Name: Shashank Sinha, M.D. | Evaluation and Management of Cardiogenic Shock in 2025
Uploaded: 2026-01-07T14:26:51.000Z
Duration: 49 min 39 s
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Well, thank you for that very kind introduction and thanks very much for hosting me.

It's truly been my honor and privilege to connect with friends and colleagues and meet new ones during my brief time here.

What I hope that we can do over the next 45 minutes is really engage in a conversation, a conversation about a life threatening condition you all are intimately familiar with and treat and manage every day.

But I want us to understand what are the challenges improving outcomes in this condition?

How do we examine a standardized, team based approach to systems of care in improving outcomes in this condition?

And then what are the opportunities that are emerging for care delivery and shock based on etiology?

Importantly, as this is, you know, a clinical institution, first and foremost I want to begin with a case presentation that hopefully will resonate.

A 37 year old woman with morbid obesity, BMI of 58, that's not a typo.

With stage non ischemic cardiomyopathy, long standing persistent atrial fibrillation presents to a referring facility with sudden onset exertional dyspnea, orthopnea and paroxysmo.

She's had multiple ER visits and hospitalizations for acute heart failure in the last year and has had difficulty affording her medications.

She's seen by the ER clinician and found to be cold and wet.

She started on IV norepinephrine and subsequently transferred for further evaluation management.

For the fellows in the audience, this is the EKG on presentation.

On arrival to the cvicu, she's confused, restless, tachypneic, tachycardic, hypotensive and has poor urine output.

Her initial labs show a serum crowning of 1.9.

Lactic acid is 3 and has elevated transaminases.

Her norepi is increased to 20 and epinephrine is now initiated.

And so she's taken for a right heart Catholic with the following findings.

The PA pressure is 62 over 48 with a mean of 52.

The pulmonary capillary wedge pressure is 45.

The PA saturation is 24%, the fick index is 1.0.

The PVR is 3.3 wood units and the PAPI is 0.35.

So the decision is made to escalate to VA ECMO, something I know you guys intimately are familiar with here.

And during induction she develops a PA arrest requiring five minutes of CPR prior to cannulation.

She's noted to have minimal pulsatility of her LV a severely dilated left ventricle of 9 cm and a dilated and moderately dysfunctional right ventricle and an impella.

Her immediate post operative course is complicated by 100 episodes of VT and VF, no exaggeration, requiring initiation of antiarrhythmic therapies and complete collapse of her left hemithorax requiring multiple bronchoscopies.

Oliguric renal failure requiring consideration of crrt.

So the question that I ask all of you, and

I'd love to see a show of hands, I realize we won't be able to capture the online audience here, but

how many of you would vote for a consult advanced heart failure team for evaluation of transplant?

B consult advanced heart failure for durable left ventricular assist device with the temporary right ventricular assist device up front C continue biventricular support on VA ECMO with bridge to myocardial recovery Or D should we consult palliative care and go straight to hospice, in which case this will be a very short talk.

So we're going to come back to this case at the end, but

I'd like you to marinate a little bit on those on that case in particular.

So I had the pleasure to chair and lead the very first concise clinical guidance issued by Jack published in March of this year.

An expert concise statement on consensus statement on the evaluation and management of shock.

I really want to thank my planning committee which included my own mentors, Dr.

Naveen Kapoor and David Morrow, as well as Rachna Kartaria and Rob Roswell as well as Dr.

Hadley Wilson's support during his presidential tenure.

Now importantly, I want to distinguish where the CCGs fall within the scope of clinical practice.

You guys are quite familiar with clinical practice guidelines which really provide the most rigorous evidence based recommendations and then expert consensus decision pathways have now recently emerged on how to apply those clinical practice guidelines in your day to day practice.

But the concise clinical guidance are now new areas where there's clear, clearly gaps in our fundamental knowledge.

But clearly, you know, there are opportunities even though evidence is emerging for us to provide some expert opinion and so as to not bury the lead.

I'm going to tell you my key takeaways first and then we're going to dive into each of these in further detail.

So number one, cardiogenic shock is a heterogeneous multifactorial syndrome in which cardiac disorder results in inadequate cardiac output culminating in clinical or biochemical evidence of end organ hyperperfusion.

We know that our classic definition of a primary cardiac insult leads to progressive cycles of ischemia and inflammation, ultimately culminating in multi organ dysfunction and leading to death.

And unfortunately, despite multiple decades of research, shock remains very deadly with a mean six month mortality of greater than 50 to 60% across a number of randomized clinical trials.

Now, importantly, we've really learned in the last five years that not all shock is created equal.

