Chapters Transcript Video Heart Lung Interactions and Positive Pressure Ventilation Dr. Mark Marinescu explains the physiologic concepts of heart lung interactions in positive and negative pressure ventilation. Hey, Eric, thanks so much and uh thanks for having me. Uh So I'm gonna give a talk on heart lung interactions in uh um uh spontaneous negative pressure and positive pressure ventilation. First, my disclosures, I have no uh financial disclosures. Uh but as Eric alluded to, I'm not a content expert in heart lung interactions, I did no pig labs or stuff where I intubated pigs and measured out. Not me. I'm a practicing critical care cardiologist. So I guess I should probably know about this and I try to educate myself as much as possible for this talk, but apologies if you are a content expert. Uh And uh I look forward to reading your comments in the chat and please be kind. Uh My goals for this talk are gonna be to explain the physiologic uh uh underpinnings for heart lung in for heart lung interactions in positive and negative uh pressure ventilation and describe some of the general considerations in optimizing heart lung interactions. Uh So why is this important? And I think it's really striking that 100% of patients with hearts have at least one lung at some point in their lives. Uh and I have to bring this up because my wife is an MFM. It's not always true, but most hearts and lungs inhabit the thorax, certainly at birth uh for live births and under most circumstances, changes in the lungs affect the flow of blood through uh the heart. So that's why it's kind of important to know about it. And we think about how uh uh structures and the thorax are arranged, it typically looks something like this, but it's not a very conducive model for uh kind of illustrating how heart lung interactions work. So, for this talk, we're gonna kind of spread things out a little bit. Uh So we're gonna be talking about two circulations in series. We'll have the RV, the pulmonary circulation, the LV, and then the systemic circulation. And then we're talking about structures and the thorax. We're pretty much talking about sacks and sacks and sacks and sacks. So we'll start off with kind of our avila sacks. Then we're gonna talk about the plora as a sack and then there's gonna be the thorax uh as a sack. And I do appreciate that this is a gross oversimplification to the point where it probably doesn't truly represent physiology. I mean, there's really another sack that's between that thorax sac and the PLO out of visceral and pro flora. There's also an adjacent sac, the para cardi that surrounds the RV and the LV and that paar constrains, uh the filling of the LV and RV and results in a lot of ventricular interdependence, which is very important for interactions like pulses paradoxes that you're all very aware of. But again, for the sake of simplicity, we're gonna kind of just evaluate these uh uh three sacks for transmission of pressure. And I'll point out where the other uh sacks become more pertinent. We're gonna be talking about several uh uh pressure uh gradients. We'll talk about a trans Avelar uh pressure. Uh We'll be talking about a trans plural pressure and a transthoracic pressure. So, trans alar the pressure gradient between the inside the Avila and the plora transpleural pressure from the plea to the thorax and transthoracic pressure typically from inside the chest to outside the chest. Also, before we get too far, I think it's important to set up that we are going to be using two different scales for pressure uh measurements. As cardiologists, we pretty much are very comfortable talking about millimeters of mercury. But every time we check AJ VP, we actually switch to centimeters of water and I don't know how many times we do the conversion in our heads, but they're actually two different scales. Uh it works most of the time because they're fairly similar. One millimeter of mercury is 75% of a centimeter of water. So, especially at low pressures, they're fairly similar. But at high pressures, there does seem to be a little bit of a differential. I know a lot of times again, I forget that we're using two different scales. But when we're setting vents, uh and the pulmonologist talk in terms of centimeters of water fairly frequently. So let's start kind of going through what happens in normal spontaneous negative pressure, ventilation. And the descriptions and pressures that we're gonna use are uh a gross oversimplification. Uh But, you know, in general, we're gonna define the atmospheric pressure as zero millimeters of mercury. This has its own problematic reasons. Uh But for the sake of discussion, we're just gonna uh start there and pretty much the airwaves also exist at zero millimeters of mercury because there is a continuous open uh connection between the outside world and our Avio and at rest between the visceral pro pro pl visceral and prial plea. I got it. Uh There tends to be kind of a negative uh pressure typically around four or five millimeters of mercury. And then our intrathoracic pressure is gonna be slightly positive. Uh That's gonna be kind of gradated as you move through the dependent zones of the thorax. But uh a 1.5 millimeters of mercury is a good nice round number. It's gonna be a little bit higher in the abdomen, maybe around three. Again, this is all very dependent on the patient you're specifically talking about. And then with inspiration, we're gonna start off expanding our thorax. We're gonna reduce the intra thoracic pressure is gonna become negative, our abdominal pressure will become slightly more positive as the diaphragm shifts, those abdominal organs inferiorly. Um We're still gonna have that same negative uh uh plural pressure. Uh And initially, we're gonna have a slightly uh negative pressure in our airways. But as flow goes to zero, the pressure will then equalize uh to serum millimeters of mercury. So what does