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Ventricular Assist Device Management In The ICU

Critical Matters
Critical Matters

58 plays · Jun 12, 2019

In this episode of Critical Matters, we explore the role of the intensivist in the management of patients with ventricular assist devices. Our guest is Dr. John Greenwood, a practicing intensivist who splits his clinical time between the Cardiac & Vascular ICU and the ED-ICU at the Hospital of the University of Pennsylvania. Additional Resources: Summary of information presented during the episode kindly provided by Dr. John Greenwood: https://bit.ly/2MJdfSa HeartWare Waveforms App for iPad: https://apple.co/2NpyQEr Articles Mentioned In This Episode: Pratt AK, Shah NS, Boyce SW. Left ventricular assist device management in the ICU. Crit Care Med. 2014;42(1):158-68: https://bit.ly/2MKr3M6 Sen A, Larson JS, Kashani KB, et al. Mechanical circulatory assist devices: a primer for critical care and emergency physicians. Crit Care. 2016;20(1):153: https://bit.ly/2NoreC4

Transcript

Speaker: Welcome to Critical Matters, a sound critical care podcast covering a broad range of topics related to the practice of intensive care medicine.

Speaker: And now, your host, Dr. Sergio Zanotti.

Speaker: Over the last decade, the use of ventricular assist devices has increased exponentially.

Speaker: There are a number of devices used today for a growing list of indications.

Speaker: Patients with ventricular assist devices may come to the ICU in the postoperative period, but may also present from the outpatient setting with complications related to long-term use of a ventricular assist device.

Speaker: It is very important for the intensivist to understand ventricular assist device equipment, patient physiology, and appropriate recognition and management of complications.

Speaker: Today's episode on the podcast

Speaker: is a follow-up on our initial discussion on critical care of the cardiac surgery patient with a focus on ventricular assist devices.

Speaker: It's a pleasure to welcome back again John C. Greenwood, who's an assistant professor of clinical emergency medicine and assistant professor of anesthesiology and critical care medicine and medical director

Speaker: the Resuscitation and Critical Care Unit at the Hospital of University of Pennsylvania, Department of Emergency Medicine.

Speaker: Dr. Greenwood divides his time between critical care and emergency medicine.

Speaker: Half of his clinical time is spent working in Penn's heart and vascular ICU and the other half in a relatively new EDICU space at HUP,

Speaker: He is the editor-in-chief of the EMRA Presser Dex and has a particular interest in the resuscitation of cardiovascular emergencies, mechanical circulatory support, and time-sensitive critical illness.

Speaker: Dr. Greenwood is also an administrator and contributor to Critical Care Perspectives in Emergency Medicine, a monthly CME podcast on resuscitation and critical care-related issues that can present to the ED, and

Speaker: and of Critical Care Project, or CCP, a multi-institutional website designed to be a multidisciplinary educational resource on topics in critical care.

Speaker: John, welcome back to Critical Matters.

Speaker: Well, thank you, Sergio.

Speaker: That's a kind introduction, but I really just think of myself as an intensivist that has an interest in heart stuff.

Speaker: So this is exciting to talk about this today.

Speaker: And as we were saying in the introduction, hard stuff seems to be growing in numbers, so even intensivists who are not working at very specialized units like yours will be exposed to these devices and need to have a basic understanding of how to manage certain complications.

Speaker: Wouldn't you agree?

Speaker: No, absolutely.

Speaker: I think you hit the nail on the head over the past 10 to 15 years.

Speaker: The number of VADs that are not only at the academic hospitals but are presenting to community hospitals because of the reasons that they're being put in is also growing in a really large volume.

Speaker: having one of these patients drop into your lap can be sometimes really anxiety provoking.

Speaker: But if you understand a few basic concepts as well as are able to recognize some common complications and initial interventions that can kind of get yourself out of the weeds, you can really turn a tough ice to unite or day into a really rewarding

Speaker: a word in clinical experience.

Speaker: So yeah, this is a great topic.

Speaker: I'm glad you're kind of bringing it to your audience.

Speaker: Absolutely.

Speaker: So before we dive into specifics, I think it'd be important to outline the general situations in which VADs are considered today.

Speaker: And I think that most people will hear, oh, it's a bridge to something, but what?

Speaker: Maybe you can expand on that, but also this concept of destination therapy, which is a little bit foreign for most of us community ICU practitioners.

Speaker: Absolutely.

Speaker: So the concept of a bridge two is really that most VADs are designed to provide the patient with time until they reach some sort of definitive state.

Speaker: And that state may be recovery.

Speaker: So you think of the patient who's had a viral myocarditis and has basically acute heart failure.

Speaker: they may have a VAD placed temporarily until their heart's able to recover and the consequence of that myocarditis go away.

Speaker: There's also this concept of bridge to transplant.

Speaker: So these are patients who are young, usually have non-ischemic cardiomyopathy of some sort, sometimes familial, sometimes from other causes, who are trying to get optimized in order to be able to receive a transplant, a heart transplant.

Speaker: The last group largely is destination therapy.

Speaker: So destination therapy is usually the older individual who may not be eligible for a heart transplant, but

Speaker: They still are relatively well, and the concept or the goal is to allow them to achieve something.

Speaker: Usually it's a life event.

Speaker: So, you know, I like to think of these patients as, you know, the 68-year-old, 70-year-old patient who, you know, doesn't have any really comorbidities other than

Speaker: just one or two end organ dysfunctions, but wants to see their kids graduate college or wants to get to a point where they can go on a family trip or something like that.

Speaker: And these things are all taken into consideration when we look at destination therapy.

Speaker: So, you know, these patients do have goals in place and we'd like to try to help them achieve them.

Speaker: And I think it's important for the intensivist to understand that

Speaker: With durable VADs, we'll talk a little bit about more later, these destination therapies, people can actually leave the hospital and have a meaningful extension of their life, which I think for most of us, in given circumstances, would be a big positive.

Speaker: No, absolutely.

Speaker: Quality life is something I think all of us are more in tune with.

Speaker: So, you know, taking into consideration what the patient wants to do and helping them get there is an important part of the intensivist job, particularly with a lot of these VAD patients.

Speaker: And I guess the last comment on this, and then we'll move on to more specifics, is that the bridge might also be a bridge to a decision based on uncertainty at the moment.

Speaker: We're not sure they're a destination therapy patient or a transplant patient or a recovery patient.

Speaker: and perhaps we need time to figure out what's the next step.

Speaker: Is that correct?

Speaker: That's correct, yeah.

Speaker: The bridge to decision is a growing group of patients receiving VADs, and this sometimes falls into the bridge to transplant or maybe a bridge that they're not going to get transplanted, but we just need more information.

Speaker: So we're kind of at a – sometimes these conditions can degrade very rapidly, and we have to make a decision about how we're going to temporize the patient.

Speaker: And a durable VAD might provide us that time to get enough information to make a well-thought-out clinical decision.

Speaker: Well, let's start talking more about the VADs.

Speaker: And I always say that there's two things that I've learned, I mean, from doing this podcast is one is that my guests are always much smarter than me.

Speaker: And two is that my audience is much smarter than me.

Speaker: So this might be a little bit over my head, but I'm sure of interest for everybody else in terms of understanding the basic physics of flow.

Speaker: Could we start by maybe explaining the different types of mechanism of flow, John?

Speaker: Yeah, absolutely.

Speaker: So when VADs first started being developed, they were mostly pulsatile, pneumatically driven devices that, if you think of the development of computers, they start these massive mainframes and have now gone into literally my pocket in terms of an iPhone.

Speaker: So they've gotten a lot smaller over time, and that's through the way the technology has advanced.

Speaker: So for the most part, we don't see any pulsatile VADs anymore in the community.

Speaker: They've moved on to two separate mechanisms.

