 Today I'm going to speak about the echocardiographic differences in RV dysfunction between acute and chronic lung failure. We will, I have no disclosures at all. And basically we will start speaking about the evaluation of the RV's function, what are the anatomic and physiologic features of the RV anatomy and how we can assess the RV function. I won't cover a lot about this because Dr. Roscoe already spoke a lot of this. And later on I will follow about the echocardiographic differences and the etiology of the acute and chronic RV dysfunction, especially I will mention in pulmonary hypertension and later on how we can differentiate it. At the end I will discuss a case study. So first we have to remember that the anatomy of the RV has three anatomic units. This will be formed by the inlet apex and they follow away by the off-road track. We have to keep in mind that the RV has a free wall that is thin in comparison with the LV. And it's very important to keep in mind that interventricular septum plays important function in the RV anatomy. The RCS is the mostly of the important flow for the RV. And we have more than two popular muscles here. Especially we have to keep in mind the RV anatomy is designed to tolerate volume overload but no pressure overload. In terms of ejection fraction of the RV it's important that the RV has a complex contraction when we differentiate it with the LV in both a sequential movement from the inlet to the apex and then moving forward to the infundibular. Unlikely to the LV there is less twisting and rotational movement that contributes for the RV pressure and the ejection fraction. The RV basically is larger than the LV in volume but his mass is less than the LV. With an erection fraction that is lower than the LV function. So the LV and the RV are connected in series. The output of the right ventricle will be the input of the left ventricle. As I mentioned before, the RV is designed as a volume pole while a LV is a pressure pump. The RV ejection fraction is associated with a high complabium PBR. So this means that there is an inverse relationship when the function of the RV decrease is because there is an increase on the afterload. This means pulmonary vascular resistance. And as I mentioned before, the interventricular septum plays an important part of the function of the RV and his connection with the LV. This is named ventricular interdependence. This means the position of the interventricular septum will alter the shape of the RV and the RV. And the interdependence is basically mediated in systole while the diastole interdependence is basically relies on the pericardium. With the measure of the eccentricity index we can see how these changes can be altered. Basically, we have to remind that the D shape of the LV is one of the signs that we can see in the echocardiogram when there is an increase in size of the RV. In order to assess the RV anatomy with the echocardiogram, we have three basic views that we will name this. For chamber view at zero degrees, RV inflow outflow and the mid-shore axis transgastric. Complimentary view, we will have the long axis view and the three transgastric view that we can assess for RV basal, RV inflow and RV inflow outflow. Starting from the fourth chamber view is one of the most important views because we can have a lot of information just in one view. Using the fourth chamber view, we can assess how is the shape and the form of the RV. A normal form will be a triangular shape. But if we start seeing there is a apex format of the RV, we can say that there is at least moderate dilatation of the RV. Measuring the endiastolic area of the RV and comparing with the endiastolic area of the LV, we can see if there is dilatation or no. The normal relation is less than 0.6, but when it's higher than one, there is at least severe dilatation. Remember that the RV and the endiastolic area, more than 18 is a sign of moderate enlargement of the RV. Also, as Dr. Roscoe mentioned before, we can assess the fractional area change, the ejection fraction, the anatomic M-Mode taxi and also tissue Doppler assessment of the function with Mayo-Cardial Performant Index. Remember that the fractional area change less than 35% is at least RV dysfunction, but less than 25 will be moderate dysfunction. As he mentioned, we can also measure the tissue annular systolic velocity of the S-prime, DP-DT measurement when it's present at TR and S-train. Moving forward to the inflow-outflow view, we also can hear measure the size of the RV, but basically in the outflow track, the infundibulum and the pulmonary vein annulus. Also, this view will be important to assess with color the presence or not of tricuspid regurgitation and pulmonary regurgitation. In the inferior wall, we can measure here the thickness of the ventricle. When the RV free wall is less than five millimeters, this means it's normal, but when it's higher than five, there is presence of RV hypertrophy. Keep in mind that we should avoid the anterior free wall because there is more presence of epicardial fat. In the short axis transgastric view, we can assess again the shape and his relation with the LV and also measure the eccentricity index. The complementary view, like transgastric RV basal inflow-outflow, will help us to have good alignment with the pulmonary valve and the RVOT. In order to do a spectral Doppler assessment of the pulmonary valve, we will cover this later in pulmonary hypertension topic. Also, transgastric RV