mode of ventilation to the pathophysiology of your patient. The mechanisms of these effects are unknown but probably related to beta gas distribution of the decelerating flow. All right, question just as a reminder. In an invasively ventilated patient, what defines a spontaneous breath? The variable inspiratory time. Zero breath, fixed inspiratory time. Next question. So you'll see this sometimes. You'll have questions and they'll give you all these numbers and you expect them to ask you what the compliance of the system is. And they ask you elastance, and you're like, oh, I knew that at some point. Elastance is easy. Just calculate compliance and flip it. So elastance is one over compliance with a change in pressure of the change in volume. Okay, it's a very simple point. If you see that, just hearing this now, you'll get one more point on the test. All right, compliance measurements. Robbie mentioned some of these a little bit earlier. We'll go through them in a little more detail as I go through the next slides. So compliance change in volume over change in pressure. Elastance change in pressure over change in volume. Resistance, you've got to know this. Change in pressure over change in flow. You look and you're like, oh, which is the top, which is the bottom? For a fixed flow, if you have more of a change in resistance, sorry, change in pressure, more of a pressure drop, the resistance has to be higher. So change in pressure over change in flow. All right, compliance equations, dynamic compliance, static compliance, what's the difference? The difference is whether you have peak pressure or plateau pressure here in the denominator. Dynamic compliance is peak pressure because it includes the resistance of the upper airways. Static compliance is plateau pressure. Static compliance, change in volume, tidal volume over the difference between plateau pressure and peak. Elastance, just to drive that home, one over compliance. Spontaneous breathing. You have all these numbers. What's the compliance of the lung? What's the compliance of the chest wall? What's the compliance of the respiratory system? Simple way to think about it, it's always going to be change in volume, tidal volume over change, delta P, change in pressure. Think about the pressures at the extreme of what they're asking. So if the question is lung compliance, what's the extremes of the lung? It's the alveolar pressure and the pleural pressure. Just think about what delta P is and it becomes really easy. Chest wall compliance, what's that? Pleural pressure inside the chest wall and atmospheric pressure. Respiratory system compliance, the whole thing, what's that? Alveolar pressure and atmospheric pressure. So just think about what the delta P is, what they're asking, and then the math becomes simple. Time constants, something that you just have to know it's going to be there somewhere in some test at some point. Time constant is a concept borrowed from electrical engineering. It describes the phenomena where a given percentage of a passively exhaled breath requires a constant time to be exhaled regardless of the starting volume given constant lung mechanics. It's a logarithmic function. So what is this? The start of exhalation, the initial flow of gas out of the lung depends on the drive pressure. The difference between the alveolar pressure and the mouth pressure and the airways resistance. It also depends for a given gas volume that the alveolar pressure at the start of exhalation depends on lung compliance. So it's a relationship between resistance and compliance. Time constant, simply R times C. It's all it is, is resistance times compliance. So for any value of resistance or compliance, the time constant equals the time necessary for the lungs to empty by 63%. It's what it is, one standard deviation, one time constant, 63%. When expiratory time equals time constant, the patient will passively exhale 63% of that inspired tidal volume. All right, clinical application. Let's just make this make sense. You have an infant with small airways disease. That patient, that infant has a long time constant and therefore long airway emptying times. So if you think about the RSV bronchiolytic, that patient has a high airways resistance, long time constant, is very tachypneic, and thus the lungs don't empty adequately leading to air trapping. Okay, moving on to the next concept and one of the last concepts I'll touch on in this section, dead space. You'll see this somewhere. You'll see it later today in the question section. Minute ventilation is dead space ventilation plus the alveolar ventilation, alveolar gas exchange ventilation. So how much of the tidal volume is dead space? How much of the tidal volume participates in gas exchange? Tidal volume times respiratory rate, minute ventilation. The tidal volume is a combination of your dead space volume and the