this mean hemodynamically? Well, we have uh increased intra abdominal pressure and a negative intrathoracic pressure. So that's gonna drive press uh blood flow up into the thorax up into the uh right ventricle. And this is true for the aorta as well since you have uh uh now more negative pressure in the thorax, blood is going to be not sucked back up, but the pressure gradient driving it into the abdomen is gonna be reduced. So, what you typically see is increased, preload to the RV and increased afterload uh to the LV. And I'm sure as cardiologists when we hear increased afterload to the R to the LV, we do tend to cringe a little bit. What happens to the PV R generally with inhalation, the PV R goes up a little bit and we'll talk more about that a little bit uh later. And then because of interdependence, I I told you we bring the per card back in uh the RV will expand, the LV will contract a little bit further decreasing uh LV, preload. Although for most circumstances, this effect isn't very marked, uh maybe more marked in in volume deplete states. So if you look at what this actually means to the human in front of you, uh It was a nice study looking at the effects of increased negative intrathoracic pressure where they had people uh blow in against a resistance there. For as the resistance increase in order to get that uh same long volumes, you have to suck in much more negative. We see that in healthy patients really generating more negative intrathoracic pressure has no effect uh in heart failure patients. Uh perhaps, although that is not very clear and more negative intrathoracic pressures, there may be maybe a slight trend towards worse stroke volume at maybe much higher negative pressures. But at in, at most cases, the the effects are probably fairly minimal and you know, everyone's always healthy all the time, there's nothing left to talk about. Thanks so much to uh coming for this talk. Uh And I hope you all have a nice day, of course. Uh that would be nice, but we know it's not true. We have these things called the ventilators. And if all we had was the iron lungs of your negative pressure ventilation, we could again stop this talk right now. Negative pressure ventilation is uh uh pretty well described, but we don't just have negative pressure ventilation. In fact, we, we typically don't use that very often uh uh anymore. We have positive pressure ventilation and thus, we should kind of talk a little bit uh about that. So why do we need positive pressure or ventilation in our cardiac patients? Uh More for the non cardiologists in the room. But if you think about what happens in heart disease, you know, thinking of a typical uh example, let's say an M I where you have myocardial ischemia, maybe a little bit of a scar formation. Uh The first step that happens, I'm sure we all know relax is the energy dependent process of, of uh myocardial of the myocardial cycle. So you're gonna get LV stiffness and as you get LV, stiffness, you'll get back pressure of blood into the, at that will be transmitted into the pulmonary veins. You'll get an increased drive of hydrostatic pressure to the uh pulmonary ali and you'll start to develop some pulmonary edema. And maybe as this process continues, you get some LV dilation, maybe you get a little bit of functional uh mit valve regurgitation. You get worsening increase in L A pressure, worsening hydrostatic drive to uh pulmonary edema. And now maybe you're starting to get some impaired gas exchange. Uh and you start experiencing some hypoxia with that hypoxia comes hypoxia mediated pulmonary vasal constriction. Uh And with that some pulmonary hypertension, this uh pulmonary hypertension will then back uh pressurize the RV system. It'll start getting some worsening congestion. Uh And with that congestion, you'll eventually get an organ dysfunction and then the combination of that congestion and the primary my carnal process will increase inflammation in the system that's gonna increase avila permeability. In fact, permeability in all of your capillaries. But the Avio not excluded uh worsening pulmonary edema. And by this point with worsening and organ dysfunction, your patients probably not eating very well. They're probably laid up for a while, maybe they're nauseated, they're not getting nutrition. Then we do a little bit of cardiac surgery to them some procedures and you lose your oncotic pressure driving gradient and you're now in profound pulmonary edema. And in fact, we see this to be true. Uh up to uh 80% of trials looking at cardiogenic shock involve the use of positive pressure ventilation. So it's uh very prevalent in our uh uh uh cardiac populations. So, going back to our kind of physiologic model here, what happens uh to the lung during positive pressure ventilation. And um again, we're gonna define the outside environment as zero millimeters of mercury. Uh And when uh you're at rest, typically with positive pressure ventilation, we use some peep. So the system is always pressurized to some degree, the airwaves are never really at zero. And hence the uh plural pressures are always uh also gonna be pressurized as long as you have kind of peep up uh as well. Um the uh thoracic pressure is gonna be probably a little bit higher and abdominal pressure is probably gonna be a little bit higher as well. And then let's say we take a breath in, we deliver some uh pressure and volume of air to inflate the air waves. And that pressure and inhalation is gonna to transmit to the plea the parietal plora and to the uh thorax. Um And again, we're gonna have a uh a slightly higher intra abdominal pressure. But compared to the thorax in this situation, the uh thoracic pressure is gonna be lower. I mean, sorry, the abdominal pressure is gonna be lower than our intrathoracic pressure. And as before when blood had a pressure gradient to go into the thorax here, that pressure gradient is gonna be to go out of the