Speaker: So one is axial flow and classically these would be kind of your HeartMate II devices where they're designed as the pump is basically has a central propeller that's located within the motor itself that spins around creating a vacuum on one side so that the blood is actually pushed to the other side.

Speaker: If you think of like a submarine propeller that's kind of how it works.

Speaker: Now, these types of flow devices, the axial flow devices, have to spin at a really high RPM rate that sometimes can cause friction, heat, and particularly blood damage, which can cause thrombosis, hemolysis, and is a lot less efficient than the newer generation, which are often referred to as the third generation VADs.

Speaker: And so the VAD market in general has moved towards what's called a centrifugal flow device.

Speaker: So these are a lot smaller and they're located really just in the pericardium, directly adjacent to the pericardium.

Speaker: And

Speaker: this mechanism, the flow is actually thrown out of the VAD.

Speaker: So the blood enters into the inlet cannula and there's a basically a fan on the inside that spins around and throws the blood towards the outer walls.

Speaker: And then that is then returned to the proximal aorta.

Speaker: Now these new generation 3 centrifugal devices you may hear of as the HeartWear device or the HeartMate 3,

Speaker: are much more durable.

Speaker: They're much more efficient.

Speaker: They cause a lot less blood damage.

Speaker: And the thought is that this is the next best step in terms of where we should go in the VAD technology market.

Speaker: And is there a difference?

Speaker: I mean, so clearly it's a progression, like you said, from pneumatic to the centrifugal kind of being the different versions, 1.0, 2.0, 3.0.

Speaker: But is there a preponderance of one over the other where it's durable or a temporary VAD?

Speaker: Right, so in, I believe it was 1994 when HeartMate 2 was FDA approved, that one was the first VAD approved for basically destination therapy.

Speaker: So in the community, there's a lot more of the HeartMate 2s that are out there compared to the newer generation devices.

Speaker: Now,

Speaker: They also had their own set of complications, which we'll discuss a little bit later, but I think what most academic or transplant centers are doing in terms of VADs, they've moved to this third generation centrifugal flow device because they're a lot smaller.

Speaker: The HeartMate 3 is still under investigation, but for bridge to transplant.

Speaker: But HeartWear has been FDA approved for bridge to transplant.

Speaker: So most, I think, insertions now have gone to centrifugal flow.

Speaker: So you will still see HeartMate II's out there.

Speaker: There's plenty of them.

Speaker: But I think over the next five years, you'll be seeing a lot more of the newer generation devices.

Speaker: Okay.

Speaker: Why don't we talk a little bit about what are the different types of devices?

Speaker: Just walk us through that so that our audience can visualize all the options and the possibilities these days.

Speaker: Yeah, absolutely.

Speaker: So I think VADs come in two separate flavors for the intensivist.

Speaker: They're the temporary ones, and then there's the durable ones.

Speaker: And by temporary, I mean these are ones usually inserted by a cardiac surgeon or an interventional cardiologist or maybe even an interventional radiologist at some places or cardiology designed to provide temporary support for a patient who's had an acute cardiovascular collapse or insufficiency, might be in a cardiogenic shock.

Speaker: So from a cardiac surgery standpoint, the

Speaker: One of the more common devices would be the Centromag device, and that's basically an external VAD that's surgically implanted into the patient.

Speaker: It's a centrifugal pump.

Speaker: It can be run for a long period of time, even though it's only FDA-approved for about six hours.

Speaker: This can run for days to weeks to maybe even longer.

Speaker: It can provide 10 liters of flow at any given time, and it's usually implanted at this point for acute RV failure after an LVAD or after cardiac surgery.

Speaker: It's a large basically inflow-outflow cannula system, so it usually utilizes a 22 French outflow, and whenever the directions always can be kind of confusing, but

Speaker: It's always kind of centered on the device rather than the patient.

Speaker: So an outflow is going from the patient to the device.

Speaker: So it's a 22 French outflow cannula to the VAD itself and then a 32 French, sorry, to the patient.

Speaker: So if you have a classic configuration would be something like left atrium to the aorta or the right atrium to the PA depending on which ventricle has failed.

Speaker: Now, there's a couple other devices that are temporary that may be seen.

Speaker: So the Tandem Heart, particularly in the community, the cardiologists are particularly utilizing these more and more with the complicated PCIs.

Speaker: So a patient comes in with a STEMI.

Speaker: They go to put a stent in, and they crash.

Speaker: This is a common device used particularly for transferring the patient to an academic clinic.

Speaker: institution who may have more resources.

Speaker: These are temporary centrifugal VADs.

Speaker: They're inserted percutaneously and the blood is basically taken out of a 21 French femoral vein that is basically inserted so it's transseptal into the left atrium and then it's returned to the femoral artery.

Speaker: So it's almost like a VA ECMO type system

Speaker: But it's a little bit more durable, and that can provide support for up to about four liters a minute.

Speaker: So if your patient's in cardiogenic shock, that may be just enough to get them through their transfer.

Speaker: And we were talking a little bit prior to the podcast about something that you're seeing more frequently, which is the impella.

Speaker: And I think this is an exciting kind of technology that it also is being used more frequently.

Speaker: This is a temporary axial flow device that's inserted percutaneously again.

Speaker: And there's a couple of different types.

Speaker: So there's an assist device.

Speaker: impella that provides about two and a half liters of flow.

Speaker: There's a full support that provides about five liters of flow.

Speaker: And then just introduced, I think over the past six months, is a right ventricular impella called RP impella that can be inserted for RV failure.

Speaker: So these are a little bit different.

Speaker: in that the device actually sits within the ventricular cavity and through an axial flow mechanism sucks blood out of one compartment, usually the ventricle, and then is basically spun around and ejected out into either the aorta or the PA to provide supportive flow.

Speaker: And these also, like you said, might be a bridge to recovery, which means that they're used for a short amount of period of time with the intention of being removed once the patient's heart function improves, correct?

Speaker: That's absolutely correct.

Speaker: Okay.

Speaker: So tell us a little bit about the durable VADs, John.

Speaker: Those, I think, that are more in the realm of the specialized units.

Speaker: But like we mentioned earlier, somebody who has a durable VAD might end up in any hospital emergently.

Speaker: And I think that understanding that is probably important for all our intensivists.

Speaker: Sure, absolutely, Sergio.

Speaker: So I think it's probably, depending on where you work, you may see these right out of the OR, or they could land in the emergency department for a short period of time while awaiting transfer.

Speaker: But I think it's important.

Speaker: We already kind of went over the indications, but just knowing some of the basics about which devices are out there, what they're trying to accomplish within the patient,

Speaker: and then also kind of some of the potential complications that you could be dealing with for a few hours while you're waiting for transport to arrive.

Speaker: So I think that one of the

Speaker: most important concepts of any VAD itself, particularly an LVAD, is that VADs are preload dependent and afterload sensitive.

Speaker: So VADs are not smart devices at all.

Speaker: Like they are not like pacemakers that can change the number of impulses per minute or anything.

Speaker: They are set and whatever's going on with the patient will impact the ability of that VAD to work.

Speaker: So it will suck blood out of one

Speaker: basically box, which is usually the ventricle, and move it to another box, which is bypassing that ventricle to usually the aorta.

Speaker: So if there's no blood in the left ventricle, then the VAD won't work.

Speaker: So that's what I mean by saying they're preload dependent.

Speaker: Now, if I took a set of pliers or a clamp and added pressure to clamp the aorta, obviously the VAD wouldn't work all that well.

Speaker: because it would be up against a very high afterload.

Speaker: So the efficiency or ability of that VAD to work is dependent upon the patient's afterload or blood pressure to be within a certain range, but that doesn't make it impossible to work.

Speaker: So preload dependence, afterload sensitivity is an important concept.

Speaker: And then

Speaker: We're going to touch briefly upon the different variables that you might see on the bedside console or the patient controller, but the only thing that actually can be prescribed by a physician or a VAT engineer or whatever is the speed.

