Let's kick off this with a brief talk about non-mortensive shock in patients who present with pulmonary embolism. These are some of my disclosures as it relates to this particular talk. First of all, what is non-mortensive shock? I mean, I think as a cardiologist in the group, I mean, we have known about non-mortensive shock as it relates to in the acute MI space. And this is from the shock trial and registry. The definition is patients have a low cardiac output, but a preserved blood pressure. And the systolic blood pressure being greater than or equal to 90 millimeters of mercury without the use of pressors. So blood pressure is OK, but they have a low cardiac index, and that's why it's called a non-mortensive or a non-ipotensive shock. And at least in the acute MI space, what we have known for the past couple of decades is if your patient has non-mortensive shock, this symposium has been about shock, and we clearly know shock is a bad state. But what if your blood pressure is preserved? And one of the ways the blood pressure is going to be preserved is that the patient compensates, has a high peripheral vascular resistance, and somehow maintains the blood pressure. It's been shown in the acute MI space that patients who are in non-mortensive shock have a high risk of hemodynamic deterioration. They have increased need for vasopressors, so they may not present with hypotension, but they may progress to hemodynamic deterioration need for vasopressors. And it's also been shown in the MI space that these patients also have a high in-hospital mortality, somewhat similar to that of a hypotensive shock. And the recommendation in patients with an acute MI shock is for aggressive management. Using this background, let's apply this to the PE space. In terms of PE, I mean, ESE risk stratification of acute PE, we classify PE as a low, intermediate, or a high-risk PE. And the classification is largely based on whether the patient is hemodynamically stable, and on RV dysfunction on TTE or CTPE, and also looking at biomarkers such as cardiac troponins. But what you can see here is there is a great emphasis on hemodynamic stability to classify patients as whether they are unstable, which becomes a high-risk PE, or whether they are hemodynamically stable. So what about patients who are intermediate-risk PE, who by definition are not hypotensive? We looked at some of the data to evaluate the incidence of non-motensive shock in patients who are, by definition, not hemodynamically unstable. This is data from the flash registry where we showed that a third of the patients had a cardiac index less than or equal to 2.2, but their blood pressure was not hypotensive, greater than or equal to 90 millimeters of mercury. And the question was, can we predict non-motensive shock in these patients who are otherwise, like if you see them on the floor or in the ER, their blood pressures are OK. And at least, I mean, that's what we get told all the time, that their blood pressures are OK. Can we predict non-motensive shock in patients who present with pulmonary embolism? Using data from shock, we came up with the composite pulmonary embolism shock score. And the components of the shock score includes markers of RV function and ischemia, which includes elevated troponin, elevated BNP, moderate or severely reduced RV function. This also includes a marker of clot burden. How much is the amount of clot in the pulmonary artery? Mainly central PE. And are there other things that can potentially make the patient unstable? So markers for potential additional clot embolization, such as concomitant DVT. And is the patient currently compensating by being tachycardic? And so all of these go into this composite shock score. And each of them get one point. And what we showed from this analysis was this composite PE shock score predicts a non-motivated shock. And the higher the score, greater was the incidence of non-motivated shock. You can see here, if you have a score of six, the incidence of non-motivated shock is close to 60%. And one of the advantages of the CPES score is that it's PE specific. For example, if you consider an 82-year-old female who presents with UTI and found to incidentally have a small sub-segmental PE, if you use the S-PESI, which is what the guidelines recommend, just by her age, she gets a point. And she's classified as high risk. But we clearly know that by taking care of that small sub-segmental PE, you're not going to improve the prognosis on this 80-year-old female with UTI. If you use the CPES score on the same exact patient, her CPES score is zero, clearly indicating that the PE is not what's driving her high risk. The other question has always been, we know non-motivated shock in AMI space is bad. But how do we know that if you have non-motivated shock in acute PE, this is actually bad for the patient? So this is some of the data that we published looking at non-motivated shock in patients with intermediate PE who were treated with anticoagulation alone. And again, as you see here, the higher the score, the higher the risk of primary composite outcomes, which was a combination of in-hospital mortality, hemodynamic deterioration, and cardiac arrest. So if you have a high CPES score, there is a significant increase in the risk of hemodynamic decompensation and also in-hospital mortality. And what we did was to categorize the CPES score as high versus low. So anybody with a CPES score of three is considered a high CPES score. And what we showed here was high CPES score, patients had worse outcomes, including increased risk of in-hospital mortality, increases of cardiac arrest, and increased risk of hemodynamic decompensation. In fact, our PERT team in the last few years, we use this score on 100% of our patients. So everybody will get a DVT scan bedside by the pulmonary fellow. Our cardiology fellow is doing an echo. So we have all of this information in every one of our patients. And if the score is three or greater, many a times we do more than just anticoagulation alone. And we also showed more recently that the CPES score adds incremental value, even over the ESC risk categories. The ESC risk categories sees cardiac troponin as one of the variables that are used to re-statify patients. And we know in many of our hospitals, we have changed our assay from a regular troponin assay to a high-sensitivity