Cardiogenic Shock: Initial Assessment and the Shock Team Call With Dr. Anu Lala

This discussion about bedside evaluation of cardiogenic shock, a state of cardiac dysfunction leading to hemodynamic instability and end-organ hypoperfusion, covers how to understand a patient’s physiology and humanity, manage their illness, and make a rapid but thorough evaluation. CardioNerds Co-Founder Dr. Daniel Ambinder, a structural fellow at Johns Hopkins Hospital, and Dr. Anu Lala, director of the AHFT Fellowship and associate professor of medicine and cardiology at Mount Sinai Hospital, lead this talk with Drs. Mark Dela Cruz and Mark Belkin, advanced heart failure and transplant cardiology fellows, University of Chicago, and Dr. Karan Desai, general cardiology fellow, University of Maryland.

Dr. Daniel Ambinder:
Hello, CardioNerds family. In this discussion we learn from Dr. Anu Lala about the nuances with identifying cardiogenic shock, classification, and initial steps in management, namely the Shock Team call.

CardioNerds is an independent, fellow founded platform with the mission to democratize cardiovascular education. The views expressed here do not necessarily reflect the opinions or policies of our employers.

And now time to get Nerdy. Looks like we have a quorum on the call. We have the CTICU, we have cardiac surgery, we have advanced heart failure and of course we have Dr. B., who is our ECMO cannulation on-call doctor for today. Let’s go ahead and get started.

Dr. Mark Dela Cruz:
Thanks. We’re a little worried about our patient whom I think is in cardiogenic shock and it looks like our newest shock algorithm at CardioNerds Medical Center tells us to contact you. We have Mr. C, a 63-year old man with a history of hypertension, diabetes, CKD Stage 3, and severe multivessel CAD, who underwent a four vessel CABG two weeks ago. He was admitted to our cardiology floor service on the ward overnight after presenting with progressive shortness of breath, lower extremity edema and found to have elevated BNP, AKI and the chest x-ray showing bilateral pulmonary edema.

On admission, troponins were mildly elevated but flat and his EKG had nonspecific T-wave changes. Overnight, he got 40 milligrams IV of Furosemide, and then 80 milligrams IV with minimal urine output. And this morning, his maps have been falling and are now in the low sixties. His extremities are now cool to the touch; remain elevated and his lactate came back elevated also at 2.5. Looking at my algorithm here, it asks me for a SCAI classification and based on what I see, I would say he is a Stage C. Any advice on our next steps?

Dr. Mark Belkin:
This sounds like a case for the CardioNerds. Friends, welcome to our CardioNerds critical care series. This is series co-chair Mark Belkin here with CardioNerds, Karan Desai, and Dan Ambinder. We’re now going to start our journey into this growing specialty of cardiology by looking at the initial approach to cardiogenic shock.

For this episode, I have the distinct honor of introducing my co-fellow Dr. Mark Dela Cruz. Mark is a current advanced heart failure fellow at the University of Chicago with myself. We actually differentiate ourselves as DLC for Dela Cruz and Belkin at work. In this podcast we may be referring to him as DLC, myself as Belkin, to keep the Mark’s straight. He obtained his Bachelor of Arts degree at the University of Pennsylvania after which he went on to obtain his medical degree at the University of California, San Francisco. He continued to internal medicine residency also at UCSF where he participated in the Clinical Research Pathway. He served as the heart failure hospitalist for a year before coming to Chicago for general cardiology fellowship at the University of Chicago and is now in his advanced heart failure fellowship. His current research focuses on heart transplant immunology, particularly on the interplay between the gut microbiome and heart transplantation outcomes. Born and raised in Manila, Philippines, Mark also maintains an interest in Filipino cardiovascular health and is an avid traveler. Mark or DLC, welcome to the show.

Dr. Mark Dela Cruz:
Thank you for this generous introduction and for inviting me to join what should be a fun discussion about taking the Shock Team call and initial management of cardiogenic shock. I am doubly excited since today I have the distinct privilege to introduce a personal idol of mine, totally fangirling, is our expert discussant, Dr. Anu Lala-Trindade. Dr. Lala is an advanced heart failure and transplant specialist at Mount Sinai Hospital in New York City. There she wears so many more hats.

She serves as the director of heart failure research and as data coordinating center leadership for the NHLBI Cardiothoracic Surgery Network. A prolific educator, Dr. Lala has won numerous teaching awards and leads the fellowship program in advanced heart failure and transplant. A physician scientist par excellence, she has authored numerous peer reviewed scientific publications and is the principal investigator for a number of clinical trials in heart failure. She serves as the deputy editor of the Journal of Cardiac Failure and also serves on local and national committees and the American Heart Association, American College of Cardiology, Heart Failure Society of America, among others, devoted to advanced heart disease. As if all those hats weren’t enough, she’s also the loving mom of two beautiful young children, a lifelong Indian classical dancer and Bhangra dancer who founded the Johns Hopkins University JOSH dance troupe, and she previously tried her hand at a standup comedy. Dr. Lala, is there anything you can’t do?

Dr. Anu Lala-Trindade:
Oh gosh, I don’t know if I deserve all that, but I feel so very lucky for…I don’t know, the life that I’ve been given, the family that I’m a part of, and for what I’m able to do for a living. Today in particular I feel lucky to be on this most coveted CardioNerds series amongst all of you. I just really want to congratulate you all and this entire enterprise on shaking things up and doing things differently and recognizing that we all receive information in different ways. I’m honored to be here and thank you for having me.