volume of gas that participates in the gas exchange, and thus physiologic dead space is going to be the sum of the airway or anatomic dead space, and those terms are and can be used interchangeably. Don't get fooled by that. Airway dead space is anatomic dead space plus the alveolar dead space. This is one of the equations you just should memorize, okay, and remember or review it right before the exam. VDVT or the dead space ratio is the difference technically between the arterial PCO2 and the mixed expired CO2 divided by the arterial CO2, PACO2. The mixed expired CO2, if exhalation is constant and is linear, that is equivalent to what? N-tidal CO2. So the questions that you will see, they will give you PACO2. They'll give you N-tidal CO2 and have you calculate VDVT. They're not going to confuse you and mix you up on mixed expired versus N-tidal, okay, so just use N-tidal. All right, last point I'm going to make here is just the summary here, a schematic of the different ventilation perfusion relationships. On the left side, shunt perfusion is low VQ, low ventilation to normal or increased perfusion. This here is the world of oximetry. These are the patients who are desaturated, okay. Normal VQ.8 and the right side here, dead space ventilation where you have high ventilation to normal perfusion or it could be normal ventilation to decreased perfusion. This is what? This is the world of capnography. These are the patients that are hypercapnic. These are the patients that have some problem with pulmonary perfusion, whether that be pulmonary hypertension, pulmonary emboli or other entities and those you'll see a little bit later. Okay, with that, I intentionally went a little quickly and I'm going to save five minutes to go through cardiorespiratory interactions, which is an hour talk of itself, but I want to hit a few key points because this is included otherwise on the syllabus here today. So if we go through this in the next five minutes before Theresa starts doing jumping jacks and tells me to stop, we have two sides of the equation. One is O2 supply, same as O2 delivery. Oxygen delivery, DO2, is a product of cardiac output and oxygen content. The formula you should all know, it's on the slide there. Don't worry about the coefficient of 1.34. Sometimes it's 1.32. You'll see a change. Don't get fooled by that. O2 demand or O2 consumption is the amount of oxygen used for aerobic metabolism. O2 consumption is cardiac output times the arterial venous O2 content difference, okay? To increase oxygen delivery, you can increase oxygen content, which could be increasing the hemoglobin transfusions, increasing the saturation and or the PaO2. You can increase cardiac output. You can do that through cardiac interventions, fluid and vasoactive agents, and I'll be discussing later this afternoon for another talk. Or what we're going to go through here now is how you can use the ventilator to optimize cardiorespiratory interactions, or at least try to avoid inhibiting or worsening cardiorespiratory interactions. Terms of decreasing O2 consumption, there's two things. Decreased patient-worker breathing or maintaining normal thermia for those patients who are febrile. If you look at this in summary, O2 delivery, again, the product of cardiac output and oxygen content. Oxygen content, a product of hemoglobin, O2 binding or saturation, O2 dissolved or PaO2. And cardiac output here is the product of heart rate and stroke volume. And stroke volume is affected by preload and afterload to both ventricles, as well as contractility of both ventricles. I'm going to skip that and jump to this slide for time. On this slide, this is the schematic of the relationship between right atrial pressure or intrathoracic pressure and systemic venous return. So blue is the patient's baseline, whatever that happens to be. If the patient has an increase in right atrial pressure by increasing the patient's PEEP, going from negative pressure breathing to positive pressure breathing, what you see is the increase in right atrial pressure results in a decrease in systemic venous return. Straightforward physiology. So how do you manage this situation clinically? What do we do? We volume load. Give a fluid bolus. How does a fluid bolus affect this relationship physiologically? What it does is it shifts that curve, that line, upward and rightward. Thus, for the same right atrial pressure, you end up with an increased systemic venous return. So to summarize, increases in intrathoracic pressure generally decrease cardiac output by decreasing RV preload. Fair question, right? Fair concept there for a question. The effects on PVR are going to vary and it's going to be based on lung volume, and I'll get to that in just a minute or two. So in general, the best strategy for the failing right ventricle is to limit intrathoracic pressure. Ventricular interdependence, complex