And in fact, non ami shock has now emerged as a very important entity.

And this has been shown in the nationwide inpatient sample shown here in the red on this graph that has risen exponentially.

And you can see the geographic variation, particularly here in the south, in hospital mortality as it's varied from 2004 to 2018.

Now, shock is a very common cause of admission and mortality in contemporary cicus.

This is data from the Critical Care Cardiology Trials Network.

And so a consortium was convened of a number of clinicians, investigators and regulators a few years ago to look at unresolved issues in shock.

And importantly, we're going to turn our attention to systems of care and the role of the specialized shock team.

How should we actually define and classify shock?

Well, the original shock trial published by Judy Hockman and colleagues in 1999 looked at definitions of hypotension or hypoperfusion noted at that time to be cool extremities, oliguria and tachycardia.

But that has now evolved from the Society of Cardiovascular Angiography and Intervention, which is now used to really classify the severity of shock that facilitate more effective communication and risk stratification.

I think it's very easy to identify those who are at risk or those who are in extremists and require VA ecmo.

But B, C and D, there remains a lot of confounding.

And B in particular has been a subject of a lot of scrutiny.

And as it's defined by scai, it's really a patient who has evidence of hemodynamic instability without hypoperfusion.

We're going to come back to that concept in a little bit in the concise clinical guidance.

The modification we actually made was that B should actually represent both evidence of hemodynamic instability or isolated hypoperfusion.

This would classically be described as SKY C in the previous classification.

And I'll explain a little bit of the rationale for that when we look at sort of sky shock validation, both by Jake Genser and colleagues at the Mayo Clinic, Benedikt Schraga in Germany and David Baron at Senterra, which was done prospectively.

You can see the stepwise associated increase in mortality which provided some contemporary evidence and support.

And then more recently the Shock Academic Research Consortium has provided a classification for shock stratifying into STEMI vs.

Acute on chronic secondary etiologies and post cardiotomy shock, which really won't be the focus of at least today's exam and discussion.

But additionally important modifiers looking at ventricular involvement and key specific etiologies are important.

And I will highlight this entity of mix shock which we increasingly see more common and is very deleterious and associated with worse outcomes.

Number three is that early recognition is absolutely critical.

All of you have seen this two by two, either Diamond, Forester or Stevenson classification that really helps us with invasive hemodynamics identify the patients who are cold and wet, but

a number of other etiologies which can only really be elucidated through invasive hemodynamic monitoring.

Congestion is common in both AMI and heart failure shock as shown by the shock working group several years ago with bi week congestion being the most common, followed soon by right sided congestion.

And importantly, elevated right sided filling pressures or elevated pulmonary capillary wedge pressures are associated with the need for cardiac replacement therapies or with death.

Now, just like we said, not all shock is created equal, not all heart failure shock is created equal.

And when we looked at this in the Critical Care Cardiology Trials Network de novo, namely conditions like acute myocarditis actually seem to emulate AMI shock both in terms of their outcomes as well as their resource utilization.

This was independently sort of investigated and corroborated in the shock working group.

And note that native heart survival is a more common outcome seen in these patients.

this is perhaps one of the key slides, is that a new paradigm has really emerged, right?

The classic teaching we all learned in med school that AMI shock associated with an acute ischemic insult leading to hypotension followed by hyperperfusion and congestion is a later finding is reversed 180 degrees with acute or chronic heart failure shock presenting with congestion.

Then hypoperfusion with hypotension is a much later finding, which is an important concept that we need to convey to all of the clinicians, which is what leads to this point, which is that you need a very low index of suspicion for heart failure shock.

The majority of that is actually captured at least in its earliest stages on the wards where sometimes there can be ascertainment or misclassification bias or in step down units or in the ER before they necessarily make it to an icu, whether that's heart failure or cardiac ICU focused.

And then this issue of time being tissue is absolutely essential.

The first 24 hours really does dictate outcomes.

And as you can see from the Sankey diagram, SKY B patients or Sky C patients will deteriorate to skyd at similar levels.

And then after that these horizontal bars really indicate that SKY isn't really providing much discriminatory capacity or risk stratification for these patients.

We've now developed an app that allows clinicians in real time to be able to track this information and be able to communicate them on their shock team calls.

Hopefully one of the key contributions that emerged from this concise clinical guidance is this golden hour of critical care, right?

And to provide a roadmap of key milestones that should be accomplished either in the ER or on the wards and evaluating these patients.

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Shashank Sinha, M.D. | Evaluation and Management of Cardiogenic Shock in 2025

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