Speaker: So you can control how fast that impeller is spinning around.

Speaker: But the rest of the stuff is basically feedback you're getting from the patient in terms of how that FAD is actually working.

Speaker: So if we want to go ahead.

Speaker: No, so I was going to say that I think in terms of understanding this is very important.

Speaker: And like you mentioned, John, a.

Speaker: flow or our output is going to be directly proportional to the speed that we can set, the only thing we can set, and inversely proportional to the difference in pressures between the inflow and the outflow, which is basically governed by our preload and our afterload, correct?

Speaker: That's absolutely correct.

Speaker: So if we had to look at some of the current devices, we talked specifically about one axial flow and then a couple centrifugal flows.

Speaker: So the axial flow device, the HeartMate 2, is the flow that it can provide is usually anywhere between 3 and 10 liters a minute.

Speaker: Now, one thing about flow is that when you look at the bedside console, it tells you the flow on the VAD.

Speaker: That's not the actual flow.

Speaker: It's not exactly like what a patient's cardiac output is.

Speaker: It's a calculated number that's based on the power as well as the set speed of the device.

Speaker: So it's an estimate, but it's not perfect.

Speaker: And the other reason for that is because the patient may also be ejecting blood out of the aortic valve.

Speaker: So there's only a fraction that's actually going through the VAD itself.

Speaker: So whenever I see a flow number, I'm always kind of like taking that with a grain of salt.

Speaker: Obviously, we want it to be within a certain range, but you have to take it into clinical context.

Speaker: Now, remember, I said axial flow devices are a lot less efficient.

Speaker: So the speed of the VAD, particularly HeartMate 2s, is a lot faster.

Speaker: So it spins at about 8,000 to 10,000 RPMs.

Speaker: Now there's this other term called pulsatility that you'll see, and the way I like to think about that, that's the sort of the native contribution of the heart.

Speaker: So remember, our hearts are pulsatile, they're not continuous flow.

Speaker: We have a pulse pressure on the monitor.

Speaker: So the higher the pulsatility, I try to explain that to my fellows and residents as that's kind of how much native contribution your heart is providing to the patient's cardiac function at the moment.

Speaker: And that can fluctuate up and down.

Speaker: And normal for HeartMate 2 is usually between a number of like four and five.

Speaker: There's also an estimate of power.

Speaker: So the power is termed in watts.

Speaker: And again, the HeartMate 2 is the axial flow devices.

Speaker: So I put all this information in the handout and so I'll try not to get too much into the specific normal ranges just because you can refer to the handout and take a look at it.

Speaker: Now, so again, we're talking about the variables of the VADs.

Speaker: That's flow, speed, pulsatility, and power.

Speaker: Those are the four main things that if you call a VAD engineer or coordinator in the middle of the night, they're going to want to know about that patient.

Speaker: So if we move to the centrifugal devices, those are the heartwares, the HeartMate 3s, and in general they provide a similar rate of flow, so usually above three liters, three to eight, three to six liters a minute.

Speaker: But the one thing you'll notice is that the speed's a lot less.

Speaker: The RPMs are usually set much, much lower, about 25% of what the HeartMate IIs are.

Speaker: So they're about 3,000 RPMs, give or take 1,000 RPMs in general.

Speaker: The cool thing about the HeartWares is that their patient console actually provides some waveform data.

Speaker: So you can actually see how pulsatile the patient is through the waveforms that are on the screen, as well as some of the numbers that you get.

Speaker: So I encourage everyone to, if you have an iPad, definitely check out the Heartware Waveforms app on iPad.

Speaker: You can go to the App Store and search for Medtronic or Heartware and it'll come up, but this is a really cool educational tool that you can actually go through and you can change certain settings on the simulated VAD and see how it responds and see how the patient would respond.

Speaker: So it's a great little

Speaker: educational tool to go through and kind of get more comfortable with the settings of the VAT and certain clinical conditions, like if a patient has a GI bleed or hypovolemic or hypertensive, you can kind of see how the VAT will respond in those clinical scenarios.

Speaker: So definitely worth a little bit of time.

Speaker: And we'll put those in the show links.

Speaker: There'll be a link, I mean, to that app alongside some references that John has provided and the summary that he referred to.

Speaker: So I think that an important concept here with understanding...

Speaker: these settings, the flow speed, the PI, the power, is really that if we have a call to a VAD rep, which is an important part of troubleshooting, that information we need to know and be able to translate.

Speaker: But also, as we'll talk a little bit more, I guess, when we talk about hemodynamics, is that

Speaker: changes in these parameters are probably more valuable than the absolute number, like you said, and these changes, depending on which direction and which combinations, might point us down different differential diagnosis, right?

Speaker: Absolutely, yep, that's correct.

Speaker: And one thing I forgot to mention too, HeartMate 2 also, if you go to their website, you can literally play with HeartMate 2 controller and it'll walk you through how to see the alarms and stuff like that.

Speaker: So it's another sort of teaching tool there.

Speaker: But absolutely, your VAD engineers or your VAD nursing coordinators, they're going to want to know those basic settings.

Speaker: And if I could

Speaker: get one thing across to the audience.

Speaker: Talking to a family member, the family members of these patients literally know everything about their patient's VAD.

Speaker: They go through extensive training on how to kind of work with it, know what the alarms mean.

Speaker: So if you have any questions whatsoever, don't feel embarrassed about asking patients' family, hey, have you had any alarms?

Speaker: Can you show me, you know,

Speaker: Go through with the family member, have they had any complications in the past?

Speaker: They are a wealth of information, particularly related to the patient's history with that VAD.

Speaker: So utilize family liberally if they show up to your ICU.

Speaker: Excellent.

Speaker: And I think that, like we mentioned at the beginning, there's two situations in which most intensivists get exposed to these.

Speaker: But we believe that in a lot of community settings, it might be an immediate post-operative period of somebody who is being bridged to either a destination therapy transplant or being moved to another hospital.

Speaker: So why don't we start talking about that transition from the OR into the ICU?

Speaker: In our last podcast that we did together, John, we did talk about

Speaker: importance of appropriate handoff and I presume like in any other situation there are particular aspects of the handoff in this patient population that are important.

Speaker: Do you want to start with those?

Speaker: Absolutely.

Speaker: So in terms of important things on this handoff in addition to kind of the usual operative course why the device was implanted is going to be critical.

Speaker: Was this a planned or an unplanned

Speaker: initiation of VAD therapy.

Speaker: Now again, usually common things being common, over the years the most common cause for a temporary VAD is postcardiotomy shock.

Speaker: So we did a CABG, the patient couldn't come off bypass, and so we put in a temporary VAD to bridge him to recovery or to some other surgical plan.

Speaker: that's going to happen the next 24 to 48 hours.

Speaker: Now, hopefully for the patient, this was a planned intervention and maybe this was advanced heart failure bridge to recovery or destination, and we're going to walk through kind of what the goals are in that immediate post-operative period.

Speaker: So at the end of their OR course, sort of after the VAD's implanted, your post-operative TEE is going to have a lot of really important information that you're going to want to get from your cardiac anesthetist.

Speaker: And the important parts of that TEE are going to be the evaluation of the LV cavity and size.

Speaker: So oftentimes, after the VAD

Speaker: is implanted.

Speaker: They'll titrate the speed so that the LV's end diastolic diameter is less than 10 millimeters or whatever number they decide to go to, but that the cavity is decompressed.

Speaker: And they're also going to want to make sure that the septum is in the midline and it's not bowed towards the RV or bowed towards the VAT itself.

Speaker: So these VADs are actually positioned so that the inflow to the VAD itself is right in the apex and pointing towards the mitral valve.

Speaker: So you want to ask, hey, was the VAD positioning okay after insertion?

Speaker: You're also going to want to know about what the aortic valve was doing after the VAD was implanted.

