 Our next speaker is Sam Simone Lalanset, Dr. Lalanset is a cardiologist. Currently he's conducting critical ultrasound fellowship in your institution. I'm sure he's using full advantage of your mentorship. We'll start his pre-recorded lecture. I believe Dr. Lalanset will be available to answer questions at the end of our session. Thank you very much. Greetings everyone, my name is Jean-Samone Lalanset. I have completed my training with cardiology and I am currently a critical care fellow at the University of Montréal and Montreal Heart Institute. It is with great pleasure that I have accepted the invitation to discuss about the perioperative and clinical role of liver transplant of a girl ultrasound or more exactly, liver transgiastric abdominal ultrasound. I don't have any conflict of interest for this talk. The main objective of this talk will be to review abnormal IVC, hepatic vein and partal vein imaging using transgiastric abdominal ultrasound to understand the clinical significance of abnormal Doppler findings in the liver and to talk about the partal vein pulsatility index. Let's focus on IVC and hepatic veins. As Dr. Lalanset well explained in his presentation, IVC and hepatic veins you can be obtained from a transgiastric view by rotating the probe to the patient's right. Around 0° the IVC can be seen in short axis along with the three hepatic veins. Around 90° along axis of the IVC can be obtained with one of the hepatic veins. IVC and hepatic veins digust examination can be useful in many ways. Dynosis of rib ventricular systolic and diastolic dysfunction and pulmonary hypertension, assessment for IVC stenosis or obstruction in liver transplantation or transplantation, ECMO and artificial R, ruling out abdominal IVC tumor or thrombus when an abdominal compartment syndrome is suspected or intraoperative monitoring during renal cell carcinoma surgery involving the IVC. Looking at the size of the IVC and the hepatic vein flow may identify the mechanism of hemodynamic instability. The presence of a reduced means systemic venous pressure secondary to hypovolemia or a pure vasodilatatory shock. IVC will often be small and the hepatic vein flow will be normal or increased. There is increased resistance to venous return. The IVC will be distended if the obstruction is located at the junction of the IVC and right atrium or collapse if it is secondary to an abdominal compartment syndrome. However, in both cases, hepatic vein flow will be abnormal with greatly reduced velocities or even no flow. Finally, in the context of a cardiogenic etiology, IVC will be dilated. The hepatic vein flow will be abnormal with reduced systemic to deltic ratio and permanent at real reversal velocity. Now, let's see how it can be useful with real cases. Here is a 37 years old man who had a fountain procedure for congenital heart disease. He became unstable after winning from cardiopulmonary bypass. A view from the IVC was obtained before and after correction. A pulse-wave Doppler of the hepatic vein was mostly normal before cardiopulmonary bypass. But velocities were greatly reduced after. This finding in combination with a dilated IVC is compatible with the IVC stenosis post-fountain procedure. The possibility of an IVC obstruction or stenosis should always be verified after a procedure involving manipulation of the IVC. In brief, a shock state with a dilated IVC and increased resistance to venous return can result from an extrinsic process such as tamponade with RV and a ribatrium collapse, abdominal compartment syndrome when you have collapsed IVC and the free fluid, or from an intrinsic process. Think about it in any surgical procedure where the IVC has been manipulated. This is an example of a nitrogenic IVC stenosis. Note the reduction of flow before and after the correction. Here is another case. After a mildly complicated cardiac surgery, a 42 years old developed a refractory shock on post-op D3 in the ICU with tachycardia, acidosis, epoxemia, and increased abdominal pressure. As we can see, the IVC collapsed on the echography. On the CT scan performed on the other patient extended mesenteric ischemia with part of venous gas as present with secondary compression of both the IVC and ARTA, causing an abnormal compartment syndrome. In the yellow circle, we can see that both the ARTA and IVC are barely visible because of the massive compression in this case. IVC imaging can also be useful to identify problems, especially in at risk population. Here is a large mobile cloud scene on surface echography on a patient recently decandulated from ECMO. Up to 46% of patients