Transcript
Speaker: Welcome to Critical Matters, a sound podcast covering a broad range of topics related to the practice of intensive care medicine.
Speaker: Sound provides comprehensive critical care programs to hospitals across the country.
Speaker: To learn more about our programs and career opportunities, visit www.soundphysicians.com.
Speaker: And now your host, Dr. Sergio Zanotti.
Speaker: Mechanical circulatory support is an increasingly important strategy for the treatment of cardiogenic shock and other subsets of critically ill patients.
Speaker: In today's podcast episode, we will discuss temporary mechanical circulatory support and its implications for critical care.
Speaker: Our guest is Dr. Bindu Akhanti, a practicing pulmonary and critical care physician.
Speaker: Dr. Akhanti is the medical director of the Heart Failure ICU and director of critical care for the Heart and Vascular Institute at Memorial Hermann Texas Medical Center in Houston.
Speaker: She's an associate professor at the UT McGovern Medical School in Houston as well.
Speaker: Dr. Akhanti is a master educator, a phenomenal clinician, and an avid researcher focusing on mechanically circulatory support and pulmonary hypertension.
Speaker: We are honored to have her as our guest today.
Speaker: Bindu, welcome to Critical Matters.
Speaker: I'm so excited to be here.
Speaker: Thank you for inviting me, Sergio.
Speaker: Thank you.
Speaker: Well, I know this is a topic that you are truly passionate and very knowledgeable about, so I'm sure this will be a feast for myself and for our listeners.
Speaker: But before we start, maybe as an introductory comment, could you tell us, Bindu, why do you think it's important for intensivists outside of cardiac ICUs to know about this topic?
Speaker: I think most of us that went into ICU medicine are really the original shockologists, right?
Speaker: We love when we are able to appropriately diagnose, manage, treat, prognosticate, and at the same time, look at the big picture and go,
Speaker: In this patient, this is the diagnosis and we are capable not only of trying to save them, but seeing what that future looks like.
Speaker: For most physicians, you know, it comes naturally, right?
Speaker: When you see a patient with lactate of 10, you're like, okay, this person is really super sick.
Speaker: But the reason every single intensivist needs to know about temporary MCS is that
Speaker: Recognizing which patient is in shock is one thing, but that's a global diagnosis.
Speaker: Buried in every patient that is in shock is the possibility that this could be a patient in AMI cardiogenic shock, or this is a patient in cardiogenic shock with other etiologies.
Speaker: This is a patient with biventricular failure.
Speaker: And if we don't know the phenotype at the get-go and what are all the available resources,
Speaker: then how are we going to take care of that person with shock, right?
Speaker: So it's, you know, we all have a solemn duty to serve.
Speaker: And one of the ways that I've been really rewarded is to be absorbed into the advanced heart failure team here at UT McGovern and Memorial Hermann.
Speaker: As a pulmonary critical care physician, you know, there are very few PCCM docs that do this.
Speaker: But we've been doing this for about 12 years and the lead heart failure cardiologist, Dr. Carr, and the cardiac surgeon, Dr. Gregorick, when they first looked at us, they said, you know what, we do see this value that medicine intensivists play a role in this evolving field.
Speaker: along with our other disciplines, right?
Speaker: Like cardiovascular anesthesia plays a huge role.
Speaker: They take care of these patients upstairs in the OR, bring us brilliantly managed patients that are truly like, you know, we look at that ABG and go, wow, base excess of zero.
Speaker: This can't get better than that, right?
Speaker: But I think for the intensivist in the trenches, for me to look at a patient with shock and not only be able to diagnose what is the appropriate phenotype,
Speaker: And for me to relay this information to the other intensivists nationally and in your podcast internationally, this is a privilege.
Speaker: And thank you for picking this topic because this is only going to advance more.
Speaker: And whether or not you practice MCS critical care, I think that knowing what is available will help you save lives.
Speaker: Not to mention that it might be coming to your ICU anytime soon, right?
Speaker: Because it's also exploding.
Speaker: Yeah.
Speaker: Yeah.
Speaker: And it may not.
Speaker: One thing that I see when we do these national conferences or teaching is that it may not come to your ICU, but it's very fascinating that you may be covering for this patient in one of those nighttime shifts.
Speaker: And I think that's
Speaker: Nothing makes an intensivist more uncomfortable than a device that they don't know or understand.
Speaker: And I think that's in our DNA as an intensivist, right?
Speaker: We walk in, we're like, I know that's the CVVHD machine, that's the ventilator.
Speaker: And then what is this?
Speaker: How does it work?
Speaker: How do I use this data?
Speaker: And I hope that over the next few minutes, we can kind of talk about this in buckets and simplify it.
Speaker: And hopefully I'll give you a lens through which you can look at this field of MCS critical care and see it more approachable at least.
Speaker: Perfect.
Speaker: So just, I mean, in terms of basic definitions, before we dive into the different types of devices available today, what do you consider temporary mechanical circulatory support?
Speaker: So before we can talk about temporary mechanical circulatory support, I think we need to make sure that we all have an understanding of just cardiogenic shock, right?
Speaker: For us, it's simply cardiac pump dysfunction.
Speaker: You have hypoperfusion and tissue hypoxia.
Speaker: So we know despite what has been done, mortality is significantly high and as high as 50%.
Speaker: We used to say that, you know, metastatic lung cancer, those are like rapidly killing.
Speaker: They are.
Speaker: But AMI cardiogenic shock, especially when you don't diagnose it soon, is a very good thing.
Speaker: the mortality is even higher.
Speaker: So then you dive a little bit deeper and then you go cardiogenic shock with hemodynamics.
Speaker: If you have a cardiac index of less than 1.8 liters per minute per meter square without support, okay,
Speaker: And that's cardiogenic shock.
Speaker: But if you have less, it's still less than 2 to 2.2 liters per minute per meter squared.
