I'm gonna talk about gas exchange. So we'll be able to go into a little bit more detail I already introduced some of these concepts about about shunt and dead space We'll go into a little bit more detail about these concepts now here same disclosures Here's the board outline for gas exchange Understand the mechanisms that match ventilation and perfusion understand the concept and calculation of pulmonary shunt and the venous admixture method Concept and calculation of dead space in the lungs know how the po2 Influences carbon dioxide transport and how pco2 influences oxygen transport by the blood won't have too much time to talk about this You know the factors that determine the alveolar po2 Concept an estimation of ventilation perfusion mismatch and the mechanisms that increase the a a po2 difference or the a gradient so Gas exchange right all about a function of ventilation and perfusion This is the sort of hallmark idea of ventilation perfusion mismatching two ends of the spectrum as IRA alluded to the far, right? We have this concept of interpulmonary shunt ie a lung unit that is not getting any ventilation, but still receives perfusion Hallmark findings of interpulmonary shunt Hypoxemia, right as well as now you've got loss of loss of lung volumes. They're Decreased in pulmonary compliance with the loss of an expiratory lung volume other side of the equation is alveolar dead space This is ventilation without perfusion Hallmark findings here are increases in our co2, right? So more difficult time with co2 clearance and as IRA alluded to Differences between the co2 you may measure that's coming out of the lung and the co2 that you might see In the bloodstream or the pco2 now remember Those are the two extremes right shunt complete shunt and complete dead space but really what we see in the intensive care unit or these VQ mismatch regions in between right where we have VQ regions less than One that are on the side of interpulmonary shunt VQ regions greater than one or that are on the side of increases in dead space and the classic disease process Right that increases both shunt and dead space is acute respiratory distress syndrome That's the hallmark finding of the disease that we have elevations in both dead space and elevations in interpulmonary shunt and hypoxemia So as we think about ventilation perfusion matching, it's important to remember Like what's happening in the alveoli in these different circumstances? So what we see on this graph is the pco2 in the alveoli relative to the pa o2 in the alveoli in this circumstance There is no Ventilation, but there is perfusion. So what's that? All right, that's shunt So what does what's happening in the alveoli the alveolar gas most closely? Represents the gas you would see in the mixed venous system i.e Right a low pa o2 in that system and an elevated pco2 Opposite is dead space where we do have ventilation but no perfusion So what's happening in the alveoli the alveolar gas most closely represents what we would have here in the atmosphere of inspired air, right? Relatively high pa o2 and it'll or high po2 and low pco2 Now when we think about hypoxemia Right. It's important to remember that there are multiple mechanisms of hypoxemia that we might encounter Right four main mechanisms of hypoxemia two are very easily correctable and two are not so easily correctable Right hypoventilation and low inspired pa o2. Those are relatively easily correctable the less easily correctable are the ones that land patients in our intensive care units, right the intrapulmonary shunt and Ventilation perfusion mismatching. So let's start here on the far left with hypoventilation So why is it the hypoventilation can cause hypoxemia? Well, this comes down to another equation that you absolutely have to memorize, right? Which is our alveolar gas equation where the alveolar pa o2 is the fi o2 times atmospheric pressure minus the pressure water Minus here it is, right the pco2 divided by the respiratory quotient so if we go through this sort of illustrative exercise of we have a rise in our Pco2 from hypoventilation from 40 to 80 you substitute 80 in here instead of 40 right now I have a drop in my alveolar pa o2 to 50 But if we simply increase the amount of fi o2 by a relatively small amount I eat put them on 30 put the patient on 30% fi o2 is compared to 21% fi o2 I've now overcome What we would see from the increase the drop in po2 that would come from an increase in the pa co2 Can be overcome very easily by just a small amount of oxygen The same holds when this low inspired oxygen characteristic ie that we often see at altitude, right? So why is altitude important? Well, the atmospheric pressure is what changes as we go up in altitude, right? So if we are at an altitude of 3,000 meters the atmospheric pressure may drop to 500 Again, I have a drop in my alveolar pa o2 down to 45 But if I put the patient on a small amount of