thorax, you're gonna have less RV filling and the same is true on the aortic side uh where you're gonna have uh uh less RV preload. But you're also gonna have uh a driving pressure of blood out of uh the thorax, less transmural aortic pressure and hence less of the afterload. This is starting to sound maybe a little bit better. We're not gonna talk about the pulmonary vasculature just yet. We're gonna go back to that in a little bit. Uh But we're gonna start off kind of talking about how the Avio R pressure is transmitted to the thorax. And again, we're talking about sac and sack. So under normal circumstances, you have your Avio uh they're hooked up to a ventilator. Uh you deliver some amount of positive pressure, the lung inflates and it takes up more room, the thorax, it pushes the chest wall open and that is going to generate a pressure in the thorax. You exhale, that pressure goes back down. But if we change the situation a little bit, for example, uh we uh reduce the AV compliance, for example, in A R DS. Uh now all of a sudden uh that pressure, that same pressure that we deliver to the Avio result in much less uh increase in your lung vis. I mean, we all have a R DS patients who have 30 centimeters of water of positive pressure and you're only putting 100 mils of uh air into their lungs. Uh So you're gonna have less transmission of that airway pressure to the thorax in poorly compliant lungs. Uh Conversely, maybe you have a patient with emphysema who have unbelievably good compliance and that pressure will be transmitted a bit more efficiently moving from how that pressure is transmitted uh to the thorax. How does that pressure end up affecting uh circulation uh uh in the human. And uh one thing that came up more in my critical care training and almost not brought up in my cardiology training was how Venus return works in the body. I'm not sure why. That's the case. I assume it's because uh the Venus system is a cardiologist, least favorite vascular system next to the lymphatics. But uh uh it's just not something that at least in my training, uh we covered a lot, but in my critical care training, this was covered quite a bit. Um And the model they use is the heart's pumping, it sends blood to your organs and from your organs, it enters your Venus pool. And within this Venus pool, you kind of have these two places where it can live, it can live in this pool called the unstressed volume. And this other pool called distressed volume and blood, the venus blood can move between these two pools. And then what happens is in the human, you have this force, this mean systemic feeling pressure, which I'm not really sure where it comes from, but it's defined as the pressure in the veins during no flow or death. And it's what kind of drives the blood up to the right atrium. So this force pushing it on the veins, I imagine in reality, it comes from muscle contraction and valves and intra abdominal pressure. But it's what kind of uh uh pushes the blood returning back up to the heart. And then you have your right atrial pressure. And it kind of makes sense that if you have a pressure gradient from the veins to the heart, the pressure in the chamber you're going to is going to oppose that uh return. So the way uh in critical care, they define kind of the Venus return is the whatever this means, m filling pressure is minus the right pressure and you can do things to kind of modify your venous return. For example, give IV fluids or uh maybe steroids and shift some of that blood into distressed volume. Uh you can modulate the systemic uh uh feeling pressure, although I'm not quite sure how uh and that would uh then uh enhance your venous return. So there's a curve, the guten curve. And this one, I do maybe recall a bit more from my cardiology training, a Venus return curve. And this was initially described by a physician named uh in the fifties. And he had this weird experimental model of dog hearts uh kind of removed and using mechanical pumps to keep uh uh a flow constant. And then he'd use these things called sterling resistors which are hollow collapsible tubes. He just raise them up and down to change right atrial pressure and uh graft the effects of Venus return. And what he found was that a right pressure of zero return was maximized and as the right pressure went to the mean systemic filling pressure, uh the uh Venus return went down to zero or nothing and you would have no cardiac output. Now, this kind of, again, intuitively seems weird to me, it's not the way I kind of think of it. We have plenty of patients with pressures of 20 their uh Venus return isn't zero. But uh this is uh uh a commonly uh uh uh conceptualized way of thinking about Venus return. And you know, if we look at something like the Frank Starling curve, this is a curve on comfortable with and familiar with. And I understand this one talking about the effects of preload on cardiac output. And here's kind of the inverse where more preload equals more cardiac output. But if you think about these two graphs really, because we're dealing with a circuit and series, your Venus return has to be equal to your cardiac output and your cardio output has to be equal to your Venus return. So the Y axis is essentially the same. And if you think about your right HL pressure and your preload, I mean, here they were specifically referring to the left HL pressure, but they're kind of similar. So your uh uh X AX is similar as well. So you can superimpose these two graphs and where they intersect is the idea that this represents your cardiac output. And then you can use this type of graph called the guiding curve. You can change your contractivity, you can change your stress to volume and figure out where your new cardiac outputs are gonna be based on change in uh in contractivity and uh your LV uh and RV, filling pressures. Now, you know, in some ways, this feels right to me. I mean, in post