All right. Good morning. Welcome to this session. I'm Hilda Nugent with the Professional Development Committee. A couple of housekeeping items. Make sure that you complete your evaluations in your app. And then complete the final evaluation. So just make sure you've done all the sessions that you've attended. And then the final evaluation, submit that, and you'll get your certificate. That needs to be done by September the 9th. Otherwise, I understand that it's locked down and can't get the credits. I don't know. Also, if you're interested in going to Nashville and speaking, we will be opening up for abstracts on August 14th. So on the website, there's some information about submitting abstracts, the things that the committee looks for related to your abstract. There's also a video. So if you're interested in that, we would love to have your submission. And now it's my pleasure to introduce our speaker, Dr. Barry Swerdlow. Dr. Swerdlow is an Associate Professor for the Nurse Anesthesia Program at Oregon Health and Science University, and a longstanding adjunct clinical faculty member in the Sanford University Department of Anesthesiology. Please join me in welcoming our speaker as he presents, Why CRNAs Should Learn TEE for Non-Cardiac Surgery. Dr. Swerdlow. Thanks very much, Hilda. Let me put this down. So I don't think I've ever spoken in a room quite this size. It's really pretty intimidating, firstly because I can't see anyone because the bright lights are in my eyes, and secondly because there are a lot of seats out there. So anyone who wants to move forward, I promise you I won't bite. Please feel free to move forward. And if you can't hear me, say something because I tend to speak a little bit softly. In any case, one of my quests in the last number of years is to teach TEE to CRNAs because I really think it has a significant place in the diagnostic modalities that are used for non-cardiac surgery. The last published percentage of CRNAs in practice cardiac surgery is about 25%. On the West Coast, it tends to be a little bit less than that. But regardless, most CRNAs practice non-cardiac surgery. And I really think that a significant role for TEE is its use in non-cardiac surgery. Although it was developed for cardiac surgery, I think it plays a very significant role in the diagnosis of adverse events that occur during non-cardiac surgery and should be used semi-routinely, in my opinion, for that purpose. So with no more ado, let me get started here. This is the usual disclaimer. So the learning objectives for this endeavor today are to identify the major uses for TEE during non-cardiac surgery, to summarize the risks associated with TEE use, and we'll spend a fair amount of time to discuss cases on the basis of what TEE can offer in the setting of non-cardiac surgery. Can you hear me okay? Yes. Okay, good. Perfect. Okay. So how many of you... I can't even see your hands. This is terrible. So just basically, do a lot of you use POCUS during your routine endeavors in non-cardiac surgery? Yes. Okay. How about TEE? My guess is no. We did a workshop last year at the AANA convention in Seattle, and it was an interesting turnout, but most people who don't practice cardiac surgery, don't provide anesthesia for cardiac surgery, don't have a fair amount of experience in TEE, although it's been recommended both by the NBCRNA and the AANA as areas of expertise that should be part of your diagnostic armamentarium. So the general reasons to perform a test are basically because it changes what you should do. If you're going to order a serum selenium level, your surgeon's probably going to ask you, what the hell are you doing that for? So it should change what you're going to do. And a good example is a CTA to diagnose pulmonary embolism. The risks should outweigh the benefits, and... Excuse me. Benefits should outweigh the risks. Sorry about that. And when you use a CTA, one of the potential problems is contrast-induced nephropathy, and you should have a reasonable suspicion of a pulmonary embolism. So, excuse me. I don't know if I can go backwards here. Can you go backwards on the slide? I pressed the button twice. How about if I... Yeah, good. Thank you. So you can see in the diagnostic algorithm for pulmonary embolism, high-risk PEs, patients who are high-risk for a PE, you go ahead and perform the test because the benefit outweighs the risk. Those patients are likely, more likely than not, going to have some abnormality on their finding, and you take the risk of doing the CTA, whereas if they are low-risk, you perform a test which has substantially lower risk, namely a D-dimer assay. Okay. So you perform a test because the benefits outweigh the risks, and so we're going to ask ourselves what are the major utilities, what are the major uses for TE in non-cardiac surgery, what are the material risks, and what are the alternatives, sort of like what you ask a patient, what you provide to a patient in the way of informed consent, when you go ahead before their anesthesia. So let's just talk about cases. I think putting things in the context of what you're used to doing will impress upon you the incredible utility of this minimally invasive diagnostic modality. So these are all, so far as I recall, real cases, although the TEs are not necessarily the TEs that were associated with the cases. This is a 46-year-old woman who was undergoing a hepatic lobectomy. Her preoperative renal function was impaired. She was on furosemide. Her blood loss at the point of the procedure when I became involved was about 2 liters. She had received 8 units of PAX cells in replacement, as well as a fair amount of crystalloid and other blood products and colloid. Her blood pressure was low. She was on vasopressors. Her heart rate was high. She was aneuric. And the question was why. And so we performed a TE. Now, for any hepatic resection, in my opinion, you should have a TE as a monitor. You'll see why in a minute. The nice thing about having a TE as a monitor is you're not just taking a snapshot. When we put down the TE in this case, we had an image that was associated with that moment. But if you have a TE from the get-go, you have a picture of what the patient looked like before, during, and after. It's a motion picture. And that's a much more valuable set of information than a simple