Speaker: And that's, you know, shock still with a low cardiac index with support.
Speaker: You know that this is a patient that may need to go on something more than your optimal medical management.
Speaker: And before we even go into temporary mechanical circulatory support, I think it's really important that we come down to what is that optimal medical management, right?
Speaker: Our goals without MCS is simple.
Speaker: We want to increase the systemic perfusion.
Speaker: We absolutely want to take care of the plumbing with enhancing the coronary perfusion.
Speaker: We want to reduce the left ventricular filling pressure and the oxygen consumption.
Speaker: And most importantly, by doing all of this, we hope that we don't take this patient that has a hemodynamic problem and convert it into a hemometabolic problem.
Speaker: Dr. Kapoor's F1000 paper has really, really very, I think like the clarity of one image sticks to my mind where it is just
Speaker: You have a hemodynamic problem, which is just the index.
Speaker: But the minute that you have passive congestion of the liver, the kidneys are done, and now you deal with the mesentric, you know, the anisarca, and then now you have like a complete metabolic problem, right?
Speaker: So now how do you take that patient with those goals, right, of increasing the perfusion and enhancing coronary perfusion?
Speaker: What does medical management look like?
Speaker: Yes, we want to take them to the cath lab, do the plumbing.
Speaker: Yes, we want to give medications such as inotropic support so that we can improve the systemic perfusion.
Speaker: We want to make sure that their rhythm is adequate.
Speaker: We want to make sure that they're well diurezed and unloaded.
Speaker: And with all of this, if your index is more than 2.2, then you don't need temporary MCS.
Speaker: But to even get to that point, we are assuming that in the ICU, we've already done the EKG, the chest x-ray, the arterial blood gases.
Speaker: We already know with the surviving sepsis guidelines and stuff that we have the central line
Speaker: We are trying to understand our central venous side.
Speaker: You have an arterial line.
Speaker: And then you look at your preload, squeeze, afterload, rhythm.
Speaker: And in combination, is there anything else such as a pericardial constraint?
Speaker: It's really, really important to not just look at it at a single parametric method, right?
Speaker: So for instance, if you have tamponade, your entire hemodynamic variables and how you interpret them changes.
Speaker: And then if you have optimized your preload, if you have optimized your afterload and squeeze,
Speaker: and at the same time rhythm and that pericardial constraint.
Speaker: And despite that, you have evidence that this person is in cardiogenic shock.
Speaker: Then your next best thing is, have you phenotyped it in terms of the staging, right?
Speaker: Like we'll talk about univentricular and biventricular, but do you know what kind of shock it is?
Speaker: Yes, it is cardiogenic because I've ruled out everything else, okay?
Speaker: What kind of staging does this patient have in terms of cardiogenic shock?
Speaker: So the sky classification is one that is most likely, you know, most of us are using.
Speaker: And basically this, the Society of Cardiovascular Angiography and Interventions came up with, there's five stages of shock.
Speaker: There's A, B, C, D, E. E is what you and I as intensivists, we see it without even going into the room, right?
Speaker: We look at that base excess.
Speaker: We look at that bicarbonate.
Speaker: We look at before we even get the lactate with the physical examination.
Speaker: You know this is a patient that is an extremist.
Speaker: But what does that look like?
Speaker: That's a patient that is stage E, is hypotensive.
Speaker: The patient is on maximal support.
Speaker: The patient is about to have a rest and they're in full-on shock extremist.
Speaker: And the next stage before that is stage D. And that's the, you know, deteriorating phase and the stages of doom, right?
Speaker: And that's a patient that basically is actively deteriorating, requiring multiple pressors, or you are actually on mechanical circulatory support to maintain the perfusion.
Speaker: The stage before that is stage C. And if you notice, I'm going backwards because we are intensivists.
Speaker: The only way to get attention is you go from E to back.
Speaker: And stage C is the patient that you walked into in the morning and you got that feel that like, hey, let me get some things right.
Speaker: But the stage C hemodynamic profiling and understanding of that is incumbent upon our intensivist really getting the SWAN in place and getting that SWAN plus ECHO plus the physical exam and all of that together.
Speaker: So if your systolic blood pressure is low, your perfusion is low, and the other thing is, you know, your index is dropping, it's less than 2.2, your wedge pressure is elevated, that's the number 15.
Speaker: Your right atrial pressure to the wedge pressure ratio, right?
Speaker: So that's like a easy, crude way of saying what's coming into the pump is not being squeezed out of the right ventricle.
Speaker: So that ratio...
Speaker: If that is more than 0.8 and then pulmonary artery pulsatility index, that's basically, you know, a crude way of also saying is like is the right ventricle working and that's PA systolic minus diastolic divided by CVP.
Speaker: You will see about 2,000 papers on this, but basically each that PAPI is validated to be low in each different disease states.
Speaker: For instance, if you have a patient with PAH, the PAPI number that differentiates what is crude RV failure is different than patient with post-LVADR.
Speaker: So for sky classification for your states, the classic, you know, this is a patient that's really going into cardiogenic shock and we want to take care of the PAPI number is less than 1.85.
Speaker: So then you go, okay, that's great.
Speaker: But what do you look for in the labs and biochemical markers that remember that hemodynamic problem going into hemometabolic problem?
Speaker: That's where we are looking at the lactate levels.
Speaker: your creatinine levels, your LFTs and your BNP that is rising.
Speaker: And I think at the bedside, all you have to do is open the sheets and touch their feet, right?
Speaker: They tell you a lot about the perfusion of the patient.
Speaker: And then stage B is your systolic is low, your MAP is less than 60, pulse is more than 100, your index is still more than 2.2, your renal function lactate, all of the more preserved, B and P is elevated.
Speaker: And this patient may or may not have entered your ICU yet, right?
Speaker: And then stage A is a patient that is at risk.