oxygen or here the climber on a small amount of oxygen, right? Now I can restore that alveolar pa o2 Easily overcome with even a couple of liters of oxygen as an example So if those aren't the two causes low inspired pa o2 or hypoventilation, right? Then now we get back to the ones that land us land them in trouble VQ mismatch and interpulmonary shunt and the characteristic finding here is here we have an elevation in the a a gradient or the difference between the alveolar pa o2 and the pa o2 that we measure in The bloodstream, right and how do we calculate the a gradient simple goes back to that alveolar gas equation, right? So we plug all of our values into the alveolar gas equation barometric pressure pressure of water the fi o2 that we're giving The measured PC o2 and the and the respiratory quotient and so under normal circumstances, right? P big a o2 or alveolar pa o2 is about a hundred the pa o2 we measure in the bloodstream is about 80 under Healthy adult conditions, right? So a normal a a gradient is generally around 20 Although this can have some age dependence younger age patients older older patients may have higher a a gradients But when we have a patient with significant disease let's say RDS for example and we go through this illustrative exercise of a patient that has a pa o2 of 60 on point 6 fi o2 with the PC o2 of 60 now We see that their P big a o2 or the alveolar o2 should be through is 352 yet What do we measure at the at the bedside? We see the P P little a o2 or the alveolar? Arterial o2 is 60. So the a a gradient is significantly elevated in this patient at 292, okay so One of the most important components right that can elevate an a a gradient. We have an elevated a a gradient We should be thinking about VQ mismatch and intrapulmonary shunt. What's the concept behind intrapulmonary shunt? Well, it's this idea right that I might have a normal lung unit with blood that goes by it It gets oxygenated and then the pa o2 on the other side is relatively high Equivalent to what the sort of capillary po2 would be but I have this lung unit, right? That does not receive any ventilation. So it's the venous blood that's coming by right and so this can be Conceptualized into what becomes the shunt equation, right? So we think about the determination of shunt we have our total cardiac output and our our mixed venous content, right? What we see in our pulmonary artery Some component of that cardiac output hopefully most of it right is going to the pulmonary capillaries and will be Oxygenated and pick up oxygen based upon the pulmonary capillary oxygen content But there is some component right that does does not participate there in that gas exchange I either shunt component where it does not pick up any oxygen at all Alright and based upon this cardiac output then mixes on the other side and you have your total oxygen content of the arterial blood that you see as the combination of the two and in fact This can be this concept can be used to actually quantify the degree of shunt with the shunt Equation as long as you know all the components, right? So what are the components that you need to know? We need to know the total cardiac output, right? You need to know the The oxygen content in the capillaries, which is estimated by the alveolar gas equation, right? and the components that go into the alveolar gas equation, you need to know the arterial content in the Arterial system ie we need an arterial blood gas and then you also need a venous blood gas to know the arterial content in The venous system so to do that to calculate the shunt to calculate shunt true shunt, right? We need cardiac output and we need all these other components I even need a PA catheter for example to be able to do this They may still ask you this conceptually, but of course, this is not the reality of right of what we do hit the bedside anymore one of the most important points though is that remember that Intrapulmonary shunt is not correctable with 100% fi o2 ie no matter how much oxygen I put in that system, right? It's not going to diffuse because there is zero ventilation that's going to that lung unit, right? We so to to really measure the true shunt fraction you have to do the shunt equation on a hundred percent fi o2 If we don't do it on a hundred percent fi o2, then it's a combination of intrapulmonary shunt and ventilation perfusion mismatch, right? So what do our the our hypoxemia metrics that we may use at the bedside or at least theoretically might exist Tell us about the mechanisms of hypoxemia. So shunt equation on a hundred percent fi o2 That's the only thing that's going to tell us truly what the degree is of pure Intrapulmonary shunt if we do the shunt equation on less than a hundred percent fi o2 Then this is the combination of shunt and VQ mismatch and in fact That's the same with the AA gradient you get similar information the degree of height of the degree