Dr. Mark Dela Cruz:
We’re just so lucky to have you and thank you for the kind words. Dr. Lala, before we even get to ask what a shock call is, we wanted to get back to the basics. How do you define cardiogenic shock?

Dr. Anu Lala-Trindade:
Such a good question Mark, it’s always so good to go back to the basics. I had the good fortune of training under Judy Hockman at NYU, whose career in clinical trials really took off with the shock trial that was published now in 1999. That evaluated emergency revascularization therapy for MIs that were complicated by shock. I bring this up here because it forms an explanation for why we consider cardiogenic shock more so in the setting of acute MI and how things have changed. I’m hoping we’ll talk a little bit about that as this episode continues.

But that trial really was patients who had ST elevation MIs or Q-wave infarction or a new left bundle branch block that were complicated by shock due to LV dysfunction. The shock was confirmed in that clinical trial, both by clinical and by hemodynamic criteria. I’m sure we’ll talk a little bit about what those different criteria are and how they’ve evolved over time. But I think it’s interesting because now with the advent of percutaneous coronary interventions, heart failure related cardiogenic shock is more and more prevalent, and this includes nonischemic ideologies of shock.

It’s important for us to keep that in mind when we’re thinking about shock, cardiogenic shock, obviously, what the parameters are that define it and what the substrate is to begin with. When we talk about what the definition of shock is at least in the clinical trial there, a systolic blood pressure of less than 90 mmHg for at least 30 minutes or the need for supportive measures to maintain a systolic blood pressure of over 90 and end organ hypoperfusion. So how is this defined? And this has been carried over the years. That is defined by cool extremities or a urine output of less than 30 milliliters per hour, and a heart rate of over 60 beats per minute.

Those are the clinical criteria. There are also hemodynamic criteria that have evolved over time, but at least originated in that trial with a cardiac index of no more than 2.2 liters per minute, per square meter of body surface area, and a pulmonary capillary wedge pressure of at least 15 mmHg. So maybe we’ll start there because that’s how I think of shock being the most well defined. This is now over 20 years ago.
Then we can talk, hopefully later on in the episodes, as to how that definition might have evolved over time.

Dr. Mark Belkin:
Wow, Dr. Lala, that was great. I really enjoyed how you spoke about the history of how we define cardiogenic shock and how it came into prominence specifically with the shock trial. You mentioned already a couple things like cool extremities and low blood pressures. Obviously, when we think about patients and we are talking to our trainees and teaching, we first think about history and physical exam often before we’ll get lab tests back or before we can get other testing back. What features of the history and physical exam are you looking for?

Dr. Anu Lala-Trindade:
Thanks so much Mark. This is easy, I get to say thanks Mark no matter what the question is. But this is my favorite part really of the assessment. I think with hemodynamics they’re so attractive and we often look to Swan numbers as opposed to patients to form our diagnoses. There’s just so much vital information as you alluded to that can be obtained simply by speaking to and examining a patient.

When I walk into a room, for example, I take note of the position the patient is in from the get-go. Are they in the chair? Or are they in the bed? Are they upright? Is the head elevated or are they lying flat? Then I just scan them head to toe while I introduce myself and try to get to know them. Where they live, who they live with, get them talking. Of course, if they’re not intubated or in extremis. I look at things like, are they on oxygen? Are the jugular veins elevated? Are they tachypneic? Are they able to get a sentence out? I tend to hold their hands and feel pulses. I get a good sense of where the patient is. Is the pulse thready? Is it strong? Is it founding? Is it fast? Is it slow? Is it regular? Is there pulsus alternans? I think you can get a lot out of that assessment, so that’s something that helps me.

Then as I spoke about earlier, I feel arms and legs. I really believe in the power of touch, in making a connection in an assessment. I know that’s a little bit tricky in COVID times, but I still stand by that. I think that’s critically important. And that’s where you get some of that, are they warm or are they cold? Then I feel the precordium. I feel for appointed maximal impulse. I feel for an LV heave that’s how I start. Is the point of maximal impulse displaced? Is it diffuse? Can I feel an RV heave? Then I auscultate. I listen. Are they tachycardic? Is there a gallop importantly, which we know is specific to low output states? I listen for murmurs, and you auscultate over each of those valves, and it can be helpful to guide what might be going on. Is there aortic stenosis? Is this obstructive shock? Is this severe mitral regurgitation in the setting of an acute MI? Or is this functional mitral regurgitation that is worse because the patient is really congested.

Then of course I auscultate at the apex, the axilla as well, to see whether it’s radiating, and you get a feel for what’s going on in the heart. I then ask the nurse how much urine they’ve been making on an hourly basis. I’m abbreviating my physical exam, of course, but I don’t want to belabor the point. I always feel the liver, see if I can feel the palpable edge. You look for ascites, things like that. But skipping over to my quick assessment of cardiogenic shock, I look then to see how much urine they’ve made as I mentioned, on an hourly basis. One thing I hope to emphasize over the next half an hour or however long you’ll tolerate me talking is looking at trends, right? Not looking just at snapshots, because that’s so critically important.

