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Dr. Venu Menon and Dr. Edward Soltesz discuss cardiogenic shock and strategic opportunities.

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Talking Tall Rounds®: CCF Cardiogenic Shock Team Initiatives

Podcast Transcript

Announcer:

Welcome to Cleveland Clinic Cardiac Consult, brought to you by the Sydell and Arnold Miller Family Heart, Vascular and Thoracic Institute at Cleveland Clinic. In each podcast, we aim to provide relevant and helpful information for healthcare professionals involved in cardiac, vascular, and thoracic specialties. Enjoy.

Ashley Bock, MD:

Good morning. I'm going to start with a case presentation this morning. This is a 68-year-old female. She has known ischemic cardiomyopathy. And she presented to us with shortness of breath, volume overload, and tachycardia. And subsequently, developed monomorphic VT and ICD firing that prompted transfer from our floor to our heart failure ICU. Her background was notable for ischemic cardiomyopathy. Her EF is 25%. She's had an ICD placed previously. She has known unrevascularized three-vessel CAD, but was deemed not to have any viability on viability testing. And so, further revascularization was never pursued. She had what was notable for CKD stage 3, with a baseline creatinine of 1.5 to 1.9. But we'll talk about that in more detail. VT and then a history of Guillain-Barre actually requiring IVIG, hyperlipidemia, and thyroid disease. She had not had any prior sternotomies. She was on guideline-directed medical therapy, including metoprolol, spironolactone and ramipril.

Ashley Bock, MD:

Here's her chest x-ray. On presentations, you see she has an ICD there and pulmonary congestion. Her EKG is notable for a left bundle morphology. She just had one lead. She did not have a biventricular device. Here is her echo. Her echo is notable for a dilated LV, as you see there. You can see that her mitral valve does not completely collapse, consistent with functional MR. There you see on color, her MR. Her RV actually looks okay in this view. Here's just another short axis view of the ventricle, which is dysfunctional, with global hypokinesis and centrally directed MR jet. Then here, you see a better picture of her RV function, which is relatively well preserved, and then her ICD lead there, as well.

Ashley Bock, MD:

In terms of her hemodynamics on admission, her blood pressure was notable. It was 86/55, so she was hypotensive. Heart rate is 77. Then I think most important to note, were her hemodynamics on admission. You see here, her RA pressure was elevated at 25. PA pressures were also elevated, with a mean PA pressure of 50 millimeters of mercury and a wedge of 32. Her initial SvO2 was 46 with a cardiac index of 1.6. All very concerning in this woman who had kind of done okay for quite a while, with chronic heart failure. And now presenting in an acutely decompensated state.

Ashley Bock, MD:

Here are her cath films from previous. She had severe three-vessel coronary disease. She has some left to right collaterals noted on her cath. As I mentioned before, really deemed not to have any targets for revascularization and really didn't have any viability in any certain territories on viability testing. One of our biggest concerns with her acute presentation, in addition to her hemodynamics was, she had evidence of end-organ dysfunction. Her creatinine was elevated above three. As you see here, she had had a baseline of near 1.5 prior to that. Obviously, in a difficult spot.

Ashley Bock, MD:

In terms of the questions that we asked ourselves at this time, what are the next steps for this patient? What additional support can we provide? What is the role of a multidisciplinary team in this setting? With that, we'll continue.

Venu Menon, MD:

We have known the impact of acute heart failure in the setting of an ICU admission for more than 50 years now. This is data from Tom Killip from Bellevue Hospital in the 1960s. A time when we had acute myocardial infarction and no treatments for it. You can see that when you presented to Bellevue in 1960, if you had rales on your exam and you had a low blood pressure, we call that cardiogenic shock. The mortality rate was about 70%. Unfortunately, that hasn't really changed too much.

Venu Menon, MD:

About a decade later, when we discovered the use of the right-heart catheter, this is data from Kanu Chatterjee, Diamond and Forrester from the Cedar Sinai CCU. We would take these folks who came in with an acute myocardial infarction, put a Swan in them. Based on the hemodynamic profile, you could essentially draw four quadrants. What you can see in the unfilled circles are those who survived the hospitalization and in dark circles, those who died. You can see that those who die, really are focused on this right lower quadrant, where a cardiac index of less than 2.2 and a high wedge pressure. This is our baseline definition of shock, as a construct today.

Venu Menon, MD:

There is another group here, which is hypoperfused and has a low wedge pressure. Something we've come to recognize as RV infarction and plays a major role in our management and choice of decision making in terms of supportive devices, as we talk about it later today. The components of shock are hypotension ... You can see, I haven't put a number to it. And we will not be utilizing a number to it in our shock algorithm. But hypotension is classic in this setting.