Speaker: So when you put this together, so you have a methodology and you say, okay, I have a patient with cardiogenic shock.
Speaker: I have this kind of profile.
Speaker: And then you say, how do I know that somebody needs to be augmented with temporary MCS?
Speaker: To know why we need to do that, we already know that the mortality is high, that's great.
Speaker: But what is it that actually happens that causes this mortality, right?
Speaker: We know that once it becomes a hemometabolic problem, lactate is going up, then the pulse pressure is narrowing, and then you have a PEA that will happen, right?
Speaker: But that's, I think, for me, that's the high-hanging fruit.
Speaker: Obviously, we want to save lives, but that thinking has not helped us.
Speaker: Because we all knew that like that was going to happen, but the mortality still remains high.
Speaker: The mortality remains high wherever, right?
Speaker: Like, you know, they have fantastic, it's like COVID.
Speaker: Yes, you came to a COVID ECMO center, your mortality was still high, right?
Speaker: Because the reason is it's like minutes matter.
Speaker: It's when you put in the MCS also matters.
Speaker: And that when is incumbent upon the shockologist, which is you.
Speaker: Because you have that premonition based on either your training or your ears at the bedside or simply your intellectual understanding of how the human body works and you can see it before it happens.
Speaker: And what is about to happen, because I think we know a coding patient is sick, but that's too late.
Speaker: So we need to really dive into our resources and
Speaker: in that stage C to stage D as intensive as and rapidly escalate.
Speaker: I'm not talking about MCS, guys.
Speaker: I'm talking about getting them into the ICU, floating a swan, really understanding mixed venous, really trying to phenotype, okay, what's the problem?
Speaker: Where is the problem, right?
Speaker: If we don't do it, you're going to have refractory arrhythmias, and then you're going to have that intractable VT, and now you're stage E and pulling them back is going to be much harder, right?
Speaker: So in the timing aspect of MCS is where we as intensivists, I think, play the highest role.
Speaker: I know how privileged I am.
Speaker: I absolutely know that.
Speaker: I recognize the privilege and hence I'm here.
Speaker: I know that I get to sit here with all the devices and all these intensivists that are supported by advanced short failure MCS guys,
Speaker: The MCS surgeons, the perfusionists, the amazing nurses.
Speaker: But I'm here to tell you that even these patients in our unit sometimes don't make it because the patients come to us far too late.
Speaker: It's a STEMI that has burnt out the wall of the ventricle, right?
Speaker: Like, yes, we can decompress, but it would have been much nicer had we not gotten to this point.
Speaker: And then so we know how STEMI minutes matter, but the cardiogenic shock minutes matter is just this evolving paradigm with cardiogenic shock teams.
Speaker: So you all have to be able to, at the bedside, figure out, is this an RV dominant shock?
Speaker: Is this a by V shock?
Speaker: Is this an LV dominant shock?
Speaker: Because your management then kind of dictates what type of MCS can you advocate for this patient?
Speaker: So, so far we went over the sky classification and what is classic C, D and E, and we focused on let's go full blown into D and E, right?
Speaker: Like let's really figure out that C, D so we don't get to an E. Now, what are these profiles in cardiogenic shock?
Speaker: One crude way that I've taught over the years in the MCS unit is I look at the human body as a series of test tubes.
Speaker: We get blood into the right atrium.
Speaker: Right atrium puts blood into the right ventricle, then in the PA, then into the lungs, then into the LA, then the LV and the aorta.
Speaker: So if we had a swan and we had these numbers, you just kind of write it out.
Speaker: What are my numbers saying?
Speaker: Let's just say, for example, my CVP is 20, okay?
Speaker: And then my PA pressure is elevated.
Speaker: Then in the left atrium, my wedge pressure is like 10, okay?
Speaker: right and the chest x-ray does not show any pulmonary edema so then you already know that the blood is going into the right atrium it's going in through the pulmonary artery so there's no obstruction there so the rv is trying to do its job but there is no way that this blood is going back into the left atrium and you know that there is no pulmonary edema so more than likely this is severe pulmonary hypertension
Speaker: Now, why does that matter for cardiogenic shock?
Speaker: Because if you go and put in a balloon in this patient, it ain't going to work, right?
Speaker: The blood actually needs to enter the left atrium.
Speaker: So you may want to do some inhaled nitric oxide, squeeze the ventricle a little bit, do some pulmonary vasodilation or call one of us that do pulmonary arterial hypertension therapies and go, hey, can you phenotype this patient?
Speaker: Is this PAH?
Speaker: Can you start the therapist, right?
Speaker: Now, similarly, let's take the same patient.
Speaker: CVP is elevated, right ventricle is filled.
Speaker: You saw the echo.
Speaker: You're focus trained.
Speaker: You looked at the TAPC and you're like, dude, this ventricle ain't moving.
Speaker: Then you looked at the pulmonary artery.
Speaker: Again, pressures are elevated.
Speaker: Then you did the wedge pressure.
Speaker: And if your wedge pressure is 20, let's say, and your CVP, I'm going to just give you a big number, 25.
Speaker: hey, you know, this is not working.
Speaker: This patient not only has RV, it looks like, you know, and then you look at the LV on echo and you look at an LVEDP, that's also elevated.
Speaker: You're like, oh, this is a patient in Bi-V shock.
Speaker: And that's the most common kind that you're going to see other than because the LV ones are probably already in the CCU.
Speaker: But the Bi-V ones can mess with you.
Speaker: They're going to have kidney.
Speaker: They're going to have a creatinine that is elevated.
Speaker: They are going to have ascites.
Speaker: They are going to look like, okay, this person is clearly septic, right?
Speaker: And then you're like, okay, that's great that we come up to diagnosis of sepsis, but why is my CBP like 25?
Speaker: This is distributive shock, right?
Speaker: Then you're like, okay, so CVP elevated, wedge pressure elevated, CVP over wedge pressure ratio is elevated.