Looking at the trends of urine output over the past several hours and then of course blood pressure, I look at pulse pressure. I’m not a huge fan of only being given the MAP on rounds. Our fellows who round with me will tell you that. I think Corinne Hammo is a previous CardioNerds and she just finished rounding with me and knows that as well now. I look at that pulse pressure as just another marker of cardiac output. All these things together tell me a little bit more about a patient, hopefully while I’m engaging with them on some level to get more collateral, personal information as to their recent history. Who were they before they came into the hospital?

Dr. Karan Desai:
Dr. Lala, that was an amazing overview of the exam and the thing that most resonated with me was that you said you were making a human connection with the patient while doing a full assessment of the patient’s critical condition. One of the things you mentioned was pulsus alternans and that was amongst a whole bunch of pearls that you had given us here. Can you just delve into that a little bit on how pulsus alternans informs your evaluation of a patient that’s critically ill?

Dr. Anu Lala-Trindade:
I think this stems for when I was a heart failure fellow at the Brigham, we had a patient who came in, in shock after transplant due to not having taken her immunosuppression medicines. These kinds of scenarios, and I’m sure you guys have felt the same way when you’re at the bedside, you never forget those experiences. I remember feeling her pulse and she truly had pulsus alternans. That’s when you’re palpating the pulse, this is an alternation of one strong and then a weak beat without a change in the cadence or the cycle length and that can be a marker of low output as a marker of increased resistance to ejection from the LV. I always think that’s interesting to look for.
Of course, this is distinct from what you might feel if a patient was an atrial fibrillation where you might feel different intensities of the pulse palpation. But this is really…you’ve got the same beats, like I said, the same cadence but you’re actually experiencing a strong and a weak pulse alternating.

Dr. Karan Desai:
Thanks Dr. Lala for that assessment and that description of the exam. And as you mentioned, this is the critical aspect of our initial evaluation. The definition of cardiogenic shock that you provided us is quite broad. Systolic blood pressure less than 90, potentially using vasoactive to maintain a systolic blood pressure over 90, and evidence of end-organ hypoperfusion, and the exam will really narrow in what’s going on pathophysiologically for the patient. At the same time, we want to make sure that we have the right inputs, the right data to inform our next steps. So, what labs and imaging tests are most helpful in evaluating cardiogenic shock for you?

Dr. Anu Lala-Trindade:
Yeah, thanks Karan. It’s so important because I don’t mean to say that the physical exam is all you need of course, you do need other information. I think in terms of labs, markers of end-organ perfusion, as you mentioned, are very helpful to me and that also includes a lactate. So, looking at the renal function, looking at the liver function as perhaps it could be either hypoperfusion or congestion for that matter, but recently the lactate has indeed been shown to have prognostic significance in this setting.

Though, the tricky thing is that we’ve yet to really establish what the optimal thresholds are in this setting. But for me again, the trends are most important. I really try never to look at one number in isolation. Where has the lactate been trending, for example? If you have an isolated lactate level of six, an hour ago was it eight? And then it’s different from whether it was two an hour ago. Similarly, with the creatinine and the liver function tests, and of course, other things like white count, hemoglobin, all these things come into play that you need to look at in an integrated way. I think that’s the critically important part of cardiogenic shock assessment is integration of information rather than hanging on one piece of data at a time.

Then of course, imaging chest x-ray in terms of pulmonary effusions or infiltrates, edema, heart size. An echocardiogram if available for you in that acute setting. You’re not looking to do a completely elaborate echocardiographic test, but really what is the assessment of left and right morphology and function? Is there an intracardiac thrombus? Are there regurgitant or stenotic valvular lesions? Is there an outflow tract obstruction that’s maybe dynamic? And then there’s a lot of interest in getting…or estimates of filling pressures, and it might just be my naivete or ignorance, but I’m not particularly convinced of that method for now, but I always have hope. I’m always humbled every single day. That’s just my approach here is that I don’t look at estimates of filling pressures by echocardiogram.
But important on the echo is what does the RV look like? Is there significant RV dysfunction? Because we all know, you all know this, that RV dysfunction is really a marker of illness severity, and we know that it also contributes to poor or worse clinical outcomes.

It can limit total cardiac output. It also can promote systemic venous congestion and of course, end-organ function as well as it pertains to the kidney and the liver. I think that’s really important, and it also plays into if that patient’s going to escalate or deteriorate, rather, further and then potentially need short term or durable mechanical circulatory support. That RV assessment is going to be critical. Then of course, there’s the PA catheter and hemodynamic assessment and monitoring, which I’m sure we’ll talk about.

Dr. Daniel Ambinder:
Thank you so much for that Dr. Lala, that was incredibly comprehensive. We’re all just going gaga over your emphasis on the RV. Dr. Lala, I also love how you emphasize looking at trends and not just relying on snapshots and time which is something that applies to all of cardiology whether we’re tracking somebody in the hours of a hospitalization to decades of their lives, they go through different phases of their cardiac care.