Speaker: So was it opening or was it not and did the surgeon decide there was some degree of aortic insufficiency so they electively stitched closed the aortic valve?

Speaker: That's going to be an important piece of information as it's going to obviously impact kind of what you're seeing on the monitor and also kind of the flows that are going through the VAD itself.

Speaker: You're also going to want to know a little bit about the outflow cannula.

Speaker: So all these VADs, so blood goes into the VAD, it goes out of outflow cannula and is returned to 99% of them returned to the proximal aorta.

Speaker: So how did the outflow cannula look?

Speaker: Was it compressed at all?

Speaker: Was it kinked on closure?

Speaker: Was there good flow going through it?

Speaker: And then lastly, what the right ventricle look like.

Speaker: So all of a sudden you're in this clinical condition where this patient might have been getting by with, if there were an elective placement, with a cardiac index of about 1.5 for the past year, and now all of a sudden you're flowing four liters a minute.

Speaker: that right ventricle is now left with dealing with a lot more venous return.

Speaker: So you want to know, was the right ventricle functioning okay?

Speaker: Was it dilated at all coming out of the OR?

Speaker: And then obviously, what are the vasoactives that are on at the moment?

Speaker: So as you move from your cardiac anesthetist to your cardiac surgeon,

Speaker: you're going to want to say, hey, what are your hemodynamic goals here?

Speaker: Like, what do you want your blood pressure to be?

Speaker: What's the goal flow?

Speaker: And then what's the current speed?

Speaker: And were you happy with it coming out of the OR?

Speaker: And likely they'll have some specific requests related to those types of titratable things.

Speaker: So I think in the immediate post-operative, like you mentioned, one of the biggest challenges probably in the first hours, like any of our cardiac surgery patients, is the hemodynamic management.

Speaker: Can we dive into a little bit of that, John?

Speaker: Sure.

Speaker: So blood pressure management usually coming out of the OR is by arterial line, usually a femoral radial arterial line.

Speaker: And the patients themselves usually don't have that much intrinsic heart function to begin with.

Speaker: So they can't generate a meaningful pulse pressure.

Speaker: So what that means is when you look, obviously, when you're looking up the monitor, you'll often see a relatively flat A-line tracing.

Speaker: You may see little blips here and there in between with each beat, and that's your aortic valve opening, and that's a good thing.

Speaker: But you might not see all that much activity.

Speaker: Now the other trouble with that is that sometimes that can make it really challenging to get a pulse ox because there's not that much variation in flow so the pulse ox sensors can get really confused as to what's going on.

Speaker: So you may be left with doing some frequent blood gases right off the bat to make sure your oxygenation's at target.

Speaker: And so I've mentioned for aortic insufficiency, the surgeon may have elected to place what's called a park stitch.

Speaker: They may come out and be like, yeah, we put a park stitch in because of moderate to severe aortic insufficiency.

Speaker: And what that is, is they basically take a suture and they suture through the aortic valve leaflet so it stays closed to prevent excessive aortic regurgitation.

Speaker: So if you hear someone say park stitch, that's just what they mean by that.

Speaker: Now, in general, I think most would agree that the MAP goal after NALVAD placement is somewhere between 70 and 90 milligrams of mercury.

Speaker: And that's a pretty consistent number because most of the VADs, when they're designed, they're designed using these pressure flow curves, using the afterload of the patient and a normal filling pressure.

Speaker: So they operate most efficiently, usually within that range of 70 to 90.

Speaker: Now,

Speaker: Over time, you may relax that goal and allow a little bit of a lower MAP goal, but in the initial, in the first few hours after they come out of the OR, I really try to keep it within that range so that I can try to keep as much constant as I can.

Speaker: And remember, like we were talking about, and Sergio, like you nicely pointed out, that the VAD performance and flow is directly related to the afterload, or what some people call the pressure head.

Speaker: So keeping good control of the MAP after surgery is important.

Speaker: Because what can happen is if the patient starts waking up and maybe you weren't ready for them to be excibated quite yet, they can get hypertensive, that can really drop your VAD flows down and has been implicated in an increased incidence of acute ischemic stroke, excessive bleeding, and in some cases, pulmonary congestion, heart failure type symptoms.

Speaker: In addition to your arterial line, you're also going to take a look.

Speaker: Most of these patients will come out with a PA catheter that you can use to titrate your inotropes.

Speaker: Usually a patient will be on some form of inotrope, whether that's epinephrine or milrinone, vasopressors, and that's also still really helpful in identifying things like postoperative tamponade, loss of domain, as well as RV dysfunction or failure.

Speaker: Now,

Speaker: If you do find yourself in a situation where the patient's getting more hypotensive or you go to the nurse and check in, like, hey, I'm going up on my norepinephrine, my vasopressin, my pressor requirement's going up,

Speaker: and you take a look at your VAD bedside controller and you notice that the VAD flows are dropping, things you want to start thinking about is, hey, am I losing volume?

Speaker: Is my patient bleeding?

Speaker: Or is the flow dropping because the left ventricle is underfilled and maybe the right ventricle is dilating?

Speaker: And so you might want to get a quick echo or TEE.

Speaker: And then lastly, sometimes, particularly in these bridge-to-decision patients, they may be overweight or in some cases morbidly obese.

Speaker: And the reason they're bridge-to-decision is because they need to lose weight before heart transplant.

Speaker: They can have a really stiff chest wall.

Speaker: And after closure, that can sometimes impact the

Speaker: patency of the outflow cannula or what's often referred to as loss of domain.

Speaker: So they have this new device that's occupying real estate within the mediastinum and when you closed up that sternum things get compressed somewhat unintentionally or they may swell over the first few hours out of the OR and if that swelling causes compression of the ventricle or the right ventricle can create a tamponade like phenomenon that's called loss of domain.

Speaker: They may not have

Speaker: traditional tamponade with fluid around the heart, it may just be an extrinsic compression from the chest wall itself.

Speaker: And with any of these devices in the cardiac surgery, I think that anticoagulation and potential bleeding are always also a fine line that we need to manage.

Speaker: And I'm sure that it's very important in the immediate post-operative situation.

Speaker: Can you comment a little bit on that, John?

Speaker: Yeah, so in

Speaker: In the early post-operative phase, usually anticoagulation will be started somewhere between the first six to 24 hours after you're sure that the patient's not actively hemorrhaging after they come out of the OR.

Speaker: Anticoagulation strategies really vary depending on the institution.

Speaker: Most places will start the patient on some form of antiplatelet, and usually that's aspirin.

Speaker: Some places even use platelet function tests to

Speaker: determine whether or not they need to be on some other antiplatelet as well.

Speaker: And then the other side of that is the work on therapeutic heparin with a bridge to Coumadin therapy.

Speaker: Now, the usual outpatient target INR, somewhere between one and a half to two and a half,

Speaker: But depending on the device, maybe higher or maybe of the previous complications, an INR of three.

Speaker: So it would be important to talk to your cardiac surgeon about what their goals are for anticoagulation, whether that's initial PTT goals, and then obviously bridging to more longer-term anticoagulation with Coumadin, what their target INR is.

Speaker: So bleeding in general though, whether or not it's in the acute postoperative phase or as an outpatient, is the most common VAD-related complication.

Speaker: In fact, about a quarter of VAD patients will need some sort of surgical intervention as a result of either postoperative bleeding or outpatient bleeding.

Speaker: And the most common locations are largely mediastinal, the thoracic pleural spaces, as with most post-cardiac surgery or post-cardiotomy patients.

Speaker: But the longer the patients are on VADS, the higher risk they're at for mucosal bleeding, particularly GI bleeds, whether it's upper or lower mucosal bleeds, such as epistaxis.

Speaker: And so those are going to be the ones that usually present coming in through your emergency department

Speaker: And so there's some reasons for that.

