 Good afternoon everyone. I'm Jaco Moreno and one of the staff from the Toronto General Hospital and I'm going to be presenting this tea for management of non-cardiac transplant. I have no disclosures to disclose with the audience and the objective of this presentation is going to be to have a better idea on how to use the transasophageal echo in the non-cardiac transplantation and how to use the transasophageal echo as a rescue tool in those situations. The first case that we are presenting is a kidney pancreas transplant on a 46 year old male that has a past medical history significant for hypertension, dyslipidemia, polycystic kidney disease with chronic kidney disease, umperitoneal dialysis and history of celiac disease and alpha thalassemia. The trans thoracic echocardiography pre-op will show a normal left ventricle, normal right ventricle and no varbular abnormalities. An indication in this situation for transasophageal echo was hemodynamic instability once the transplant started. As we can see in this example we start with the picture on the left side of the screen. We have a left ventricle and a right ventricle from a four five chamber view, um, midasophageal view where you can see perfectly like as the left ventricle is very reduced inside, very hyper dynamic, same principle can be applied to the right ventricle and then the image on the right is a sun view over the mitral valve and the LBOT tract where you can see the yellow flow acceleration which represents flow acceleration through the LBOT and a posteriorly directed jet into the mitral valve. It will pay close attention to this image. We can see that the patient has a very thick ventricle and then when we see like the septum is enlarged anything more than 1.1 centimeters is considered hypertrophied and then you can see that during systole you have the anterior mitral valve leaflet occupying like the LBOT tract. When that happens and as you will know this is considered sun and in that situation that can cause a lot of hemodynamic instability. If we go to the stomach, to the transgastric view, short axis of the left and right ventricle, we can see how those two ventricles are reduced in size, how they are completely collapsed, it's what we call like the fish mouth and then this situation was happening with norepinephrine at 0.2 mic per kilo per minute with a blood pressure that was 79 over 43 and a tachycardia, sinus tachycardia of 118 bits per minute. So what should we do? So we approached the anesthetic team, we recommended them to actually give a bolus of esmolone, one liter bolus and then we were able with that to reduce the norepinephrine from 0.2 to 0.05 with another quid pressure, this astoic was into the one-tenths and as you can see in that image, this left ventricle is not so hyperdynamic now, it's not so empty and it's working much better. If we go up to the middle of a GL view again, we have this four chamber view in the left side where you can see how both ventricles now feel and how they are contracting fine but not in a hyperdynamic manner. How if we put color now, there is not so much flow acceleration to the LVOT, we cannot see any mitral regurgitation either. If we go to the long axis view, the arctic valve is an ideal image too to assess for LVOT acceleration like in the five chamber view that we got before and then as you can see here, there is very minimal mitral regurgitation, there is a little bit of flow acceleration in the LVOT but nothing compared to before and as you can see in the lower image and the 2D, you can definitely see that the anterior mitral outlet is not getting sucked into the LVOT. When we measure, here is the ideal image to measure the thickness of the LV because it's comparable to the parastinal long axis in the transterrathic and we measure a set of 1.55 centimeters. Anything more than 15 millimeters is considered severe septal hypertrophy and it should be measured in endiastomy. So we left the probe in the patient just in case that they needed to assess the patient and then unfortunately like 40 meters later, we will call in because the patient is again unstable, they have been giving more fluid but then it's not enough and the patient is dropping the pressure again and the requirements of Norepia are increasing. When we come in the CVP we realize it came down from 15 to 7 and again when that happens as you can see again both ventricles hyper-dynamic to try to compensate that super thick left ventricles very anti-hyper-dynamic and as you can see again we can see some and then we can see flux generation in the LVOT and we can see again mitral recogitation. So what we decided to do in this situation is give another leader of volume and as you can see it's a little bit better still very hyper-dynamic but basically our management and our recommendation is to run a little bit of esmolol even if it's necessary an esmolol infusion to slow down those patients and fulfill them. The patient did fine after the surgery. So the second case that we're going to be presented here is a single lung transplantation patient. This was a 60 year old male that got a previous history of a known small cell lung cancer requiring chemo radiation complicated with ARDS and unfortunately for the patient pulmonary fibrosis requiring a single lung transplant and on the time of the case. Other significant past medical history the patient got hypertension, coronary artery disease with a PCI, requiring a barometrial stent to the LID and OSA or C-PAP. The pre-op trans thoracic echo showed by caspid aortic valve and an aortic valve area as close of one centimeter to the square but normal main gradients of 19 and a left ventricle rejection fraction mildly down to 52 percent moderately down a right ventricle systolic function and mild to moderate a caspid occultation with dilatation of the ascending order at 43 millimeters. In this situation the surgeons