concept here. Can't do that justice in the amount of time I have, so I'm simply going to make this one point. The left schematic here is normal situation. The right schematic is the patient with RV diastolic hypertension, diastolic dysfunction. We have now a hypertensive dilated right ventricle that simply impedes on the left ventricle, reducing left ventricular preload and thus left ventricular output. Next concept, you will see the some way, shape or form on an exam. It's going to be there. It's really perfect for test taking. We'll walk through these four schematics. The first schematic here, baseline normal spontaneous quiet breathing. We have a systemic systolic pressure of 100 and a left ventricular pressure of 100 as well, and thus the transmural pressure is essentially zero. If we now have a patient here who's in respiratory distress and has an exaggerated inspiratory effort, their mean intrathoracic pressure in this schematic we'll say is minus 25. So for this situation, for this patient to still generate that same systolic systemic pressure of 100, the transmural pressure that needs to be generated here is 100 minus the negative 25 or 125. So in this situation, we've made it harder for that left ventricle to pump blood because it has to overcome the negative intrathoracic pressure. You now take that same patient with cardiomyopathy, acute myocarditis, whatever it is, intubate the patient such that their mean intrathoracic pressure is now positive 20. We have unloaded that left ventricle because the transmural pressure needed now to get the same systolic systemic pressure of 100 is 100 minus a positive 20 or just 80. So positive pressure ventilation reduces left ventricular afterload and improves left ventricular function. Lastly, side comment here, vasodilators, mirinone for example. In this situation, we systemically afterload the patient such that the systemic systolic pressure is now only 80. And but nothing else has changed in the sense we go back to quiet breathing with the mean intrathoracic pressure in the schematic of zero. We now have a transmural pressure of 80 minus zero or 80. Okay, so mirinone's effects and intubation's effects physiologically ends up with the same beneficial component or outcome for the left ventricle. So in terms of the left ventricle, increasing intrathoracic pressure increases cardiac output by decreasing LV afterload. The effects of positive pressure ventilation on LV preload are variable and are based on the patient's intravascular volume status as well as RV effects. All right, last couple of points here. The dominant effect of positive pressure ventilation on cardiorespiratory interactions is always the mean airway pressure. That's what matters. Any effects due to phasic changes, delta P, tidal volume are minor and must always be balanced by the mean airway pressure. Frank Starling curve, not going to go through it here. Make sure you know it. Make sure you know the relationships here for both normal ventricular compliance and decreased ventricular compliance and how changes in volume affect changes in pressure. And if you have questions, we can go through it at the break. Last point I'm going to make is the effects of lung volume on pulmonary vascular resistance. This mirrors the schematic Robbie showed earlier. If you look at PVR on the vertical axis and lung volume on the horizontal axis, in terms of large pulmonary vessels, when the lung is adalactatic, the resistance in those large tortuous vessels is high. As the lung opens up and over distends, the resistance in those large vessels falls. If you look at the small vessels in orange and you look at the insert here, as alveoli get over distended, they compress the surrounding capillaries, leading to an increase in PVR in the small vessels with over distension. But what we care most about is total pulmonary vascular resistance, which is going to be at the lowest point at functional residual capacity. Okay. All right. Take home points as I conclude. You need to know the concepts of mechanical ventilations, not individual modes with the exceptions I mentioned earlier. You need to know the basic equations. You just have to have those memorized. You don't want to waste points on something that is straightforward. You just have to know. Time constants, port and point, just have to remember 63% of the tidal volume is exhaled at one time constant, and time constants are time C. In general, mechanical ventilation works against the right ventricle and in favor of the left ventricle as a general rule. And lastly, pulmonary vascular resistance is minimized at FRC. So thank you for that whirlwind tour. And we'll be back a little bit later with some more concepts. I think I'm going to turn it back over to Robbie now.

mechanical ventilation

APRV

oscillator

airway pressure

lung compliance

pulmonary vascular resistance