develop venous thrombolabalic complication during or after ECMO therapy. It is important to recognize this complication as they can be devastating. Now let's go back to medical school with a review of the central venous waveform and how it translates on the hepatic vent flow. First, we use the EKG to localize C-stalli and diastalli. The atrial contraction happens shortly after the P-wave and corresponds to the A-wave of the right atrial pressure waveform. The same A-wave appears on the hepatic vent flow. The X-descent secondary atrial relaxation is located in C-stalli and corresponds to the S-wave on the hepatic vent flow. The venous return at the end of C-stalli raise the atrial pressure giving the A-wave on both the right atrial pressure waveform and the hepatic vent flow. Finally, the Y-descent secondary to cuspid valve propane is located during the diastalli. The D-wave is the hepatic vent flow equivalent. In case of increasing right atrial pressure, the X-wave will become blunted and the same thing will happen to the S-wave on the hepatic vent flow. The V-wave may become more permanent too. As our V-function deteriorates, now the progressive disappearance of the X-descent and the S-wave with a predominant D-wave. The hepatic veins offer a favorable angle for Doppler interrogation as you can see on picture A and are located really close to the IVC and right atrium as you can see during a surgical procedure on picture D. Consequently, it is a good place to evaluate the venous feeding of the right ventricle. Here on picture C, the Doppler tracing illustrates an abnormal SD ratio inferior to one compatible with a mild RV dysfunction. This case demonstrates how we can integrate all this information. This 73-year-old woman with heart failure secondary to mitral and truchuspid regurgitation was referred for mitral valve replacement and truchuspid valve replacement. On the top left corner, the stomach appears severely taken on T-gout secondary to venous congestive. On the monitor pulmonary hypertension is present as you can see on the yellow pulmonary artery curve. The central venous pressure is also elevated with predominant V-wave visible on the green curve. On the mid esophageal for chamber view, both atrium are dilated and RV dysfunction is present with an RV free wall strain of minus 15.7%. Accordingly, the hepatic vein Doppler is compatible with a CVR-TR and RV dysfunction as the S-wave is completely reverse. The IVC and the hepatic vein flow can also evolve as complications occur or therapeutic measures are taken and can be monitored during the case. This case of a 77-year-old man of Pancabage is a great example. After the induction, the patient was stable on norepinephrine and hepatic vein Doppler was normal with S and D ratio over one. During the procedure, the patient was hypotensive and required idols of norepinephrine. The hepatic vein Doppler show S-wave inversion compatible with CVR-RV dysfunction and the patient was successfully treated with ionotrope. Interestingly, at the end of surgery, the IVC, visible on the bottom right, started to collapse with increased hepatic flow velocity. The last Doppler signal was associated with visor dilatation because there were no blood vessels. A CVR vasoplegia secondary to the procedure was diagnosed and treated with vasopressor. This case emphasizes the importance to reassess the situation and ecographic data when the patient becomes unstable. Now let's talk about the portal vein. Starting from the IVC view, the right portal vein can often be viewed with an angle between 50 to 70 degrees and minor manipulation. The portal vein can be identified by its ecodance sheet and a typical laminar or monophasic velocity between 15 and 30 cm per second. Portal vein imaging has many applications. We can use it for monitoring right ventricle dysfunction associated with venous congesta, evaluation of response to medical treatment, abdominal compartment syndrome, mesenteric ischemia with portal venous air, hepatic artery and portal vein stenosis in liver transplantation. In this presentation, we will mainly focus on the two first points. Previously, we talked about the manifestation of RV failure on the right at a low pressure curve. We also talked about the equivalent on hepatic vent Doppler with S-blunting then reversal as the RV dysfunction progresses. As the venous congesta and secondary to RV dysfunction appear, the portal Doppler will become more and more positive. I will not address the hepatic Doppler in this talk as Dr. Bourbier-Souigny, who is an expert, will talk about it better than me in the next presentation. With