Part 1: Waveform Basics Originally broadcast Tuesday, February 23, 2021
Medtronic is pleased to offer this dynamic, virtual event on the integration of HVAD™ System Waveforms and Logfiles into clinical practice. This two-part series provides an opportunity for HVAD clinicians to share case studies with the goal of providing deeper insight into the physiologic basis of HVAD Waveforms and Logfiles as tools for patient and device management.
Featured Faculty
Michele Kassemos - Moderator Marketing Product Consultant Mechanical Circulatory Support Medtronic
Michael S. Kiernan, MD, MS, MBA Medical Director, Ventricular Assist Device Program Assistant Professor, Tufts Medical Center
Marwan F. Jumean, MD, FACC, FSCAI Interventional Heart Failure Cardiologist Associate Professor, UTHealth
Jennifer Pavone, MS, RN, AGACNP-BC Director, Transplant Operations NYU Langone Health
Brief Statement HeartWare™ HVAD™ System Indications For Use: The HeartWare™ HVAD™ System is indicated for hemodynamic support in patients with advanced, refractory left ventricular heart failure; either as a Bridge to Cardiac Transplantation (BTT), myocardial recovery, or as Destination Therapy (DT) in patients for whom subsequent transplantation is not planned.Contraindications: The HeartWare System is contraindicated in patients who cannot tolerate anticoagulation therapy. Warnings/Precautions: Proper usage and maintenance of the HVAD™ System is critical for the functioning of the device. Serious and life-threatening adverse events, including stroke, have been associated with use of this device. Blood pressure management may reduce the risk of stroke. Never disconnect from two power sources at the same time (batteries or power adapters) since this will stop the pump, which could lead to serious injury or death. At least one power source must be connected at all times. Always keep a spare controller and fully charged spare batteries available at all times in case of an emergency. Do not disconnect the driveline from the controller or the pump will stop. Avoid devices and conditions that may induce strong static discharges as this may cause the VAD to perform improperly or stop. Magnetic resonance imaging (MRI) could cause harm to the patient or could cause the pump to stop. The HVAD™ Pump may cause interference with automatic implantable cardioverter-defibrillators (AICDs), which may lead to inappropriate shocks, arrhythmia, and death. Chest compressions may pose a risk due to pump location and position of the outflow graft on the aorta — use clinical judgment. If chest compressions have been administered, confirm function and positioning of HVAD Pump post-CPR.Potential Complications: Implantation of a VAD is an invasive procedure requiring general anesthesia and entry into the thoracic cavity. There are numerous known risks associated with this surgical procedure and the therapy including, but not limited to, death, stroke, neurological dysfunction, device malfunction, peripheral and devicerelated thromboembolic events, bleeding, right ventricular failure, infection, hemolysis, and sepsis. Refer to the “Instructions for Use” for detailed information regarding the implant procedure, indications, contraindications, warnings, precautions, and potential adverse events prior to using this device.Caution: Federal law (USA) restricts these devices to sale by or on the order of a physician.Waveforms Disclaimer HVAD Waveforms and logfiles do NOT conform to a single, classic appearance, and are not intended for diagnostic purposes. In addition to Waveforms and logfiles, other measurements, as determined by the physician, are used to assess a patient’s condition. Waveforms and logfiles represent pump performance and should be considered in their clinical context.Virtual Disclaimer The information shared at this event may include Medtronic confidential business information and personal data, including the identity of participants, that is subject to protection under applicable privacy laws and regulations. For these reasons, neither audio recording of this call nor screenshots, photos, or videos of the content are permitted, except by the organizers. Please note that your login/ID/name may be seen by others. By registering to participate in this event, you agree to keep Medtronic business information confidential and you consent to the disclosure and use of your login/ID/name and to audio and/or video recording of this event by Medtronic for use at its discretion. Medtronic will comply with applicable privacy laws and regulations and its data privacy policy which is available at www.medtronic.com/us-en/privacy-statement.html
Yeah, yeah, yeah, this place Mhm, yeah! Mhm, Mhm, Mhm, Yeah, Mhm, Mhm, Mhm Yeah, yeah, yeah, yeah, Mhm, Yeah! Mm hmm. Yeah, yeah! Mhm, Mhm, Mhm, Yeah, yeah, yeah. Good. Good afternoon. Good evening and good morning. Wherever it is around the globe, you're joining us from today. Welcome to the first virtual Medtronic, EMC s waveform boot camp. My name is Michelle Casinos. I'm a former bad coordinator and a market programming specialist with Medtronic, M. C s. And I'm pleased to serve as your moderator for today's webinar. The H fad waveform, at its most basic, is simply a visual representation of blood flow through the pump. The real art, however, of waveform analysis lies in an understanding of the constantly changing dynamic between a patient's physiology and the pump here to discuss both the art and the science of waveform analysis are three distinguished faculty. Dr. Michael Karenin is a medical director of the VAT program at Tufts Medical Center in Boston. Dr. Marwin German is an interventional heart failure cardiologist at the University of Texas Health Science Center in Houston. And Miss Jennifer Pavane is an acute care nurse practitioner and the director of transplant operations at N Y. U Langone Health in New York City, New York Welcome to all of you. And with that I'll turn it over to Dr Karen. Great. Thanks so much. Michel, Can I see the slides, please? Excellent. Terrific. Well, welcome, everybody. I couldn't have said it better than Michelle is. You're probably where there's gonna be a two part series. So just to present the lay of the land this evening waveform basics. We're going to start with a brief didactic session for about 15 minutes. That really talks about how wave forms are generated and what they mean to me. If you understand wave forms, it means that you have a really strong understanding of the physiology of continuous flow devices. And it's just as Michelle stated. I think one of the main strengths of this device is the value of the information provided to us in wave forms. You know, the old saying goes that a picture is worth 1000 words, and this isn't just a picture. This is a real time dynamic display regarding the patient pump interaction, and it provides insight not just into the patient condition, but what's going on in the pump and they can assist with patient management and oftentimes with with device and patient optimization. And, of course, the waveform varies across a number of different clinical conditions that will review in the cases after the death Tax succession. Yeah, and then case two in two weeks. I'm sorry. And in the second presentation, we'll talk a little bit more about log file analysis and then get into a number of more complicated cases as well. Oh, all right, give me one second as I take control of the screen here. Here we go. So again, from a basic perspective, understanding the normal contour and profile of away form is displayed here. Uh, and just in terms of the different nomenclature that we'll be talking about So we have the peak, the peak, the peak flow versus the trough flow, and the pulse utility is the difference between the peak and the trough. What's presented on the H fat monitor is in green. Here is the average flow over time, so that would be the 4.5 liters per minute. There is a rule of two's whereby in general we want the overall pulse it till it