So let's do ACS, so acute coronary syndrome. So basically here, I want to kind of focus on first talking about when you suspect somebody with a heart damage, myocardial injury, kind of going through a differential diagnosis of it, then talk more specifically about acute myocardial infarction, talk about treatments for type 1, differentiate treatments between STEMI and unSTEMI, discuss the complications of acute MI, and then focus on cardiogenic shock. All right, so I want to emphasize this. The easiest way to figure out if a patient's heart is damaged is to check a troponin level, right? If the troponin level is elevated, there's some reason why it's elevated. There's some stress on the heart. It doesn't normally just hang out in the blood, right? And most of these are not due to a blocked artery. They're due to direct myocardial injury. And here is a list of all of them over here. Some are cardiac. If you have myocarditis, if you have an inflamed heart, you're probably going to leak troponin, right? Or if you got punched in the chest because of trauma, you're going to have myocardial injury. And both of those are going to cause troponin elevations, right, or stress cardiomyopathy or whatever. Or if you have non-cardiac injury, so for example, if you have sepsis, imagine if you're shredding your kidney, your brain, and every other organ, your heart's going to get damaged too. And so you're going to have myocardial injury from that as well, and troponin elevation. So those are systemic causes. That's on the right here in the blue. On the left is the ischemic causes. That means the heart itself is not getting enough oxygen to support its function, right? And even with this, there's an algorithm. One possible cause is acute coronary syndrome, which I'll discuss later, but basically an acute thrombus is blocking blood flow to the heart, right? And the other ones are non-ACS causes. So either like hypoxia or increased demand or something else, right? So if you want to focus more on myocardial infarctions, that's when you have a thrombus in the artery. There are three types for acute coronary syndrome, right? There's a STEMI. So what a STEMI is, is basically a patient comes in, they have signs of a blocked artery in their heart, maybe chest pressure, shortness of breath, and their ECG shows ST-segment elevations. That's a STEMI. A non-STEMI is the same thing, except there's no ST-segment elevations. That's the only differentiation between the two of them. And then the third thing is unstable angina, where the patient has acute coronary syndrome, they have all the symptoms of it, but their troponins aren't positive. Nowadays, unstable angina is extremely rare. Why? Because their troponin assays are so sensitive that even you could detect troponin in somebody walking down the street. All right, so unstable angina, I haven't seen it in my ICU, I think in about 15 years. All right. So just to back up and talk about how the pathogenesis of corneal atherosclerosis develops, basically the first step is you develop intimal thickening, and you have increased cholesterol, and eventually inflammation forms there, calcium gets deposited, and then an atheroma develops and it breaks off. Platelets don't like that, and then they'll start aggregating around there, causing blockages of blood flow. And interestingly enough, these tend not to be obstructive lesions. So the ones that most likely cause acute coronary syndrome are like 20% blockages, or 30% blockages. It's not the old, heavily calcified one that's 90%. Why do I bring that up? It's because you can't just stress test everybody out of this, right? You can't just put everybody on a stress test and say, okay, you're more likely to have a heart attack than you. It's because it's really the things that are not flow limiting. I think you know how to diagnose STEMIs and NSTEMIs at this point, but just to go over it, you have to have symptoms of acute coronary syndrome, chest pressure, shortness of breath, et cetera. Maybe you have hemodynamic instability if you have alterations in heart function, right? Like if your EF stops dropping. In the ICU setting, you might have detect ST segment changes on telemetry, or maybe you'll see a new arrhythmia. And then you could also do laboratory and imaging studies. You could measure troponin. If it starts going up, you might suspect it. Or you might do echo and see a new wall motion abnormality. But to diagnose a type one MI, these are the things that are required for diagnosis. Your troponin must be elevated. And then you have to have one of these things. You have to see that the patient has symptoms of ischemia, new ECG changes, new wall motion abnormalities, and you can do this on a POCUS or an all echo, or you could do a cardiac cath or a cardiac CTI to see it. In the ICU specifically though, it's hard to diagnose. So in my world, in the cardiology world, there are so many studies that talks about acute coronary syndrome. None of them are in the ICU. And they're all in patients who come to the ED or an outpatient, and they present with chest pain. But there's only 14 studies that have talked about patients who've developed acute coronary syndrome in the ICU setting. And they're more likely to develop acute coronary syndrome