Speaker: Now, this may be due to super therapeutic anticoagulation, and that's possible.

Speaker: These patients often can fluctuate, and you want to keep relatively tight control of what their anticoagulation targets are.

Speaker: But VAD patients also develop a secondary coagulopathy from kind of the mechanism of the VAD itself.

Speaker: So if you think about

Speaker: how blood is handled as it goes through the vat, it's going through a spinning device that can cause a lot of shear forces on your platelets as well as other blood products.

Speaker: So it can basically create what's considered an acquired von Willebrand syndrome that can cause platelet dysfunction.

Speaker: that makes them at higher risk for not being able to form a clot properly.

Speaker: And so they're at higher risk of bleeding.

Speaker: So something that considers you're trying to maybe provide, if your patient's bleeding, how you're going to address that clinically might be due to more platelet transfusions, fibrinogen transfusions, something like that.

Speaker: I mentioned as an outpatient, patients have more increased incidence of GI bleeds.

Speaker: And the reason for that is so when you move to like this pulsatile flow state, which is a normal heart, to a continuous flow state with a VAD,

Speaker: there's pretty much an equilibration of pressures between the arterial and the venous side, particularly at the capillary level.

Speaker: So these patients are really high risk of developing AVMs, and it seems to happen most frequently in the GI tract.

Speaker: And so it's not uncommon that we'll have patients who are now anticoagulated and come in with these massive GI bleeds, and it's found that they have AVMs in their colon or even in their upper GI tract, which can be a little bit more challenging.

Speaker: So, definitely something to think about in the hypotensive patient who comes in from the outpatient setting and maybe has a bleed or has a concern for bleed.

Speaker: This may be due to an AVM.

Speaker: So, how you might want to start or address that may be something to be discussed before if your patient's ramping up to become a VAD center.

Speaker: Now, in terms of general goals, I think hemoglobin targets are kind of the usual range.

Speaker: around 8 to 10 milligrams per deciliter for most VAD patients.

Speaker: And like we mentioned at the beginning, a lot of these patients might be potential candidates for transplant.

Speaker: Are there any important considerations in terms of transfusions and selection of type of blood?

Speaker: I think that's something that a lot of times people who are not exposed to these patients is something that we don't consider as well.

Speaker: It's a great question, Sergio, and this is a really important point.

Speaker: So when the patient comes in, if you're talking to family members or the patient trying to figure out why they have the VAD placed, if they are a bridge to transplant, it's important if you're going to transfuse them with anything that they get leuker-reduced radiated blood products because obviously you don't want to increase their PRA risk or their ability to receive a transplanted organ.

Speaker: every transfusion, I'm sure we've all heard, every transfusion is like a mini transplant.

Speaker: So the amount of antibodies they're exposed to goes up exponentially with each transplant.

Speaker: So we really try to avoid red blood cell transfusions if at all possible.

Speaker: However, the caveat to that is if the patient's in front of you and is exsanguinating, you have to keep the patient's best interest in mind, and that may require blood product transfusion.

Speaker: Now there's a lot of people that are uncomfortable with this anticoagulant patient because they're like, oh well can I reverse them because I don't want the VAD to clot off.

Speaker: And that's probably a perpetuated myth.

Speaker: So there are one or two small studies that actually looked at VAD thrombosis with reversal of anticoagulation and a number of these in this case series were result of GI bleeds.

Speaker: And

Speaker: In none of them did the patient have an acute thrombosis of their VAD with reversal of the anticoagulation.

Speaker: So how I approach this is I'm not using PCC to reverse their Coumadin because of the increased thrombosis risk of that.

Speaker: But using something like FFP and vitamin K, stuff like that to temporarily reverse their anticoagulation is perfectly safe.

Speaker: And obviously, this is all done in conjunction with the VAD team.

Speaker: But certainly, don't feel like your back's against the wall.

Speaker: You can reverse them if they're bleeding excessively and unstable in front of you.

Speaker: And I think that a point that maybe be the opposite extreme of the situation, but I think is important for our audience, is that you can have acute thrombosis of your VAD, even in the presence of a therapeutic or super therapeutic INR.

Speaker: So that should not lead you to the conclusion, oh, it's probably not thrombosis because the INR is four.

Speaker: Correct?

Speaker: Correct.

Speaker: Yeah, that's a great point.

Speaker: So about five years ago now, in New England Journal, there was a report of increased risk of or increased incidence of thrombosis, particularly with the HeartMate 2 devices.

Speaker: And this created quite a scare in the VAD community.

Speaker: And since it maybe changed some of the practice strategies for anticoagulation and particularly around HeartMate 2s.

Speaker: So if you're concerned about thrombosis being like you have low flow alarms, high power,

Speaker: Some things that you can do, look for things like hemolysis, so if the patient has new hematuria, you can send an LDH or even a plasma-free hemoglobin and get a quick echo because oftentimes you'll see a distended left ventricle if there is in fact a VAD thrombosis.

Speaker: But these patients can certainly be therapeutic on their anticoagulation.

Speaker: We do know that any coagulation, the coagulation cascade in all these patients is all thrown off, so it's certainly a risk even if they are therapeutic.

Speaker: So why don't we dive into some of the common complications that occur with these patients?

Speaker: And I think for our audience, it's important to recognize that these complications can occur in the immediate postoperative period, but also can occur in patients who have the VAD for a longer period of time.

Speaker: Want to start with right ventricular failure, John?

Speaker: Sure, that sounds like a great spot.

Speaker: So RV failure is an important one to keep an eye out for, particularly in the early perioperative period, and sometimes even up through the first month after patients had a VAD in place.

Speaker: And this is from a number of different reasons that are a number of different causes can actually lead to a patient developing right ventricular failure after a VAD.

Speaker: So after the LVAD is put in, there's often a change in geometry of the right ventricle.

Speaker: So you're now mechanically unloading what used to be a dilated left ventricle and causing the septum to kind of shift over more towards the free wall, the LV.

Speaker: And what this will do is essentially it expands the size or dilates the right ventricle sometimes, which allows for increased venous return due to the VAD now contributing to the patient's cardiac output.

Speaker: Now these patients also often have underlying secondary pulmonary hypertension from chronic heart failure or maybe even their underlying disease.

Speaker: So it kind of is a double whammy on the right ventricle.

Speaker: So you have increased RV afterload that's at the baseline or maybe even worsened temporarily in the postoperative phase from hypoxemia or maybe some pulmonary edema.

Speaker: And now you've also given it a new increased flow load to deal with.

Speaker: And in a tenuous patient, this can be a really challenging physiologic scenario for the right ventricle to deal with.

Speaker: So things that might cue you in and maybe a patient who's having a slight increase in vasopressor inotrope requirement when you get called to the bedside, take a look at the VAD console itself.

Speaker: If the flows have dropped, if there's minimal pulsatility, that can give you a sign that the left ventricle is empty.

Speaker: And sure, this may be due from under-resuscitation,

Speaker: But if you take a look and you see that CVP climbing, you have to be concerned about RV failure and even tamponade.

Speaker: So if you look at the hardware, let's say it's a hardware device and you can actually see the waveforms on the device itself, you'll notice that the waveform will often be flat.

Speaker: And if you have a flat waveform on your VAD bedside console, that's a concerning sign that the LV is empty.

Speaker: And oftentimes, the analogy I put is, so when your heart's doing more of the work, you're more pulsatile, but when the VAD's doing all the work, you're less pulsatile, and that waveform might even be flat.

Speaker: So that flow waveform is going to be a nice little bedside tool or bedside sign to look for in terms of how much is the VAD contributing versus how much is the patient's native left ventricle contributing to cardiac output.

Speaker: So if you are concerned about early right ventricular failure, some standard interventions that you can do to kind of help improve the physiologic scenario for the right ventricular to perform and maybe even recover.