e to be about two leaders. So plus or minus a leader above and below that average flow. And then we generally want the trough flow to be greater than two liters per minute, which you certainly want to avoid as a trough flow. That hit zero, which would equate to stagnation or below zero, which would mean in German records, didn't flow through the valve from the aorta. So this is a real life depiction of what a normal age fat waveform should look like again. Regular pattern between the peaks with the smooth Sinus oil wave. So, of course, regular intervals indicate a scientist rhythm If a patient has an arrhythmia, and we'll see some examples of that at some point, um, would indicate, um, you know, potential atrial fibrillation, or PVCs or some other abnormal arrhythmia in terms of pulse Attila the this would demonstrate a low pulse utility state, normal flow but low pulse utility and then finally, high pulse utility. And we'll talk about what these different patient conditions may reflect in the cases. Remember, that is true with all continuous flow. L VADs that the flow on the screen is an estimation. It is not a directly measured flow in pump flow is estimated by the pump speed, which we, of course, set a directly measured power and then an entered viscosity setting using the patient's hematocrit. And it's actually that is something that helps improve the accuracy of flow estimation and centrifugal flow devices. And if that is abnormally set, then of course our flow estimation would be off. So, for example, if the patient was anemic and it wasn't and then received a blood transfusion and that hematocrit was not appropriately adjusted, then you could have a falsely elevated flow because the less viscous the blood, the thinner the blood to hire the flow estimation, the thicker the blood to hire the hematocrit, the lower the flow estimation would be. And then, of course, we know that for a given speed within a normal range of power should be, and that is really helpful for troubleshooting as well. If a pump is running at a higher than anticipated power for a given speed, that could alert us to a condition such as a bad thrombosis, versus if it's lower than anticipated power, which would equate to a lower than anticipated estimated flow that could alert us to potentially obstruction somewhere along the circuit. Mhm and always remembering that the, you know, the interaction between the patient and in the pump and anything that's really affecting filling of the left ventricle is going to impact filling in the L VAD and the degree of pulse utility. As we move through the talk, we're going to talk about two different pulse utilities. We're gonna be talking about pulse utility within the L VOD. And that's all the devices presenting on the monitor versus patient pulse utility, meaning actual pulse utility in the arterial system. And there is, of course, a correlation between those. But they are very distinct, and there could be a case where the patient is very pulse a tile and the VAT is not pulsate tile. And we'll talk about what different scenarios could could create that type of condition. So, of course, the device speed, um, impacts the loading characteristics of the left ventricle. If the device is set very high, then the LV is going to be maximally unloaded. The devices are pre load sensitive and again, anything that leads to under filling of the left ventricle is going to lead to reduced, uh, filling and contract Ili or pulse utility through the L VAD. So the conditions, such as hyperbole, mia right heart failure in Tampa nod The devices are after load sensitive. It can be affected by increased blood pressure or hypertension. So increased map is going to lead to potentially increase pulse utility and reduced L VAD flows and then finally contracted. Pretty. So every patient will have a different amount of residual contract, I'll reserve, and they're left ventricle. Some patients will have a very dilated left ventricle with extremely reduced ejection fraction and have very limited pulse utility no matter what. While others may have a higher contract, I'll reserve and have higher pulse utility even at some higher speed settings. So looking now in terms of the three factors that impact the pulse utility and the flow through the device, so that's impacted by the pressure difference between two chambers. So that's the left ventricle in the aorta. So we have a valve lys conduit, the L VAD, with the continuously spinning rotor that is pushing blood from pressure chamber one the LV to the aorta, and the pressure difference in those chambers varies across the cardiac cycle as the LV contract. So this is an LV pressure waveform. And so when the LV contracts and we have systolic ejection, the pressure difference between the left ventricle and the aorta is going to be decreased. So what we call the Delta P will be, at a minimum, insistently and a maximum and diastolic. And it's that difference in pressure across the cardiac cycle between those two chambers that leads to the pulse utility in the flow waveform characteristics that we're seeing on the H Vac monitor. It's really important to understand this is another way to graphically to pick that, but now, also adding, what we see in the Blue Line is the flow wave cartoon of the flow waveform profile. So the device flow is equal to the rotor speed, which is fixed. Uh, it's proportional to that divided by the pressure in the actually in the outlet, the order minus the inlet. So that's the Delta P. So this is ice of Olympic contraction with systolic ejection the green of the left ventricle. So in a normal person without an L VOD, of course insistently, the aortic valve will open when the LV exceeds aortic pressure and will close when that drops down so insistently. If there is no static lesion, the pressure in chamber one is equal to the pressure in chamber to there is no gradient, so this fixed pump will now be pushing blood in a maximum when there's no gradient. In contrast, in diastolic Leah, normal aortic diastolic pressure of 60 LV diastolic pressure of 10, we now have a gradient of 50 and diastolic, so flow is going to decrease because there's a larger pressure head that this fixed motors pushing blood across. So again, as this is why there's flow variation across the cardiac cycle, this may not be going through the aortic valve, but as the LV contracts, it is going to augment blood flow we're thinking about it is squeezing blood flow through the L VAT itself. This is highlighting that relationship, and what happens as we increase VAT speed. These are pressure volume loops. I won't spend too much time here, but in the Black loop again, we have ice of Olympic, Um, contraction. With systolic, a direction appears. What we have is systolic pressure, and then we come back down we have end diastolic pressure or volume. As we ramp up speeds across these different colors, we can see that we are unloading the LV because there is a reduction in the volumes. The end, diastolic and systolic volumes, a reduction in stroke volume the faster we're, uh, putting the speed on these devices. And, importantly, a reduction in the end systolic pressure and what occurs here as we see what we call an uncoupling between the LV in the aorta as we go up in speed. So in Panel B in this scenario, when the LV pressure exceeds aortic pressure, we would see the aortic valve opening regularly with each cardiac cycle. As we go up and see, we'll see partial aortic valve leaflet tip opening, not full excursion of those leaflets, and then eventually we'll see full uncoupling where the LV pressure no longer exceeds aortic pressure in D. N. A. And that's what we call an uncoupling. Our full unloading at the left ventricle in the aortic valve is no longer opening, and so a real life example of this in one of our patients that had a bad interrogation there was concern that there was obstruction of flow. So we put a pressure a pigtail catheter into the L V. And in fact, we we we diagnosed