I definitely think that this is something that may dovetail with what you tell us next. But a common issue that we run across is a missed diagnosis of cardiogenic shock in patients with either undifferentiated shock or non-overt signs of shock, or maybe early cardiogenic shock. We learned with Dr. Mark Drazner in episode 142, little plug there, that if they’re cold, they’re cold and if they’re warm, they still might actually be cold and still…
This can be seen in acute to compensated heart failure patients in which their poor perfusion status is not noted or in undifferentiated shock patients where the cardiac etiology is not quickly identified. Dr. Lala, what tips and tricks do you have for us to not miss this important diagnosis, because early cardiogenic shock is not something any CardioNerd wants to miss.

Dr. Anu Lala-Trindade:
Yeah, thanks Dan. Gosh, it’s so funny how so much of your style stems from your personal experiences at the bedside. When you ask a question like that, I think about what I teach fellows and what I remind myself of when I round, is I think cardiogenic shock is particularly scary in younger people, because they are so good at masking things. They have so much reserve, oftentimes, maybe they don’t if they’ve got a history of heart failure, but they may just not look as sick as they are.

This woman that I was alluding to in the beginning, who came in acute rejection cardiogenic shock after transplant, she was a young woman, and her exam was actually very subtle. She had a “normal blood pressure” by conventional means because her systolic blood pressure was in the 120s, but her diastolic pressure was up in the hundreds, and so that’s just one thing that you want to keep note of is what is that pulse pressure? Don’t look at just MAPs because it becomes easy to be fooled by that. I think that’s helpful.

I think oftentimes like you said, a patient may not necessarily be cool to touch. There could be two processes going on. I guess before I answer even that question, we’re so indebted to Dr. Drazner and his mentor and my mentor, Dr. Lynn Stevenson for helping us to profile these patients, right? Based on congestion and perfusion. And Dr. Hockman, to your point, would also always remind us of the inflammatory cascade that’s encountered in all kinds of shock which can lead to basically cytokine mediated systemic vasodilation. This in fact, if you would recall, I’m sure you guys were exposed to this as well, it was something that we encountered not infrequently in cases of cardiogenic shock amidst the COVID pandemic. Where in patients could be under perfused, but warm on exam by virtue of widespread systemic inflammation.

I think this scenario points out, again, the importance of integration of information. And forgive me if I’m like a broken record but not taking any one data point in isolation, no matter what it is, whether it’s cold extremities or an elevated lactate, or a low-mixed venous on the PA catheter which so often is just considered the gold standard. Every piece of information has to be integrated into one clinical picture.

This goes back to the aspects of the physical exam that we spoke about. What is end-organ function looking like? Not just by lab markers but by actual urine output? What is their mental status? Do they seem like they’re a little bit more lethargic? Can you get an idea of what their baseline is? Then of course, we already talked a little bit about the echo and the imaging findings, et cetera. But I think if you have a high index of suspicion, it won’t mislead you, if that makes sense. I think not being quick to make an assessment is also important. Taking your time, putting pieces together and then making an assessment. And you may be wrong.

Gosh, I’ve been wrong a lot, but we get better with time. We start to recognize patterns and then it comes quicker to us, it comes more easily. I don’t know if there’s any one piece of information that I could say, “Hey, this is someone who has mixed shock, or this is someone who has early shock or undifferentiated shock.” But rather I would just make that point again of integrating all these pieces of data. I hope that makes sense.

Dr. Mark Dela Cruz:
No, I think that totally does. Taking a lot of these pieces back but integrating in the way that I’m thinking about the patient that we presented at the very beginning of this episode. We have a 63-year-old man with severe multivessel CAD recent CABG, so recent basically ischemic cardiomyopathy, presenting with signs and symptoms of significant congestion.

Now I’m thinking about it along the lines of all the signs and symptoms of acute decompensated heart failure that you mentioned, so I think something that I also try to do in my practice is to think of the human dynamic profile on the two axes as famous and defined by Dr. Lynn Stevenson, as you mentioned.

With the two axes being volume status and perfusion status. For volume status, and I think our patient is clearly wet. Now, what’s our perfusion status, right? Warm or cold? I think in this particular case he has evidence of poor end-organ perfusion with cool extremities. That narrow pulse pressure that we mentioned. Elevated lactate. And acute kidney injury. I think putting it all together, it’s all concerning for that low slow state.

Dr. Daniel Ambinder:
Love that explanation, Mark. Our patient is likely in the cold and wet profile and if I was taking this call, I would certainly be concerned that the patient is in cardiogenic shock. Next, let’s consider the severity. In 2019, the Society for Cardiovascular Angiography and Interventions, a.k.a. SCAI, released a consensus statement on the classification of cardiogenic shock. This is the latest classification following UNOS and INTERMACS.

Dr. Lala, how do you classify cardiogenic shock when evaluating a patient? Would you briefly describe the different classifications and give us your approach to using this to actually move the patient’s care forward?

Dr. Anu Lala-Trindade:
Thanks so much for asking. I think these tools provide a framework in our brain, right? Cardiogenic shock is such an acute adrenaline filled circumstance for us as clinicians, and so it’s important when we have these classifications and these schemes and these definitions for us to keep our thoughts somewhat organized amidst the chaos that’s happening when you have a really sick patient in front of you. I do think that these classification schemes are helpful.