snapshot. So this is a patient who was hypotensive and received a lot of volume. And what I expected to see was right ventricular failure. In a patient with chronic kidney disease who received this amount of volume, despite two liters of blood loss, what I expected to see was right ventricular failure. What I saw was this. This is a transgastric short axis view. It's basically a mid-papillary view. I don't know if you can appreciate that. On the right, is there a laser pointer here associated with this? I guess not. If I can get a laser pointer, it would be helpful. But on the right-hand side, you see the LV on the upper left, the RV. What you can appreciate here, I wish I could play this. Can you play that video again? Great, thank you. What you can appreciate is that the LV cavity, even in end diastole, which is after it's filled significantly, it's filled to the maximum, is very small. So despite my misgivings, the diagnosis was a low preload. LVEDV is the definition of preload. It's the maximum volume of the left ventricle after it's been filled due to hypovolemia. Despite the fact that they had given eight units of PAX cells and a lot of crystalloid and colloid and other blood products, this patient was simply hypovolemic. So the answer to their question was this patient did not have RV failure. This patient needed more intravascular volume. These are snapshots. That's the patient on the left. Actually, it's a patient with LVH and normal volemia. And the same view, transgastric, short axis, mid-papillary view of TE, which is not difficult to obtain. Upstairs the last two days had students and CRNAs performing TEs, and there's a four-view protocol which we use to teach it. And this is one of the main views. It's not difficult to obtain. There's a lot of voodoo around TE, which in my opinion is nonsense and not based upon the fact that it's a difficult skill. It does take some expertise to use it over and over again, and that's why you should start with normals and move on to pathology, like any other diagnostic modality. But in any case, the LVEDV on the left is a normal volemic LVEDV. The LVEDV on the right is what this patient had. A hypovolemic, and you can see one is small and one is large. I mean, you don't have to be a rocket scientist to figure this out. So let's do another one. This, again, is a use of TE for patients who are hemodynamically unstable, i.e. they have a low blood pressure usually. This was a 66-year-old man for a lap coli. He had a number of preexisting comorbidities. He was induced in a standard fashion for general anesthesia, and post-induction he became hypotensive. That hypotension did not respond to volume set of vasopressors, and the question was why. So we put down a TE, and we saw this. Unlike the last patient, this patient has an LVEDV, which is very reasonable. It doesn't need any more volume. In fact, the contractility is the same view as the transgastric short axis mid-papillary view. And this patient doesn't need volume, doesn't need anything to help him with contraction, because MAP equals cardiac output times SVR. If the stroke volume is normal, then this patient must have a low SVR. And there are only two things that cause SVR to drop acutely. One is drugs. By acutely, I mean minutes. And the other is anaphylaxis. So this patient simply needed enolephrine. Okay. So compare low preload and low afterload. So this is what our first patient looked like. That's what our second patient looked like. And this takes all of about, if you have the TE set up, and in the patient, you're watching a motion picture, which is hard to do until after induction, although you can place these probes ahead of time. They usually don't. Usually these are performed in general anesthesia. But if you're watching the situation develop, it takes you about 30 seconds to make a diagnosis, or a minute. So it takes two minutes. Who cares? It doesn't take a half hour to get a half-baked diagnosis from a urine sodium. You're looking at the preload in the transgastric view. So let's do another one. So this was a 75-year-old man for an open AAA resection. It's a vascular procedure, but done in the general operating room. He had some comorbidities. He was induced in a standard fashion. He was given a balanced general anesthetic, whatever that means. They put the cross clamp on, and immediately the patient became hypotensive. They started some dopamine, and the patient stayed hypotensive. They had a PA catheter in. The PAD was 16 torr. They ran an amnestic level of background anesthesia. The EBL for the procedure up to that point was about half a liter. It had been replaced with an adequate amount of crystalloid and colloid. And the patient's hypotension didn't improve immediately with ephedrine or phenylephrine. So why was it, and what should they do? So that was the pre. This is a motion picture. This is the pre-cross clamp view. Nice LVEDV. Same view. It's a transgastric short axis view. Nice contractility, all segments. This is the post-cross clamp view. And you can see this is a ventricle where the anterior wall at the very bottom of the screen is not thickening and thinning. And the anterolateral wall is actually dyskinetic. So can you play that one more time? Or maybe the next slide has one. I don't remember. Yeah. So that's the pre-cross clamp. And if I can get a laser pointer, if you have one, it would be very helpful to me. But if you look at about 6 o'clock there, that's the anterior wall. And look at the anterolateral wall. It's actually moving outward during systole. That's the anterolateral wall. That's at about 4 o'clock. So at 6 o'clock, it's not getting thick and thin. Unlike the inferior wall, which is at the top, which is getting thick and thin, the anterior wall is not. This is somebody with a proximal LED lesion, which was perfusing their anterior wall, which became problematic with application of the cross clamp. So if you can do it, if they haven't made an incision yet, you should take the cross clamp off. If they've made an incision, this is not somebody whose hypotension will respond to fluid. This is somebody who needs more inotropy. Conceivably, if it's okay with the surgeon after they do the repair or the aortic aneurysm correction, they can put an interior balloon pump in. This patient needs to go to the cath lab. Oh, I did. This