LVAT patients oftentimes I'll see uh the right Atal pressure go up uh and the cardiac output starts going down and I'm thinking, oh, is this because I'm impairing my Venus return, the pump is doing what it's doing. I've programmed the speed. That's not what the problem is. Um But it still kind of in some ways also doesn't feel right with my observ patients. And there is some criticism about this approach. Uh Certain people believe that actually confused his dependent and independent variables. And in fact, it's not the right pressure that drives Venus return. It's the cardiac output that drives right H pressure. And as the cardiac output goes up, you're clearly sucking more blood through the system. Uh you're gonna drop your right pressure and you're gonna increase your Venus return just because you have more blood active in circulation. Uh The converse argument would be that cardiac output really doesn't drive Venus return because the Venus pool is so compliant and so big, you could put as much cardiac output there as you want and things will remain static, but there's a little bit of uh contention as to how to think about uh Venus return. Uh So what what happens in real life in patients? Not just the conceptual understanding as a study of the effect of positive pressure, ventilation on uh venous return and vine loaded cardiac surgery patients. And here they graph for a number of cardiac surgery patients to write l pressures and looked at the change in right pressure compared to the change in cardiac output. And you can see that it pretty much goes around zero where the 2 may not be dependent. Of course, this is a preload uh replete in the individual. There was a nice Scandinavian study as well that looked at pressure monitoring in the plora next to the pericardium uh in uh the plora in other locations and then your airway pressure in CV P. And what they noted is that changes in your airway pressure transmitted most to your pericardium, uh sorry, most to your plural pressures, but uh less to your pericardial pressure and your Venus pressure with only about a third of the change in airway pressures actually resulting in change in central Venus uh pressures. So where do I come down on this? It remains unclear to me how much positive pressure ventilation actually, in reality does affect Venus return, it seems like increases in airway pressure, confirm minimal change to right at pressure. And remember we're dealing with different scales, right? So a change in centimeters of water is gonna be less in millimeters of mercury. And it's also unclear to me that increases in right atrial pressure, decrease Venus return in certain situations. It seems like it does, but in other situations, it seems uh uh like it doesn't and all of this discussion don't take into account things like ventricular interdependence and how changes in Venus return affect cardiac output from uh those uh standpoints. Uh Perhaps the truth is that it's different in different people and uh the patient's volume state uh may make a big impact on whether or not positive pressure or ventilation will impact Venus return. And in fact, we see this looking at pulse pressure variability, we use that as a marker of fluid responsiveness. So in a volume down state, uh uh um the changes of positive pressure ventilation on uh Venus return may be more pronounced uh than in the volume replete state. Looking at some other studies, this was a classic uh study by Grace and Greenbaum that looked at patients with cardiac dysfunction and their response to peep. And kind of goes along those uh uh lines where if your uh uh wedge pressure was 12, you had your best cardiac output at low or minimum peep or ze zero peep. If your wedge pressure was higher, your best cardiac output was at modest peep. Uh And if you had a very high wedge pressure, your best cardiac output was uh at high peep, although not high peep, by today's standards, reaching a max of uh eight. And you know, again, some real world data, this is uh from that same study I showed earlier where uh now instead of using uh a resistor to induce negative intrathoracic pressure, we use uh resistance to exhalation uh to induce uh positive intrathoracic pressure. And we see in healthy uh patients, we see a decline uh in uh a stroke volume with uh uh increasing peep. But in patients with half breath, the stroke volume actually goes up which again may be a healthy patient volume down a heart failure, patient, more volume replete. I think the effects of positive pressure ventilation on afterload are a little bit more clear. There was this study that was done in uh 2016 in Greece, very small study looking at cardiogenic shock and they actually randomized patients to intruder balloon pump alone or intruder balloon pump plus positive pressure ventilation. And the patients who had the inter balloon pump and positive pressure ventilation had improvements in urine output, improvements in wedge pressure, improvements in uh uh pressure dosing and uh uh some data from uh studies looking at percutaneous metro valve repair where uh steadily increasing the peep resulted in decreased left in systolic volumes and increasing coa links. So there's clearly a benefit to the LV uh from the reduction in afterload from peep effects. Although I guess it could be preload as well. Hard to say. All right. So I said I'd talk about pulmonary vascular resistance as we're gonna talk about it. We're done with kind of the preload uh afterload, bit and just a little bit of review. Uh The LV in general is volume sensitive and pressure resistant. Uh What that means is you can drive up the RV, afterload under most circumstances pretty high without developing profound cardiogenic shock. But if you give the L VA ton of volume, especially in a weak state, uh it has a harder time handling that the RV. On the other hand, is the inverse is very pressure sensitive uh and more volume resistant. The