Speaker: And then you say, if my pulmonary artery pulsatility index is also low, right, that's a BIV shock.
Speaker: What about a patient with LV dominant shock?
Speaker: Now, this person usually is pretty straightforward.
Speaker: Your CVP is low.
Speaker: It may be less than like classic, like, you know, 14%.
Speaker: Your CVP to wedge pressure ratio may be less than 0.86, and your papi may be preserved.
Speaker: Now, that's a beautiful case of LV dominant shock.
Speaker: Now, if you take a patient with LV dominant shock and he's in your ICU and the blood pressure is low, you add some levo, you add some vaso, of course the blood pressure is going to increase, right?
Speaker: Right.
Speaker: But that patient at the end of the day, that LVDP in front of you is going up.
Speaker: And you know, let's assume that this is an AMI shock.
Speaker: In front of you, this balloon that we call the left ventricle is increasing, is increasing, right?
Speaker: And then you have the mechanical complications of AMI.
Speaker: Whether it is your mitral regurgitation, whether it is VSD and in worst case, the free wall ruptures, right?
Speaker: And there's nothing you can do.
Speaker: Yeah, you give pressers, but those were not adequate because the pressers can only go so far.
Speaker: What that patient really needed, ideally was already she had gone to the cath lab.
Speaker: But then that is a patient that you started inotropic support and it was not quite working.
Speaker: And you decided that that's a patient that I may need temporary MCS on.
Speaker: Right.
Speaker: And that's when going into the question that Sergio is asking is,
Speaker: tell us about temporary MCS.
Speaker: And so we can't talk about temporary MCS until we get these alphabets done.
Speaker: So we're done, now let's go into the words.
Speaker: And that's when we go into what are the kinds of temporary mechanical circulatory support devices available.
Speaker: Sergio, is that a good starting point for us?
Speaker: So we talked about the sky classification.
Speaker: I think the indications are very important to emphasize the importance of time-sensitive interventions, right, and how time really has a tremendous implication on final patient outcomes.
Speaker: And let's review now.
Speaker: Once we made a decision that our patient is in shock, we, as you explained, have looked into the phenotype, have classified as best we can, and are feeling that our patient is going to need more support.
Speaker: What are the options we have today in terms of temporary support for that patient?
Speaker: So there are many, I mean, you know, you can just Google temporary MCS and you'll see everything.
Speaker: But I want you guys to go back to your algorithm and separate it now into, am I dealing with an RV failure patient?
Speaker: Am I dealing with a by V patient?
Speaker: Or am I dealing with an LV failure?
Speaker: First of all, just, you know, and now we have shock extremists, right?
Speaker: out of all of these in your ICU, in a patient that is about to code or is coding, the number one device that you need to know about is the Veno Arterial ECMO, right?
Speaker: It can be placed in the intensive care unit.
Speaker: You can just drop in five French sheets in the artery and the vein to get the patient ready for cannulation.
Speaker: The patient can be immediately supported.
Speaker: It takes blood from the vein.
Speaker: So if your drainage cannula is all the way up in SVC, it drains from the SVC and IVC.
Speaker: If your drainage cannula from the femoral is just in the IVC, then it's draining from the IVC, taken to a pump, right, a centrifugal pump, pushed through a membrane or an oxygenator into the femoral artery back in through the aorta.
Speaker: This will enable you to provide temporary perfusion in the setting of complete cardiopulmonary failure.
Speaker: So in shock extremist, the first device is VA ECMO.
Speaker: The way we know arterial ECMO works is obviously it's your classic cardiopulmonary bypass that you would do in the operating room.
Speaker: It's typically the return cannulas, which is going into the aorta or about 15 to 22.
Speaker: And the drainage cannulas can go up and, you know, the cannula sizes go.
Speaker: It differed depending upon the body habitus of the patients, 18 to 21.
Speaker: Now, what are the advantages?
Speaker: It has a membrane, right?
Speaker: So if a patient is also having hypoxemia or along with other etiologies such as PE and stuff, you know, you're able to oxygenate the patient.
Speaker: The second thing that I need you to know about Vino-RTG-LECMO
Speaker: the one that is done in the ICU, as from intensivist perspective, is if patients have peripheral arterial disease, imagine putting in a complete obstructing cannula in the femoral artery, right?
Speaker: That leg will become ischemic.
Speaker: So you typically put in another small catheter to perfuse the distal leg.
Speaker: The reason I'm telling you all about it is if you are...
Speaker: If you're part of a hub-and-spoke model, the patient is cannulated and they're about to take the patient, you need to watch these legs to make sure they don't get ischemic.
Speaker: What are the disadvantages of veno arterial ECMO?
Speaker: We just talked to you about limb ischemia.
Speaker: Of course, they'll need anticoagulation.
Speaker: So, you know, all of the everything that can happen does happen, will happen the more you do, just like in ICU, right?
Speaker: Right.
Speaker: Now, who are the patients you can do it in?
Speaker: If the patient has severe aortic insufficiency or if the patient truly has sepsis and distributive etiology, no amount of three liters flow is going to be able to augment that patient, right?
Speaker: It's just it's not enough three to four liters.
Speaker: Sometimes, you know, central ECMO can give you all the way up to 30.
Speaker: six, seven, if you can, depending upon the cannulas, but peripheral, like most, you know, they write four to 10 liters sometimes support, but maybe maximum, like, you know, we, we've the bedside 4.85.
Speaker: With the sweep gas, we can remove the CO2 and add oxygen, right?
Speaker: The sweep gas can go up.
Speaker: And if you have significant dead space that can help.
Speaker: So your VA ECMO can help you in RV failure, in BIV failure, and in LV failure, meaning if a patient is coding.
Speaker: But the minute that you put these patients on VA ECMO, you wait for the shock extremist to kind of die down.
Speaker: Is it just RV, meaning the lungs are okay?