inflow has better alignment for Tapsi, tissue Doppler of S-prime, and tricuspid valve assessment. Moving forward, we have to keep in mind that the general etiology of the dysfunction of the RV will be basically related to pressure overload, volume overload, or RV ischemia that will develop RV dysfunction followed by RV dilatation that later on in time will create tricuspid valve, annular dilatation, and tricuspid regurgitation. Remember that the severity of the TR is not directly related to the RV dysfunction. Other signs of RV dysfunction in echocardiography will be increase of the right atrium pressure, decrease of the LV preload, and signs of venous estasis. Moving forward for causes of pressure overload, the most frequent will be left heart failure, followed by pulmonary hypertension and pulmonary embolus. Volume overload will be mostly for tricuspid regurgitation, pulmonary regurgitation, or ASD. The pathophysiology after we have an increase on the RV after load will be RV dilatation followed with an RV voltage increase that will increase later the oxygen demand of the RV developing a RV ischemia. When this RV ischemia happens, that is decreased on the LV preload with decreased on the systemic blood pressure that also will contribute with more RV ischemia due to decrease in the coronary perfusion to the RV. As Dr. Roscoe mentioned very well, we see in thoracic surgery, we have a lot of new circumstances that will increase the pulmonary vascular resistance. So maybe we have a patient that has COPD, MFISEMA, or any respiratory disease that has mild or moderate pulmonary hypertension. But just the fact of having hypoxemia, hypercarmia, one lung ventilation, increase of PIP, or reperfusion syndrome will increase the risk of worsening this pulmonary hypertension. Special situations will be protamine reaction, pulmonary embolism, or extensive low lung resection, for example, a pneumonectomy or Velovectomy. So why is so important the pulmonary hypertension? Pulmonary hypertension is the most common cause of chronic pressure overload of the RV. And the RV will adapt with increase of the afterload through multiple compensatory mechanisms. Those are RV, hypertrophy, and increase of the venous pressure, specifically with increase on the right atron size. Regarding the 2018 world symposium of pulmonary hypertension, the definition is a mean pressure higher than 20 millimeters of mercurium. And we can differentiate using which pressure and pulmonary vascular resistance if this is related to isolated precapillary, isolated postcapillary, or mixed. Also, we can have diagnosis of pulmonary hypertension where when our systolic pulmonary pressures is higher than 30, or the transpulmonary gradient is higher than 15. The ratio between mean pulmonary arterial pressure mean pulmonary pressure less than four is a robust estimator of significance on pulmonary hypertension. And predicts also hemodynamic complications specifically under general anesthesia. So regarding the profiles, sorry, I have to move back. In 2022, the new European guidelines by the SOCIETE of European Arterial Surgery by the European Society of Cardiology, they cut off the diagnosis of pulmonary hypertension, decreasing the pulmonary vascular resistance to higher than two wood units. This means 160 dimes in order to do a early diagnosis of pulmonary hypertension and prevent later diagnosis and progression of the disease. There are five profiles of pulmonary hypertension regarding the WHO. Those will be group one with idiopathic pulmonary hypertension. Group two is basically related to left heart disease. And in pulmonary part, we will have group three secondary to lung disease or hypoxia. And group four is secondary to chronic pulmonary embolism. So what are the recommendations for assessing pulmonary hypertension with echocardiogram? First, we have to assess if there is any presence of trichospy regurgitation and the velocity of this check. When it's less than 2.8, there is low probability of having pulmonary hypertension. But when it's higher than 3.4, there is a high probability. Using the Bernoulli equation, we can assess the RBSP. But also we have to complement with two more echo signs of pulmonary hypertension. First, we have to take a look on the ventricles and see how is the ratio between the RV and the LV basal diameter. When this is higher than one, there is signs of pulmonary hypertension. The eccentricity in this and the new one could be TAPSI versus the systolic pulmonary arterial pressure ratio less than 0.55. Pulmonary artery, when we assess, we have to assess for pulmonary acceleration time. When this is less than 105, there is high signs of pulmonary hypertension. As Dr. Roscoe mentioned, the presence of mid systolic noshing and early diastolic pulmonary regurgitation velocity more than 2.2. When the diameter of the pulmonary artery is more than 25 millimeters, it's also a sign of pulmonary hypertension. And later on, when we take a look in the venous system, we can see when the IVC diameter is more than 21, and there is an increase in the collapse during the inspiration. Right atrium area at end systole and more than 18 as well. In order to have better alignment with the pulmonary artery, we will have different views. First, we have to start with the upper esophageal or the arch between 60 and 90 degrees where we can measure the acceleration time. If there is no presence of pulmonary regurgitation using this equation, we can have the numbers for mean