Venu Menon, MD:

This compensatory tachycardia. And again, note while tachycardia is a common component, we have a number of people in the ICU who are bradyarrhythmic because they're pacemaker dependent. And chronotropic incompetence can often mask tachycardia in this setting.

Venu Menon, MD:

But the bottom line is, you have to have end-organ hypoperfusion. Just because you have a blood pressure of 80 and you're doing the New York Times, you're not in shock. You have to have end-organ hypoperfusion. And so, when we look at shock as a construct, we define it as an ineffective cardiac output to meet demand in the setting of an adequate intravascular status.

Venu Menon, MD:

There's a number of definitions for shock in the literature. What you can see is it actually been only three randomized clinical trials of shock, the SHOCK trial, the IABP-SHOCK II trial and the CULPRIT-SHOCK trial. And the SHOCK trial was the only one where we actually used hemodynamic criteria. And you actually needed a Swan to go in. All of these other studies had a component of blood pressure and hypoperfusion that made you enroll into the study. Something similar to what we will be using in our protocol later today.

Venu Menon, MD:

I had the privilege of working on the SHOCK trial and we published a number of hemodynamic papers in the early days. And what we found was that a hemodynamic profile of shock is heterogeneous. That you did not need a low blood pressure to definitely be in shock. There were normal-tensive people who were in shock with hypoperfusion. And that systemic inflammation played a marked role in the setting of shock.

Venu Menon, MD:

And so, although the construct of shock was one of an acute systolic failure with a reduced ejection fraction and a reduced stroke volume. There is a significant component of vasodilation that is highly heterogeneous, varies from patient to patient, needs to be measured. And as a result, warrants hemodynamic monitoring, including placement of a Swan.

Venu Menon, MD:

This is the latest SCAI classification from earlier this year. I think it's a very nice classification to say that all shock is not the same. They grade it similar to how we do it in valvular heart disease, A, B, C, D, and E. A being those at risk. People with classical shock actually start here. They're people who have hypoperfusion. We are beginning to put support on them, but then they tend to deteriorate. And then when they deteriorate, we add on further supportive devices. And finally, they're an extremist, we're doing CPR. We have them on an ECMO. These are apples and oranges. And to compare them across clinical trials, you need some sort of a classification like this. And this is going to be extremely useful going forwards.

Venu Menon, MD:

We were very quickly able to actually validate this. This is a paper from Jacob Jentzer at Mayo. We looked at this classification at the Mayo Clinic. Over 10,000 patients in JACC last month. And you can see that this classification, that it's simple. Just the presence of hypoperfusion really identifies someone who's at risk in the unit. And then you go onto refractory shock. There's a huge mortality difference. And this gap is where intervention has the promise to probably alter outcomes in this otherwise dismal disease.

Venu Menon, MD:

This is data that Paul Cremer and I have contributed to. This is the Critical Care Network Registry. Just out in Circ. This is a snapshot of CCU admissions across the United States in 30 hospitals this past year.

And what I want to show you is that shock is extremely heterogeneous when you see it in the CCU. Cardiogenic shock is a predominant cause, but certainly other forms of shock coexist. And when you actually look at the cause, although all our data is in acute myocardial infarction in shock, you can see that AMI shock is only 30% of what we see in the CCU today. A large proportion of shock that we see is non-ischemic or ischemic without AMI, like the case that Ashley showed you today.

Edward Soltesz, MD, MPH:

Overview of some of the devices that we use for acute MCS. And I want to just focus on some of the surgical devices that we have. But when we take a step back and look at what are the goals of acute mechanical circulatory support? We have to realize that first and foremost, we want to restore end-organ perfusion, adequate end-organ perfusion. We want to unload the injured ventricle, both pressure and volume unloading. And then we want a bridge to either recovery or potential transplant or a durable device implant.

Edward Soltesz, MD, MPH:

We want to talk about saving the patient, saving the heart, and then saving a life. The concept, however, being that not all of these are interrelated. In the sense that some devices don't necessarily save the heart, but may save the patient. And other devices may save the heart, but not necessarily the patient. We have to understand devices, in particular, and how we utilize them throughout a patient's course in cardiogenic shock.

Edward Soltesz, MD, MPH:

The ideal mechanical support, Jerry talked a bit about this. We want to ideally provide a device that can do it all. That can do it all, but can also be ventricular specific. We don't want to provide bi-ventricular support when we only need left ventricular support. We want something that's easy to insert and remove, that's biocompatible, allows patients to walk around. And is, of course, inexpensive.