RV typically can handle huge, swift uh shifts in volume uh without much difficulty. But if you increase RV, afterload, it becomes less happy. The uh pulmonary vascular is similar to the RV. And that it's a unbelievably compliant system with very low vascular resistance compared to the systemic uh circulation. In fact, you know, when you exercise, you can increase uh your cardiac apathy or pulmonary veins tremendously. But there's almost no increase in pulmonary uh pressures as a function of that uh decrease that rapid decrease in pulmonary vascular resistance. So, in normal uh healthy individuals, uh what kind of defines a lot of the pulmonary vascular resistance and uh a lot of it is going to be the effects of the pulmonary arterials and the small Avelar capillary vessels. So, the pulmonary arterials uh they exist in this interstitial space. Uh And when the lungs uh inflate uh that in interstitial space is kind of pulled apart that stretches open these pulmonary arterials, thus decreasing uh uh uh pulmonary uh vascular resistance in these arterials. And you see that by the blue line going down with increases in total lung capacity. Conversely, the uh small arterial capillaries, uh the opposite thing happens where as the uh lung inflates, the transmural pressure of the Avio uh increases. And this is true in both negative pressure ventilation and positive pressure ventilation causing collapse of these small capillaries uh with increasing lung capacities. They would be thinking how is that possible in negative pressure ventilation? Remember in negative pressure ventilation, the plural plural pressure drops significantly in inhalation. Uh but the avila pressure goes to zero uh as flow stops. So there's going to be uh a zero avila pressure, negative intrathoracic pressure or negative plural pressure. There's gonna be a driving gradient to collapse those Avelar uh uh or uh uh capillaries. And it's kind of more intuitive why there's a positive transmural pressure gradient in positive pressure ventilation, you're just shoving air in into the uh Avio. So these are kind of opposed and it kind of forms this U shaped curve where the lowest pulmono vascular resistance is at uh a functional residual capacity. What is functional residual capacity? You might ask for cardiologists uh it's gonna be and exhalation. So you have this wide range of capacity of your lungs, you pretty much spend your entire life in the title volume zone. I know some of you might not have thought about this since internal medicine or med school even. Uh and uh functional visual capacity is is an exhalation. It's important to remember that in both positive and negative pressure, ventilation, exhalation is a passive process in exhalation. Kind of everything just recoils down of its own accord. And at end exhalation, everything has kind of reached this state of homeostasis where you've kind of optimized your arteriolar expansion and your small capillary collapse. So that's where that's gonna be uh where your uh lowest pulmonary vascular resistance is. Um So thinking about positive pressure of ventilation that would suggest that under ze, where you're allowing passive recoil, that's zero peep, that's gonna be your best pulmonary vascular resistance. Of course, we oftentimes don't use ze or almost never use ze. In the modern era, we kind of shift this curve over by adding constant positive and expiratory pressure. So uh in positive pressure, ventilation right off the bat, we are not gonna be in our most optimal zone uh regarding pulmonary vascular resistance. So, uh you know, again, going back to our model, we think about this, we're putting air into the airways, we're inflating them. And as we discussed, as we inflate them, we're gonna collapse those uh small pulmonary arterial capillaries, uh or aar capillaries. We're gonna get uh a compression, we're gonna increase our PV R with increasing lung volumes pretty easy. Everything makes sense. Uh uh We're done with pulmonary vascular resistance. But uh and and it seems like, you know, the obvious thing would just be to use less peep, less pressure sometimes if we use less peep, less pressure. Well, unfortunately, then we get a Leis and that's just as bad. So not only do we have a U shaped curve within the respiratory cycle, but we also have this U shaped curve uh between adleta and over distension where we're kind of using peep to find where that Nader is recruiting the most number of AV units and preventing over distension. So again, this is something that's understandable, right? And I feel like maybe we can come to a solution on this. If you just find where the of that Purvis will be fine, optimize the peep and we uh optimize our pulmonary vascular resistance. But alas is not that simple because of gravity. So, within the lung, we pretty much divide our lung into different west zones, which are really just kind of dependent states. And uh in the bottom of the lung, literally, just because of gravity uh in the dependent zones, you have your highest uh arteriolar pressure, which is going to keep uh those pulmonary uh Avelar capillaries open in all stages of the respiratory cycle. Um However, at the apex in zone one, because uh the pulmonary art artery pressure is so much lower, just given the height above the R A and the height above uh the, the uh pulmonary arteries in the lung apis those uh uh small vessels can remain collapsed in all stages of the respiratory cycle. Uh So, you know what happens in inhalation is these kind of marginal uh uh Avio they collapse as well. So you have this uh variability in the optimal lung volume as you move through the different zones. It's not gonna be straightforward, it's gonna be heterogeneous and a lot of this was done in a, in standing patients. The same thing is true in supine patients. And as I, as I thought about this, it kind of got me thinking because we all have those cardiovascular patients