wanted to go straight on ECMO to the transplant so the decision was not to perform a TE unless necessary but unfortunately after induction the patient became extremely amodynamically unstable. In a situation with a patient with pulmonary hypertension and hypotension we always need to assess the performance of the right ventricle. In this case we tilted the probe from Amida Sofaxial 4 chamber view into a modified 4 chamber view where we exposed the right ventricle. Then the right ventricle function was evaluated in this case by fraction and a change which was 22 percent considering that like moderate RV dysfunction. On the right side of the screen we were using a right ventricular strain of the free wall which is 0.84 accurate with MRI for measuring systolic function of the right ventricle and we are using that using the technology of the speckled tracking. The RV strain was down in the mid and apical free walls of the right ventricle where the normal value should be always below minus 25 percent. The calculated right ventricle ejection fraction was 32.5 percent. When in normal conditions it should be above a 45 percent at least. Whenever we have a bad ventricular, a bad right ventricular function it's always a good idea to check for the degree of tricuspabric agitation. We knew from the pre-op transtorathic that it has like mild to moderate tr but then whenever you have at least moderate tricuspabric agitation the RV function is always going to be overestimated. As in this example the venacontractor was measured as 0.5 consistent with moderate tr and by measuring the tr you can to measure the right ventricular systolic pressures and as we know like it was mild pulmonary hypertension. In this case the pulmonary systolic pressures were estimated at 51. So the next step that we took we went into the Stomach transgastric X-plane over the short axis of the LB and we are presenting on the right side a 90 degrees and face view of the LB from the lateral aspect and then then we assess the left ventricle ejection fraction and it was moderately down, no mildly down as expected by the pre-operative transtorathic echo. We use the same string technology for the left ventricle and we were able to calculate an ejection fraction around 40 to 43%. It was consistent with at least a moderately down LB function. In this image you can present anything that is is the bull-sized view and anything that is red means that you have shrinking of the longitudinal strain of the left ventricle and anything that is blue is the ones that are a little bit dyskinetic and instead of actually shrinking they are even getting a little bit bigger which is showing you the zones of the left ventricle where the left ventricle is not performing appropriately. We then went to the aortic belt in the long axis view normally at 130 this situation was 146. As you can see here there is flow acceleration through the aortic belt. We already knew there were some gradients. There is a little bit of aortic recogitation too as you can see in the static image on the right side of the screen and you have it there. That's the yet coming towards us so we measure that the venacontract that was only 0.2 and we did the relationship between the yet and LBOT and it was all consistent with mild aortic recogitation and moderate aortic stenosis. This is a short axis view of the aortic belt where we have the known the left and the right coronary cusp and as you can see between the left and the right coronary cusp over here there is a raffy that's the bicuspid aortic belt and as you can see that's the only place where the aortic valve is actually opening okay. We did the gradients velocity 0.4 m per second and main gradient only 16 but those are under anaesthetic conditions. The aortic valve area that we calculate was 1.4 and not 1.0 as calculated in the pre-op trans thoracic echo. We decided to go to the intratrial septum from a bicable BU, coronary sinors, right atrium, left atrium, intratrial septum just to be sure that we didn't have any hypoxia here with a crystal clear with the scale and there was no PFO here. So what should we do? So we have a patient with moderate right ventricular dysfunction and unexpected moderate LB dysfunction probably related to mild hypotension after induction. We knew that the patient have moderate stochastic agurgitation and there's an estimation of moderate aortic stenosis. So the final decision was to cannulate the patient and went into BA Yakmo centrally. So after the single lung transplant was performed the next step is how to win this patient from BA Yakmo. This is something that I'm going to reserve for the fourth case that we are going to be presenting today and I will show you how to use transasophageal echo to win from ACMO. So the third case that we are presenting today is going to be liver transplant patient 67 year old female with n-stage liver disease secondary to fulminanepathic failure and past medical history is significant for hypertension chronic kidney disease. The patient got a trans thoracic echo preoperatively which showed a small left ventricle asymmetric left ventricle hypertrophy with a septum of 15 millimeters, left ventricle ejection fraction which was normal, some systolic anterior motion of the anterior metal leaflets and pressure gradients post balsalva up to 94 millimeters of mercury. The right ventricle was normal and there was only trivial tricuspid agurgitation and most importantly there was no mild agurgitation. So the indication in this case to do the transasophageal echo was because we knew all that high risk for some high risk for LVOT gradients as we saw in the previous case of the kidney transplant patient and we just wanted to have good interoperative monitoring. So in this patient what I want to do is check the left ventricular function, check the left ventricular thickness as you can see here there is severe asymmetric