There are many of them as you already alluded to, so when you’re thinking about acute MI shock, that’s different from heart failure cardiogenic shock, which is what it sounds like this patient has. Maybe he has a history of coronary disease, a recent CABG, a low ejection fraction, a backdrop of an ischemic cardiomyopathy as you mentioned who is now low output and progressing into cardiogenic shock. They’re a little different and we’ll talk a little bit about that, but I think AHA/ACC defines this by stage C/D heart failure. And then our NYHA class will say, okay this is a 3-B to an ambulatory class 4 patient to an advanced class 4 patient. And then they’re the INTERMACS profiles that are trying to capture those more advanced New York Heart Association class patients. And those go from one to seven. I’m sure you guys have covered these so forgive me if I’m belaboring the point, but INTERMACS one profile is developed with the intent of understanding who would benefit from mechanical circulatory support.

So, one, is the crash and burn. They’re in front of you. They need MCS. You’re petrified. You’re calling your attendings, et cetera. Two are those patients … Again, this is coined by Dr. Stevenson and others, two are those folks who are sliding fast. They’re on two inotropes and they’re still not perfusing. They’re fattening is still getting worse. They still have low level lactates, et cetera. Three are those patients who are now stabilized but they’re on inotropes. INTERMACS profile four are those patients who have symptoms at rest. I think of them as they’re like ambulatory NYHA class four patients. And those lines are not by any means really set in stone they’re more in the sand if you will, but then there’s INTERMACS profile five that is exertion intolerant, or sometimes we’ll call it the walking wounded. INTERMACS six and seven are the less sick. You think of them as you’re like NYHA class 3-B folks, so exertion-limited is six and really advanced class 3 patients are seven.

We typically think of one, two and three as being a little bit clearer because they’re requiring vasoactive substances or mechanical circulatory support for stabilization. Whereas four almost sits on its own for me and then you’ve got five, six and seven, which are like the less sick. In terms of the SCAI shock stages I think it’s really nice because they proposed a five-stage classification system, specifically targeted at the classification of cardiogenic shock.

We’ve talked a little bit about all these other classification schemes, but this one is really for cardiogenic shock. E is those patients who are an extremis, and I think of them as overlapping with INTERMACS profile one. There’s a nice state-of-the-art article in Journal of Cardiac Failure, senior authored by Navin Kapur and first authored by a number of wonderful junior folks and fellows like yourself that shows a really nice overlap of all of these classification schemes.

Coming back to the SCAI shock stages, you’ve got E which is extremis which I think of this overlapping with INTERMACS profile one. Then you’ve got D which is deteriorating. To me that’s very much like the INTERMACS profile two. They’re deteriorating, they’re sliding fast despite support with vasoactive substances. Stage C is classic cardiogenic shock. That to me is like in between INTERMACS profile two and three if you will. And then interestingly, stage B is like the beginning of cardiogenic shock which I think you guys nicely tried to touch on in the previous question, and that can be a little bit tricky. Then moving back even further, A are those patients who are at risk for cardiogenic shock.
I think it’s nice when we think about these things in a more systematic fashion, and you can see how there’s so much overlap between these different classification schemes. For me it helps me think about which therapies I’m going to grab for or think about next. Who do I need to engage with next? Is it a CT surgeon? Is it one of my interventional colleagues, etc.?

Dr. Mark Belkin:
Dr. Lala, you really brought those classifications to light. Sounds like all these classifications have their value, but the SCAI criteria is perfect for organizing our cardiogenic shock admissions. Just typically backtrack though, you had alluded at the start of the episode to a recent article in the Journal of Cardiac Failure, a state-of-the-art review addressing heart failure related cardiogenic shock in comparison to acute myocardial infarction related cardiogenic shock. How do you incorporate these ideological classifications into your evaluation and how do they add to the illness severity classifications we just discussed?

Dr. Anu Lala-Trindade:
Yeah, thanks so much Mark. I’m biased, obviously, you know I love this journal and I love this issue and this state-of-the-art article in particular because, importantly, it highlights the difference between acute MI shock and worsening heart failure cardiogenic shock as we’ve already talked about.

The clinical trajectory of acute MI shock is different from heart failure shock. Acute MI shock is characterized by an abrupt presentation. You have this abrupt event that leads to cardiogenic shock in otherwise previously potentially stable and maybe ambulatory patients. Whereas patients with chronic heart failure may have multiple decompensations that can then slowly progress to a pre-cardiogenic shock state or a frank overt cardiogenic shock state, where you need to do something promptly in order to get them back to an ambulatory state.

When you think of an acute MI cardiogenic shock, you think, “Okay I need to get this patient back to native heart recovery.” Whereas in heart failure cardiogenic shock, you may be thinking, “Okay, is this patient now a candidate for advanced therapies?” Am I thinking about a left ventricular assist device? Or am I going to think about it for the patients with the history of heart failure, particularly with reduced ejection fraction, am I moving to heart transplantation? Is this patient a candidate for heart transplantation?

I think that’s the key distinction for me that’s brought out in this state-of-the-art paper that I hope people will take away from it. For me, it’s also challenging with the SCAI classification thinking about stage A. Who is at risk for cardiogenic shock? It’s someone who really fits into that acute MI category, where they don’t have symptoms maybe going in, but because they’ve had an acute particularly, anterior MI, they’re at risk for cardiogenic shock.