the portal Doppler tracing, we can calculate the portal ventosatility or PVPI. The PVPI is the ratio of the difference between maximum velocity and minimum velocity and the maximum velocity. Now let's see how these notions are related to practice. This is a 34-year-old woman postcardiopulmonary bypass after a rose procedure. On the top corner, there are giant V-wave on the CVP curve. Those giant V-wave are also seen on the hepatic vent Doppler associated with S-blunting. The portal Doppler shows abnormal pulsatility associated also with giant V-wave. Dysamodynamic and ecographic findings are compatible with significant RV dysfunction and venous congestion and should be addressed. This other case of a 76-year-old woman postcabbage and mitral valve replacement is a great example of how we can integrate ecographic data to other clinical information. Even if the central venous pressure, the pulmonary artery pressure and the RV function were normal, before the cardiopulmonary bypass, she developed RV dysfunction with elevated diastolic RV pressure, abnormal portal Doppler and abnormal venous Doppler, hepatic main Doppler surgery. The transcranial Doppler signal indicates the presence of high-intensity transient signals compatible with arrombolitis also embolised in the right coronary artery and lead to post-op RV failure which was treated with ionotropic support. It is interesting to visualise the RV dysfunction in its consequences with ecography. However, it is also useful to use the ecographic to monitor the response to different interventions. As you can see in this case of a 22-year-old woman with a dark male tree-leaf ventricular with revised implantation. Before the procedure, she had pulmonary artery pretension, elevated central venous pressure and severe ventricular dysfunction. The portal Doppler is also markedly abnormal with severe venous congestion. The procedure was performed by Dr. Lamesh at the Montreal Heart Institute. She was treated two times with inhalated vessel dilatators namely merinone and epoprostenol. This mitigation helped with pulmonary pressure without major effect on systemic pressure as you can see on the left graph. The portal pulsatility was also reduced. After the procedure, normal flow was restored in the portal vein. Blood loss was a minor. She was with epinephrine and NO. Her flu balance was very negative with minus 3.4 liters with the help of hemophiltration and lassox. Consequently, she was extubated two hours post-op in the ICU in a stable condition. The prognostic value of the portal vein pulsatility has been studied by Dr. Dono and his team. In this article that includes 115 cardiac surgical patients and published in the British Journal of Anesthesia in 2019, they observed that abnormal portal or splendid vein pulsatility indicated artery dysfunction and post-op complication. In fact, for predicting post-op major complication, namely acute kidney injury, significant bleeding, surgical re-invention and death, after multivariable analysis, portal flu pulsatility after casual pulmonary bypass was the best predictor with a node ratio of 5.13 was better than systolic RV dysfunction. In addition to this, they also published the British Journal of Anesthesia in 2022. The association between portal Doppler pulsatility before and after cardiopulmonary bypass were assessed on 373 cardiac surgery patients. The outcomes were time on life support after surgery and major complications after surgery, major bleeding, re-invention, severe acute kidney injury, dead and prolonged mechanical ventilation. In this study, the presence of a portal pulsatility fraction over 50% or ppf50 before or after cardiopulmonary bypass was associated with a longer duration of life support. The presence of a ppf50 after cardiopulmonary bypass was also associated with a significantly higher rate of major complication of 4% versus 20.3%. In conclusion, TGAS can maximize the potential of the EE without additional costs. It can be a great tool for unstable patient, especially when the heart is normal. Portal eye pretension is highly pronostic before and after cardiac surgery and TGAS represents a new area of resurgent period operative anesthesia and critical care. Thank you for listening. Thanks to the symposium organization for the invitation. Don't hesitate to communicate with me if you have any questions. Special thanks to Dr. Daneu who is a great mentor and exceptional clinician and researcher, but mostly one of the kindest and most passionate colleagues. Thank you everyone. Thank you so much for excellent lecture. I'm sure it will provoke even more