pulmonary pressure. But if there is presence of pulmonary regurgitation, we can use the early peak in order to estimate the mean pulmonary arterial pressure using the Bernoulli equation. Other views will be the transgusted RV-modificated view and the mid-ascending artery arch, short axis. I want to mention especially the presence of acute pulmonary embolismo because there is two signs that are specific and especially pressure in this situation. One is going to be the McConnell sign that is specifically related to a dyskinetic mid-RV-free well with apical sparring of the RV and the 60-60 sign. The 60-60 means there is RV systolic pressures less than 60 and an acceleration time less than 60 milliseconds. Why is those RV speeds going to be low? Because there is no time to drive ventricle to compensate the increase of the pulmonary pressure so he cannot generate higher RV speed. In summary, we will have two causes that will increase the RV pressure over low, greater left causes of pulmonary hypertension or chronic causes of pulmonary hypertension or chronic respiratory disease. Those patients undergoing respiratory failure, thoracic surgery or develop api will increase the RV pressure over low and then a diastolic dysfunction and systolic dysfunction with RV dilatation. Later on, we should have to get the diagnosis between chronic and acute. Basically, we have to remind the chronic we will see signs of pulmonary hypertension. We will see specifically adaptation like RV hypertrophy and increase the right age and size. But maybe those are not present when there is sorry when there is also sorry sorry when there is right ventricle dilatation. So finally, what is the importance and the impact of the RV dysfunction? Because it is direct associated with an increase of mortality. A low ejection fracture and outlet change is associated with postoperative morbidity and mortality. And acute failure has mortality rate from 44 to 86%. Okay, later on I would like to follow the study case. So this is a patient of 49 years old that has been basically presenting between 6 and 12 months of decrease of tolerance to exercise that's undergoing to surgery. I won't tell the surgery because here I would like you guys to interactively help me to do the diagnosis but here definitely we can see there is an increase on the side of the RV with an increase on the size of the right atrium. We can see how the interventricular septum is flattening towards the left side and the same with the interatrial septum and there is presence of apex forming of the RV with pericardial effusion. So we start doing measurements. We can see here our RV is dilated that is also increased on the thickness. Our top set is decreased with an anatomic M mold to 1.5. Later on we put color but basically I cannot see anything. I cannot say anything about this view because it's not adequate. So we move forward to inflow outflow view. We are still having supporting elements of RV dilatation and our annulus of the RVOT is going to be almost 29 millimeters. So my first question is how long is this situation have been happening? Acute, crony. I need more information. I will wait. I'm just waiting for the poll so I'll share the results to you in a second here. Okay. I'm going to end it. Share the results. 63% said chronic. Okay. Rated we have very smart people here or we need more information. Okay. So we need more information. We have to see if this patient has pulmonary hypertension or not. So we put color here. We have to assess if there is presence of TR or not. I can see two jets here. So we have to take a decision later on. We follow to another view. We measure these two jets. Both looks like moderate between moderate and severe. We are not convinced. So we go to modification and we see a complete jet of severe tricuspid regurgitation. And we assess. There has been a contract of 0.7. We measure our RBSP is 59. And there is an incomplete spectrum, of course. This patient in pre-operative he has a mean pulmonary arterial pressure of 46. And maybe this is really incomplete. But we have to rule out left side causes, right? So here we can see our LV is affected definitely with a D shape. Our coronary sign is dilated as well. This is a sign of increase on the venous system. With an intraventricular septum really moving towards the left side. And the same with the inter-terial septum. We have to rule out how is the inferior vena cava. We can see a huge vena cava with reversal flow that complements the diagnosis of tricuspid regurgitation is severe with inverse systolic flow here. So the third question is which one of these auctions will be that cover signs of volume overload in this patient? Okay, everyone's just voting and I'll just give them about 10 seconds to link. Okay, great. Okay, I'm going to close the polls. Thanks for everyone. Okay, perfect. So we have option one. Of course, everything is dilated. The interventricular septum is in diastole. Basically, we can see there is a signs of volume in this patient. Okay, so we assess the left side of the heart. That is mitre regurgitation looks like mild with a MR fraction of 29%. With diastole, that is function of the left ventricle type one. The function is 48%. So maybe our LV is still working well. We move forward to transgastric and we can see this huge RV. There is signs of ascites here as well. We found right lung with a lot of fluid here. And the left lung is also collapsed with a lot of febrile diffusion. So later on we follow to the assess the pulmonary valve. There is a huge pulmonary artery with pulmonary regurgitation. So we can see here there is mid systolic notching presence of PR. We measure them acceleration time that is 99 milliseconds. So there is consistency for signs of pulmonary hypertension. So which one of these two options will have signs of pressure overload? Okay. Voting is open. We'll give people about 10 seconds. Okay. I'm going to close the poll in about 5 seconds. Thank you everyone. Okay. Great. Perfect. So we have signs of pulmonary hypertension with chronic compensation mechanisms like RV hypertrophy. So what is the diagnosis of this patient? 