Speaker: We don't really need an oxygenator.
Speaker: We don't really need this cannula in the aorta.
Speaker: Then you need to ask yourself, yeah, VA ECMO is a great right ventricular assist device because it's suctioning blood right out of the vein, right?
Speaker: But anything you can do to de-escalate or downsize into a smaller, more sophisticated, you can do.
Speaker: The same thing is for LV failure.
Speaker: is on Veno-Arterial ECMO.
Speaker: And, you know, when the New England Journal trial came out, it's like VA ECMO in cardiogenic shock, there is not significant help.
Speaker: We were like, of course, we know that.
Speaker: Like it was only supposed to help when the patient is like deathly ill and dying, and then you're supposed to change it over.
Speaker: What do I mean by that?
Speaker: If you remember back when
Speaker: When I say back, back, back, back into med school with the PV loops, I know you guys do our PV loops really well with the lung, with ARDS, right?
Speaker: But the PV loop of the heart, where you can see in cardiogenic shock, right, the PV loop moves to the right.
Speaker: Your end diastolic volume is going up, your blood pressure is coming down, it moves to the right.
Speaker: In VA ECMO, it doesn't bring it back to the left.
Speaker: It moves it even more to the right.
Speaker: So think of like, you know, in ARDS, how the limb becomes flattened and then, you know, your entire loop is getting, you know, wider and wider.
Speaker: So in the cardiac loops with VA ECMO, the endostolic, right, your LV is actually having to work harder because you have a hose in the aorta.
Speaker: So what you want to do in these settings is you support the patient, of course, you know, work with your cardiology colleagues and you say, okay, so I have a patient, I immediately supported them, but now I have it, this is AMI cardiogenic shock.
Speaker: So you've taken them to the cath lab, you worked on the culprit lesion, and then you say, where is my problem?
Speaker: So let's look at the test tube method, right?
Speaker: So right atrial pressure is up, RV pressure is up, PA is up, LA is up, LV is up, LVEDP is up, but the aorta, the mean arterial pressure is low because your LV is big, right?
Speaker: So all you have done with VA ECMO is you bypass from the right atrium to aorta bypass.
Speaker: This LV is not being unloaded.
Speaker: If anything, there's a possibility that you may be harming it.
Speaker: It's incomplete LV unloading.
Speaker: So you have to figure out
Speaker: Right now, your temporary support devices, if you have isolated LV, you can put this patient on the impeller support system where it takes blood from the left ventricle and puts it over the aortic valve.
Speaker: Right here, left ventricle suctioning blood through the pigtail catheter and putting it over the aortic valve.
Speaker: So it's an LV aorta bypass, whereas a VA ECMO was what?
Speaker: Right atrial aorta bypass, right?
Speaker: So you are really addressing it where the problem is with the impeller.
Speaker: So a typical scenario may look like this.
Speaker: Patient is in shock E. You astutely call your team.
Speaker: The patient was put on VA ECMO.
Speaker: You again see that, okay, the VA ECMO is put in, but now the patient's LV is getting bigger.
Speaker: Their pulsatility, pulsatility is their systolic divided by diastolic, is very small.
Speaker: Let's say it's less than 10, then it's not unloading.
Speaker: You put a echo probe on and there's smoke in the ventricle.
Speaker: And they're not ejecting.
Speaker: Yes, they're on anticoagulation.
Speaker: You're like, hey, you know, we need to, because you want to preserve muscle function, then you want to vent the ventricle.
Speaker: You surgically as well, there's like an LV sump that the surgeons can put in.
Speaker: It's not, it impella, it's just the current available percutaneous approach, right?
Speaker: So you unload and then you say, hey, my lungs are fine.
Speaker: I've unloaded it.
Speaker: Do I really need the veno arterial ECMO?
Speaker: Then you come down on the veno arterial ECMO, the flow, and you see you maintain the blood pressure over the next two, three days.
Speaker: It looks like the pressure is being maintained.
Speaker: The patient is ejecting well, then you can decannulate that person.
Speaker: Now you've taken an AMI cardiogenic shock.
Speaker: with low index in shock extremists supported them on VA ECMO plus impeller then changed it over from an acpella like ecmo plus impeller to just an impeller device as let's say a bridge to recovery that's called btr bridge to recovery the other wording that is used is bridge to decision so you're trying to figure out btd
Speaker: And the other thing people use is bridge to transplant or bridge to LVAD.
Speaker: Either way, the problem that I need you to recognize is it's not just supporting the patient, timely support.
Speaker: It's at the same time, parallelly thinking, where am I taking this patient?
Speaker: How do I get this patient home?
Speaker: I think, Bindu, you made a very important point in terms of whenever you start somebody on mechanically circular support, you're thinking of your exit strategy, right?
Speaker: And you talked about bridge to transplant.
Speaker: Not everybody's a candidate for transplant, obviously.
Speaker: You talked about bridge to recovery, which is those patients who we think have a decent chance or a chance to recover.
Speaker: But you also mentioned
Speaker: the bridge to decision, which is something a lot of intensivists, I think, don't always appreciate, that sometimes it's unclear what the trajectory will be or should be, and the buying time to make that decision of what the next step is can also be very powerful.
Speaker: Could you comment on that a little bit?
Speaker: Yeah, I think this is when the intensivists actually have the most crucial goals
Speaker: player status when you work in a large team called the heart team approach.
Speaker: You have already stabilized, you put in your groundwork, just like the interventional cardiologist that did the plumbing and that tried to see and that put in the patient with the MCS or the surgeon.
Speaker: You as the intensivist are able to talk to the family, you bridge that connection and
Speaker: And I think one of the things that I've noticed is the same working understanding of recognizing which septic patients won't make it.
Speaker: We tend to apply that to the heart failure patients.