that the valid was appropriate, uh, functioning appropriately because we, in fact see, the LV is maximally unloaded uncoupled from the aortic waveform. Uh, in this clinical scenario indication of a normal state for someone with an L VOD. And so the last series of cartoons again will run through quickly to drive this home. But this is a flow pressure relationship. So when Delta P is at a minimum, insistently flow will be the highest. It will be the lowest again in diastolic when the pressure gradients the highest. And then you can see whoops with this cartoon as we play it that the that there's variation in the flow profile. So there indeed is pulse a tile flow through the device that varies across the cardiac cycle, and we can think about that is the Frank Starling relationship. So anything that's going to again decrease LV filling is going to result in less contraction of the L V and a decrease in the amount of contract or pulse utility that we're seeing in the l that so here we see in either in an under filled left ventricle or ventricle that's being, uh, overly unloaded by an L VAD. We may see a low pulse style state in Converse and LV with a high pre load or one. Perhaps that sub maximally unloaded because we haven't adjusted the l that speed appropriately, we can see higher pulse utility. This is what we see again, real time on the monitors so we can see in panel one at a low speed 2200 RPMs. We have a low flow state of 1.7 liters per minute high pulse utility. You can see here we're not meeting the rules of two, so the trough flow is at zero, and in cases it's dipping below some evidence of regurgitation flow. With the ramp speed study, you can see gradual augmentation of mean flow to 4.7. But importantly, what I'd highlight here is the relationship that in fact, while average flow increases peak, systolic flow remains relatively equal. The thing that is changing is you see that the trough is rising. So what we're augmenting at higher speeds, in fact, is a raising of the trough flows And that's what results in augmentation of the overall mean flows in these devices. And that very much correlates with what we see in the patient's pulse utility and the arterial system. So this isn't a review of physiology of CFL. VADs will start on the right panels. Here we see again, the different numbers in the bottom are different steps in a ramp. Study is we ramp up the speed of device. There's very little change in systolic blood pressure. What changes more dramatically is the increase in diastolic blood pressure. And because of that, we see increases in mean arterial pressure, which is really important because if we're doing a ramp study, we need to be cognizant of the impact that they can have on the map. Because we know that high map can lead to other complications, such as stroke in these patients and again, as that occurs, we see a narrowing of the arterial pulse pressure. So again, decreased pulse utility in the VAT may in fact translate to decrease pulse utility in the patient in that setting. And that's what we're seeing here. This is a patient of mine on post op Day one or two I went to check on in the intensive care unit and we see that there is low pulse utility. The patient was having intermittent suction events. In fact, you can see that reflected in the wave form on the left as well. This is an A line pressure tracing 2700 RPMs, and then we decrease the speed to 2500, and immediately you see an opening up of the arterial pulse pressure so you can see that there is higher amplitude pulse utility in the A line tracing and that correlated exactly what with what we're seeing on the H Vac monitors. So there is a wealth of information on those waveforms that does, in fact, reflect the physiology we're seeing in patients. And this is the summary cartoon again, which just shows that you've probably seen this before. But what we want to avoid is the regurgitate region of the L VOD speed setting, where flow is dropping to zero or below. We want our patients to be in a normal pulse. It'll range, avoiding higher speeds that can cause Parsons partial suction events. So we want them to have a little bit of a cushion whereby, if they're if they're flow, wave forms really dampened things such as positional changes. Orville Salva from a cough or straining using the bathroom can decrease acutely pre load to the left ventricle and cause intermittent suction events versus full on suction. So we do want some comfort zone and have the patients in the region of normal pulse utility okay, so moving forward into our cases as we go through the cases and we think about how do we categorize different patient in bad conditions? We tend to group these in two by two boxes not too dissimilar to how we think about acute heart failure. Namely, is the patient wet or dry? Are they cold or warm in likeness? To that, we think about are the high pulse utility low pulse utility, high flow versus low flow in different combinations of those those two metrics. So let's review that a little bit, and then we'll talk about the case is, uh, so the first this with the example of a lower flow lower pulse utility state? And as I mentioned previously, anything that affects under filling of the L VOD will lead to a low flow low pulse utility state, and that could be bleeding. Hyperbole. Mia Right Heart failure Tampa Nod I will highlight two things that we'll talk about in the next. Webinar are obstruction, and in fact, this leads to high patient, pulse utility low device pulse utility, because if you're obstructing flow through the device, there'll be very little pulse utility in the H vats. The device isn't seeing pulse utility, but in this setting, in fact, the aortic valve could be opening regularly because all of the cardiac output is going through. The patient's native circulation in our case is, well, you know, Alaska, other moderators. You know, what other clinical information do they want to diagnose these different conditions? So what's the value? Be it echo the physical exam, invasive human dynamics to help troubleshoot and diagnose what we're seeing in the wave forms. Next. Quickly, we have low flow high pulse utility. Uh, I think most commonly we think about, um, under unloading by the L VAD, we need to optimize the device and think about if there's room to augment speed here, the speed is already 2700, so we may think about hypertension. What's the what's the blood pressure is a room for patient optimization in this setting. Next, we have high flow, low pulse utility. Most common is is the is the dreaded thrombosis, which we don't see too commonly, and it often has a very unique way form. Sometimes it can reflect his aortic insufficiency again will cover a I and in boot camp two. And then lastly, we have high flow, high pulse utility, generally the least worrisome of of the states that I think you know, we don't think about as commonly. But one thing to consider again, as if it's a noticeable change over time in your patient, is to do a screening echo because it could reflect recovery of LV function or increase contract illit e of the left ventricle itself. So with that, we're going to transition now and into our cases, and I'll call in Dr Julian, uh, first. And this is a patient to give us his thoughts. But this is a patient that I saw in clinic who came in, um, reporting really symptoms of or prosthesis. So told us that generally was feeling well, No, no real dystonia, but was getting intermittently lightheaded When, when standing and walking across the room. So this is what we saw our nurses saw when we connected it to the monitor. And, of course, again, it's not just a picture, it's not a static picture. These are real time waveform. So we'll advance and happen to take a video of what happened when the patient went from sitting on the examination table. The standing in the room. So, Dr Julian, if I can let me have you walk us through what you're seeing here and what your thoughts are, Um, Thanks, Mike. Again, I want