of intrapulmonary shunt and the degree of VQ Mismatch will will be seen with the AA gradient But we don't use most of these right at the bedside. What do we use at the bedside? Well, we think about things like the PF ratio or the SF ratio or the oxygenation index or the oxygen saturation index and one of the important points is that all of those metrics in fact Can be more can be impaired with any of these four mechanisms of hypoxemia. Okay Now why oh I why PF ratio well, they tell you slightly different things, right? They all reflect the degree of hypoxemia But we've had a shift at least in our pediatric ARDS thinking to try to think about the oxygenation index In addition to just the PF ratio because it captures the degree of respiratory support that's needed To achieve that degree of oxygenation and you have this patient who you've just intubated Let's say who's on a PIPA 5 with a PA o2 is 68 fi o2 0.6 and the initial mean airway pressure is 8 Patient has a PF ratio of 100 we would characterize that as relatively severe hypoxemia or severe ARDS You wait an hour, right recruit that lung and the PF ratio now goes up to 240, right? Has that patient's lung disease severity changed dramatically in that one hour period likely not right the actual component of the lung injury So that's where the oxygenation index comes into play because the PF ratio does tell you a little bit more about the response to therapy while the oxygenation index is capturing the overall cost to achieve that degree of oxygenation and that's conceptually the the idea of why Oxygenation index was incorporated instead of the PF ratio at least into the pediatric ARDS definitions Although that's not necessarily universally accepted certainly not in the adult world Okay, that's oxygenation. So let's switch now to the other side or Shunt let's switch to the other side of dead space and remember dead space Hypercarbia hallmark clinical finding and in particular a large difference between the airway and the arterial co2 So dead space is all about co2 removal adequate co2 removal requires us to have an effective Alveolar minute ventilation right now What do we set we set the total minute ventilation on the ventilator right in a passive patient based on the rate and the title? Volume right, but that title volume is not all Going to the alveoli, right? There's a component of that title volume that goes to dead space and as we think about the dead space There's two major components as as Ira was alluding to there's anatomic dead space and alveolar dead space now under conditions of health We have almost no alveolar dead space, right alveolar dead space Develops when we have problems with pulmonary perfusion things like microvascular thrombosis we have impairments and cardiac output like pulmonary hypertension or a pulmonary embolus as an example, or Perhaps how we might be managing the ventilator right where we have over distention for example, right with a deke with an increase in pulmonary Vascular resistance and a decrease in pulmonary blood flow the anatomic dead space classically is fixed Although when we put somebody on the ventilator We may introduce more anatomic dead space right with the tubing and things like that that we apply on the ventilator and so Remember not all minute ventilation is the same, right? So if I want to think about co2 clearance, right? And I have this patient all receiving eight liters per minute a minute ventilation I'm not going to necessarily get the same amount of co2 clearance because that co2 clearance is dependent upon me Overcoming at least the anatomic dead space assuming that the health and of the patient is the same or the Patient doesn't have significant amount of lung injury So these three different conditions all with a minute ventilation of eight liters where I have, you know One condition of a very low tidal volume to let's say this is an adult patient with 250 ml is a tidal volume at a rate of 32, right my effective minute ventilation in the alveoli is Much smaller than it would be if I used a tidal volume of one liter For example and eight breaths per minute right because I overcome that anatomic dead space right with that larger tidal volume Now, of course, I'm not advocating that this is what we do, right? There's lots of harm if we ventilate patients with a very high tidal volume its effect on the lung mechanics, etc But co2 clearance is more effective with the larger tidal volume than it would be with the lower tidal volume And this is the balance that we have to play when struggling against mentally introduced lung injury Now, how can we measure dead space? Well, there are sort of three classic ways to measure dead space One is based upon the Douglas bag and measuring mean expired co2 directly as as IRA was alluding to So this is based upon that equation that IRA had put up there of total VD VT The bohr-enghoff Estimation equation is equal to