Speaker: So oftentimes, if they're not already on, inhaled pulmonary vasodilator like epiproxenol or in some cases nitric oxide, we'll get that started.

Speaker: Assuming they still have a reasonable blood pressure with minimal vasopressor requirements, an inodilator like milrinone is often started relatively quickly.

Speaker: And if you don't have enough blood pressure to start milrinone, ramping up your epinephrine as your inopressor, if you will, is an important initial step to kind of support that right ventricle.

Speaker: if it's struggling.

Speaker: You may even need to paralyze the patient to minimize your intrathoracic pressure if things start really getting out of hand.

Speaker: And obviously early surgical consultation, getting your cardiac started, hey I'm really concerned about this right ventricle, because it's not uncommon that they'll put in a temporary RVAD so you're not maxing out on your vasopressors

Speaker: and really flogging the patient early on.

Speaker: You know, a right ventricle with new liver congestion, liver failure, those VAD patients never do well.

Speaker: So it's something to really stay on top of.

Speaker: Now, one other small point that's worth touching upon is, let's just say the patient's doing great, and the surgeon comes by, and this happens every now and then, and they're like, I want the vasopressors off, they look great, turn off the epi, let's get them extubated, looks great.

Speaker: Sometimes with rapid de-escalations, and particularly after extubation, that's a high risk time for the right ventricle, and you can have delayed right ventricular failure.

Speaker: So moving away from a positive pressure, positive intrathoracic pressure environment with intubation mechanical ventilation to a negative inspiratory pressure system can also hit the RV with increased preload and lead to progressive overload and failure.

Speaker: And we've had a couple of these at Penn where everything looks great, they get extubated, they even get downgraded to the floor, and day four, day five, they come back not looking well, and it's just that they're

Speaker: right ventricle pumped out.

Speaker: So definitely something that you're not out of the woods at even after the patient's extubated and transitioning out of the ICU.

Speaker: So I think something to always keep in mind and obviously the ultimate treatment I think for RV failure, we're unable to really get it better with the interventions you mentioned, would be to go to a right ventricular assist device, right?

Speaker: Yeah, that's correct.

Speaker: And that's our preferable sort of route or exit strategy, if you will.

Speaker: Okay.

Speaker: So why don't we talk a little bit about this suction episodes or suck down, which I think is something very particular to the VAD world that a lot of us might not be as familiar with.

Speaker: Yeah.

Speaker: So there's a...

Speaker: This is fairly common.

Speaker: You can get into this situation.

Speaker: So suck down is just a generic term used for if, like I said, these VADs aren't very smart.

Speaker: So the VAD knows to suck things into it.

Speaker: And if the left ventricle is underfilled, well, it's going to just suck in myocardium.

Speaker: So suction events can occur when the LV is too underfilled and the VAD starts pulling in the septum or

Speaker: usually the septum, into the VAD itself and the VAD can't flow.

Speaker: So what does that mean?

Speaker: Well, it means you're usually going to get either a low flow alarm with the VAD itself and you may see power spikes along with it because it can't suck anything in, or can't suck a fluid in like blood.

Speaker: Or if it's a temporary VAD, you may notice that the cannula is coming out of the patient into the Centromag or chattering.

Speaker: And this is something very similar or analogous to chattering of an ECMO circuit.

Speaker: that's a pretty much a suction event and that means your left ventricle is under filled.

Speaker: So VAD flows in particular can change

Speaker: increase if the patient gets hypotensive though.

Speaker: So your vasopressor titration can affect the performance of your VAD in the sense that if the patient's afterload goes down, well all of a sudden the VAD's like, wow this is really easy, I can flow a lot more and empty out your LV.

Speaker: So again, highlights the importance of keeping that map range pretty tight.

Speaker: And then obviously other reasons that your LV can become small, whether or not it's tamponade, excessive chest wall swelling for loss of domain, RV failure.

Speaker: These can lead to an underfilled LV and suction events.

Speaker: So these should be taken quite seriously.

Speaker: I think most of the time your initial intervention for a suction event or a low flow related to a suction event is going to be a small fluid bolus to see if you can increase that preload and distend the LV a little bit more.

Speaker: But you may also decide to increase your MAP target and in some cases, let's just say you just need a little bit of time, you can even turn down the speed of the VAT itself.

Speaker: So the way I kind of approach these suction events is I bring my ultrasound to the bedside and if you're savvy with bedside ultrasound, it's a great tool to look at the left ventricle.

Speaker: It's not impossible to see the heart after cardiac surgery with a surface echocardiogram.

Speaker: So looking at the LV cavity size, if the cavity size is a one-to-one ratio with the size of that inflow cannula, that's a high-risk patient for suck-down.

Speaker: And then obviously you're going to do a couple other diagnostic tests to figure out why the LV is empty.

Speaker: So looking for low flow alarms with high power spikes, even things... Sorry, Sergio.

Speaker: Even a suckdown event can even cause tachydysrhythmias, particularly wide-complex tachycardias, VTAC, when the septum gets sucked into the VAD.

Speaker: Those are all complications of an underfilled LV in the setting of a fixed-speed VAD.

Speaker: And I think that, like you said from the beginning, it seems like a lot of our differential diagnosis really ultimately will pan out to what do I need to act on, my preload or my afterload, right?

Speaker: And the underfilled LV, like you said, could be because we need to increase the preload, or it could be because we need to decrease the afterload of the LV, or it might be a problem with the right ventricle.

Speaker: And all these things are going to come in recurrent.

Speaker: So I think that we need to be really always thinking about this as we intervene on these patients.

Speaker: No, totally.

Speaker: So suck down is a symptom.

Speaker: It is not a diagnosis.

Speaker: So suck down or a suction event is going to lead you to try and figure out what else is going on.

Speaker: Excellent.

Speaker: And you mentioned arrhythmias, which I presume are obviously very common in this population, but also something that can be exacerbated by all these foreign devices into the heart.

Speaker: Can you talk a little bit in general terms of what we should be concerned about with arrhythmias in the immediate post-operative period, John?

Speaker: Yeah, so common things being common.

Speaker: So atrial fibrillation, post-cardiac surgery, or post-VAD placement is common.

Speaker: I usually, and I think most, will consider early intervention on post-operative AFib in durable VAD patients, largely because they may be highly dependent on the atrial kick for forward flow.

Speaker: So we'll often initiate, start with a bolus dose of amiodarone to try and help

Speaker: get the patient back in the sinus rhythm, even a couple of boluses of amiodarine 150 milligrams IV, because obviously the loading dose is about five grams.

Speaker: It'll take you forever to get there.

Speaker: But if you're weaned off of your vasopressors and your inotropes, early institution of a beta blocker is also a common intervention in these patients.

Speaker: And a lot of times the atrial fibrillation goes away, but sometimes it doesn't.

Speaker: It can cause some hemodynamic or flow issues.

Speaker: Now ventricular arrhythmias are also fairly common and these can be caused by a number of different issues.

Speaker: So we mentioned kind of suck down itself and in the immediate post-operative phase it may be caused by the inflow cannula malposition.

Speaker: So again getting back to

Speaker: your post-operative echo.

Speaker: Suction events can cause irritation of the septum causing VTAC and the intervention for that is a simple fluid bolus.

Speaker: But also these patients are oftentimes have dilated cardiomyopathies so they're at high risk for VT just by the nature of their end-stage heart disease.

Speaker: So

Speaker: You know, if the one thing that's important, I would say that remember, if their ICD is still in place after they had their VAD placed, put a magnet on it so that they'd stop getting shocked.

Speaker: This is one thing that you can fix and address as you're starting your antiarrhythmics.

Speaker: The VAD is generally supported or the left ventricle is supported now with a mechanical device.

Speaker: So it's not like a native heart VTAC.

Speaker: You have a little bit of time.

Speaker: A little bit of time.