to just confirm 11 thing that you said that the strength of this pump is the dynamic display that you get when you're seeing the patient. So your description is Ortho synthesis, the initial wave form that you look at. Um, if you're gonna look at flowing possibility demonstrates the low flow low positivity at baseline. When the patients sitting. You know, this is typically suggesting that the pre load on the pump is low. Whether it's because of volume issues, um or not. Then if you play it if you as you play the clip again, you can see those negative deflections And I don't know if you can point those, uh, to the audience. Um, that is basically indicative of suction. So, um, you know, again taking a step back and looking at the clinical scenario, Are we dealing with an inpatient post up or we're dealing with an outpatient. And you you said that the patient came into clinics as an outpatient setting with somewhat earth prosthesis. So my thought process are we dealing with volume issues? Are we dealing with a G I bleeding acute blood loss? Are we dealing with a high rpm state? Um, and we need to back off on the RPMs. I mean, those are the thought process of having, and then you always supplement this with in addition to the clinical scenario. Um What what the echo looks like as well when you see those patients in clinic. Yeah. Perfect. So I'll tell you that, uh, you know, to answer your questions. He actually looked to me to be You've Olympic. He did not look dry. His GDP would say it was visible just at the level of his clavicle sitting upright. You know, you can see it nicely when he was supine, but certainly didn't look flat. It wasn't elevated, so I would definitely say he looked you bulimic. The speed, you know, in the setting was was 29 20 I believe, which you know is is a reasonable speed. Um, so in, you know, in that setting to your comment, you know, are feeling in this setting was that he was you bulimic in that we we did, in fact, adjust his feed. So we dropped it down by 100 RPMs, and this is now the waveform. And again, we're seeing this real time live in clinic, really immediate changes. And so this to me assisted impatient optimization avoided unnecessary medication changes. But let me ask you, in terms of everybody does this a little bit differently. So, um, you know, you and I have worked together in the past. I would say that this is something even within our own group. I think people do it differently, but I try to in every bad patient. I see I will. Once they're on the monitor, I'll do a couple of physiologic maneuvers. I will ask patients to stand up. We call these bad Ortho static vital signs, even if they're asymptomatic to see if there's any flow dampening with or without suction. And then I'll often ask them to perform of El Salvador maneuver to see if we're provoking any any suction or or or dampening of the wave form, or are those things that you feel are helpful or do routinely? I'm glad that you've mentioned this. So, um, I don't I don't do this routinely on every single patient if they have no symptoms. So my question to you is, um if we leave patients who apparently have evidence of suction here and there even though they're asymptomatic, do they have long term, uh, effects or adverse effects from that, that we have to preemptively do something about it before we adjust it? Or is it just to make sure that we have a pretty reform, uh, you know, you know, fulfilling the rule of two that you just mentioned. Yeah, it's a great question there, you know, the answer is, we don't know the answer. Um, you know, I think there's certainly concern that subclinical suction events may be related to long term risk of adverse events, whether or not it could be causing, um uh, you know some uh increased year forces things that could lead to approach from Biotic State or ingestions if it occurred. Uh, so there is the ongoing post market approval study for Medtronic and a subsidy called Apogee, where hopefully, you know, data is being collected. And I hope there's a wealth of data that Medtronic has, and that's exactly the right question. Do these subclinical suction events translate to adverse outcomes? Or am I overreacting? Because, frankly, if I see intermittent suction, even if it's a symptomatic and it doesn't look like the patient's dry, I do react to that, and I will make a speed change to avoid suction. But if the patient's feeling great, maybe that's not the right thing to do. But there is a wealth. I think we're just at the tip of the iceberg and how we utilize his way for him. So hopefully we'll get those answers. You know, in the you know, the 6 12 months is is some investigators start to utilize Medtronics datasets. So let me throw one question back at you. So I I, in this setting, felt very comfortable going down in the screed. In optimizing this patient just by the way, forms and not getting an immediate follow up echo. You know, if echo is available, I'd probably have it done on the next visit to take a look to make sure that there was no changes. But do you get an echo with with each speed adjustment, or would you be comfortable allowing the wave forms to guide your optimization? Looking at that way from I'm okay with just leaving the patient as is and following up based on symptoms because, you know, that way form looks like everything is looking at that. Coupled with my clinical examine, how the patient is feeling, I think is sufficient enough to leave the patient alone. Okay, well, I'm gonna I'm gonna stick with you for a second. Just as we talk about patient optimization and walk us into the second case before I do just three slides. So this is actually a patient that I walked into again in the early postoperative period in the intensive care unit. Very regular pattern here. And in fact, um, the ICU team, um, didn't, you know, highlight that there was any abnormal pattern and the Elvis we actually have to do some education with the with the clinical staff in the unit and say no, that this is, in fact representing a near full suction event that's occurring intermittently. And so we walked the speed down from 3000 to 2900. This is a patient who had been having struggling a little bit with some early RV dysfunction. But you can see at 2900, uh, there's still partial suction not as dramatic. And then at 2800 again, still, on the higher speed side, we have a normalization of the waveform normal Sinus oil pattern. Absence of a suction events but still relatively low pulse utility in the setting of right heart failure. But again just highlighting the instantaneous changes you can see in the patient in bad condition when making these speed adjustments. But for you case, too, so we have a 30 year old, you know, post op Day two who had some hyperbole? Mia. Due to a bleeding event in that setting, the patient had developed some suction events or the staff acutely, while waiting for blood transfusion decreased the l that speed to 2100. You know you walk into the unit and this is what you see on the monitor. You know what? What is your assessment? What are your thoughts? Can you walk us through it again? Looking at that wave form? Um, with the clinical scenario, you're looking with an acute. So this is a cute post op. That's number one. There is evidence of, uh, of some high Polina from active bleeding. But looking at that wave form that way form, you know, gives you a low flow, high possibility waveform. And whenever you see that, um, you know, this is either indicative in my mind, You know, the most two most common things in the outpatient setting is high blood pressure. But in the inpatient settings, probably especially acutely. A Q Post op is probably low RPMs on the pump. So I think going up on the RPMs and by itself should should allow the recovery of that wave form. Um, for this patient. Yeah. Now, I would fully agree with that, but just to bring up this, uh, you know, again, this table for the audience in terms of troubleshooting that high pulse, a tile, low flow