the pco2 Minus the mean expired co2 over the pco2 and a Douglas bag is collecting the co2 that's being exhaled and you can calculate the mean expired concentration on their Cumbersome difficult for us to do in in reality at the bedside Volumetric capnography is an alternative way where we can get an average of the mean expired co2 and then there are simpler and sort of more crude approximations either coming from the alveolar gas equation the corrected minute ventilation or time-based Capnography, which I'll allude which I'll cover here in a second so why is it that with dead space we see a large difference right between the The co2 we measure at the airway and the co2 that we have in the bloodstream Well, here's the sort of concept behind it if I have a normal situation here, right where I have the venous oxy venous venous blood you get a Diffusion of the pco2 across the alveolar capillary membrane and that pco2 is exhaled So if I have all lung units that have normal amounts of perfusion, right? Then there is an equilibration that happens here in contrast if I have no Perfusion to this lung unit right then there is no pco2 that's getting to that lung unit The concentration of the pco2 there is zero compared to the to this to lung unit model of 40, right? and I see that the end tidal co2 is is Net effect is significantly lower at 20 and I have a large difference between the pco2 and the end tidal co2 How can we calculate this? Well one way would be volumetric capnography So volumetric capnography is different than time-based capnography, which is what we use Classically at the bedside in that it is integrating the co2 and the volume together Okay, it still has the same classic phases of the time-based capnography curve oops phase one here Which is our anatomic dead space right where you don't see any increase in co2 co2 on this axis Right and tidal co2 here pco2 here and this is the exhale tidal volume So you don't see any rise here at the beginning of exhalation. That's our anatomic dead space. This is our alveolar plateau phase Right, and then this is that mixture between phase 1 and phase 3 or phase 2 so I can I can compartmentalize the various different components of Ventilation here with volumetric capnography where this area Z is my total dead space ventilation of anatomic dead space this area X is my alveolar ventilation and this area Y is the L is the alveolar dead space fraction Now We don't use volumetric capnography much, right? instead what most of us use at the bedside is time-based capnography and as IRA was alluding to In a circumstance where I have a normal appearance of time-based capnography with a flat portion here Ie I have a nice true alveolar plateau Then the end tidal co2 that is this point a right more closely reflects the mean Expired co2 which is functionally the area underneath this curve Okay But if I have a circumstance like what you see in the dotted line Right of somebody that's got airway obstruction or lower airway obstruction where I don't necessarily achieve that alveolar plateau Right, then the calculation of the mean expired co2 using the end tidal co2 is not really valid So you have to be very careful in calculating dead space from the end tidal co2 Circumstances of significant lower airway obstruction where you don't have a flat alveolar plateau. So this and Tidal co2 based estimate in fact is not truly VD VT It is called a VD SF or the alveolar dead space fraction and it most closely represents the alveolar dead space not Physiologic dead space of VD VT and if you think about it conceptually we have 35 as a normal end tidal co2 We have 40 right as a normal PC o2 that AV DSF turns out to be about 8 or 9 percent, right? Not 30 percent of a normal VD VT that we see But what we know is that this fraction this alveolar dead space fraction is relevant, right? It is associated with mortality even after controlling for the degree of hypoxemia so this is on all ventilated patients if you stratify patients by their degree of hypoxemia i.e A surrogate for intrapulmonary shunt, right? Patients with higher dead space have much higher mortality all ventilated patients and even the subset with ARDS So this highlights that concept that both dead space and hypoxemia Dead space and shunt are important concepts in the sort of prognosis of our critically ill patients It may also help us determine therapy, right? If we see a patient that has significant elevations in dead space We have to think there is a problem with pulmonary perfusion for this patient. Where is that problem coming from? Is it an impaired cardiac output? Is it microvascular thrombosis, for example for somebody with ARDS? Am I over distending their lung for example in how I'm applying my peep strategies, for example in the ventilator Okay, and that's it. That's gas exchange in 20 minutes

gas exchange

ventilation

perfusion

intrapulmonary shunt

dead space

hypoxemia