who are very humanly and stable and then you go to turn them and you tell the nurses no, no, no, please don't turn them and they tell you no, we have to turn them every two hours uh to a avoid bed stores and you turn them and then they crash and their pressures start escalating. And, you know, again, I'm married to an OBGYN. So I'm thinking, grab a uterus, you know, there's a venus return problem, get them onto their left hand side and I do that and it never makes any difference. And I wonder if what's going on is every time we turn these patients, we have dependent zones of the lung that move from kind of maybe a West zone three to a west zone two. They're now in play perhaps. Uh but they haven't recruited yet. And then you have all these other sections of the lung that warrant play that gets smushed from the dependence and the weight of the thorax. And you have this transient increase in pulmonary vascular resistance each time you turn a patient. This is just a hypothesis. I'm throwing out there, not basing any data. But I, I wonder if this at least has some impact on why some of our patients are humanly unstable, tend to crump like when nurses turn them because they can't really come up with a better other reason, those ones, they are paralyzed, right. It's nothing to do with them. Um Or at least not to do with them volitionally. So what's the best strategy uh for uh ventilators, especially protect the RV? Um uh uh uh who was one of my Cleveland Cli uh Cleven Clinic, clinical Care fellows uh will uh know uh Matt uh who's one of our fellows who published uh this paper recently looking at optimal uh respiratory uh the therapies for right uh ventricular support. Uh uh this is an A R DS but, you know, in some ways grossly applicable to all patients. And not surprisingly, he found that the existing literature is characterized by small, simple uh small sample size increases application of treatments across studies and very deporting results and essentially doesn't help us terribly in trying to optimize uh respiratory uh settings. There are various ways you can try to uh uh look at physiological uh aspects to optimize recruitment and de recruitment. Uh You can look at pressure volume tracings to try to optimize the uh peep or the compliance is best. You can actually uh uh try to measure the compliance in the recruited segments as you bring the peep down and then try to figure out which segments are most optimal from a compliance standpoint but what I typically use is in vine control ventilation, looking at the airway pressure during like a constant volume control recruitment. And if that pressure wave form is concave, especially towards the end of the breath, that means towards the end of the breath, the delta pressure to recruit more volumes going down and you still recruit segments in play. It should probably go up on your peep. Conversely, if that curve is a concave, that means that towards the end of the breath, as your uh pressure is increasing, you're delivering much less volume and you're probably over descended. And if your uh uh airway pressure is flat, uh then that probably represents the optimal uh peep, at least in terms of uh recruitment. Uh and the recruitment, there are other strategies people use uh rich was telling me that uh at least for the prevention of valley or ventilator associated lung injury, esophageal manometry is used here to uh uh measure a surrogate for the uh transpulmonary pressure and then optimizing the vent settings to achieve good transpulmonary pressures. Although I'm not sure how much of effect this will have on RV, preload and afterload for the reasons I've discussed before. It may be helpful in evaluating for auto peep. Uh I know our electrophysiologists have been uh very patiently listening through this talk so far, but I have something for them. Electrical impedance tomography where uh uh this is an up and coming technology we use 32 electrodes placed around the thorax and a band. And then using uh uh uh an current kind of cycling between them, they'll uh define an impedance map throughout the thorax and using uh algorithms kind of define areas of uh uh a collapsed lung and hyperextended lung. And what's nice about this is uh you can define these regions through the dependent zones, even though you're only looking at a narrow area and try to optimize uh your peep and pressure. That way, we actually looked at incorporating this uh at the University of Rochester. But in the cardiac population, it seems like overkill. But certainly for a pulmonary uh population, we're trying to minimize them later induce lung injury. Uh uh Maybe that makes sense. We also have hypercapnic uh hypoxic vasal constriction. Uh This is a normal physiologic response uh uh initially to poor oration kind of makes sense. You're not getting oxygen into the avi oli, you get upstream pulmonary vasal construction and shun the blood to better Avio segments. Of course, this isn't helpful when all the Avio are bad. Uh because it's drive up PV R. Uh Obviously, you should try to mitigate hypoxia and hypercapnia. Uh And interestingly, alkalosis may lessen the effects of this at least transiently. But uh it's, it's unclear if that's a uh robust response uh on the topic of hypoxic mediated uh vasal constriction. Uh uh I don't know if, if you guys call it as well. But sometimes you've refer to oxygen as the poor man's flow land. Uh for the same reason you give it and it will reduce PV R. Uh Of course, the problem with oxygen is we know that oxygen increases reactive oxygen species and it has had long demonstrated negative effects on uh uh outcomes. Uh both of lung disease and cardiac disease. So we should try to minimize that. There's also pulmonary vaso dilators, uh things like in nitric oxide and op prostin. And although uh there's certainly uh uh a role for these therapies. Anyone with primary pulmonary arterial hypertension or secondary secondary