Then for those patients with chronic heart failure symptoms, severe cardiomyopathies, those patients are also at risk for cardiogenic shock. One thing I’d love to share with you guys that anyone who’s rounded with me at Sinai will tell you is I always like to ask myself the question, given the scenario you guys described in this patient, someone with multiple comorbid conditions, an ischemic cardiomyopathy, who’s coming in with a worsening heart failure episode, just at the outset before you tell me that he’s not responding to diuretics and it seems like he’s cool. The question I ask myself is, “Would I be surprised if this patient developed cardiogenic shock tonight?” If the answer is no, then I need to think of what my backup plan is. What am I thinking about this patient? So, he is 63. Is he a transplant candidate? How bad is that CKD? Is he going to be able to get just a heart alone? Is this patient a LVEDP candidate?

Would that be in line with what this patient would want? And obviously you can’t do this for every patient all the time, but you could start thinking that way. I think if we get into the habit as clinicians of, “Would I be surprised if something terrible happened to this patient tonight?” I think it just increases your level of alertness. It makes you make sure that you’re crossing your Ts and dotting your Is. That’s a question I love to ask myself that I hope others will find helpful too, because it just allows for a sense of preparedness.

Dr. Daniel Ambinder:
Thanks Dr. Lala. Unfortunately, this patient that was initially described by the ELC was having limited urine output and really the initial attempts at intravenous diuretics didn’t work. As we learned in episodes 153 and 154 on diuresis … So please listen to these episodes. They’re featuring doctors Nick Smith, Angela Wagley, Nisha Galotra, Matthew Sparks, Michael Falker and Kelly Arps. It was really well done. What they went through there was, there were multiple reasons why patients may not respond to IV diuretics including renal venous congestion, or renal hypoperfusion.

Dr. Lala, I think the team was asking themselves that question that you just mentioned, “Would I be surprised that this patient went into cardiogenic shock?” And they were not. But that next question about what to do next I think the team needed some help with. What they did is they reached out to the shock team. Now there is a ton of buzz about shock teams. Can you explain to all our listeners, all the CardioNerds out there what they are, why we use them, and if right now is the appropriate time for the team to be calling the institution’s shock team?

Dr. Anu Lala-Trindade:
Yeah, Dan that’s such a good question, thanks for asking, because you’re getting at the “Now what?” Which is what we all want to know. I think cardiogenic shock is truly a clinical scenario that really requires multidisciplinary input. That’s between heart failure, it’s between interventional cardiology, cardiothoracic surgery, electrophysiology, honestly, sometimes when indicated. Also, the cardiac intensivists and or even cardiac anesthesia depending on the clinical scenario. But once activated … and each institution has their own take on this. A nice thought-provoking paper that’s in circulation I think in 2019 senior authored by Stavros Dracos who’s just another wonderful guy that you guys should definitely talk to on CardioNerds if you haven’t already. He just shared the experience at Utah where there was an advanced heart failure doc, an interventionalist, and a CT surgeon who all came together for any decision around patient management in anyone there was a suspicion for cardiogenic shock.

Essentially there is an activation. That can happen by any centralized process. At Sinai, we have an administrative support call center whereby any cardiogenic shock patient even at referring hospitals, calls the call center, then activates the shock team. That involves getting one of us on the heart failure team, one of the CT surgeons, and one of the interventionalists all on the call at the same time with the referring physician to talk about the clinical scenario. It affords a measured discussion. And everyone has their own vantage points. When you have different people providing their own expert opinion and input, then I think you’re able to come away from the scenario with at least an initial plan that is an integrated plan. Many people have proposed that the heart failure cardiologist is like the initial screen, but I think it could be either one of those people quite frankly.

The important thing is that we’ve got experts from different fields within cardiology and CT surgery coming together for the purposes of A, confirming is this cardiogenic shock, what’s the backdrop, and then what’s our plan moving forward. That could be a discussion of survival benefits. Is there benefit to doing short-term durable, mechanical circulatory support? Is this patient a transplant candidate as we talked about? I think it addresses the concern of delaying care. I think oftentimes the concern with having a multidisciplinary approach and a shock team, if I wait to coordinate the care amongst cardiology and CT surgery and heart failure, I’m going to lose time and time is myocardium and end-organ perfusion.

But I think multiple studies and multiple institution’s experiences have shown us that multidisciplinary approach in fact doesn’t delay implementation of critical decisions, it actually ensures an appropriate level of support and importantly it allows for a planning of care escalation. A number of centers have shown, actually, the improved outcomes associated with shock teams at respective institutions and Sinai is one of them. I’m sure you guys have shock teams at each one of your institutions as well, but I’m a huge proponent of this effort to get people of different expert opinions together at the same time. It also allows us to keep in mind what tools are in our armamentarium, so that’s the essence of the shock team.

Dr. Mark Dela Cruz:
I think it’s just so great hearing about the shock team, that it’s so great to see that communication really does improve outcomes and that in this particular case we finally have another intervention that does decrease mortality and cardiogenic shock. Of course, multidisciplinary teams like this work best when they’re used properly. As an expert frequently on the line from these calls Dr. Lala, what are the pertinent details that you’d recommend we make sure we include if we’re in the preparing end of the call or listen for on the receiving end?