in the ICU setting. Why? If you, let's say, come in with an abdominal abscess, and you have a hyperadrenergic state, and you have a hyperinflammatory state, well, that stuff leads to ACS, right? So 14% of ICU patients in one study develop ACS, which seems a little bit high to me, by the way, but just leave it at that. This is just one study here. Develop it. But in many of them, ACS was not detected, or not detected till later. And it's because it's harder to list the symptoms. If somebody's intubated, they're not gonna tell you they have chest pressure, right? And the signs are less specific. If somebody's developing hypotension, well, it could be due to sepsis, it could be due to hypovolemia, it could be due to a number of things. And at least in this study, 80% of MIs were missed initially. So you have to have a higher index of suspicion, especially in somebody who has a history of coronary heart disease. All right, for patients with STEMI, I think at this point, all of you know this, but if you have SC segment elevations in the pre-hospital setting, almost always these patients need to be reperfused immediately. There's two options, you can use thrombolytics if you're in areas that are two hours away from a cardiac cath lab, or preferably we prefer emergent cardiac catheterization. In the ICU setting, there is less data for these things, but most patients can't be on thrombolytics because of contraindications due to something else. And even some patients can't even get a PCI because you have to give anticoagulation and antiplatelets for them. So even some patients with STEMIs, you can't take them to cath lab. But if you can, the treatment of choice is PCI. One question that comes up often in my world is how many arteries you fix. Most patients who come in with STEMIs, they have disease more than one vessel. You definitely wanna fix a target, but at some point you wanna fix the other arteries because they're more likely to thrombose as well. And so this is one study called the COMPLETE trial published a few years ago, which showed that you have improved outcomes basically. If it's a non-STEMI, you have a little bit more time to think. Most of these patients need cardiac catheterization, but they don't need it emergently. You don't have to rush them over to the cath lab and get their artery open within 90 minutes. You have some time to think. And there's definitely no benefit to thrombolytics. So the timing of when you take them to the cath lab depends on how they are. If somebody's complaining of hemodynamic instability, well, I guess you don't complain of hemodynamic instability. If you complain of chest pressure, shortness of breath, palpitations, diaphoresis, et cetera, and you think it's from their heart and it's persistent despite medical therapy, well, in those cases, you might wanna take them to the cardiac cath lab earlier. If they have hemodynamic instability, you might wanna take them to the cath lab earlier. If they have arrhythmias, you want them to take them to cath lab earlier. Those are the kind of things that we think about in terms of timing. And so some people use these terms and you might hear them in your ICU, where if you're hemodynamic unstable, you need immediate invasive therapy. You must go to the cath lab right away if you have an end-stemmy. Otherwise, you might consider early invasive therapy, maybe a strategy. Maybe you need to go to the cath lab within 24 hours, delayed, maybe within 48 hours, and then you're not gonna see this as much, but a schema-guided strategy in patients who are very low risk, which wouldn't be in an ICU. You wouldn't take them to cath lab at all. All right, so this is a summary slide that I really, really like, and the reference is in that corner there. So it's by Deepak Bhatt and published in JAMA in 2022. I have it there for your reference, but I just wanna go over it because I think we have enough time for it. If you have a stemmy that's present on ECG, you have to treat with antiplatelet and anticoagulant therapy first. And then you go to the cath lab if it's available immediately. If not, you'd consider thrombolytics. And then if you have an obstruction, you just treat them for the obstruction by PCI and then medical therapy. And if not, then you treat them for other causes. If it's an end-stemmy, you basically perform a cardiac catheterization, but you have a little bit more time to think, and it's usually within 24 to 48 hours. And if you don't have high sensitivity components that are elevated, then you diagnose unstable angina, which again, I don't see very often. And so that pathway is not as important for ICU practice. Here's a list of all the anticoagulant and antiplatelet therapies that I could think of, at least as of a year ago. And it's divided really into anticoagulants and antiplatelets and patients with acute coronary syndrome need both. Let's go for the first one, which is aspirin. It's been around forever. This is just one trial that was published a few years ago, talked about what dose you should use. You can use any dose you want, basically. All right, I'll just speak louder. So the dosage doesn't matter, but in general what you do is you want to load for the 162 milligrams to 325 in the first dose, but then