to left heart failure or whatever. Uh And certainly a role in patients with heart transplants or LVAT placements in other conditions. It's uh uh less clear, certainly inhaled viso dialers improve PV R and oxygenation transiently. Uh uh But their effects on long term outcomes are not very robust. Um And uh they certainly won't do very much for mechanical induced changes in uh pulmo vascular resistance. Uh Certainly given the difference in cost and lack of security of any single agent. If you're gonna use one inhale, the perros, probably prefer to inhale nitric oxide just given the very uh high costs. So, modes of delivering positive pressure ventilation um will start off with the high flow uh nasal cannula, which has really been a game changer. And for those who don't think about high flow nasal cannula frequently, it's a marvel of, of engineering. Uh And, and it's able to deliver constant high flow oxygen. And by giving very high flows, typically, we, you use between 10 and 40 liters per minute, you wash out all of the air in the oral pharynx and that we're able to deliver a very constant level of fio two to the patient and humidified as well, which is definitely better than the dry air we have in Rochester. It's probably a little bit better here. Uh um uh But uh uh oh and given the fact that you're giving all of this flow, uh you're also gonna have some peep effects and that peep effects are actually linear. Uh And you can routinely uh get peep uh around 7 to 10 centimeters uh of water. However, that peep uh effect isn't constant to the regul to the respiratory cycle. I can CPAP because you're giving constant flow but not modulating flow. When you inhale, that pressure is gonna dip back down and then come back up in exhalation. So that's gonna kind of differentiate that peep effect from something like CPAP where you're maintaining the same continuous pressure uh of air and oxygen. And as we already discussed, you're gonna get the beneficial effects from preload, afterload and from improvement in oxygenation. And then similar to CPAP, we have BIPAP but different in BIPAP, we can set both in respiratory pressure and respiratory pressure. So much more similar to our ventilator. Uh And this is a uh preferred strategy for things like clearance of CO2. However, avoid very high respiratory pressures, typically greater than 20 centimeters of water is, is best practice to avoid the risk of gastric inflation. Because unlike an ET tube, you're not directing the pressure into the airways, it's kind of going everywhere into the oral pharynx. So, uh uh certainly one of the best uh trial names uh uh ever. The three CPO trial uh looked at standard of care versus CPAP versus non-invasive positive pressure ventilation. And interestingly, they found uh no difference between CPAP and non invasive post pressure ventilation benefits uh from that compared to standard uh therapy but no major physically significant change in survival. However, uh uh for CPAP uh compared to both by pa and center therapy, there was improvement in uh arterial blood gasses and improvement in respiratory distress. And I know at our hospital when uh when uh we talk about putting people on non-invasive positive pressure ventilation, everyone always reaches for bipap because more is more. Uh but uh I would argue that in patients who do not have increased work of breathing or significantly increased work of breathing, uh and who do not need assistance with CO2 clearance or already uh uh um uh hypercapnic, that CPAP is gonna be better because in bipap, you have to match the patient's respiratory rate to deliver the positive pressure and inhalation. And that triggering uh is sometimes challenging and that can result in patient ventilator, uh negative interactions for a CPAP. It's kind of simple. It's easy. It's one constant pressure. The machine doesn't have to think very hard. Uh And you still get those beneficial pressure uh effects without driving the uh uh intrathoracic pressure much higher from those high inspiratory pressures. When you think about high flow versus non invasive positive pressure ventilation, the data is not very good. There's a small study looking at need for reintubation after extubation and found those have been different. Uh There's another small study that looked at prolonged uh intubation time and high flow nasal canula did worse compared to non invasive uh positive pressure ventilation. After exhibition of that population, there are future studies ongoing looking at high flow versus non-invasive positive pressure ventilation uh for pulmonary edema. But that, that is not out yet. Uh factors associated with intolerance of non-invasive positive pressure ventilation. I'm not gonna read this to you, but I will bring up a point that I've observed in clinical practice when patients are failing noninvasive pressure ventilation and especially if they've been on bipap. I know I've had a number of cases where when you go to intimate, they've had a profound aspiration. This kind of makes sense when you're in cardiogenic shock. Uh your gastric motility is all the way down. Maybe you've been on tube feeds before your post cardiac surgery. The stomach is filling up. Uh uh but it's a regular routine postoperative patient right. So things initially are just kind of following the protocol and then uh you go to intubate them and their tummy is full. I always advocate uh if you have the time to get an abdominal x-ray uh in these cases, or I'll even pocus their stomachs with the ultrasound. And if they don't really have a, a nasal gastric tube prior intubation, I'll put one in to decompress them. Uh just in case, especially if they have evidence of gastric uh dilation because we've had a couple of, of pretty negative uh results. So talk about invasive positive pressure ventilation. Uh In general, there's no single optimal mandatory strategy in cardiac pathology. SMV is probably wrong