assay. And even just that change in the assay will change the category of these patients. So now we know non-mortensive shock in PE patients will mean that these patients are sicker. Can we predict the non-mortensive shock non-invasively? So in other words, most of this data I showed you, we took the patient to the cath lab, did a right heart cath, and measured the cardiac index. But if you're doing that step, it's invasive. Can we do this non-invasively? So these are some of our publications looking at, can we predict non-mortensive shock in acute PE patients non-invasively? This is purely looking at McConnell's sign on an echo. Can this predict non-mortensive shock? Here you can see the specificity is somewhat limited. It has a good sensitivity, 88%. And the specificity is only 53%. But if the patient does not have McConnell's sign, it's very unlikely that they're going to be in a non-mortensive shock. What are the other ways we can non-invasively predict, while the patient is in the floor or in the intensive care unit, whether the patient is potentially in non-mortensive shock? One of the things that we can do on the floor is an LVOT VTI. And of course, we have been training our fellows to do this bedside. So what we showed in this analysis is if LVOT VTI is less than or equal to 15 centimeters, it has a good sensitivity and also specificity for predicting non-mortensive shock in these group patients. We have also looked at CO2 gap as a predictor of non-mortensive shock. And CO2 gap is looking at the difference in CO2 in the mixed venous versus arterial blood gases. And we have shown that this actually nicely correlates with the cardiac index. CO2 gap greater than 6 millimeters of mercury is considered abnormal. And finally, we published some data looking at IVC contrast reflex. All these patients are getting a CTPE. And if you see a lot of IVC contrast reflex, we showed that this is also predictive of non-mortensive shock. Something that can be done at the time they are getting a CTPE. The specificity was around 93%. And specifically, the positive predictive value is 97%. Let's put this to test. I'll just share one quick patient example. So 45-year-old female, cardiac arrest, respiratory failure. She has a history of asthma, woke up with shortness of breath, took her NEBS, and the boyfriend called EMS. But upon arrival, patient was in PERS. She was intubated, two rounds of CPR. She was admitted to ICU. So this was not PE, but this was asthma exertion observation. So she was treated with steroids, NEBS, and antibiotics. Extubated day two to a high-flow nasal cannula. CTPE on day one was negative. And she was in the hospital for a long time. On day 11, she becomes acutely tachycardic. Blood pressure is slightly lower, 90s over 60s, but immediately rebounds back within the next five minutes. And you can see that she did not miss any doses of DVT prophylaxis. For whatever it's worth, she was on lower nonstance of UF, and fractured at a heparin. On the widest, her heart rate is tachycardic, but the blood pressure is now back to baseline 130s over 80s. She's a bit tachypneic, and 93% on room air. And these are some of her labs. And there was a high suspicion for PE. They did a PE scan. And you can see here, she does have, as it plays through, a saddle embolus with the complete occlusion of secondary branches of the right and left lung, and early right heart strain. There is also something there. And I'll be circling something in the RA, which was actually missed by the radiology read overnight. So that's Claudine Transit in the right atrium. But anyway, we got a call in the middle of the night. Blood pressure is now stable. Let me see if I can see what they said. Blood pressure is now stable. We'll go out. We got a call in the middle of the night. They said, oh, by the way, she's doing OK. Blood pressure is now stable. And she does not have a high oxygen requirement. In fact, she's satting at around 93% on room air. So traditionally, we would have seen these patients and said, she's stable. Maybe we just anticoagulate. We said, based on all the information we had, we said, emergently transfer to our hospital. And the reason we did this was that we used the enhanced risk stratification. Does she have right heart strain? Yes. Does she have a large clot burden? Yes. Is it centrally located? Yes. Are her biomarkers troponin and BNP positive? Yes. Does she have a DVT? She did have a DVT. Is she tachycardic? Yes. And the CPES score, in our case, was the maximum six. And the CPES score will tell us that a normal tensile shock prevalence is between 58% to 100%. A risk of death is in-hospital death is 40%. Cardiac arrest is 40%. Risk of hemodynamic deterioration is 40%. So she comes to our CCU. She had a radial A-line placed. And we're seeing this on the monitor. Very low pulse pressure. Now she's hypotensive. From being seemingly normal, she's now hemodynamically decompensated. She was started on dobutamine and Lebofet for low blood pressure. So we immediately took her to the cath lab. We do a detailed hemodynamics pre- and post-procedure. Here you can see our PA systolic is around 55. Our cardiac index, despite being on some dobutamine, is 1.5. And we did mechanical thrombectomy. And you can see the amount of clot we took out. And at the background, you can see my fellow, which has a satisfied look on his face. And what's more important is immediate hemodynamics. So you can see our heart rate immediately came down. Our PA pressures are normalized. Our cardiac index is still better. There is a 30% increase, but that's not normalized as yet. And 36 hours later, you can see that RV is much better. So just to conclude, in terms of normal intensive shock in acute PA patients, at least the data supports that one in three patients with intermediate risk PA are in normal intensive shock. And if you go by usual measures of hemodynamic stability, you're going to miss these patients. They have worse outcomes, similar to acute MI, normal intensive shock patients. And there are multiple ways to predict the normal intensive shock. And hopefully, future trials will find out whether using this normal intensive shock and applying therapies for them will have a significant benefit in terms of their outcomes. Thank you.

non-motensive shock

pulmonary embolism

CPES score

risk stratification

hemodynamic deterioration