Dr. Anu Lala-Trindade:
Thanks so much Mark. We’ve covered a lot of it from the biologic perspective, but what we haven’t really covered is getting to know the patient to whatever extent possible prior to their presentation, prior to that cardiogenic shock phone call. Who are they outside of the hospital? Who do they live with? What do they do for a living? Did they see doctors? Are they on medicines regularly? What is their support system? Do we know anything about their wishes in terms of goals of care, etc.?

I think in addition to all the key points that we’ve already talked about, I think this is a really crucial piece of information to get, because we can ultimately reach out for whatever device it might be, whether it’s an Impella or a balloon pump or … or a total artificial heart even at one extreme. But we’re not going to be serving the patient if we don’t recognize who they are as much as we possibly can. Recognizing obviously that some of these patients are in extremis and we don’t have the time to obtain that information. But to whatever extent that we can, I would just want to remind our listeners and myself, we can all use a reminder is, recognizing that these patients are people prior to coming in with shock. Integrating our approach with who they are as individuals I think is really key.

Dr. Mark Dela Cruz:
Thank you so much for that. I think that’s just so beautifully stated. I think in the throes of these stressful situations, particularly as either trainees, or young physicians, making and preparing these calls, calling a huge group of individuals, and other providers, it’s so easy to get so caught up in the minutiae of these fine details and forgetting who the patient is. At the end of the day, we’re here to serve people and make people feel better so that they can get home to their families and live healthy, productive lives. I think bringing that back to who the person is I think is such a beautiful sentiment and I think yeah, we should be saying it more of these shock calls.

Dr. Anu Lala-Trindade:
Yeah, what are we seeking to allow for? Of course, improved survival, but also a return to independence and a return to hopefully restored or even improved quality of life.

Dr. Mark Belkin:
Wow. Yes, totally agree. That was beautiful. Bring it back to our case, what would you say to the caller on the other end of the shock team line?

Dr. Anu Lala-Trindade:
Yeah, thanks Mark. Sounds like you guys have nicely described that this patient is indeed under perfused on the backdrop of having a preexisting cardiomyopathy attributed to ischemic causes. Without going into too much nitty gritty here, the recent CABG, did one of the vein grafts go down? Is this something that we should potentially see as what tipped him over in this scenario? Is there an acute on chronic ischemic event that tipped him over? But in addition to that, I still want to think about the short term and then the mid to longer term and this is all within the context of the hospitalization.

In the short term, how can we best support this patient? I think it again depends on trying to better understand what’s going on. The troponins were flat, so it’s unlikely to have been an acute ischemic event with maybe like the LIMA going down or something like that. It sounds at least this is more a chronic myocardial injury attributed to chronic heart failure. Initial stabilization, whether that is inotropic support or based on then taking a little bit further what we think the end game is for this patient. This is a patient with however many years long standing or maybe not so long-standing ischemic cardiomyopathy.

It would make me wonder as to whether we should be thinking about advanced therapies in someone like this. Because importantly, and this is another thing I always talk about on rounds, is when you are starting inotropes on a patient, we know inotropes are associated with worse mortality, worse outcomes. We have trials of chronic heart failure patients being tried on inotropic therapy to actually improve outcomes and it showed indeed the opposite.

Whenever I start an inotrope on a patient, I think about what my end game is. Am I doing this for palliation? Am I doing this because they’re truly diuretic resistant and that’s a data free zone, which I’m sure you guys have already covered? Or am I doing this now because I’m considering advanced therapies? I think that’s an important point to keep in mind. Really what’s this trajectory is what I’d love to know about this patient. But it sounds like it may be reasonable because this patient is not responding to diuretic therapy, although I could argue, depending on their home dose you might be able to escalate it even further, it would be reasonable to get more information.

Whether that’s through a hemodynamic evaluation, a class 2A, to get a right heart cath in this scenario. I also think that right heart caths or PA catheterizations are underutilized in this scenario. This is a patient who you could say is going into shock if you will, maybe like a SCAI B or even an INTERMACS four. I think a PA catheter with an assessment of hemodynamics would be helpful.
Going back to how we started out, the shock trial, again, albeit in the acute MI setting. So, different scenario. Everybody had chemodynamics monitoring. So, I think it’s really important, and there’s some recent data also alluding to the fact that those patients who are managed with PA catheters in this scenario, in the shock scenario, may have better outcomes.

Dr. Karan Desai:
Thanks, Dr. Lala. That leads me into my next question, which is, we’ve basically taken this entire call so far without any invasive hemodynamics. This patient is headed up to the CCU, aka the Shulman unit, and the general fellow is already setting up the Swan-Ganz catheter. And she’s going to ask us what information we’d like.

Dr. Lala, I have two broad questions for you. A lot of shock team algorithms require invasive hemodynamics when making the call. Do you believe it’s necessary to have those invasive hemodynamics before making the shock call? And broadly, because we’ll be covering this in a future episode, how is that invasive hemodynamic information going to guide your next steps?

Dr. Anu Lala-Trindade:
Yeah, thanks. I think that’s a really important question. Do I think that you need the hemodynamic assessment prior to the shock call? In broad strokes, I would say no, because I think oftentimes, you’re getting referrals or calls from people who may not have access to doing a PA catheter or experience doing it. I would say if there’s a clinical suspicion for shock that clinicians in general should feel like they have access to an expert team to help them in the evaluation of that diagnosis. I guess that’s the first part of your question.