Speaker: Now, if the patient remains in VT for a long period of time, this can cause you some hemodynamic issues.

Speaker: But as you're giving some medicines, it's okay to turn off or put a magnet on that ICD for a short period of time while you're trying to make some interventions.

Speaker: And as I mentioned, similar to the AFib,

Speaker: Beta blockers, amiodarone, and lidocaine are usually considered first-line medications in these acute postoperative and even some of the long-term durable VAD patients.

Speaker: So we talked about a whole set of common complications.

Speaker: Like we were talking before we started recording the podcast, the list of complications is very long and a lot of that will be referred to in some of the links in the show notes.

Speaker: But what I wanted to go next, John, is to

Speaker: To think about from the standpoint of addressing a patient who's unstable or let's call it a crashing bad patient, there's clearly two tools that I think are very useful in the immediate assessment.

Speaker: And one of them is understanding the control box alarms or what's changed.

Speaker: And the other one is the use of echo.

Speaker: Can you walk us through those two in the setting of somebody who has changed a status or is, quote unquote, unstable or crashing?

Speaker: Yeah.

Speaker: Yeah, so bedside ultrasound is absolutely your best friend.

Speaker: And so if there's a patient who's really doing unwell, the ultrasound is the first thing I'm bringing to the bedside.

Speaker: And in the immediate post-operative setting, so we're talking about within the first 12 to 24 or even 48 hours, if a patient is crashing in front of me, I'm looking for a tamponade, looking for all the complications we mentioned before.

Speaker: But if

Speaker: If their map starts to drop and we're maxed out on pressers and we're still at a map of less than 40 and I'm concerned that they're not perfusing, I'm calling cardiac surgery to bedside to do basically a bedside sternotomy so to open the patient back up.

Speaker: Oftentimes this is not a time to continue to provide excess amount of vasopressors.

Speaker: It's usually a surgical issue and that needs to be addressed either in the OR or even in some cases at the bedside, not a medical management point.

Speaker: So taking a look to see if there's any fluid around the heart or if the RV is bowing out are things that are going to be really helpful on bedside ultrasound.

Speaker: And I think in general, you know, one of the sort of algorithms that we follow is using that MAPA-40 as kind of your threshold to start thinking about is the patient perfusing anything at all?

Speaker: So post-operative stroke is a, I mean, it's just a killer for these patients who have a VAD.

Speaker: And particularly if they're destination, what's the point if they don't have a neurostatus or if they end up coming out with a stroke?

Speaker: You've just put a $100,000 device in someone who's not going to be able to use it to its full effect.

Speaker: So really staying on top of this and in the crashing patient, you know, thinking about early reopening is really, really important.

Speaker: But let's just say that, you know, it's not in the immediate postoperative phase.

Speaker: Maybe this person came in through the emergency department.

Speaker: I think one question often is, is it okay to do CPR on these patients?

Speaker: And so, you know, what I usually say, or at least how I educate my emergency physicians about this is, okay, you treat this patient almost like a tracheotomy patient, a tracheostomy patient, right?

Speaker: So, you know, in the tracheostomy patient, they come in respiratory failure.

Speaker: They still have a set of lungs.

Speaker: And they still have a trachea.

Speaker: So if the trach's not working, intubate them.

Speaker: Use their native lungs.

Speaker: Well, in the case of a VAD patient, if the VAD patient's crashing and hemodynamically unstable, they still have a native heart.

Speaker: So use it.

Speaker: Early initiation of inotropes, epinephrine to try and maximize their native cardiac performance is going to be what you're going to try to do right off the bat.

Speaker: And oftentimes this just involves a small fluid challenge followed by vasopressors and inotropes.

Speaker: And while you're waiting to get in contact with the VAD team,

Speaker: Now if you do that, and even after about one minute, if there's still minimal flow, and this can be assessed by Doppler if you don't have an A-line in place, so a bedside Doppler in the brachial artery is the usual recommended place to listen for actual flow.

Speaker: If there's minimal flow and the patient's MAP is less than 40, go ahead and start CPR.

Speaker: There used to be a large myth that was put out that you cannot perform CPR on patients with a VAD, and that's just not true.

Speaker: There are a few small case series that looked at post-mortem patients who died after who also had a VAD.

Speaker: and who received CPR, and not a single one of them had a VAD dislodgement.

Speaker: Now, certainly, it's going to be something you're going to worry about if you have to do CPR, but it's not a contraindication.

Speaker: So for your ER providers, it is absolutely okay to do CPR.

Speaker: We do it in our ICU as well.

Speaker: You want to protect the brain if you're trying to get this patient out of this acute event.

Speaker: So establishing some form of flow is better than no flow at all.

Speaker: And what about understanding what changes like in flow and power or in the PI might mean in terms of potential diagnosis?

Speaker: Can you talk a little bit about that, John?

Speaker: Yeah, sure.

Speaker: So I do have my own like internal algorithm on how to approach this differential diagnosis.

Speaker: And in the show notes, there'll be a little, a fairly simple algorithm on different alarms that you might get at the bedside.

Speaker: So yeah,

Speaker: To go through particularly, I think probably flow alarms are the most common and most important.

Speaker: So with low flow alarms, you're going to think of a couple of different things.

Speaker: So low flow can be caused by obviously hypovolemia, which we talked about a little bit with LV size.

Speaker: Don't forget, hypovolemia may also include hemorrhage as well.

Speaker: So an unrecognized GI bleed is something that I've gotten fooled on before, will also cause a hypovolemic state, obviously, and low flow alarms.

Speaker: Arrhythmias and inflow-outflow cannula obstruction will also often cause low flow alarms.

Speaker: And then obviously your right ventricular failure and tamponade in the immediate postoperative phase is something you're always going to be concerned about.

Speaker: Now, the flip side of that are your high flow alarms.

Speaker: So this means all of a sudden the VAD is still at the same set speed, but the flows are going up.

Speaker: And you may see this like it.

Speaker: So, for example, on your HeartMate 2s, oftentimes a high flow is it won't even show the leader's permit anymore.

Speaker: The monitor will actually have three plus signs, which means it's

Speaker: it thinks it's flowing a lot.

Speaker: It may not be, but it thinks it is.

Speaker: And if you see this, you're going to want to be concerned of a vasoplegic state.

Speaker: So that might be from something like sepsis or

Speaker: something even more insidious and concerning, which would be a rotor thrombus or a VAD thrombus.

Speaker: And the reason why you get high flow alarms here is largely because, remember what I said in terms of the VAD flows are not actual flows.

Speaker: It's not like it's doing a thermodilution like a PA catheter or something like that.

Speaker: It's estimated or calculated based on the power and the speed in which it's set.

Speaker: So if all of a sudden the VAD feels like it's working really, really hard to achieve that speed that it's set for, and that could be because there's a big clot jammed in the rotor, that'll give you high flow alarms.

Speaker: So high flow alarms or low flow alarms could mean a VAD thrombus and worth further investigation.

Speaker: Now if you want to move over just quickly to pulsatility, so remember it's like kind of the contribution of the native heart, the contractility of the blood moving through the VAD as opposed to whether or not it's just straight continuous flow.

Speaker: Things that can give you high pulsatility, I think the most common thing we see is hypertension.

Speaker: So if all of a sudden the afterload on that VAD is really high, it's going to make the LV distend a little bit more because less blood's going through the VAD.

Speaker: So the heart's going to become more contractile.

Speaker: You're going to have a high pulsatility as a result of that.

Speaker: In the outpatient world, you may see as a patient who's a bridge to recovery as their heart gets better, well, that means it's going to contract more.

Speaker: So you're going to see high pulsatility, and sometimes some electrical malfunctions can cause high pulsatility alarms.

Speaker: And then to the opposite side, low pulsatility.

Speaker: Getting back to kind of your low flow, so hypovolemia, poor LV function, recent changes in speed.