Edward Soltesz, MD, MPH:

And when you look at it from the ideal hemodynamic device, we want to look at a system that's going to bring our Frank-Starling curve. It's going to operate on the left side and on the bottom. Meaning it's going to increase mean arterial blood flow or perfusion. But at the same time, reduce myocardial oxygen demand.

Edward Soltesz, MD, MPH:

These are our devices that we have that are sort of surgical devices. Not going to talk too much about CentriMag, but we'll focus on ECMO and Impella.

Edward Soltesz, MD, MPH:

When we look at these from the perspective of their ability to unload the ventricle, you can see that ECMO does not provide any unloading. Whereas, CentriMag is surgically placed biventricular or univentricular support device, can provide full unloading. But of course requires a sternotomy.

Edward Soltesz, MD, MPH:

Our immediate focus when we're faced with a patient who needs acute MCS is what part of the heart needs support? How much support is needed? And how quickly do we need to provide that support?

Edward Soltesz, MD, MPH:

And here is the menu of devices that we have. And again, some of these are appetizers and some of these are main courses. But we start on the left side with counterpulsation balloon pump, as Jerry had spoken about. We have left, LV-specific devices. As you can see, ECMO is not in that category. Because it's not an LV-specific device. We do have an RV-specific ECMO circuit that we can utilize, mainly surgically. But when we look at ECMO, it really falls into the biventricular pulmonary support categories.

Edward Soltesz, MD, MPH:

And, of course, Impella you can see. And the various configurations of Impella, whether it be RP or CP or a 5.0 device. Can be ventricular specific. But many of the percutaneously placed devices do not provide pulmonary support. And that's where ECMO and various configurations of CentriMag and TandemHeart can.

Edward Soltesz, MD, MPH:

We can also look at the degree of mechanical support provided by all these devices. With balloon pump really providing partial support. And on the far right side of the picture, you can see ECMO and CentriMag. And I have the lungs there, because it provides full cardiopulmonary support.

Edward Soltesz, MD, MPH:

Now, hemodynamics of all these devices, I think are important to understand. Because if you look at a balloon pump, it can decrease pressure, but does increase the volume. If you look at TandemHeart, increases pressure, but significantly decreases volume. ECMO, sort of the worst of these devices. It increases pressure and LV volume. And Impella decreases pressure and decreases volume.

Edward Soltesz, MD, MPH:

I'm not going to spend too much time on balloon pump, because Jerry already covered this. But I do want to focus a bit more on ECMO. Here's our circuit. It's a rotaflow pump. Low cost, small, connected to a Quadrox oxygenator. And if you are of the Mercedes driving type, you'll use this. This is the Maquet Cardiohelp. It's about $8,000 or $9,000 more than the device that we have as our homegrown pump.

Edward Soltesz, MD, MPH:

The disadvantages of ECMO are extremely important to understand though, as a mechanical support device. Because, as I mentioned before, it'll save the patient. But it won't save the heart. There's minimal LV unloading, there's poor coronary perfusion, there's no reduction in left ventricular work. And there's actually relative cerebral hypoxia present. Especially if you're cannulated peripherally. And more importantly, to someone like myself in the MCS sphere doing LVADs and transplants, we cannot decouple the LV from the RV. Meaning it's very difficult to understand when you wean ECMO, the individual contributions and damage to each ventricle.

Edward Soltesz, MD, MPH:

Here you can see the human dynamics of ECMO. And Jerry showed this. As you increase flow, you significantly increase LV pressure and volume. And there are, of course, complications associated with ECMO. Some of which have been mitigated by the newer pump, the Quadrox oxygenator. Which has decreased our pump thrombosis and oxygenator problems. And limb complications, which have been mitigated by requiring antegrade profusion sheets and, or axillary cannulations. But we still have a lot of neurologic and dialysis events. A lot of this is related to homolysis. If you look at all of our devices, you can see that ECMO is just below cardiopulmonary bypass as the biggest driver of homolysis. And on the far left side, you can see various Impella devices. Then of course, static blood. Cerebral hypoxia is a problem, especially when you are perfectly cannulated, you get the Harlequin or North-South Syndrome problem.

Edward Soltesz, MD, MPH:

We've tried to mitigate limb complications by requiring a distal perfusion catheter or sheath, or cannulating directly the femoral or axillary artery. Spectroscopic monitoring of the limbs is also important to understand any complications that may be occurring. And more recently, we've also been using axillary ambulatory VA ECMO. Some of you may have taken care of a few of these patients recently who have gone directly to transplant.