state, this is really what's in the differential. You know, and I would argue that continuous suction is a very it's not. This is still a very smooth regular profile to me. It doesn't have the jagged, irregular appearance of of suction. So it argued that that continuous suction is probably not what I define as a high pulse utility state. It's it's somewhat of a unique waveform, but certainly thinking about hypertension in the ambulatory setting. And then again, whether or not there's some room for that optimization and and and going up on the speed, which certainly when you're talking about a speed of 2100, you would think there is some room to be able to do that. And if you look at the human dynamics, you know, this is the beauty of post ill patients who have the swan in place, where you can see that the P diastolic is high. The CPP is driven by a high diastolic, so you can argue that you don't need an echocardiogram. In this scenario, you have evidence that the LV is not being unloaded, the wage pressure is high and the way form is consistent with that as well. Yeah, thank you and I would point that out to that other information, I would agree you don't likely need an echo to diagnosis with your exam if the J V P is to someone's ear, which should be with the C v p of 20. But, you know, just to point out again, this pulse utility is translating to native Pulse utility. So this L V is not adequately unloading. And because of that, we're seeing regular opening of the aortic valve where what we generally like to see is, you know, intimate and opening. No one knows what's right, but historically, we've kind of talked about opening of the aortic valve, every couple of beats or so to help flush out the aortic root to prevent stagnation. And from this formation, which could be an itis for stroke. So we do like to see the aortic valve opening intermittently in patients when possible. Uh, and this is just the final result. The speed was increased. I'm sure that, you know, this patient was also diaries. It was patient and pump management. I don't think the speed augmentation by itself got the CVP from 20 you know, down to normal. But certainly the echo show that the LV was now adequately decompressed, Um, and not dilated. And we have normal bad parameters. Great. I'm gonna move on to Jennifer if I if I may. So, Jen, on this next case, case three. Um, if you can tell us what you're seeing here, we have a 60 year old again. Early, postoperative period day, too. Speed is 2600. But if you can just tell us on this, I'm going to advance the slide one here just to highlight the irregularity of this of this wave form. And if you can describe for the audience what this represents, how would you describe it? So what I see here is, um, and base the patients at their baseline flow of 4.5 leaders, their powers normal at 3.9. Um, the frequency is regular, but the pulse utility here is variable. You have, um, some areas right there on the left hand side of your of your wave form there that are different than the rest. So what we're seeing here is completely normal. And this is when levar is turned on. So, love, Ari, um is a feature that you can turn on and off on the pump. The every 60 seconds for two seconds at a time, the pumps going to slow down 200 RPMs below it, set speed and then ramp up for one second, 200 above its set speed. And that's going to wash out the pump. This is completely normal. Expected when LeVar is on, I turn it on on all of our patients. I think it's great. Yeah, thank you so exactly. Exactly. Right. You know, in the European trial they had access to LaVar e from the get go. It was more recently released in the US We to turn it on, you know, coming out of the operating room as you mentioned, it helps to wash out the device as well as the left ventricle in. In is, one more potential mechanism to prevent night is for Claude North rhombus formation to reduce the risk of adverse events. So with that, we will transition into the next question for both, like so, are there any patients that you worry about turning this feature on patients with really marginal RV function? Or it doesn't matter? You just do it blankly on every patient. We've been doing it on everybody. We have not seen any acute human dynamic impact. That's a great question. I've had lots of people, you know, I have been a different roundtables where people have asked it. But there's nothing in at least in the European experience or in the literature or what our surgeons report seeing in the operating room. Why? Why doing this when it's occurring once a minute, it's a three second cycle. Why it should lead to any acute human dynamic. Instability. Uh, but I will say it again. It's not. I've been called to the bedside a number of occasions. It certainly is a curveball. And people, if they're not aware of the love ari particularly. We've been using the H bad for years, so when people haven't seen it before, they're wondering what is going on. It's certainly an irregular appearance. We have this experience. Yeah, we have the same experience. We There's really no one that we wouldn't turn it on. Um, when we first got it available are historical patients we chose to turn on and there was one patient that had a decent amount of suction, had some precinct apple events. We weren't sure what to do, so we didn't turn it on on him. But I don't think it would have made any human dynamic impact on him. So for going forward, it's on on everybody, you know. In the post market approval study, we are hoping to be able to look at the impact of LaVar recycle and reducing risk of adverse events. But the problem is, it's not. It's observational. It's not a randomized not comparing LeVar Ian to Lombardi off. So some of that analysis is going to be somewhat limited. And it was one of a number of different interventions in this apogee sub study that was utilized to help standardized care and reduce risk of adverse events. It's hard to tease out the contribution to decrease stroke risk if, in fact, that's what we see in the most contemporary experience with this device. Um, other things to consider, though, as it relates to seeing a regular irregularity in the in the H bad wave form patterns are arrhythmia related, or what we're labeling is E K G related, most commonly atrial fibrillation. But you can't see it with ventricular arrhythmias, namely by Germany and PVCs. You can often see float real time across the monitor versus the non arrhythmia, or 90 kg related. So LeVar is what we just discussed about and then thinking about positional results, which would be partial suction events in section in session two. We'll look at the impact of the balloon pump on H fat wave forms, and we'll talk more about suction and even some respiratory variation, which you can see not uncommonly in the early postoperative state in the just like we see respiratory variation in right heart human dynamics. In fact, sometimes you can see that on the H fad monitor as well. All right, so we have a couple questions. If it'd be okay to take a couple questions right now from the audience. Great, Great. Um, 11 question the first one is, Does the bump or the plateau sometimes present in the waveform had end diastolic have a known interpretation. Uh, do you do you all on the faculty? So I'm assuming that means in terms of the Contour, whether it's a sign, use oil versus sometimes we see an occasional more abrupt or jagged appearance. You know, I would say, um, well, we're certainly again we're certainly learning. I mean, that's a great question for machine learning technology to look at these patterns. One of the things I've seen in my experiences, if well, I'm thinking specifically of a patient of mine who has an abnormal. The geometry of the LV is abnormal was dilated, but they had a prior aneurysm resection. And because of that, the L VAD was somewhat malp positioned, um, and so that one that patients more pulses style than the normal patient because the L V is inadequately