is the same. So, okay, segments. Can you back up one step? I actually can't see that too well. Can you go back one step? Okay, great. So that looked normal, and segments 7 and 12 are abnormal. Severe anterior hypokinesis and anterolateral dyskinesis. Yep. Yep. Okay. So, this is a third example of someone whose diagnosis of hemodynamic instability was sorted out rapidly, efficiently, without any risk by TE. This was a healthy young lady who was scheduled for a total abdominal hysterectomy. She was healthy. She was induced in a standard fashion. She was given an antibiotic ahead of time, before incision. She had a pen allergy, so they gave her clindamycin. And post-induction, she became hypotensive, despite fluid challenge, reasonable doses of vasopressor, large doses of vasopressor, and even some epinephrine. The question was why? And she, her AA gradient was increased. She had decreased pulmonary compliance, and the question was why? And so, this is what her transgastric view, this is, in my opinion, the transgastric short axis view is the go-to view to start your diagnostic pathway with TE. And this is a, again, left ventricle is on the, is most of that, most of that film. That's a normal-appearing LV, and since MAP equals cardiac output times SVR, that's, oh, shows you what I know. No? is one that causes the stage to blow up. I don't want to press that one. Okay. So this is basically a normal transgastric view. It's the LVEDV is nice and normal. Contractility looks normal. And because, and most importantly, the LVEDV is normal. The LVESV, the end systolic volume is normal. The stroke volume is normal. The heart rate's reasonable. So the cardiac output's reasonable. This is MAP equals cardiac output times SVR. This has got to be a patient with low SVR. So in about a minute's time of looking at this and staring at it, making certain your eyeballs aren't crossed, you figured out that this is, the problem here is a low SVR. And it could be a low SVR from anesthesia, or it could be a low SVR because of anaphylaxis, but it's an acute problem. Now this wouldn't be just anaphylaxis. This would be a volume resuscitated anaphylaxis. But you've given this patient two and a half liters of fluid, as I recall. This is a patient who's received fluid. The LVEDV is normal, and the SVR is low. And you've sorted that out in a very short time period definitively. So again, I think this is the last example I have of its utility for hemodynamic instability. This is a 66-year-old gentleman for an X lab for an acute abdomen. It looks like he has air underneath both diaphragms. He has some preexisting problems, rheumatoid arthritis, hypertension, and failure. He's on a number of drugs, including a monoclonal antibody. He had a preoperative TT, transthoracic echo, showing an EF of 50%. And he was induced with etomidate and a few other medications. And post-induction, his blood pressure sagged despite turning down his SIVO, giving him some fluid, treating him with ephedrine. And the question was, why? Does he need additional volume, inotropia, or vascular tone? And so we did a TE. We had the same view. This is a transgastric short axis mid-papillary view. You can see both papillary muscles there very nicely. I don't know how to do this with a laser, but one papillary muscle about 4 o'clock, the other's about noon. You can see them over here in the diagram. And you can see on this view, can you play it one more time? Great. The things that are getting thick and thin are at 7, 12, 11, 10. But 8 and 9, 8 in particular, is not getting thick and thin. It's getting a little bit thick, but not very much. This is septal hypokinesis. I'm waiting for the film man. Can you make the advances slide just a little bit, one step? Right, septal hypokinesis. The LVESV is elevated, so the encystomic volume is elevated, that means the stroke volume is decreased. This is hypotension in somebody who's been induced that is not related to a low SVR. This is somebody who has a low cardiac output. They specifically have a low cardiac output on the basis of new, presumably new, you don't know if it's new because, again, it's not a motion picture here, you've just put down the probe, septal hypokinesis. Treatment is an inotropy, additional fluid may worsen the problem because it'll distend your ventricle. The LVEDV, the preload, is adequate, you don't need to distend, you shouldn't distend the ventricle further. In fact, if this is ischemic in etiology, distending the ventricle is contraindicated. It's not just not indicated, it's contraindicated because it will increase myocardial oxygen consumption. So that's what I just said. So the utility of a TEE in non-cardiac surgery, number one, is to sort out issues related to hemodynamic instability. Ideally, it's to sort them out before they become grossly unstable and you need to rescue them. So that's why putting down a TEE and watching it is a great idea. If there's an issue with cardiac output, then the question is, is it an issue related to preload, contractility, or cardiac afterload? If there's not an issue related to cardiac output and there's hemodynamic instability, i.e., hypotension, then your problem is related to SVR. And if it's an acute change in SVR, there are a limited number of things which cause an acute change, decrease in SVR. So another issue that's easily addressed or rapidly and definitively addressed by TEE is oliguria. So this is a 72-year-old man for a small bowel resection. He'd had a splenectomy in the past. He was basically healthy otherwise. He had some reasonably normal laboratory values preoperatively, had a family history of malignant hyperthermia. They provided anesthesia as TEVA with no triggering agents. The patient's blood pressure and vital signs preoperatively were reasonably normal. There was questionable SV segment depression in lead II, not seen in other leads. Then the patient became oliguric, and they asked us, they'd given them enough fluid, they'd get fluid challenges, they may have even given them Lasix, and the question is, why is this patient oliguric? Again, if you had a TEE, and you know the answer, you could avoid the patient becoming oliguric. But at this point, we put a TEE down, and this is what it showed. Can you play that back again? I clicked twice, not knowing. This is what's called a four-chamber