Edward Soltesz, MD, MPH:

And it's a unique configuration where we actually place a graft to the axillary artery. And through that graft, place a cannula into the artery. And what that does is prevents hyperperfusion syndrome of the arm. Which has really led to some problems in the past of just direct axillary cannulation.

Edward Soltesz, MD, MPH:

Left ventricular unloading is important with ECMO. And Jerry has talked about this. Balloon pump, Impella, or direct surgical vent are our options. And we've seen improved outcomes when we do vent ECMO.

Edward Soltesz, MD, MPH:

So our paradigm shift in LV unloading really has occurred over the past few years where we've moved from inotropes and anticoagulation to balloon pump usage to sometimes apical cannulation, or even a septostomy. To now really utilizing an Impella, an ECPella circuit as a true venting strategy.

Edward Soltesz, MD, MPH:

But it's also not just vent. If we put an axillary five liter Impella, that's transition to the next device. And that's important. Many studies have characterized this on unloading with Impella as more than likely the most ideal unloading strategy. But unfortunately, ECMO, the outcomes are still poor for cardiac ECMO. If you use that as the only device.

Edward Soltesz, MD, MPH:

So when do we use it? We use it in severe biventricular failure. We use it in someone who's failing before our eyes. Someone who's crashing and burning and we don't have facilities readily available to place a ventricular specific strategy.

Edward Soltesz, MD, MPH:

Unfortunately, there certainly are pros and cons. But the lack of LV unloading and the inability to decouple the LV on the RV really make ECMO not the most ideal MCS device for saving the heart. It'll certainly save the patient, but we need to transition to the next device. And that next device usually is an axillary placed Impella. Jerry has focused on this already, but the key here is the axillary device. And now the 5.5, which we placed last week in the first US patient here at the Cleveland Clinic last week. The Impella 5.5 device allows us to fully unload the left ventricle. Allows patients to ambulate. And actually can be used well beyond a month to two months in duration. And it has the lowest homolysis rate of any device we have, especially the 5.5. But of course, it requires a trip to the operating room for at least the surgical device. And you need fluoroscopy and you need echo to place it. We do have a number of temporary right ventricular assist devices. I'll just briefly talk on these. Everything from the ProtekDuo to a surgically placed CentriMag.

Edward Soltesz, MD, MPH:

Here's the way we cannulate a temporary right heart support in the operating room. We put a graft at the pulmonary artery, put a cannula through that so it doesn't kink going through the ribs. And we cannulate either the internal jugular or the femoral vein as the inflow to the device. And we can connect it either to an oxygenator or just a pump. If you do an oxygenator, of course, it allows you to warm the blood, but also oxygenate the blood. So patients who are bleeding may benefit from that. This is a percutaneous strategy where it's a ProtekDuo proprietary catheter. Cannula that goes in, inflow is into the right atrial holes. Outflow is out the tip of the cannula in the pulmonary artery.

Edward Soltesz, MD, MPH:

And then of course the Impella RP, which is a percutaneous device. Which is a very nice device, but unfortunately doesn't allow patients to ambulate.

Edward Soltesz, MD, MPH:

I think the easiest, obviously, is if the chest is open, we place it surgically. And if the patient's chest is already closed, we're really leaning toward a ProtekDuo.

Edward Soltesz, MD, MPH:

Really, what I want to focus upon is our tailored shock strategy. Which is we cannulate patients who are crashing and burning for ECMO, understanding that we're going to protect the limb with the reperfusion sheath. We're going to provide some form of LV unloading, whether it be a balloon pump. And then we want to move them within the next 12 to 24 hours to thinking about ventricular specific support. So we bring them to the operating room, put an axillary Impella in. At that point, we can either wean the ECMO, which oftentimes we can. Because the majority of patients don't need full biventricular cardiopulmonary support. Or we wean the VA ECMO and add an Impella RP or some other form of right ventricular assist. Or occasionally, we go from VA to VV ECMO. Or on rare occasions, we continue ECMO support and with the Impella.

Edward Soltesz, MD, MPH:

In summary, I would say there's no single device for all situations and conditions or time of a patient's cardiogenic shock episode. ECMO is expensive strategy to rescue a patient. It's not ideal. I mean, inexpensive strategy to rescue a patient. But it's not ideal for recovery of the ventricle or ambulation. Impella is good to recover the left ventricle, but it doesn't help the RV. It does, however, allow us to test the right ventricle and know if we can go right to a durable L vent. ECMO Impella, our ECPella strategy is very good and has proven to be one of the better strategies we have. But the key is to continually reevaluate our MCS strategy with the goal to achieve ventricular specific support. Thank you.

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