10 seconds. Thank you everyone. I'll close the poll in about 5 seconds. Okay. This patient has chronic pulmonary hypertension. And he is undergoing pulmonary and dark therapy. So following I'm going to show you the pictures after the surgery was performed coming up. We can see here the inter-atrial septum is a little bit towards the left but it's more released on the pressure on the right atrium, the same with the RV. We have persistent of course tricuspid regurgitation. That tricuspid regurgitation is still there. We measure the RBSP with an incomplete Doppler around 2035 but even though the right atrium pressure right now is a 15 and we started with 25 almost. This is working properly. The IVC is smaller. Pulmonary artery is a little bit decreased. The main PA even though we still have pulmonary regurgitation. In the trans-gastric view we can see how is that released in the interventricular septum with decreasing the size of the RV but of course we're still having chronic signs and the patient is doing really well right now the RBSP R33. No other complications so thank you so much for coming and listen to me if you have any questions. Sorry about the if you didn't understand nothing because my language is not perfect English so should I stop sharing? That would be great Selene. Thank you so much. Great presentation. Thank you. Thank you very much Selene for that. That was great. Great case. Thank you for that. So we have actually finished the session with the three presenters. We are now open to a Q&A from the audience. Several questions were actually trying to be answered to the team. I have actually that has been placed in the panel for Alex Kamayas. They are asking how reliable is the formula for estimating the fusion volume in patients with prior thoracic surgery or for localated or complex fusions when we use TE for long old rason. Hi, thanks for the question. Basically the two references I've put have not directly answered that question. In one of the references the method used to validate the formula where we were using just the surface area alone was in chronic effusions of cardiac surgical patients. They didn't mention if these were loculated effusions or complex effusions. However, I think that the locules formed after the effusion formed most likely it will remain distributed in the same way it would have. Most likely it's going to be accurate. If the locules are caused by adherences from past surgeries or past pleural disease then I'm not sure that the fluid will distribute the same way so I don't think you could use the formula. I'm not sure if you could use the same method that was described with the depth the distance of the proximal depth and the distilled depth of the probe times the maximal surface area. This was validated by actually instilling normal saline in the pleura of patients undergoing surgery. Of course this is likely that it's because of the way it was validated. I'm not sure you can use these formulas in complex very loculated effusions. Okay thank you very much for that Alex. For Dr. Roscoe, actually one of the questions from Stefan Boushev was asking what's your first choice for inotropic drop support there is RV dysfunction I actually mentioned that his first choice is epinephrine but they say that it's one of the most toxic inotropic that you could use so you did actually answer him but I would like to ask you because again like for me and then we have been at Toronto General we know what it is I think epinephrine is most of the times like our first choice so what would you have to comment on options as mill renon or WDM. Yeah thanks for that question having worked in quite a few different centres each centre has their own choice and there doesn't seem to be any difference in patient outcome with whatever you choose I think the important thing is to choose what you're most familiar with titrating on a patient so if you've never used mill renon it's probably not the time to first start using mill renon and also who's going to be taking care of this patient post-op it's probably the ICU and it's probably the nurses on ICU and if they've never seen a syringe of dobutamine before then don't be using dobutamine for the first time because it's not just your intra-operative management of the patient it's who's going to be looking after them for the next few days on ICU and they've got a bit familiar with titrating those drugs as well so it generally comes down to an institutional preference Yeah I definitely agree so for Dr. Martin regarding your presentation this actually question is not posted on the audience but in your experience Salin what do you think, under general anesthetic which will be the best way to estimate pulmonary hypertension because we are talking about cut-off values but when those patients are under general anesthetic those mean pa