view. It's a metesophageal four-chamber view. It's one of the four protocol views that I teach when SRNAs are learning TEE or CRNAs are learning TEE. You can see, I know it's a terrible imagery, but I put a line up there, that a portion of the RV free wall isn't beating. So this was a new finding, and it's related probably to RV ischemia, and the vessel that supplies the right ventricle always comes off the RCA, unlike the inferior wall, which most of the time comes off the RCA. If I can advance this, if I click it, I'm afraid it's going to do something terrible. Great. So the situation is more complex than hypovolemia in a patient with a small bowel obstruction whose third's facing. This patient has adequate preload. You look at their LV, and you can look at their LV in this view, too. It's the area that's blackened out on the right bottom. The LV-DV is adequate, but most importantly, the right ventricle is achinetic. It's not beating. That wall, even though it's a thin wall on the RV, should get thick and thin. It doesn't. And you can confirm this in other views. This RV achinesis, it's due to RCA ischemia. The treatment is to afterload reduce the RV, okay, and to provide inotropy to it with an ionodilator, like milrinone or amrinone, and take the patient to cath lab if you can. Additional fluid, again, in this setting of oliguria is not only not indicated because the LV-EDV is adequate, but is contraindicated because it will worsen ischemia. So you've made a diagnosis rapidly. You've made a precise diagnosis rapidly and definitively. You've prevented a problem by fluid overloading this patient. And you've treated the patient appropriately based upon that diagnosis very, very efficiently. So I just think this is a two-chamber view. This is also one of the protocol views. That's the LV you're looking at at the bottom screen, the LA on the top, the mitral valve in between. And you can see that the anterior wall is beating very nicely. It's getting thick and thin. But that area that's yellow, which is the inferior wall, is not getting thick and thin. Don't look at the endocardial movement. Look at the thickening and thinning of the myocardium, which is equal to contractility. You can see it's not contractile. So this is the same patient. This is a patient with right-dominant anatomy. In other words, not only does their right ventricle get fed by their RCA, which happens in everybody, but their inferior wall of the left ventricle gets fed by their RCA, which happens in about 70% to 80% of people. And concurrent with their RV ischemia, which is causing their oliguria, which you're going to treat appropriately with an inodilator and maybe take the patient to the cath lab later, depending upon if they're stable enough and if the surgeon allows it, they have inferior wall dysfunction. So we can go to the next slide. You can look at this slide a little bit longer. You can see that the, that area is not getting thicker and thinner, whereas the bottom portion, the opposite side of the ventricle, the anterior wall, is getting thicker and thinner. And you often see a hyperkinetic wall when you see a hypokinetic wall on the opposite side. Okay, again, another example of oliguria, 56-year-old man for a Whipple, he was a little bit overweight. He had obstructive sleep apnea. In California, that's a little bit overweight. In the rest of the world, that's significantly overweight. He had a CRIT of 35%, which means he was anemic. He had a transthoracic echo consistent with his hypertension, showing grade one diastolic dysfunction, and a reasonably full ventricle. After five hours of surgery, he had a blood loss of about 1,200 cc, which was presumably replaced what they believed to be a correct volume. But the patient became increasingly oliguric, despite fluid challenges and despite LASIK. Sound familiar? This is not an unusual situation. You have a big case, you have some blood loss. You've given what you think to be a reasonable amount of fluid, and your patient stops peeing, and your question is, why? And so the blood pressure looked okay, the heart rate was a little fast, but who knows why? Pain, volume, it could be lots of things. The CVP, whatever that means, was up a little bit. But why is this patient oliguric? Do they have ventricular dysfunction, is their preload adequate, and what do you do about it? So these are all questions that are common questions, they're questions which you can address definitively and efficiently with TEE, and you guys should learn it. There's no reason in 2024 that you guys shouldn't be using TEE routinely during significant non-cardiac surgery. Accept availability of the machine, and permission to use it. I'm not blaming you, but I think it's something that you do need to learn. I think this should be an opportunity for you to use it. So that's what their TEE looked like. This is a transgastric short axis view. You can see the LVDV is tiny, it's tiny. Their preload is low. You made that diagnosis in, as my wife would say, milcoma nix, in two seconds, okay? So that's a transgastric view, the structure on your right hand side, can you play that one more time? Structure on the images right hand side is your LV, your RV is above, the LV cavity is very tiny, you could freeze this, you could actually measure a fractional area change, you could calculate an ejection fraction, but you don't have to. You can eyeball that, you can say, my patient's oligarch because they need volume, okay? So let's advance this. Low preload, they need volume, the contractility here is normal. So the preload is low, it could be other things in addition to that, you won't know until you correct the preload. The SVR can be low, you're not looking at SVR here, okay? But until you correct preload, that's the, you won't know, okay? The treatment is volume. So a third use of TE, very common during non-cardiac surgery, is my patient ischemic. And the example I gave here was someone having a carotid done, I'm sure a lot of you do anesthesia for carotid endarterectomies, they're not necessarily done in the heart room, they're done in the general operating room by vascular surgeons routinely. The pre-op ECG was remarkable only for insignificant Q waves in some of your inferior leads but not all of them. The patient had general anesthesia. The patient developed a Mobitz 1 