Speaker: And I am going to argue that I,
Speaker: Even though you may be right, I mean, only trials will have to show this, I would argue that in a developing field such as mechanical circulatory support, you cannot tell me that this guy that was admitted five times for heart failure that now has come in is on temporary MCS should proceed to either withdrawal of care or comfort care because studies have shown when you are admitted this many times, these patients' mortality is high.
Speaker: Yeah, well...
Speaker: Studies have also shown that heart failure patients that keep going home will die.
Speaker: They should have been supported and taken from stage C and referred to a durable LVAD program sooner too.
Speaker: Do you see that?
Speaker: So I am asking you, or rather persuading you, to think of it as you know 30% of cardiogenic shock
Speaker: The other 70%, the chapters are being written, and I am going to stay here and say, the more the intensivists can escalate at a faster rate, the mortality will only improve for the patients with temporary MCS, and in which case, the survival over the next 10, 20 years will improve.
Speaker: So,
Speaker: don't need to think of every patient and go, well, I don't want to offer ECMO because this guy is not going to get transplant.
Speaker: I want you to look at it as what are the terminal conditions the patient has?
Speaker: Okay, if the patient has leukemia, lymphoma, metastatic cancer, advanced elderly age that is non-functioning, all of those, of course, those are the easy buckets.
Speaker: Then the pristine candidates are the easy bucket as well, right?
Speaker: Like 28-year-old comes in peripartum cardiomyopathy, is in state of shock.
Speaker: Boom, like everything, right?
Speaker: Everything.
Speaker: We do everything and we do it well.
Speaker: It's the gray bucket.
Speaker: The 66-year-old that has come in and out of the hospital, has mild AKI, was a smoker up to like five years ago.
Speaker: I just humbly ask that you don't take that burden on you.
Speaker: You reach, at least if you're an institution that offers hard programs, then you're probably not, like you're doing this already, but share the burden.
Speaker: Sharing the burden enables you to consider alternative viewpoints.
Speaker: So for instance, Sergio, brief, brief, very brief exit, durable LVAD.
Speaker: In the early 2000s, the rematch trial came.
Speaker: The rematch trial showed that in patients that are not transplant candidates, the optimal medical management group, and remember this, you know, save and solve trials and all those trials were out.
Speaker: We were on ACE inhibitors.
Speaker: We were on diuretics, right?
Speaker: Then that trial showed, despite optimal medical management, the survival was only 8%.
Speaker: 8%, guys.
Speaker: And the survival went to 24% at two years with the first generation LVADs.
Speaker: And this one was barely, I mean, you know, in terms of the number of patients, right?
Speaker: It was not that many.
Speaker: It was like 68 and 61.
Speaker: That trial really started the LVAD.
Speaker: programs everywhere.
Speaker: So right now, optimal medical management, maybe these weight loss medications will change that curve, has improved from 8% at two years with this life-saving, billion-dollar industry and everything, right?
Speaker: Has improved.
Speaker: But I ask this one of my favorite questions I ask our fellows,
Speaker: They're like, oh, it's 70%.
Speaker: I'm like, try like, you know, try 24, 30, maybe like in the best of hands, like maybe a little bit higher.
Speaker: So optimal medical management in end-stage heart failure has a long way to go.
Speaker: So who are you and I at the bedside in just one passing, this guy is never going to get a durable LVAD.
Speaker: We have to try the bridge to recovery.
Speaker: We have to try or at least give due justice for bridge to decision.
Speaker: And at the very least, take this hemodynamic, hemometabolic problem, support them in ideal situations, and at least bring it back to where you can say, I just have this problem and I'm going to try to see and then have a very tight ballgame, like in X number of weeks or X number of days, if this doesn't work, we have nothing else.
Speaker: And that you can only really do with a heart team approach.
Speaker: So that's for LV failure.
Speaker: So you really want to be able to say, I want to have an exit.
Speaker: I really want to be able to support them.
Speaker: So we talked about the impeller.
Speaker: We talked about VA ECMO.
Speaker: intra-aortic balloon pump.
Speaker: And I think you know that this is the most commonly used counter-pulsation device.
Speaker: It sits nicely in the descending aorta and it improves coronary perfusion and cardiac output.
Speaker: There are
Speaker: There's some data whether it actually augments cardiac output or not.
Speaker: But, you know, for you, literally in most of the ICUs, IABP is available.
Speaker: I want you to think about it as augmenting systemic perfusion and some coronary perfusion.
Speaker: It's very easy.
Speaker: Everyone knows how to do it.
Speaker: And I think that's a simple enough thing.
Speaker: And I advise my shockologists, you all,
Speaker: Next time the patient is on balloon pump, look at the waveforms.
Speaker: There are so many resources online to learn the waveforms.
Speaker: And I think if you're a student, which you are, that's the reason you're listening right now.
Speaker: You will really, it's physiologically, it makes sense, right?
Speaker: Dicrotic notch, it augments, then, you know, what happens to SPP.
Speaker: Now, what is the third device?
Speaker: So balloon pump, I'm just saying, you know, you guys know it.
Speaker: ECMO, we talked.
Speaker: Impella, we talked.
Speaker: Now, Impella, there's two, right?
Speaker: There's the Impella CP, and then there's the Impella.
Speaker: Right now, we use the 5.5.
Speaker: What is the main difference?
Speaker: The Impella CP is emergently usually placed in the cath lab, and it provides support, but it's a much smaller amount of support compared to the bigger 5.5.
Speaker: So the 5-5 needs a surgical cut down, axillary graft, but if the patients for some reason don't have a good upper extremity anatomy, it can be also suited stratically into the aorta.
Speaker: Surgeons are able to place it.
Speaker: then these patients experience direct ventricular unloading.
Speaker: They do need anticoagulation.
Speaker: Limb ischemia can happen.
Speaker: And sometimes aortic valve can be damaged.