unloaded. Uh, and it is kind of a funny contour because there's almost partial obstruction, not suction. But there's kind of a partial obstruction from an acceptably positioned, um inflow cannula. So abnormal, I would say inflow cannula positioning would be something that can result in in an abnormal contour. Uh, in that setting, I don't know, marijuana or Jen. Do you have any experience or thoughts with that? Yeah, I don't think it has a clinical significance as much I think we we, uh you know, we have experience with, you know, a pickle calculation and non April calculations for age fats and and, you know, I have to go back and look and see if there is a specific distinction between the location of the pump, as you said and the the the contour of the wave form. But I don't really think much of it other than what you just said. Great, thank you. One additional question was in your in your practices and your experiences. Do you find that there's one finding or, um, condition that that is present in the waveform that is sort of, um, typically overlooked or underappreciated? Let's say like they're cute and you were talking about the ICU, sort of missing, um, missing section. Is there something just in your experiences that is often kind of underappreciated or goes unrecognized by? Maybe just teams kind of floating by the, Let's, say, a patient in the ICU, I I would say it's probably suction. It's the dynamic nature of suction where you could miss it if you turn your back. And that's why I you know, I do like, uh, provoke a ble maneuvers to see if we can precipitate it. But, you know, I had one case that sticks out in my mind about a patient that was having limited working with working with PT was very limited. Um, because every time they stood up, we were seeing VT on the monitor. Uh, and in fact, you know, no one is looking at the h God monitor because the telemetry box kept ringing. But if you folks, when we focused on the h bad monitor when they stood up, you clearly saw that they were having a suction events, which was the precipitous for the ventricular arrhythmia. And then by simply walking down that speed, uh, there was resolution of that condition. And now you know, the patient was working, uh, fine with PT without recurrence of those events. I think what's most important here that we have to drive home is that wave forms tell you so much about your patient. Um, if something is wrong with your patient, if you look towards your wave forms, you can find answers. Um, so I think that's it's not one particular thing that I think is underappreciated. I think as a whole, you have to look at the pump. Um, and it gives you a lot of clues to what's happening. Great. Thank you, Echo. That put it in the context of everything we've talked about the echo, the human dynamics and the physical exam. You can't look at them in isolation, that is for sure. But they certainly supplement all of our other diagnostic skills and capabilities. Great. Okay. So, General, stick with you. This really a continuation of the earlier case. So, uh, get 43 year old, different patient, but a similar scenario here. 43 year old now post op, Day eight. Uh, we have a speed of 2600. Pulse utility of four liters flow of about four. So 3 to 4. So what are you seeing here? Because you got called, actually, because the bedside nurse was concerned that the patient was having was tachycardic. Yeah, so that's definitely what it looks like. Each peak is a cardiac cycle. So, um, this these give you a lot of insight into what's happening with the patients. E k. G. Um, Their flow is normal. Their power is normal. Their frequency is, uh, pretty fast here and there. Possibility is, is, uh is okay, But what if super important here is the time scale. So normally, we're looking at a 12th time scale, and this is 20 so this patient is actually completely fine. Um, they're not tackle, Kartik. If you hit that time scale button on the bottom left is how you can see that we are at a different interval than were normally looking at. And then, actually, if you look at the power curve, you can actually see that levar is on here, even even easier than you can see in the flow. Um, curso. I people tend to just look at flow over time, but I think looking at power over time is also a key. Um, it gives you an extra hint into what's happening. So what you need to do here is just hit that time scale. Um, and we can see, um, I think it's on the next slide. That Yep. Over time. So you can change this. You can go out 10 seconds, 20 seconds an hour. You can go out today is, um And what's particularly helpful here is that let's say you had a patient who was, um g I bleeding and was very hypovolemic. Got a couple of units of blood. You can actually see that response over time. So using these time scales to see what's going on with the patient is very, very helpful. Great, Yeah, totally agree. And so what? We're going to focus next session a little bit more on those other ways of trending data, which are the log files. And then again, here are the different timescales, and again, this can. We can be fooled when this is extended out to 20 seconds, but I do find it helpful in some circumstances, particularly when we're looking at arrhythmias or if we're feeling that we're seeing frequent PVC. So it's not uncommon in clinic that I'll change and this will be on an as needed basis. But if the patient's feeling some palpitations intermittently, I may open up this time scale to 20 seconds and see if we're able to capture PVCs more frequently. This last window is a little bit more. It's not totally static because it's 60 minutes. It's not. What it's not showing is the wave forms, but what it's showing and the red is the peak versus the trough. And so this is one of our patients, so it's more commonly utilized in an inpatient setting because it is collecting sick. In here. It's a full 60 minutes worth of data, but what you can see, it's about 40 minutes ago we had a speed increase. And so that's why we're seeing a reduction in pulse civility of about, you know, 4 to 5 leaders in an amplitude here now, down to two or three following that speed adjustment that was made so again, just one more potential tool that can be helpful at times to help. Look at the degree of pulses style changes over a really recent period and then log files extend out a bit further. So case five here tomorrow. And if I may, I'll jump back to you for this one. So again, early postoperative state in a 55 year old speed had initially been a 28 100 with a normal power. Three leaders of positivity. It was, in fact, recognize that the device was having a continuous suction. So do in the acute setting again, the speed was dropped down to 2000 RPMs. Um, and now, with no with that background, what are you seeing here? 2000 RPMs. And what should you be seeing? Um, with the speed that low. So again, if you remember the first case I think with the second case, that represented a low RPMs, but the it should low flow high possibility. Um, here you see a low flow low possibility. So it's a little bit different. Um, And again, when you see that at that low rpm, you always have to think Okay, in the immediate post operative period, Why is this happening? Am I dealing with again looking at the pump? And what is the pump seeing from? From? It's from From a volume perspective. So which means that the lvs under filled there's either because of an extrinsic compression or because the volume is significantly down or because the RV is not moving blood to the L V side, um, to the L V. So these are the three things that I think about in the postoperative period. Obviously, in patients with the in the I C, you can always look at the tail. You see if they have any arrhythmias. The waveform doesn't suggest that, but it's it's a regular waveform, so that's the differential. So if you tie again that piece with the clinical scenario, which is the patients hypertensive. But you see that the CPS 20 the p A diastolic is 20. So you have