and SMV is a mode where you have mandatory breath of the machine gives you but allows you to take your own breaths whenever you want. But those breaths will be completely unassisted. So what's gonna happen is you're gonna get all these variations between intrathoracic pressure in both positive and negative uh uh breathing probably uh increased mechanical work of breathing for these ineffective uh breaths. Uh And uh uh overall just a more chaotic system. Uh although not backed by, by studies, this is kind of the generally perceived wisdom in general ventilatory settings are used for any patient is otherwise good in the cardiac patient, typically less than eight mils per kg. And it's important to monitor how the patient responds to your ventilatory settings. It's also really important to watch for auto people as this can lead to uh human collapse, especially in in uh uh conditions where patients are preload dependent. I'm sure not gonna talk about ventilatory modes here. This is a heart lung interaction. Talk is definitely beyond the scope of uh this conversation. I will say in patients in whom you're contemplating positive pressure ventilation. If they have RV dysfunction or preload dependence, I would be very cautious about initiating positive pressure ventilation and you should avoid it if possible. This is especially true if the RV dysfunction is acute. For example, acute pe or uh acute RV infarct patients who have had more chronic longstanding RV dysfunction, for example, pulmonary hypertension will be much better able to uh uh uh work through uh uh those human uh perturbations, intra a preload quickly. When we intubate these patients, we'll use very low dose. Accommodate typically 0.1 mix per kg, mixed with low dose benzo. Uh you could consider a wake fiber optic intubation. That's not a practice I've typically uh uh used and whenever possible, we try to have cardiac anesthesia uh for the intubation and make sure you have your uh stick of neo and that be ready and try to maintain uh good uh maps. Again, it's important to minimize uh negative patient ventilator interactions as this will uh uh change these balance, these beneficial effects of afterload uh and preload reduction uh and can increase the metabolic demands. Uh If the human and the ventilator are not working well uh together who so kind of putting this all together. There are many factors uh that influence uh heart lung interactions, including uh how you're delivering ventilations, the volume status, lung compliance, chest wall compliance, which didn't even talk about uh uh but also has uh an effect, the homogeneity of the lung compliance, the pulmo vascular to RVLV function, acid base status. Uh And many of these factors are difficult to measure and tribute to the effects on the human being to varying degrees. And this kind of reminds me of something called the three body problem where if you have two masses in orbit around each other and the only force between them is gravity. You can understand this scenario from starting conditions. You have formulas and you can vary nicely and easily describe what's gonna happen over a time from an initial set of starting conditions. But if you add just one additional body, just one force, meaning interactions between them, just gravity. If you know the initial conditions, you cannot predict what your end result will be because the system is chaos. Um And if we can figure out uh how interactions will occur from starting conditions with three bodies in just one force, to think that we can perfectly predict how the heart and the lung and the ventilator will interact with each other. And every single patient a priority starting conditions is probably hubris and uh frequent monitoring of your patients is is uh required to really give them the best care possible. We can make some kind of broader conclusions. Uh in patients with V dysfunction and congestion, they probably benefit from positive pressure ventilation. In peep patients who are volume depleted, probably have more effects from impaired venous return. Uh with positive pressure ventilation. Uh the effects of positive pressure ventilation is probably more pronounced in patients with uh high lung compliance and less pronounced in patients with poor lung compliance. In RV dysfunction, the minimal uh mean pulmonary pressure, that's the combination of peep and positive pressure to achieve adequate gas exchange and recruitment uh is optimal, which is kind of stupid to say because it just says be perfect. Uh uh We should, you should always try to be uh but alkalosis may, if you get into trouble temporarily, mitigate some of the effects of hypoxic hypercapnic media vasal constriction. Uh inhaled vasodilators may improve PV R and hypoxia, especially in cases with pulmonary arterial hypertension, but won't typically help in uh uh uh A R DS long term or their causes where we have mechanical reasons for uh pulmonary uh vascular resistance elevations. Uh in patients without hypercane increased work of breathing high flow nasal canal or CPAP are good alternatives to bipap. And that's what I recommend avoid uh very high IPAP settings when using BIPAP. And if possible assess for gastric dilation prior to unplanned in patient. Um in general. Um You should use venator strategies that work in all conditions like A R DS. And they're probably appropriate for cardiac patients. And uh care should be taken when in debating patients RV, dysfunction or pelo dependent states and obvious pressure or ventilation can be used to supplement extubation and you should always try to extubate your patients every single day. Uh And if none of this still makes sense to you, uh you don't what to do. There's always ECMO. All right, thanks. Uh Thanks so much for, for being a great audience. Published June 9, 2023 Created by Related Presenters Mark Marinescu, M.D. Cardiologist University of Rochester Medical Center
BROADCASTMED