afterwards you want to go to 81 milligrams. Here's just a study that showed no difference between the 325 and 81, so that's why we tend to use 81. Patients who come in with ACS, acute coronary syndrome, they don't just be on aspirin. They also have to have dual antiplatelet therapies. This is a lot of stuff that's written here, and the reason why is because it depends on your institution which drug to use. You could use clopidrogel, you could use Prasugrel, you could use Ticagrelor, and you put five cardiologists in a room together and they will argue about which one's better. I will tell you in general, Ticagrelor tends to be used more often in patients with STEMIs because there's one study that showed benefit to it, and then another one showed that Prasugrel is better, and so they're using that now this year. Next year, I don't know what it's going to be like and which one will be preferable. It doesn't really matter. Use one of them. In general, the risk of bleeding increases as you go from clopidrogel to Prasugrel to Ticagrelor. So we've gone over antiplatelets, which is basically aspirin and the P2Y12. There actually is an IV formulation of P2Y12, Cangrelor, which we sometimes use. They tried using it routinely, but we don't use it routinely because it has high rates of bleeding. All right, so let's talk about anticoagulants. In general, most ICUs use heparin. It's just easier than something that's longer-acting like inoxaparin or other ones. If a patient has heparin, HIT, or some other reason why they can't get beyond heparin, you could use bivalorudin, which works equally as well. I don't know what just happened there, but in general, though, the combination is for patients that come with acute coronary syndrome, as long as they have no contraindications, they should be on aspirin, a P2Y12 inhibitor, and heparin. The other medications are not as urgent to use, but should be considered within 24 to 48 hours. Historically, we have talked about the importance of beta blockers and using it within 24 hours of having acute coronary syndrome. Is that common in your practice, or do you guys normally do this? The issue is, in an ICU setting, if you're coming in with hypotensive due to other causes, you can't be on a beta blocker in the first place. But even if you can, there's less evidence supporting its use in patients with normal heart function. For example, let's say you have a left circumflex that's knocked out, your EF is 45%. There's now a study that was just published in the New England Journal in March, which showed no benefit to beta blockers. The only time that you use beta blockers is in patients who have EFs lower than 40%. Patients with recurrent arrhythmias or recurrent angina, that's it. If not, then they don't need a beta blocker. That's as of March 2024. This may not have permeated your practice yet. Another thing is to consider something to inhibit the RAS system, so the renin-angiotensin-aldosterone system. Historically, we've used ACE inhibitors, especially for patients with STEMIs. Any patient that comes in with it, we give them six weeks of licinopril. That is becoming less often used. This is from the guidelines from 2013. It's probably the next iteration of it in the next year is going to favor ARB use, especially for those who have EFs less than 40% and patients with diabetes. Now also, we're switching over to Arnis, to Intresto is the brand name for it, Secubitrol, and ARB together, because those work better than ACE inhibitors. But this is the guidelines, and so that's why we kept it in this slide. MRAs are becoming used more and more often. There's several trials about it. This one, Amphibicis, specifically discusses the use of a second-generation MRA after acute myocarditis called Dapilirone. Basically, anybody with an EF less than 40% with evidence of heart failure, you should consider an MRA. And I use it early. So my algorithm is, if somebody has a low EF, I would preferentially use something to block either an ACE inhibitor or an ARB initially. Then afterwards, like a day or two later, I would add an MRA. All right, I'm going to skip this stuff, but I just want to emphasize that you could use Simvastatin, Atorvastatin, or Rosuvastatin, basically high-dose statin therapy, and you can even add ezetimide initially on to basically decrease the risk of heart attacks in the future. So this is basically a summary slide of managing STEMIs and really end STEMIs. We know that there's evidence to support use of aspirin, dual antiplatelets, reperfusing early, beta blockers if the EF is low, and then the medications I just had. For symptom relief, if somebody's coming in with crushing chest pain, you could use IV nitrates, but that doesn't reduce mortality. And then there's good evidence that heparin helps, but it's less so the longer you're in the hospital. And then don't use the other medications below. All right, I'm going to skip this because I just basically said it in the phrase. So we talked about acute corneal syndrome in 17 minutes. Now I'm going to focus a little bit on the mechanical complications of MI. And this is a slide that was published, I guess, three years ago. And it was discussing basically what happens if people get MIs and the mechanical complications of