rhythm, not a malignant rhythm, but not uncommon rhythm during carotid manipulation, except the surgeon wasn't manipulating the carotid. The question is, was the, and concurrently with that, the patient developed a little itsy-bitsy bit of ST-segment elevation in their inferior leads, at least some of their inferior leads. And the question was, is this real or is this just, you know, patient has Mobitz 1, which is a relatively benign arrhythmia. The vital signs didn't change. And the question was, is there myocardial ischemia? And the answer is, you can tell, you just have to look. So this is a two-chamber view. This is the LV at the bottom. This is the LA at the top. It's one of the protocol views. This is, you've been watching, you can put a TE down at the beginning of the case. You can watch the ventricle, and you can, what you, and this is a terrible image. I apologize about this image. Segment 10 isn't moving. Segment 10 is a kinetic, which is your inferior wall. The rest of your ventricle, can you play that one more time? Segment 10 on both the two-chamber view and the 10 and 15, actually. The 15 may be dyskinetic, but it's your inferior wall. You don't see 15 in your transgastric view. So 10 and 15 have shown abnormal wall motion. A TEE is the most sensitive indication of myocardial ischemia that you have, in terms of segmental wall motion abdominal. It's much better than an electrocardiogram. So this is LV inferior wall dyskinesis. I was correct. You can tell it's the inferior wall, and if it's the right dominant system, it's the RCA. But it's always the inferior wall, it's always the PDA. Somebody with PDA disease, and the treatment is to start nitroglycerin while maintaining the organ perfusion, your head, your coronaries, the rest of your body with phenylephrine. So the last example I want to give you in terms of utility of CPR is cardiopulmonary resuscitation. I found this clip, I really enjoy this clip, and we might have time to play some of it. This is CPR from the beginning of the century, and we've come a long ways, but we haven't come far enough, and TE can guide us in terms of our CPR administration in many, many ways. Probably the most effective way is it can tell us whether or not CPR is being done in a manner that will cause ejection of the LV. It's much better than end-tidal CO2. And the amazing part is the statistics now that people are losing TE, one of the things I did last year was work with the ER group up at OHSU to show them how to use TE for cardiac arrest situations, is that the area of maximal compression, where people put their hands in cardiopulmonary resuscitation, in 50% of the cases is wrong, is wrong. So we're doing ineffective CPR 50% of the time, and this is something that occurs not just in the cardiac OR, in fact it doesn't occur a lot in the cardiac OR, it occurs in the general operating room and in the ER. So area of maximal compression, the depth of the compression are things that are easily determined by protocol views, meaning one of the four views that we teach as beginning level of competence in TE usage are things that are appreciated very easily in one of the four views, namely the mitosophageal long axis view, which we'll look at in one second. You can tell the difference between fine VF and asystole, you can identify treatable causes of PEA very easily, and importantly you can make statements that reflect the likelihood of recovery after CPR. So this TE is very useful and it's become a standard, in my opinion, for performance of CPR, certainly in emergency rooms across the country, and in fact the American Academy of Emergency Physicians now will certify ER doctors in TE usage for that purpose. And I, this is getting a little bit off topic, to some extent although I'm happy to share my opinions with you, I have my biases, I think you guys should do the same thing. I think that there's no reason that you can't, you've done it for other diagnostic modalities, you should do it for TE. So let's show you how, so these are motion pictures on the left of correctly performed CPR and on the right of incorrectly performing CPR, and the most remarkable finding is the LV, which is on the left hand side of the screen, both screens, is emptying on the left, it's not emptying on the right, it's sitting there smiling at you, doing nothing, not ejecting out the aorta, that's because the hands are too cephalic, and when they move the hands more, that's where the, the point of maximal compression is over the aortic valve, over the LVOT on the right, and on the left it's over the ventricle, you're actually ejecting blood out through an open aortic valve, you're emptying out your LV on the left, and you're doing nothing on the right. So this patient on the right, it's maybe the same patient, I don't recall, was, is not being adequately resuscitated. You guys appreciate that? This is what's called the mid-esophageal long axis view, it's one of the four protocol views, it's a very useful view, the structure at the bottom of the screen is your left ventricle, top of the screen is your left atrium, in between is your mitral valve, and on the right hand side of the screen, where the arrow is, is your ascending aorta, and between the two arrows is your, is your aortic valve. Can we, mid-esophageal, that's what I just said. And that also shows you your point of maximal compression, your area of maximal compression, which is adjusted more caudad, and allows emptying of your LV. So this is a real utility to, you can see in this same picture, maybe a different patient, that the aortic valve, which is on the right, at about 3 p.m., 3 o'clock, is opening during compressions, the LV is being ejected, and the area of maximal compression is over the LV, not over the LVOT and aortic valve, which is incorrect, which is done about 50% of the time. It's particularly done that way in pregnant women who have big abdomens or anyone who's obese, because people think that they don't want to get into the belly, and correctly so, but you need to have a more caudad location of your hands in order to eject the contents of your LV. So there you can see at the bottom, the opening of the aortic valve and the mitral valve is closed, and likewise filling during relaxation. Bottom is compression, top is relaxation, and you're looking at the LV being ejected through