 Good morning, everyone. I'd like to start by thanking the organizers for the invitation to speak at this meeting. The topic I've been given is to cover the perioperative role of TEE and assessing right heart function in patients with severe lung disease. I have no disclosures or conflicts of interest. I will quickly talk about the lung diseases affecting the right side of the heart and how the right heart adapts or maladaps these disease processes. We'll briefly cover the management of RV dysfunction, but as this is an echo lecture and an echo conference, then the main part of this talk is going to be about the role of TEE and assessing RV function. So lung diseases can generally be divided into four main categories depending on the underlying pathology. With the obstructive pathophysiology, such as end stage emphysema, we typically get dynamic hyperinflation, which increases intrathoracic pressure, and this results in a reduced preload to the right side of the heart. As the disease progresses even further, we eventually get an increase in RV afterload. The other types of lung disease typically affect the heart just by affecting RV afterload, an increase in pulmonary vascular resistance, and pulmonary hypertension. And just to remind ourselves of the definition, so pulmonary hypertension is a mean PA pressure, more than 20 millimeters of mercury, and then it's subdivided into precapillary pulmonary hypertension, where you have a high PVR and a normal wedge pressure. You can get postcapillary pulmonary hypertension with a normal PVR and a high wedge pressure, and then there is a third type that combine pre-postcapillary pulmonary hypertension. And pretty much all pulmonary hypertension, secondary to lung disease, it's precapillary in nature. So you have a high PVR, a high pulmonary pressure gradient, and a high diastolic pressure gradient with normal left-sided heart pressures. In terms of RV adaptation, you have to take into consideration whether the increase in afterload is acute or chronic in nature. This is going to be covered in the next lecture in more detail, so I'm not going to spend any more time talking about this. Other than to say that there are significant differences in the echo findings. I think we all know the basic principles of managing RV dysfunction. You want to optimize the preload, which usually involves diresis or dialysis to bring the dilated right ventricle back down its styling curve. You want to induce measures to reduce the afterload, so some form of pulmonary vasodilators. You want to augment RV contractility with ionotropes. And then you have to maintain your right coronary perfusion pressure by avoiding any systemic hypotension, and it's usually achieved with vasopressors. So let's move on to the main part of this lecture. So in a perioptic period, there are several methods we can use for evaluating the right ventricle. Imaging modalities including CT, echo, cardiac MRI, but for an intra-optive period, echo is the most feasible. But we shouldn't use echo in isolation. We also have our hemodynamic monitoring, and we should integrate the findings from our echo with our hemodynamics to give us a fuller picture of what's going on with the patient. So what's the role of TEE? Well, hopefully it's going to help us get an early diagnosis of RV dysfunction, and we'll talk about the geometry systolic and diastolic function. And then once we've made some management intervention, then we can use TEE to assess whether these interventions have been effective or not. So how can we assess the right ventricle? Well, let's just have a quick look at the geometry. We all know the RV is quite an odd shape. I equate it to sort of like a narrow teapot, where the tricuspid valve is the inflow, and then the outflow is the spout going out through the pulmonary valves. And it's useful to know what the normal values are, what a normal sized right ventricle is, so that we can spot abnormal very quickly. How do you assess RV systolic function? Well, there's many ways of assessing it with echocardiography, which tends to suggest that none of the methods are perfect, and they all have their pros and cons. And in the intra-object period, you have to take into consideration how much time do we have to assess the RV at any moment, and how accurate and objective do we want to be with our measurements. Very rapid assessment with eyeballing takes just a few seconds, but it's not going to be as objective and accurate as something like 3D RV ejection fractions. So it's a balance of how much time we have available and how accurate and objective we want to be. So let's start with eyeballing. I suspect most people on the spot are completely normal right ventricle from a completely dead right ventricle. But it's that sort of range of dysfunction in between, whether it's mildly reduced, moderately reduced, and if you do an intervention as it got slightly better or slightly worse, that's what can be challenging with eyeballing. And actually studies have shown that even when experts assess RV function by eyeballing, they actually get it wrong about 40% of the time. So it's very quick, but it's often inaccurate and it's certainly not objective. So what I might consider mildly reduced function, the next person might consider as moderately reduced function, someone else could even think it's severely reduced function. So quick, but