septal hypertrophy involving the basal, mid anterior, anterior lateral and anterior septal walls. The maximum septum was measured as 1.6 centimeters and in this case we couldn't see some but just pay attention to the anterior leaflet of the mitral valve which is thickened distally with mild co-optations at the center. So if we put a colorful Doppler in this four chamber view and long axis view of the of the arctic valve but we can see it's a centrally a little bit more towards the anterior directed jet and we were not able to see some here. We check for flow acceleration to the LVOT at the time there was not such acceleration but instead we find mild to moderate MR but centrally directed not posteriorly directed as it's supposed to be when you have some. So we check in this situation for right ventricular function we realize about how big this right atrium as you can see in the left side of the screen was and how the intratal septum was actually bulging into the left atrium. Then we check for PFO and there was none and we put color into the tricuspid valve and when we have a big annulus dilatation with a gigantic right atrium so what you are going to expect is to have a tricuspid recogitation. So if we keep assessing for the tricuspid so we go to the inflow outflow view and we can appreciate how this RA is such like such a big RA okay and how about this tricuspid recogitation. This is severe tricuspid recogitation and definitely is the last thing that you want to have when you are doing a liver transplant. So you can do assessment we were able to measure the recogitan jet of the tricuspid valve was up to 60 milliliters consistent consistent with severe and effective recogitan area of 1.3 centimeters to the square which is extremely extremely bad for the patient. We went into the hepatic vein following the IVC and when you have a severe TR you want to know how your liver is going to be affected. When you go there you check with pulse width Doppler and then we check with pulse width Doppler we confirm systolic reversal of the hepatic vein flow. We keep examining the patient and again remember transasophageal echo can help us to determine more things during an examination included as you can see here a right side of the pleural effusion like this case. You can trace the area and determine how important it is. So if the area is less than 20 centimeters we have a small pleural effusion that's than 400 mils if it's between 20 and 40 we have a moderated effusion if it's more than 40 centimeters to the square you have a large pleural effusion. Another important utility of the transasophageal echo in liver transplantation is to determine if the patient will be able to tolerate the partial IVC clamp as per the classic piggyback technique for side-by-side cabal anastomosis. In this situation you want to pay attention to the possibility of LVOT flow acceleration and SAM in hypovolemic states. In this case there wasn't LVOT gradient neither flow acceleration and the patient was able to tolerate relatively well hypovolemia despite asymmetric septal hypertrophy of the lab ventricle. Finally you want to assess both ventricles after the clamp is released but most importantly you want to check how severe is the TR post transplant to determine how this will impact your new liver. In our case we still have like severe tachycardic vegetation with even more apathic vein flow reversal. The last case that we are presenting is a 74-year-old gentleman with adiopathic pulmonary fibrosis, double lung transplant with dyslipidemia and GERD. Normal echo is set for a partial fusion of the right coronary cast and left coronary cast of the artery valve but without AES or AI with mild pulmonary hypertension. The indication 40 in this case was after the transplant was done the surgeons and the anesthesia team was unable to win the patient from VA ECMO due to high VA pressures so we were calling and we put the probing. So that was on 1.5 liters where they got the stock because the patient got hypovolemics so on minimal ammo support we checked the right ventricular function to see how it was tolerating these VA pressures which by the way this right ventricle didn't look so great. Then we went into the stomach and assessed the LV for volume status as you can see here that we look very hyper dynamic and under feel in this situation every time that we try to win from the ECMO flows the RV will worsen its function and the VA pressures will rise. So we decided and checked the pulmonary veins. In this case the left upper pulmonary vein was assessed and we recorded high velocities in this vein. The other three pulmonary veins were seen and were normal with normal pressures. So how much is too much pressure in a pulmonary vein? So the recommendation is not to have a flow more than one meter per second not to have a gradient between the pulmonary vein and the left end through more than 10-12 millimeters per mercury and half a diameter which is going to be smaller than five millimeters those are criterias for pulmonary vein stenosis and it used to happen up to 1% interoperatively. So after the stenosis in the left upper pulmonary vein was done the velocities were back to normal. So then we needed to win from ECMO again and we started at three liters per minute and progressively we went down normally you go down by 0.5 liters per minute every five minutes until the cannulation and you need to check the whole time for RV dysfunction and the casper of agogitation. So you can see here this is a 2.7 and again you want to sit in the long axis view you want to check at the same time the patient is thermodynamically stable that you have an adequate PA-FIO2 ratio and you have a good lung compliance and always remember to check for your TR and we keep winning down to 0.3-2 liters you keep going 1.5-1 and finally off. Thank you very much for listening and I'm waiting for your questions.