the aortic valve. You're looking at what you want to see, and if you don't see it, there's a problem. And the nice thing about TEE as opposed to TTE, transthoracic echo, is it doesn't occupy the real estate of the thorax. You don't have to stop CPR to look, you can just look. So not only does it tell you, does TEE tell you the area of maximal compression, it tells you the depth of compression. This is a different view, this is a four chamber view. You can see that these bad compressions are inadequate, and good compressions are adequate. You can just look at the LV, which is that structure at the bottom of the screen, and it's emptying each time with good compressions, and I didn't look before, but I assume with bad compressions it wasn't emptying. So depth of compression is another thing that you get out of TEE. So it can guide, I think the most useful role of TEE and CPR is to guide the person performing the CPR in terms of area of maximal compression, and whether or not they're being vigorous enough with their hand movement. One other use of TEE during cardiac arrest is distinguishing fine VF from asystole. I don't know which is which, presumably the top is fine VF, the bottom is asystole, but it could be vice versa. One is a shockable rhythm, the other is not. This is a big difference in terms of prognosis, big difference in terms of therapy. TEE of this patient shows quivering, not only of the valvular structures, this is a four-chamber view. Can you play that one more time, it's a short clip. Quivering, which is muscle in what you see in fine VF, as opposed to asystole when it's not moving at all. I don't have an example of use of TEE. This actually may be an example for treatable causes of PEA, but it's useful for diagnosis of tamponade, for diagnosis of, and we'll look at tamponade in a second, all the treatable HNTs. So this is a prognostication slide. This is an article that came out a couple years ago on decision-making for patients who have acute ascending aortic dissection who present with cardiac arrest. And what you can do is you can prognosticate very well if this tamponade is in the basis of dissection. These patients have about a 60% mortality, a near 100% problem in terms of quality of life afterwards. So this is a, one of the protocol views that we teach. This is a, on the left is a blown-up view of the metesophageal long-axis view, and on the right is a transgastric short-axis view. You can appreciate the fact that there's a pericardial effusion labeled as such, except pericardial, not pericard, pericardial effusion that surrounds the heart, and if you look at the severe hypotension after cardiac arrest, there's a metesophageal long-axis view which shows an intimal flap. That's that white thing moving from left to right on the screen. So dissection, and you see a pericardial effusion. And if you do the appropriate view, this is a metesophageal long-axis view. You can see there's diastolic compression of your right ventricle, and there's systolic compression of your left atrium. So this is a patient with tamponade. So I would expect this patient's prognosis to be very poor if they have both tamponade and a dissection. Tamponade itself from other causes, malignant effusions, et cetera, is one thing, but tamponade from where you have retrograde dissection into the pericardial sac from an ascending dissection is a very poor prognostic finding. So prognostication is another use of TEE in the setting of cardiac arrest. Can we advance the slide? One more. Okay. So just to summarize, we have TEE utility in non-cardiac surgery in the basis of utility in sorting out questions related to hemodynamic instability, questions related to oliguria, questions related to myocardial ischemia, and its utility during cardiac arrest, which is very useful. The contraindications of TEE are very limited, in my opinion. Like any other procedure that's invasive, you need to have patient consent, otherwise it's assault and battery. You need to have absolute contraindications or any physical disruption in the esophagus, which are relatively rare, they exist, upper GI bleeding, and there are a number of relative contraindications as well. But all in all, most people tolerate TEE just fine. You do need to get them consented for it ahead of time. There are some risks associated with TEE, but any of you who can put down an orogastric tube have probably done, and it's a big orogastric tube. So less than 0 point, what did I say, 0.2% of complications occur if you don't include misinterpretation of data, which is true of any diagnostic monitor. Misinterpretation of data is by far the greatest risk for TEE, and what I suggest initially, once you achieve a beginning level of competence in this technique, is to make the diagnosis usually involving the transgastric short axis view, confirm the diagnosis in one of your other three remaining protocol views, and then get an expert before intervening to confirm your diagnosis, and then intervene appropriately. That way you can do no harm. You haven't intervened. You've made a diagnosis based upon a diagnostic modality, which is essentially complication-free once it's put down, and I believe it's a good way to start. So misinterpretation of data is the greatest risk. There are some risks. So those are examples of misinterpretation of data. There are some mechanical issues which can occur with TEE placement. Usually it's a non-midline placement. The most common reason to have a significant complication from TEE other than misinterpretation is when people force the procedure like any other procedure. Don't force it. If tissue doesn't give way, there's probably a reason for it. It doesn't mean you don't use a little bit of force, but you shouldn't use a lot of force. And the most common area of complication is having the probe stuck in one of the piriform sinuses. It's a non-midline insertion of the probe. So those are the areas of laceration or perforation that can occur. I've probably placed I don't know how many TEEs, but I've only seen one complication which I did not have. It was done by a cardiologist who forced the probe and lacerated the stomach. But just don't force it. Alternative to TEE, remember I talked about the fact that you should talk about the potential benefits, the risks, material risks, what a reasonable person