not objective and not that accurate. What about eccentricity index a very quick simple method. We take a trans gastric short axis view the left ventricle should look circular. If it doesn't look circular it looks oval or D shaped. Then they suggest that the right ventricle has some overload either pressure or volume or both. And down side to this it all it actually represents is an increasing RV pressures compared to the left it doesn't tell us directly about RV systolic function. And it generally occurs very late in the disease process when the RVs already on a slippery downhill slope. I think most people know what taxi is. So very old method been almost 40 years ago it was first described. And we're going to measure how far the tricuspid annulus moves from the base of the heart to the apex of the heart in sisterly. One of the problems with TE is getting the alignment because it doesn't move directly towards the probe or directly away from the probe, as it does with trans thoracic and the apical four chamber view. And if we take this example, and we em mode across here, then you can see that we're not actually in alignment. And this one gave us a value of about 18 or 19 millimeters for our taxi, which is still just about normal. But actually if we use anatomical em mode, which is now available on a lot of machines, we can get a more accurate measure of taxi and it turned out to be about 27 or 28. So you can underestimate taxi, if you just use in the simple four chamber view without the use of anatomical em mode. And the caveats the taxi well it's only looking at longitudinal function of the right ventricle, and it isn't actually representative of global RV systolic function in patients who've had their pericardium opened. So patients who've had cardiac surgery. As soon as you're open to pericardium, the taxi drops. That doesn't mean that the RV is suddenly decreased in function. It's just, you lose a bit more of the longitudinal function and you gain radial function to compensate for this. And also, although quite rare you can have regional abnormalities of the right ventricle. On the left hand side, the base of the heart is moving reasonably well, but the rest of the RV is a kinetic so this would overestimate RV function with taxi. And on the opposite side, you have what's the classical McConnell sign, the base of the heart doesn't move at all, but towards the apex is contracting, and therefore taxi would underestimate the function of this right ventricle tissue Doppler moving at the S prime velocity. It's been around for about 20 years. And instead of looking at how far the annulus moves we're going to look at how fast the annulus moves. The problem with transosoftial echo again is getting the Doppler alignment. So there's no way in a four chamber view you can aim the Doppler on this angle. So some studies have actually taken the modified transgastric RV inflow view and taken this part of the tricuspid annulus moving from base to apex using their tissue Doppler pulse wave to give you the waveform and then measured the S prime from here. The problem with S prime, you have to get good Doppler alignment. Again, it like taxi it only looks at longitudinal function and again like taxi. After your pericardium has been opened, then it's actually inaccurate measure of RV systolic function. And a few people have highlighted that in this transgastric view, it's not actually the lateral annulus that you're measuring the velocity of. It's the posterior annulus. And does the posterior annulus move as quickly as the lateral annulus. I don't sure that's been looked at fully. Okay, fractional area change. Again, a very old method, very simple method. You measure the area in end diastole, you measure the area in end systole, you take one from the other divided by end diastolic. And you're left with a fractional area change. There are a few methods where they seem to grade RV systolic function into mild, moderate and severe dysfunction based on the fractional area change values. But again, it has its problems. You have to have a good RV focus for chamber view, and you have to avoid foreshortening. Otherwise, you're going to get your areas incorrect. So I've reviewed the RV OT contribution to RV ejection, and there is significant inter-observer variability. So the intra-observer variability is fine. So if I measure it at various points throughout the operation, then actually that's a feasible method of assessing RV function. So if I measure it at the beginning, and someone else measures it at the end, and then someone measures it on ICU afterwards, then any changes in the fractional area change may be due to inter-observer variability, rather than a change in RV function. Okay, RV strain. So RV strain is a lot more objective with much less inter-observer variability. But now these techniques are starting to become a lot more time consuming. So with these strain, you have to decide whether you're just going to look at the free wall or you're going to include the septum, and if you do include the septum, you have to work out which part of the septum belongs to the right ventricle and which belongs to the left ventricle. You need a good frame rate for this, which is usually not too much of a problem with the modern technology. You have to be very careful that you've positioned a region of interest only over the RV myocardium