Speaker: But the most important thing is these patients, especially with the upper extremity one,
Speaker: They come out, they're supported, you can extubate them, you're walking them.
Speaker: And it's a good bridge to decision device because you can see, because, you know, if you're supporting them four to five liters of decompression, that's essentially a trial run of a durable LVAD, right?
Speaker: You're like, I'm going to support them, I'm going to decompress them, I'm going to see.
Speaker: If their multi-organ failure is going to get better, I'm going to see if their cacaxia is going to improve.
Speaker: I'm going to see if they're going to declare themselves, meaning like are they going to be good candidates, or maybe it's a bridge to recovery.
Speaker: Their AMI cardiogenic shock is improving, and then I'm going to be able to recover them.
Speaker: Again, it takes a sophisticated unit to know the nuances.
Speaker: I think a big part, and Sergio, I think you probably can attest to it.
Speaker: It's not about getting it right in ICU medicine that you and I are here.
Speaker: It's trying to not get it wrong, right?
Speaker: Right.
Speaker: So the more experience you have, the better you're going to be.
Speaker: And you also see that not all patients need impeller support.
Speaker: There are some patients, maybe you should have removed the impeller and the patients are recovering.
Speaker: And I think those are the nuances that you can learn at the bedside as you take care of these patients and with additional training too.
Speaker: Now, what is the entire tandem part, right?
Speaker: I'm going to, so Levanova pulled the pump, but I think the cannulas are available, but I'm going to tell you, let's say the same test tube method.
Speaker: Right atrium is up, right ventricle is up, PA pressures are up, LA pressures are up, lungs are flooded.
Speaker: But then you go to an LVEDP and the LVEDP is low.
Speaker: So this patient, let's say, has
Speaker: giant left atrial syndrome, severe mitral stenosis.
Speaker: You put in a patient, you put the VA ECMO on for temporary, they're crashing, but you didn't solve the problem, right?
Speaker: Can you put in an impeller?
Speaker: Can you, will that help?
Speaker: If the blood is not coming from the left atrium to the left ventricle, putting in an impeller won't help either, right?
Speaker: patient, what do you really need?
Speaker: You need the left atrial bypass, right?
Speaker: Left atrium, blood needs to be sucked and put it into the aorta.
Speaker: So the tandem cannula and Dr. Carr's group, Texas Heart, one of the best publications.
Speaker: And I'm so proud to be in this team.
Speaker: And I was witness to this as, you know, young faculty, like patients, you know, like he would put it on coding patients with the team.
Speaker: And I'm just like completely marveled at this.
Speaker: You take the venous, like you access venous side, you access the arterial, just like you're doing a VA ECMO.
Speaker: But your drainage cannula, under floral, you're going into the right atrium from the IVC and you're transversing the PFO, making it big, creating an atrial septostomy and you're suctioning blood from the left atrium.
Speaker: into the aorta.
Speaker: Since you're doing deoxygenated blood from the left atrium, with the VA ECMO, it's deoxygenator, so you put in an oxygenator.
Speaker: But with the tandem, since you're removing it from the left atrium, which is already oxygenated, into the aorta, you don't need an oxygenator.
Speaker: So that's what a tandem heart is.
Speaker: So tandem heart again, LV, you know, can you use it in LV, like just straight LV failure?
Speaker: Yeah, because, you know, blood comes from the left atrium to the left ventricle and causes LV ETPs go up, right?
Speaker: Like why not just suction it from the left atrium directly?
Speaker: Mitral stenosis, your classic LV failure.
Speaker: What are the reasons, what are some of the issues with it?
Speaker: In ICU, we took care of a lot of tandems.
Speaker: In the ICU, the patients are immobile, right?
Speaker: They're like, they're immobile.
Speaker: Cardiac perforation in like, you know, inexperienced hands or the patients, you know, it's a, any device carries with it risks.
Speaker: And then the other thing is when a patient is put on tandem heart and you're taking it out and the patient, let's say, has improved, now you've created a hole, right?
Speaker: So they have a residual ASD.
Speaker: So sometimes you have to go and close it.
Speaker: The most important thing to know as intensive is if you're taking care of a tandem patient is the patients are immobile compared to your other devices because it's going against the PFO, across the PFO, the cannula may migrate.
Speaker: There's another thing called the lava.
Speaker: Basically, the cannula can drain from the left atrium and the right atrium via ECMO.
Speaker: So this way you're decompressing the left side and, you know, you're immediately stabilizing.
Speaker: Again, you need to put, you know, patients need to be in the cath lab because you're putting the cannula under floral.
Speaker: So that's the last in terms of temporary MCS for left side.
Speaker: Very quickly, I'll touch upon the right side.
Speaker: A frequent question is, hey, why can't we put an R-VAD in patients with, for instance, severe pH?
Speaker: See, severe pH, yes, you can put in an R-VAD if the patient had severe pH and just something happened and the patient got pushed over.
Speaker: But at the end of the day, the resistance is high.
Speaker: So you're just giving a bypass from RA to PA.
Speaker: What you really need is that blood to go from the PA to the LA, right?
Speaker: So that's the reason RVADs typically don't help and you really need those powerful pulmonary vasodilators.
Speaker: But what if the patient has an RCA infarct?
Speaker: Then yeah, you know, RAPA bypass.
Speaker: Right now, you know, there's in terms of the cannulas, there are multiple like the tandem RVAD, the RPFLEX,
Speaker: Where else can you use them?
Speaker: Post-LVAD RV failure.
Speaker: Anything that causes an isolated RV issue, you can think about.
Speaker: And they work the same way.
Speaker: I just want you to think that they work the same way.
Speaker: Now, is there any other classification when people start talking about that I can share with you?
Speaker: One clinical pearl is
Speaker: anything before the hyphen is drainage and anything after the hyphen is returned.
Speaker: And drainage is always to the pump, meaning I am taking blood from the vein to the pump.