should know. The same thing as informed consent. You should talk about alternatives. The major alternative to TEE is transthoracic echo. The risks of transthoracic echo again are largely misinterpretation. You can't do any significant harm with transthoracic echo. You probably hit someone over the head with a probe. The advantages of TEE versus TTE are the fact that you get a better image. You have your probe in the esophagus. You don't have to occupy territory on the chest, which is very useful during certain – you always have access to the mouth except during an ENT procedure. But otherwise, if you're dealing with a general surgeon or orthopedic surgeon, you have access to the airway. So it does not require an interoperative chest wall territory. Doesn't interrupt CPR to place the TEE probe. You get better quality images. And it's free of external factors such as defibrillation pads, obesity, COPD, et cetera. Anything that's going to degrade your TTE image, your esophagus sits almost in contact with the heart posteriorly. You get a great image. It's usually very clear. It doesn't mean you don't get mucked up images sometimes, but usually it's a much clearer than TTE. That's my spiel. And I really think that all of you should, if you haven't already, made an effort to learn a beginning level of competence in TTE, which, in my opinion, involves a limited number of views to provide a maximum amount of information. So I have about 10 minutes for questions. Thank you. Thank you. No one has any questions? I can't believe that. Don't you want to know, like, I don't know. Why? Because we've looked at this. We've looked at, oh, good, somebody's coming up. I don't know the answer. I don't know anything about CRNA billing. While there was last summer, I provided one at this convention. So there are others that I know of, middle tennis. There are some online. There are TA workshops specifically for CRNAs that are available online through a couple of Midwestern institutions that I'm aware of. Good question. That's an excellent question. So I do know of some pathways to certification, but they won't work for you, unfortunately. The only true pathway towards certification is through the National Board of Echocardiography. One of the prerequisites for the National Board of Echocardiography to be certified is that you be a physician. So that's pretty dumb, in my opinion. You know, like, doesn't work. So there are guidelines for certification, which are for procedures for which there is no outside certification, but those are institutional-specific. So I don't know of any generalized pathway, but I do believe that having a workshop, and as an organization, I mean, you guys have broached certifying yourselves for more invasive procedures, for central venous cannulation, probably for PA catheter placement, for endotracheal intubation, you know, all of those things are standard parts of your anesthesia armamentarium, and in my opinion, TE should be the same way. It's just standard, it's less invasive than many of the techniques for which you've certified yourselves, and you should, just like the American Academy of Emergency Physicians, in my opinion, you should develop a pathway for certification. Go ahead. Sorry. No apologies necessary. Thank you for allowing us to understand the utility of this outside of the cardiac ORs. And I just wanted to ask more clarification in regards to the use of TEE during CPR, and if there's been any evidence in regards to injury, traumatic injury, esophageally, or in the stomach, the different areas that you mentioned that are common during that type of use. That's a really good question. The answer is there have been studies that have looked at injury, and they don't occur. You know, again, they occur only if you force the probe. The esophagus is a potential space. When you do a CT scan of the posterior pharynx, you see tissue. You don't see an opening. It isn't like the mannequins, which have an opening for the esophagus. See, you have an upper esophageal sphincter. You feel a little bit of resistance. You can retroflex, anaphylaxis, anaphylaxis the probe just a little bit to get by there. But no, the answer is people have looked at it, and there is an increased incidence of injury during CPR related to the probe. There's, you know, there are injuries related to CPR, but they're not related to the probe. Lacerating the spleen, lacerating the thorax, et cetera, but not related to the probe. Another question that I thought of was, you know, the utility of, obviously TE would be the gold standard, but the utility of Edwards monitors and utilizing flow track or other noninvasive monitors to guide hemodynamics. But I guess for valvular or wall motion issues that obviously that would be, the TE would be superior for that. But I was just curious, for individuals who may not have as much access to TE probes or them being occupied or unavailable, is that a reasonable alternative? I think that's a reasonable alternative for hemodynamics. I think that for other issues for which TE will provide you an answer, it's not a reasonable alternative. It's a reasonable alternative in terms of hemodynamics if you don't have a TE available. I think a TE gives you a snapshot and a motion picture ideally, which is incredibly useful, more useful than a noninvasive cardiac output monitor. The issue with many of those monitors also is they need to be calibrated. But you can see changes and specifically changes related to cardiac output. That's only one utility of a TE, but I'm all for using it. Don't get me wrong. I just think that TE is a much better diagnostic monitor. There's no reason, given its low risk, that you guys shouldn't be doing it. Excellent. And, of course, the TE would be diagnostic, whereas the Edwards monitors would be a trend to follow. It would be a trend. It would be helpful in terms of making a diagnosis of a low cardiac output situation or no change in cardiac output situation. But it's not as useful in my mind, in my opinion. Excellent. Thank you. You're welcome. Thank you very much. Josh Carr, University of Southern California. I think this is a wonderful presentation. I think we need more of this to be disseminated at our meeting, so I thank you very much for that. Just wanted to check in with you. You have mentioned four essential views that