and not over any of the pericardium. Most of the software is actually designed to do strain imaging of the left ventricle. So you have to kind of trick the machine and force it onto the right ventricle to get the values. So it probably takes maybe three or four minutes to start to get some useful numbers out of this. And again, you have to decide whether you want to look at just free wall or the whole of the RV. The myocardial performance index for the right ventricle, the T-index for the RV. You can use your tissue Doppler waveform that we saw earlier. It is a little bit time consuming again to do all the calculations. You have to have a very clean spectral Doppler waveform to get very accurate measurements. And the one downside to this is that when your RA pressure is elevated, that actually will give you falsely low myocardial performance numbers, which will suggest the RV is functioning okay when it may not be. And then finally we have the 3D RV ejection fraction reconstructed from 2D images. So from quite time consuming, although the technology is getting better these days. A lot of the time, the software is not on the machine, so it needs to be taken away from the machine and reconstructed offline, often requiring stitching of beats together. Some machines now do have the software on the machine and can get it down to one beat, but it is a lot more time consuming. Oh, so just to summarize, this just gives you the normal values of all those systolic RV function parameters just so we know what we're aiming for, what we're looking for. What about diastolic function? So like the left ventricle, diastolic dysfunction will occur before systolic dysfunction. So if you can pick up diastolic dysfunction, then you can intervene earlier, you make your diagnosis earlier, you intervene earlier, hopefully the RV doesn't progress down a systolic function pathway. So your RV diastolic function is evaluated using combination of trans tricuspid flow and your tissue Doppler waveforms. So it can be quite time consuming, aligning the Doppler for the trans tricuspid flow to get your E wave and A wave, measuring the ratio of E and A, measuring your deceleration time, then getting your tissue Doppler waveform, trying to get a good spectral Doppler image to measure your E prime velocity, and then putting all of this together to decide whether the RV diastolic function is normal, whether it's improved, got worse. So ideally, if you could measure it very quickly, it would be superb to make the diagnosis early, but unfortunately it is quite time consuming. And also your E velocity will change with preload. So there are some inaccuracies as well. So I just thought I'd finish off with a few echo extras. I think we all know how to calculate your right ventricular systolic pressure from our TR jet using the simplified Bernoulli equation and extrapolating to say that's the same as your PA systolic pressure so I'm not going to talk any more about this. But what if there isn't a reasonable amount of TR, then you can still actually calculate your PA pressure, you can calculate the mean PA pressure using your pulmonary artery acceleration time or your RVOT acceleration time, then slightly where you want to put the pulse wave Doppler packet either side of the pulmonary valve. But it gives you this waveform, you can measure the acceleration time, so from where the waveform starts to where it peaks, and that time can be put into this equation and that will help you calculate the mean PA pressure. This waveform also gives you a bit of other information. If there is no systolic notch, then that suggests that it's post capillary pulmonary hypertension. If you get a systolic notch, then that's then suggest if you have pre capillary pulmonary hypertension is supposed to represent an arterial reflectance wave. And the earlier the systolic notch in the waveform, then the more severe the pulmonary hypertension. What about pulmonary vascular resistance? Well, there's a few studies that have tried to develop equations to try and calculate the PVR and various echo parameters. Here's just two of them. So theoretically you could measure the PVR, you could then do an intervention, give a pulmonary vasodilator, and then you could see whether how much your PVR has dropped if it's dropped at all using these measurements. Again, a little bit time consuming. And for those advocates of ventricular arterial coupling, then there are a few studies that have looked at whether we can assess RVPA coupling using echocardiography. And essentially, there is on the numerator, there's some form of RV systolic function on the denominator is some form of afterload. And you look at the ratio, you can do an intervention and see what's happened to the ratio is the numerator still higher than the denominator as the ratio is still the same. So this theoretically allows us to monitor any therapeutic interventions, not just looking at whether the PVR is going to fall down, but as the RV function changed in accordance with that as well. So with that in mind, we've covered lung diseases affecting the right heart and how the right heart may or may not adapt to that. We've looked at the various methods for assessing RV function with TEE and their pros and their cons. And then finally, I've just given you a few echo extras that we can measure if we have enough time. Thank you very much.