pressures can be actually lower than expected Yeah basically you have to assess what is the relation between the mean pulmonary artery and the mean pulmonary systemic pressure so when there is a relation less than 25% is a high estimator for pulmonary hypertension Okay so you normally are in the OR and you are looking at this mostly you are looking at your difference between your main PA and your min arterial pressure and if it's like one fourth then it's when you start to get bored Yeah Okay there is another question on the pool for Dr. Cavallas from Stefan Langevin do you use color Doppler to differentiate atelectasis from pneumonia along the So there was one of my colleagues from Invest in Morial has done some research on this it might be tricky to differentiate really atelectasis from pneumonia based on color Doppler because the way so even with pulse Doppler you could perhaps see the hypothesis that you would have more vasodilation in some instances and others however I don't think that he was able to validate this method the way we could use color Doppler is more to differentiate some kind of an organized clot that may look solid from hepatized lung so if you see color Doppler inside this solid structure that you're not sure is like clot or dense lung then color Doppler could be useful Thank you very much I have another question for Dr. Roscoe so in your experience which will be like the single measurement that you will use to quantify RB function with PE My own preference is fractional area change and once you've done it hundreds of times you actually get quite slick at it but when you start doing it there's a bit of a learning curve to avoid the trabeculations and the right ventricle the problem with that is if I do it myself throughout the case I can follow the trend if someone else does it post upon ICU gets a different number who knows whether that means the RB is different or whether it's the interobserver variability but for my own intra-op use I prefer fractional area change I agree there is one more question for Dr. Martinez Arnaud which is one of our previous fellows and really like the general so it's asking can you comment on the role of enamel mill renon in the context of RB dysfunction I never used it before I heard there is people that use it or even though they put bolus of mill renon the problem with mill renon is you can have severe effects when you go systemically basically vasodilation in the systemic pressures as well and basically in this situation you would like to keep the systolic pressure high in order to keep that RB perfused otherwise you will lose also that relationship between the RB SP and your systolic blood pressure so in my experience we try to avoid it and I never use it in hell I don't know if the rest have more experience so I'm going to do a comment on that maybe Alex you can help us here but I read like an article that you guys published from the Montreal Heart Institute with a more than 10 years experience in JCVA about using enamel renon for RB dysfunction one of the things that was commenting on the article if I recall badly is basically like 66% of the patients do well with it but there are a couple of situations where like enamel renon is not so helpful when you have a prolonged pulmonary bypass time more than 100 minutes and when you have concomitant LB failure I mean giving it inhaled it prevents the systemic basso dilatation at a certain degree but you will have some so I don't know if you want to comment on that you have any other experiences so since my experience is mostly in the ICU we sometimes use it in the ICU but mostly it's given in the context you just described so patients that have temporary right ventricular failure when they come off bypass so it's used very often in that context when we get them in the ICU and it was just a transient thing they usually get much better after I think they would in many circumstances just get better by themselves but when we receive them they've stabilized with the inhaled male renon and sometimes we use it as a repeated nebulized inhaled male renon in patients that have isolated right ventricular failure with signs of increased right pulmonary vascular resistance we see a lot of patients responding to that therapy so yeah thank you and I think another thing that we normally don't talk about is the use of prostaglandins like in an inhaled version proposteronol for example like short actin one of the benefits compared to for example NO is like on chronic hypertrophic right ventricles it will actually increase the work of the work index of the right ventricle and it will reduce the pvr too which is another consideration thank you very much guys I think Asad Marsari now is going to actually give us the results for the pool we're just going to put up another poll I'm just curious to see how many people in the audience have access to onboard 3D software especially 3D RV EF so if you don't mind just answering that question we can get a sense of how many of us can actually translate these into clinical practice yeah as the polls open we'll just give it another 10 seconds okay and thank you for all the references that people are posting as well I will try to keep track of those and add them to the list as well okay so about 21% how many responders were there Mark can you tell from yeah 52 pretty good number of people responding so many people have some 3D reprocessing but not the RV but 21% of access to 3D RV processing so thank you