The second part of the question, which I alluded to in the answer to the last question is, yes, I want that hemodynamic assessment. If I’m thinking shock, I would like a PA catheter in place which you’ve already hopefully done in this CardioNerds CCU. And how does that information guide next steps? When I think about what is it that I’m gaining from that PA catheter assessment, well, I already have an assessment of their arterial pressure. So, I have that. But now what I’m looking for is filling pressures and then perfusion by way of either thermodilution … perfusion meaning our cardiac output. And I focus on cardiac index because I like it to be relative to the body surface area. An output of five in an 80-pound, four-foot female compared to an output of five in a six foot, 200 pound man is obviously completely different, so I would say first focus on that cardiac index.

Then in terms of filling pressures. So, you want your CVP, you want your wedge pressure, because you importantly want to think about them in relationship to each other and I’ll come back to that. You want your PA pressures, and again your systolic and your diastolic pressure, just the way I was sharing with you that the systolic and the diastolic systolic pressures are important to me as a marker of perfusion or cardiac index.
Similarly, having that PA systolic and that PA diastolic pressure is important for me to understand how the RV’s doing. What’s the RV able to handle? We all are familiar with Navin Kapur’s coined term the PAPI, or the PA pulsatility index, which is the PA systolic minus the PA diastolic pressure over the RA pressure or the CVP as another marker of RV function which I’ll get to. Then of course the cardiac index, whether that’s assessed by thermodilution or by … and I’m sure you guys are going to have more information coming on this soon, so I don’t want to steal anyone’s thunder.

But broadly speaking, what do I get from this information? I get, are they congested? Do they need diuresis? And I get, are they underperfused? It’s a confirmation of the integration of all the different things that we’ve already talked about, the physical exam, the lab, the imaging, et cetera. But importantly, as we already talked about, don’t forget that RV. I am able to categorize it as is this LV dominant shock? Is this RV dominant shock? Or a lot of times what we see in our chronic heart failure patients, is this bi-ventricular shock? This is important because it informs what therapies are at our disposal next that will actually serve our patient.

Then just really quick, coming back to that CVP to wedge ratio, the typical relationship is a CVP of five to a wedge of 10. I like using nickels and dimes, so you’ve got an intact relationship when you’ve got 0.5 and then we see that there’s RV dysfunction when you see that ratio going towards 0.6 and then overt RV failure even, at ratios that have been established at 0.86 or higher. For me, to come back, long-winded answer unfortunately to your question, but I am looking at your filling pressures, your CVP and wedge ratio, your PA pulsatility index and that’s an integration of course of the PA systolic and diastolic difference, and then your cardiac index. Then lastly, I’ll just mention that of course you want a formal assessment of your systemic vascular resistance as well, which can be mixed depending on the clinical scenario. But normal systemic vascular resistance as we know is 800 to 1200 dynes. And if we see that it’s elevated, particularly above 1600, it can be someone who’s really clamped down and may go along with that person who’s also cold.

Dr. Karan Desai:
Thanks, Dr. Lala. That was a perfect prelude into our deep dive of invasive hemodynamics. Coming up soon on an episode with Dr. Nosheen Reza and Brian McCauley of the University of Pennsylvania. So CardioNerds, make sure you please listen to that episode.

Dr. Mark Dela Cruz:
Great. Also, now that we can relax, after that shock team call, Dr. Lala, one last question from an even bigger fangirl now that we’ve spoken. And of course, a CardioNerd’s favorite. What makes your heart flutter about cardiac critical care?

Dr. Anu Lala-Trindade:
I think this is the one clinical scenario that serves as a true test of your nerves and your ability to integrate the knowledge that you’ve acquired with a really careful bedside assessment. I love that all coming together at one point. I love coming together across disciplines at the bedside in an effort to make the best possible decisions for our patients.
This is a little bit maybe off what we’re hoping to cover but from a spiritual sense, I think when you’re seeing patients at this brink of really life and death, when we think about cardiogenic shock, the grim reality is that the mortality has not changed that much. It stays at a staggering 40% to 50%. We’re of course trying our best to do more and think about it differently and recognize how cardiogenic shock has evolved over time, but from a spiritual standpoint, you’re faced with a family and a patient at that brink of life and death and I think if we can all remind ourselves of the fact that we are human and we are treating other humans in this incredibly vulnerable adrenaline-driven state, both for the patient and by virtue of what we have to do for the clinicians, I think it brings about a lot of humility and respect for what we are able to do. I think for all of those reasons, this is a clinical scenario that I deeply enjoy but also respect and am humbled by.

Dr. Mark Belkin:
Wow, what a beautiful sentiment and what a perfect way to end this conversation. Dr. Lala, thank you for taking the time to discuss the initial management of cardiogenic shock with us. We hope this helps our listeners identification and early management of cardiogenic shock and helps optimize those shock team calls. It is so important that we first laid this foundation with you on appropriate and rapt identification of cardiogenic shock. Thank you so much Dr. Lala for the fantastic teaching. I know the DLC, and I cannot wait to incorporate these pearls tomorrow in rounds.

Dr. Anu Lala-Trindade:

I’m so grateful to all of you and I’m grateful to our listeners as well who are committed to this lifelong pursuit of knowledge. An honor to be with you all.

*This podcast transcript has been edited for clarity and brevity.