you teach to the students. Yes. I think I caught three of them. Okay. I was just going to go over those. That's great. So I wish I had a simulator. Actually, we had a sim lab upstairs, two yesterday and one this morning, where I did have a simulator. The four protocol views, the most important view in my mind, and the one you should start with, is your transgastric short axis mid-papillary view. So transgastric, there's a lot of voodoo, a lot of words that sound hocus pocus here, but they aren't really. Transgastric just means you put the probe in the stomach. So you push it down to about 45 to 50 centimeters. It's no biggie. Okay? Mid-papillary, transgastric, short axis, you're talking about the axis of the LV. So the short axis means you have zero degrees axis. It's the short axis of the left ventricle. And mid-papillary, the three portions of the heart. There's the top of the heart, otherwise known as the base. Why it was called the base is beyond me. The top of the heart is called the base, the mid-portion of the heart, and the bottom of the heart, which is the apex. The mid-portion of the heart is the portion that I suggested using this protocol. And it's easy to obtain. You put it down in the stomach, and it's the first view. And it's the most informative view because it tells you your LVEDV, tells you LVESV, tells you all the walls that are part of the left ventricle, the anterior, anterolateral, infralateral, inferior, inferior septal, anterior septal, plus your RV free wall. So it looks at contractility of all your walls. So it's a very useful tool. That's number one view. Number two, three, and four views, the next three views are all mid-esophageal views. So instead of putting it down to 50 centimeters, you put it in the mid-esophagus, which is about 30 centimeters or so. Start off with zero degrees, so it's short axis, and that's a four-chamber view. You're looking at a plane that's zero degrees, short axis of the left ventricle. And the third view, second mid-esophageal view, is you rotate the probe 90 degrees and look at your two-chamber view. The advantage of that is you don't see your anterior and inferior walls very well in your four-chamber view. You do see them well in your two-chamber view. I use the mid-chamber views and the way I teach mid-chamber views as a corroborative way of imaging things that you find to be problematic in your transgastric view. So find your problem in your transgastric view. You can find nearly all the problems. There are some exceptions. You know, pulmonary emboli, it smells like a pulmonary embolus because the RV is dilated. You know, there's abdominal and salmonella septal motion, all of which you can see in the transgastric view. You can't make the diagnosis of a thrombus in the pulmonary artery outflow tract until you look there, which is not part of the protocol. But most things that occur commonly during non-cardiac surgery, you can diagnose in the transgastric short axis view. Start there and corroborate your finding in a mid-esophageal view. So the three mid-esophageal views are your four chamber, zero degrees, 90 degrees, 130 degrees, or 140 degrees, or 120 degrees, it depends, which is called your mid-esophageal long axis view. That's the view I'd recommend, for example, for CPR. It tells you whether you're emptying your ventricle. It tells you whether or not you're performing CPR in the right locale. Okay? Thank you. You're welcome. Thank you again for taking the time to present to us. For a patient that's getting an intraoperative TTE, or TEE, excuse me, and their positioning may be different than supine, like lateral decusis, or like a steep trendelenburg, would that change our four-view protocol in any significant way? No, because the relationship of the esophagus to the heart doesn't change. So your preload is your preload in whether or not you're in the lateral position or prone position. So imaging what you want to image is not going to change. It's really nice. It doesn't mean you won't have physiologic changes, but what you're viewing on TEE will reflect those physiologic changes. So you may have compromised venous return in certain positions, or you may have increased intrathoracic pressures, which result in other physiologic changes. But all of that will be correctly reflected in your TEE and specifically in the protocol views. So you can use TEE. Now, putting it in in that position, particularly prone, is a little bit of a challenge, but not as much as a challenge as needing to visualize what you're putting in, like you do with intubating someone in the prone position. I've seen it done. I wouldn't do it. That's because I'm a chicken. But, you know, putting down a TEE probe in the prone position is not a problem. That being said, I really do think a good way of learning TEE initially is to do TEE in normal patients. And some of the normal patients that I've worked with students and other people to learn TEE on are long back cases. which are done in the prone position. So put the probe in before you turn the patient and just sit there for four hours and play with it. Once it's in, you basically can't do any harm except extubating the patient. And all of you guys and gals are going to be conscious of the endotracheal tube. Unlike a cardiologist, you're not going to sit there and whack it around and extubate the patient. So you really, once you put the probe in, you really can do no harm with the probe. So move it back and forth. Do it gently. Twist it side to side. Flex the tip left and right. Enter flex, retroflex the tip. Change the omniplane angle. You'll learn all this lingo and the way to do this in literally a half hour's time. It's not a day workshop in TEE will make you, provide you with baseline competence, in my opinion. And I've done it with students. I've done it with CRNAs. It's not difficult. It behooves everyone to learn it and to get it introduced in your institution. With that being, oh, actually I have two more minutes. Any other questions? Okay, thank you very much for coming. It's been a nice experience. Thank you.

Transesophageal Echocardiography

non-cardiac surgeries

Certified Registered Nurse Anesthetists

hemodynamic instability

myocardial ischemia

cardiac arrest

diagnostic value

institutional certification

Oregon Health and Science University

educational talk