equalization of pressures. Then you look at echocardiogram and the echo shows essentially evidence of RV collapsed. So there is extensive compression. So if you put all this together, I think this is probably suggestive of, um, RV collapse. Yeah, this could This could indicate Tampa not based on based on this, based on this scenario. Yeah, perfect. I have nothing to add their um you know, I think you're exactly right. It's recognizing when this is occurring, uh, as it relates to the timing of of surgery and knowing the differentials that can occur in those different periods of time, so that again transitions us first. So here the course, if you're seeing Tampa nod, that would indicate, you know, media spinal bleeding with compression of the RV raid atrium. So the answer is evacuation of that clatter hematoma with surgery, which is what occurred in this setting. We see improvement reduction in the C V p again Doctor Julian highlighted in the slide. Before, in this setting, we had an acutely ill patients. Tachycardic, hypotensive map of 54. Now we see improvement in the blood pressure improvement in the right side of filling pressures in the echo normalization of the chambers and the bad parameters returning to a normal pulse style state. So, frankly, this is not uncommon situation. You know, surgical bleeding is unfortunately, you know, still a relatively common event. These patients are coagulate pathetic. Um, and it's not uncommon that we patients return to the O. R for evacuation of of clock. So again, it can really assist. I mean, I think this is one place where, you know, we have data here that may proceed. Other changes that we're seeing again, putting it all into context. But if you're seeing a normal pulse, a tidal wave form that now is suddenly acutely becoming dampened in the setting of of hypertension Um, you know that that that really is a warning sign to get human dynamic data for swans not in and bedside echo immediately to figure out what's going on. A lot of times in the immediate postoperative period, you may not be able to get good windows on the echocardiogram. Totally right. Have regional Tampa not, um come, you know, so stuff that you really have to go with the clinical scenario and the waveform and convince the surgeons to open the patient back up and evacuate the hematoma. Great. Thank you. Um, and so six again. This is will transition to, um you know, another somewhat similar case here, but 67 year old, uh, this is now in the surgical hand. So this is inter office is a place where I never am. But we have This is what the, you know, cardiac anesthesia, and the surgeons are dealing with. They have a patient now in the O. R. Who's on multiple i behind the tropes as well as Veysel pressers to maintain profusion pressure, obviously sedated. You know what? What are we What are we seeing here? And what are your concerns? You know, now chest is still open, right? So we're not going to be tamping Rod, But again, it's again low flow, low possibility. And it's somewhat concerning when you see that in the interpretive period, then my differential at that point number one would be You know that the RV is tanking in the in the in the or, um, as as a result that you're seeing this again. As you said, Temple has not done issue if you look at the human dynamics here from from anesthesia, you can see that the CPS 25 and the PPL pressures are high, but the P A pulse pressure is narrow. Um, so this is all suggestive, that there is no forward flow from the right side to fill the ventricle to allow the pump to function properly. And in the echo, you show that the lvs under filled. But the RV is dilated again. You know when when assessing RV function, and this is probably beyond the scope of the wave form. It's really not easy to us that's already function. But if you have to put everything together, you know, in the interact with the period low possibility, the LV volume is down. But the RV parameters of RV function, at least invasively are are concerning. Then this is most likely RV failure, in my opinion. Great. You know, I would, I would add, though this is one situation where I mean right heart failure is always really challenging clinically, and I certainly I think I would just add that the absence of low pulse it'll state by no means excludes right heart failure. I've certainly seen normal pulse utility and patients with clinically overt right heart failure. And that's probably because they're still volume overloaded and or they may be on China tropes, so they have increase. Uh, you know, left sided contract illit E. Because of the idea. Tropic support the receiving. So I wouldn't I wouldn't say, Um, you don't need to have a low flow, low pulse utility state to have somebody who may have clinically significant right heart failure. If it's there, it's kind of, you know, it's It's higher sensitivity, lower specificity type situation. So it certainly doesn't exclude that, but it can certainly indicate that you're dealing with some pretty profound right heart failure in this clinical setting. Profound is the key word here because again, it's a spectrum, right? So on the extreme end of spectrum, this is what you see when the RV tanks immediately post off. Definitely right. And that and that. By the way, it's the same reason why you know, the L V can be under filled in VF. Remember that the LV supported in the setting of a ventricular arrhythmia, but what's not supported as the right ventricle. So if you've got a fibrillating right ventricle. You're not going to push blood across the pulmonary circulation. So it's essentially VT or VF can lead to, you know, our right heart failure, acute right heart failure, particularly in the setting of high after load, uh, state, uh, in which case the LV would be under filled in that setting as well. So in terms of what was done here, the patient was already on vasopressin, an entropic support. So is Dr Julian mentioned there was evidence of persistent pulmonary hypertension. We're going to be limited, probably in our ability to go up on al that speed to further unload because of the lack of pulse utility and the risk of suction. So we're going to, you know, aggressive volume management, either mechanical with renal replacement therapy or dery sis and an initiation of pulmonary vessel dilator. So our group would use inhaled villa tree, initiating aggressive management of pulmonary support. Uh, and again, volume management. We did see a reduction in C v. P uh, improvement in the conceptual positioning. So bad RV that LV interaction seemed to improve, and we see a slight improvement in possibility. But no Marwan highlighted. This is a pretty profound case. So this is not great pulse utility, But it's better than what we were seeing a minute ago. Mhm. Perfect. So I'll come back, uh, to jen on this one. So case seven, we have a now in the ambulatory setting. So not acute. We have a patient, 55 year old now, five months out, coming in for routine clinic visit. Um, and I'll let us I'll let you walk us through. You know what we're seeing here after he gets connected to the monitor? Sure. So, um, first thing I see here is a very high pulse utility. His speeds 27 20. It's a good speed, but if you see, his baseline parameter is about five liters per minute right now, he's only flowing for his power is totally fine. Um, at 3.8, but his baseline pulse utility is three. And right now we have a possibility of about seven and our flow during diastolic. So the trough there is is almost approaching zero. Um, so we have a lower flow high pulse utility scenario here. Um, so this almost always hypertension. Um, that is the first thing that comes to mind. Um you mentioned before that the consequence of hypertension is, uh, catastrophic. You could have, um, strokes. And for us, getting the patient's blood pressure down is of utmost importance. You can see here his patients also short of breath, so he's getting no flow. His the after load is so high, the pump is not going