Speaker: So they might have been at their outpatient and got their speed changed recently.

Speaker: That's now overflowed their left ventricle, so now it's more empty.

Speaker: That can cause low pulsatility.

Speaker: And then, again, your inflow-outflow obstructions as well.

Speaker: Well, John, this has been a fascinating conversation.

Speaker: I think that, like we mentioned at the beginning, a growing population in our healthcare, something that I think more frequently our intensivists are being exposed, especially, I mean, in places that are doing a lot of heart transplant and heart failure, but also in ICUs that might use these as temporary bridges for transfer to a higher acuity setting or for recovery.

Speaker: In previous episodes, you're a seasoned guest.

Speaker: We usually close with some questions unrelated to the topic.

Speaker: You've been through those.

Speaker: So today I'm going to ask you a couple of questions that are similar but are more related to the topic that we spoke today.

Speaker: Is that okay?

Speaker: That sounds great.

Speaker: These are the hardest ones.

Speaker: So my first question is, could you tell us about your most instructive failure with dealing with these patients?

Speaker: I think that one of the things that we don't value as much as we should is

Speaker: the ability to learn from failure and embrace failure as an opportunity.

Speaker: So could you tell me your biggest fail with these patients?

Speaker: Yeah, so the biggest one's tough because I've definitely had my fair share of learning lessons, if you will, from taking care of these the VAD patients.

Speaker: You know, I think starting out as a fellow

Speaker: There was one patient in particular that always stuck with me.

Speaker: And, you know, I think the immediate post-operative patients, oftentimes you kind of know what to look out for.

Speaker: But in the outpatient world, you know, all bets are off.

Speaker: They could come in with sepsis or anything.

Speaker: And oftentimes people freak out just because there's a VAD patient in the emergency department or in the hospital and they don't take care of VAD patients.

Speaker: So, yeah.

Speaker: there was an elderly gentleman, his name was Frank.

Speaker: He was in his late 60s and was a destination therapy patient.

Speaker: And he was destination because his grandkids, one of his grandkids was graduating college and he really wanted to make it to the graduation.

Speaker: And, you know, we're very familiar with that patients getting, you know,

Speaker: dehydrated, nausea, vomiting, diarrhea, causing some problems with the flow alarms.

Speaker: And he came in kind of with a very nondescript syndrome of, like his wife said, he was just feeling weak and he was having some nausea, vomiting, and some GI symptoms, which was probably more related to poor flow.

Speaker: But I started just kind of treating him with, he was a little bit hypotensive, so we gave him some fluids.

Speaker: And then all of a sudden, his hemodynamics just crashed.

Speaker: it wasn't until about 30 minutes later that he finally had his first bowel movement and it was just a massive GI bleed.

Speaker: And I really was kicking myself and I knew you know AVMs are a common complication with VAD patients but it didn't hit me right off the bat that that's probably what was going on.

Speaker: He was getting fluid and he should have been getting blood and I should have reversed his anticoagulation and unfortunately you know he ended up doing okay but had a rocky course.

Speaker: So you know

Speaker: Sometimes out of sight, out of mind, we're not thinking about things like GI bleeds with patients who hasn't had a frank hematemesis or bloody bowel movement.

Speaker: So that's one thing that stuck with me.

Speaker: Always never forget about these bleeding complications.

Speaker: They're the most common and sometimes the hardest to diagnose.

Speaker: I think that's a great point.

Speaker: Like you mentioned earlier, a quarter of these patients will have bleeding complications.

Speaker: And just think of common things as possible causes.

Speaker: The second question I have, John, relates to something that now that you have so much experience with these patients that you know to be true, yet most intensivists who don't deal with these patients on a regular basis get wrong about this patient population.

Speaker: So it's a great question.

Speaker: And I think that sometimes when we deal with patients that are so sick all the time, we develop this, not nihilism, but this kind of thought of, yeah, this patient's not going to get better.

Speaker: They need a freaking machine to keep their heart going.

Speaker: In some cases, I think the cardiac surgery intensivist stretches into the realm of the oncologist intensivist that deal with end-stage disease, and we think they're not going to get better.

Speaker: But I definitely want to press the audience here that that's not true.

Speaker: these patients in particular went through a lot to become eligible to get their VAD.

Speaker: And there is such a rigorous screening process that goes from social to physiologic to optimizing them, leading them in.

Speaker: They, in some cases, wait for years to get their VAD on home infusions.

Speaker: So they put a lot of work into getting to this point where they can get off their continuous medications at home, infusions, that sort of thing.

Speaker: And these patients can turn around.

Speaker: And I think it's worth at least a time-limited trial to try and get these patients better and out of the ICU.

Speaker: Now, certainly, we're going to be realistic and optimistic with the family with destination patients.

Speaker: But for those bridge-to-transplant patients and bridge-to-recovery patients,

Speaker: there is opportunity to salvage these patients, so don't give up on them.

Speaker: Definitely work within the multidisciplinary culture in your ICU.

Speaker: Get everyone on board, and if that means transfer, get them to transfer.

Speaker: And in some cases, if it is available to you and the patient is crashing, it's not unreasonable to put the patient on a temporary ECMO support to get them to

Speaker: to another institution, there have been a couple of bad thrombosis patients that have recovered amazingly after getting a VAD explant implant that might have just been due to some unintended complication as an outpatient.

Speaker: But these patients can recover, so I don't want you to give up on them early on.

Speaker: These are definitely salvageable patients.

Speaker: And I think that along those lines, an area that I think in my own practice, I'm trying to be more positive

Speaker: open-minded and objective about is those patients who crash and are bridges to decision because it might not be clear, but we don't know for a fact that they won't be able to recover, that they wouldn't be a good candidate for destination therapy or a transplant.

Speaker: And I think that really, like you said, understanding that a lot of these patients do have meaningful recovery.

Speaker: and can have a prolonged quality of life afterwards, it's something that we need to really understand in the ICU.

Speaker: And I think it's difficult when we don't see these patients long term.

Speaker: Yeah, 100% agree.

Speaker: The VAD teams kind of grow with these patients, and they're much more familiar with them.

Speaker: then we might be in just this episodic care of this patient.

Speaker: But it's such a great point, Sergio, is that, you know, keeping a frame of reference in terms of what the patient's goals are and where we work within the trajectory of the patient care.

Speaker: Absolutely.

Speaker: And the final question to close, John, is what do you want every listener to our podcast to know specifically about this topic, the single most important take-home message?

Speaker: Yeah, this is a tough one.

Speaker: Yeah, the single most important topic, you know,

Speaker: I think that you have options, that this isn't an end game.

Speaker: The VAD itself isn't an end game.

Speaker: We kind of touched on not giving up, but I think keeping your eyes wide open in terms of what the goal is for the patient, I think we've all moved towards keeping

Speaker: patient goals in mind and trying to honor those patient wishes as much as we possibly can.

Speaker: So I think the last question brought up, don't giving up on these patients.

Speaker: I think that's probably the most important thing.

Speaker: And just be thoughtful about the things you're trying to accomplish.

Speaker: Be honest with the families, engage them early, and then obviously

Speaker: keeping their heart failure cardiologist and VAD coordinating team together, creating a multidisciplinary approach to manage these really complex patients is probably the most important thing when it comes to taking care of the VAD patient.

Speaker: Well, I want to be respectful of your time, but again, John, thank you, thank you for your time, generosity with all your knowledge, for preparing an excellent handout for our listeners, and for really a fascinating discussion on a topic that I think we're going to see more and more.

Speaker: So I hope to have you back on the show soon, and thank you very much.

Speaker: Oh, absolutely, Sergio.

Speaker: This is an honor.

Speaker: You have developed quite a following so far, so this is exciting to be a part of.

Speaker: Thanks again for listening to Critical Matters.

Speaker: Make sure to subscribe to this podcast on iTunes or Google Play.

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