Speaker: So it's V-A, I'm returning it to the artery.
Speaker: So it's pump focused.
Speaker: If I take it from two veins and give it to the artery, it becomes V-V-A.
Speaker: If I take it from two veins and give it to an artery and a vein, then it becomes VV-AV.
Speaker: Okay, that's one technology.
Speaker: I want you to know the nomenclature.
Speaker: The second nomenclature to really know is, is it an axial or is it a centrifugal?
Speaker: For instance, a VA ECMO, the pump is outside.
Speaker: It's a centrifugal pump.
Speaker: Whereas an impeller, an axial flow is intracorporeal.
Speaker: That's an axial flow inside the body.
Speaker: ECMO?
Speaker: extracorporeal.
Speaker: So know the hyphen method, know if you're dealing with a pump that is intracorporeal or extracorporeal inside the body, outside, and then know is it an axial flow, centrifugal flow.
Speaker: At least as you follow your patients that go on to temporary MCS,
Speaker: then you can look at it and go, hey, you know, I understand.
Speaker: I understand the classification, where they get it.
Speaker: How do you separate a univentricular, biventricular failure patient?
Speaker: What are all the MCSs that are available right now?
Speaker: And be able to draw it out for yourself.
Speaker: You would be surprised.
Speaker: You know, you can say, why can't this help?
Speaker: Tell me why it doesn't help.
Speaker: And I think you talk it out and go from there.
Speaker: Sergio, I know we touched base about Sky and then the kinds of devices and then supporting devices right and left.
Speaker: briefly about PV loop.
Speaker: I mean, I'll have to come back on your podcast, man, if you want me to do everything.
Speaker: So for sure.
Speaker: And I think that definitely we have a part two scheduled where we'll talk more about the specific management, including troubleshooting,
Speaker: managing complications, and weaning and withdrawal versus upgrading.
Speaker: But you did cover a lot of very important concepts as an introduction.
Speaker: The one thing I do want to ask you before we wrap this part one up, Bindu, is obviously in the last couple of months, at least in the clinical trial arena,
Speaker: The Danger Shock RCT was published, and I think it's definitely a landmark paper moving forward as we start to see the impact of some of these devices, temporary support in patients with cardiogenic shock associated with MI.
Speaker: Any comments on this particular paper?
Speaker: I think that, number one, it was a prospector, multicenter, open-labeled RCT.
Speaker: It was done in Denmark, Germany, and UK over the last 10 years.
Speaker: 360 patients from, I think, 18 to 90 years of age in STEMI, and the absolute reduction was about, number needed to treat was eight.
Speaker: So it was a 12.7% reduction in mortality rate.
Speaker: In fact, I was just going to sit with the fellows to go over this.
Speaker: And I think it's a good start in MCS in terms of it's the first RCT in AMI shock, which is one of the highest mortality, to achieve its primary endpoint.
Speaker: And you know physiologically it makes sense, but I think that big picture is...
Speaker: Science matters and we need to do more and more of these trials to see right patient, right support, right timing.
Speaker: And I am here to ask all of you as intensivists, if there was ever a need for us to really be in this field and move outcomes, it's now.
Speaker: And I hope more of you will join the MCS critical care community.
Speaker: Reach out if you want to learn more, obviously.
Speaker: But I think like this, we are learning together.
Speaker: So that's those are my thoughts on that, Sergio.
Speaker: Perfect.
Speaker: I know.
Speaker: So I think that we have a lot to talk about that will be in part two.
Speaker: But I do want to close the podcast, Bindu, with a couple of questions that are unrelated to MCS.
Speaker: Would that be OK?
Speaker: Yes.
Speaker: Yes.
Speaker: Go for it.
Speaker: So the first question relates to books.
Speaker: Are there any books or is there a book that has impacted you significantly or that you have gifted often to other people?
Speaker: Yeah, I think out of all the books that I've ever read, The Alchemist speaks to me.
Speaker: And I think as I'm getting older, it speaks to me a lot more.
Speaker: For those of you that read it, you must know.
Speaker: But if you didn't read it, I highly recommend it.
Speaker: And the central idea is that
Speaker: Everyone has this personal legend within them.
Speaker: And when we are young and we imagine this world full of possibility, that personal legend is like very clear.
Speaker: And the universe kind of puts clues in your way for you to be enthralled if you were to choose to see them.
Speaker: And then the universe comes together to make it happen for you.
Speaker: And I think like, and, and that's, there's a statement there.
Speaker: And I think that says, and when you want something, all the universe conspires to help you achieve it.
Speaker: And I think like, I look at my own, my, my own path.
Speaker: I mean, just like all of you, like we are, we are filled with potential and the only person that gets in the way is us.
Speaker: Right.
Speaker: Right.
Speaker: have come to realize that one of my own personal legends is to see people as having unbelievable potential and mentor them and be the miracle growth that they need.
Speaker: I mean, I'm a gardener at heart, so sorry.
Speaker: I'm not, I'm not supporting any brand, but I think that's what it is.
Speaker: Like, I hope
Speaker: I hope we really continue this improvement, right?
Speaker: So I think that book really speaks to me.
Speaker: And it's a free PDF online.
Speaker: So I don't even gift it.
Speaker: I just send the students and my mentees a link and I try to post on social media and my personal pages about it.
Speaker: It's like, it's so powerful, so powerful.
Speaker: Absolutely.
Speaker: A brilliant book, I agree, and we'll definitely put a link in the show notes.
Speaker: I think this is the perfect place to take a pause and stop, Bindu, for today.
Speaker: We definitely will continue this conversation.
Speaker: I really want to thank you for sharing your passion for this topic, your knowledge, and I look forward to part two of our discussion where we dive into the managing of complications and troubleshooting of these MCS devices.
Speaker: Thank you so much, Sergio.
Speaker: Thank you for listening to Critical Matters, a sound podcast.
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