to work harder to overcome it. And it's just backing up. His doctoral map is one of five. Um, so here we definitely have hypertension. Um, that is causing this wave form. Yeah, that's great. We see as you highlighted, we see the trough flow. That's, you know less than that to the rule of twos. It's approaching zero. So certainly in terms of stroke mitigation as well as other symptoms that you highlighted, uh, we want to We want to improve blood pressure control in the in this patient. And if the blood pressure was, you know, if we were looking at a patient who's Doppler blood pressure was 80. Then of course, we'd be thinking about whether or not there's room for device optimization, but certainly in this setting, um, we're gonna be we're gonna be targeting blood pressure first and not going up on speed because we go up on speed, we may worsen the hypertension. So blood pressure control first and then so patient optimization and then device optimization. Yep. Uh, so why does hypertension Just one graphic? This is a beautiful review if you haven't seen it by John Rich and Dan Birkoff. Um, talking about, um, waveform analysis, but highlighting again pulse a tile in the setting of a high map versus, uh, improve blood pressure control. But we talked about the Delta P across the cardiac cycle. Again, we have the left ventricular waveform so insistently in a normal patient there again is no, it's equal. There's no gradient between the L V and the aorta, the gradient of courses in diastolic when the Eric valve is closed. So we see this Delta P here in the green in the hypertensive patient, of course, we're going to see increase both in systolic, but as well as diastolic pressure. So now that that Delta p in diastolic, in the setting of a hypertensive patient, is going to be even greater, and it's that physiology that we're seeing right there, the greater difference in diastolic that's going to lead to increased pulse utility, uh, in the setting of increased after load, which will result in decreased flow. So the low flow, high pulse utility state of hypertension. With these patients, I think we probably have time for, uh, for just one more. So this is the follow up the patient received in hypertensive medication. Um, and we see improvement in the in the in the degree of pulse utility. Um, overall, with that with that therapy. Michelle, we have a We have another case we can go to. Unless there's any questions in the chat room that you wanted to afford to us. Uh, right now, Dr Colonel, I think you do have time for one more and we'll we'll check back, uh, for the questions. Okay. Perfect. So, um, this is you know, this is a you know, an important case, a classic case, a kind of a feared case that, uh, you know, you may or may not seen at some point in managing patients with l VADs. So, Mara, I'll come back to you or Jen. Really? But this is in a 71 year old patient who's at home and calls the, You know, we have a bad pager at two. In the morning that they're experiencing. Uh, you know, they're having high watt or high power alarms, you know, in their power readings greater than 10. It's pretty classic here. You know what are what are you seeing? More One before I comment on this, I just want to tell the people one weekend when I was a fellow, um, with Mike, Mike was leaving town. David was leaving. Everyone of the tough was leaving town, So they gave me that that pager and they said it hasn't gone off in two weeks and they leave town, and in two hours it starts beeping with the same clinical scenario. This patient has a high water alarm, but anyways, this is in my mind. This is a This is a thrombosis. Until proven otherwise, you're dealing with a case of very high, very high flow, artificially high flow and low possibility. Yeah, So just to comment on that, not not sticking you with a bad pager, but so importantly, this is again is flow estimation. Right? So this is a setting where the flow and the device is very different than the actual cardiac output in the patient. So because there's increased drag on that spinning rotor, it is doing everything it can to maintain that fixed speed at 25 60 but has higher power requirement. So the power is directly measured. It's chugging along, but because it's gunk it up with the rhombus, um, it takes more power to maintain a fixed speed, and that translates to an abnormally false estimation of flow. So flow through the device may, in fact, the zero or one leader permitted, and the patient could be very pulse it tile because they're not unloaded, their LV is banging away and all the cardiac output is going through the aortic valve, so you may see the aortic valve opening regularly. So this this is again a disconnect and understanding that this is not true flow. It's an estimated estimated flow. And so, you know, this is Dr Julian. Highlighted is the setting of of course thrombosis. This patient received medical the patient. You know, the first question on the phone, by the way, is you know, what does your urine look like? Are you having any dark colored urine? Hemoglobin? Yuria from analysis. Ldh is generally going to be markedly elevated in that setting. Um, and you know, the patient received medical management with a probabilistic therapy. And again, the nice thing about wave forms, as you can see, an immediate and dramatic response and improvement with the administration of of logic therapy, where the flow immediately responded, didn't normalize in the first few minutes, two hours. But five hours later, we're seeing return back to normal operating range. And, of course, you can see an irregular pattern here which may indicate, um, uh, a fib in this patient is as well. So let me, um, one point make sorry. I just want to make one point is, um you got to fix this really fast because I don't think when people are home and they call with high wants It's never like, maybe it's something Maybe it's nothing. They just bring them in because, um, the only scenario that it's not around this is if you've just adjusted the speed and you didn't address your high power alarm, and that's set to tight. But that, um, is probably not what's going on. I want everyone to think immediately about dramas and getting that patient and quickly yeah, and I would add to that I mean, this is not necessarily talk about managing adverse events, but to me it's a it's a it's a surgical condition. Frankly, unless the patient's not a candidate for that exchange, medical management leads to resolution and probably at best, 50% of cases with really high risk of recurrence. So we really reserve lyric therapy, Um, as demonstrated in this case, but for patients who are declining or not operative candidates for other reasons. But the surgical team needs to be alerted. Uh, you know, immediately. Great. Thank you guys so much. We're right at the top of the hour and we don't have any further questions. So with that, I want to thank Dr Kernan doctored Romanian and Miss Pavo not only for your time today, but for really bringing kind of Technicolor to this content. Um, the value and benefits of waveform analysis is most evident. I believe when it's presented and discussed by clinicians such as yourself. So I would like to thank you and our many participants today for your time and your attention. Um, please do I just want to remind you to take a moment to complete the survey following the end of this session, we will Listen, we want to make certain we provide programs. Um, meaningful content. We want to help you who want to help your patients. Want to help your program. So So please give us your feedback. Also. Please join us next week. Tuesday, March 2nd for part two. Beyond the basics where we really get some more great case studies and good conversation here from our faculty. Thank you so much. Thank you. Dr Karen. In Dr Dominion and Miss Pavane. Thank you so much for your time today. Very much. Mm, yeah. Mhm. Yeah, yeah. Mhm, Mhm, Mhm Yeah, yeah, yeah Mm, yeah. Mhm Yeah, yeah Mm Mhm. Yeah, yeah, yeah.