it. In the 1980s, before routine reperfusion was done, the incidence of mechanical complications was 1.7%. So out of 100 patients that come in with acute corneal syndrome, about 2% will have a complication, one out of 50, right? And then the mortality rate is astronomical at around 70%. Now, as of a few years ago, with the advent of basically emergent PCI or urgent PCI, the incidence rate has dropped to 0.27, so very low. So I see about a few of these a year in my ICU. But the mortality rate is still very high, and it's around 40%. Here are the four of them. One is a VSD. Basically what happens here is that a hole develops between the left ventricle and the right ventricle. And you have clinically severe heart failure or cardiogenic shock. And you might feel even a thrill when you examine the patient, basically a vibration when you put your hand on their chest. These patients don't do well without surgery. They're usually in cardiogenic shock, and they might need some kind of mechanical circuitry support device to support them until they go to the operating room if they're a candidate for it. The next thing is free wall rupture. This is where instead of a rupture going in the septum, it's occurring in the free wall. Have you seen this? You have? That's good. It's very rare to see this because they die right away, right? It's hard to live with a hole in your heart. The only things that I've seen is pseudoaneurysms, where it's a partially contained rupture. Maybe two layers are ruptured through, but you have one layer kind of protecting it. Those patients could be asymptomatic, but you might be able to detect it because of chest pressure, or because of an echo finding, or something else. You need to do salvage surgery for these patients, even though the mortality rate is almost 40%, 50%. The third complication is a papillary muscle rupture. This is where instead of having a rupture of the free wall or the interventricular septum, you have a rupture of the pap muscles that support the mitral valve. If that happens, you have torrential MR, mitral regurgitation. And again, that leads to pulmonary edema and cardiogenic shock. Again, this is a surgical treatment. You need to go to the operating room quickly after this diagnosis. And this is basically a summary slide talking about the mechanical complications of MRI. If you have signs or symptoms suggesting of it, which thankfully is rare now, it's less than 1%. It's 0.27%. You want to do a point-of-care ultrasound, or an echo, or something else to diagnose it as fast as possible. If you're at a specialized center, you keep the patient there, but otherwise you want to transfer the patient somewhere where they could operate on this patient. If they're unstable, that requires a shock team discussion. Maybe put the patient on a mechanical circulatory support device, and then treatment depends on what the diagnosis is. If they're hemodynamically stable, you have time to think about how to treat the patient, and then you can consider any of those treatments that are on the bottom there. I'm going to skip this, but basically I just want to point out that most of the stuff that I'm talking about is about myocardial infarctions that affect the left side of the heart, while the right coronary artery supplies blood to the right side as well. So in patients with right ventricular infarctions, it tends to happen in about 10% of cases it's hemodynamically significant, where you have signs of right heart failure. And these basically, you just need to support their RV until their RV starts working again. All right, let me go over cardiogenic shock. So John's going to talk about this more in a few days from now. He's just going to talk about basically shock in general. But still about 3% of patients with STEMIs, and a little bit less with NSTEMIs, come in with cardiogenic shock associated with their myocardial infarction, and an even greater proportion have acute and chronic heart failure. You need two things to have a diagnosis of cardiogenic shock. One is you have to have cardiac dysfunction. So if your heart is pumping at EF of 70%, that's not cardiogenic shock. It's something else causing a shock. So when you have cardiac dysfunction, it has to be both systolic dysfunction and diastolic. Basically you have to have decline in cardiac output, and you have to have increased congestion in your heart. The second thing is it can't just be a low cardiac output. You have to have systemic signs of hyperperfusion. All of you as intensivists and working in an ICU setting know this, that you need to have hyperperfusion diagnosed shock, and it's the same thing goes for cardiogenic shock. In my world, I want to emphasize that if somebody comes in with acute MI and they're in shock, that is easy to recognize as a diagnosis. They're coming in, they might be clutching their chest, their blood pressure is low. And that is the classic stereotype of cardiogenic shock, easy to recognize, not hard to figure out that they're in shock. You need to treat them emergently. Take them to the cath lab or maybe put a device in, put them on norepinephrine, et cetera. But more common, especially in America, is heart failure-induced cardiogenic shock, and that's acute on chronic. This is somebody who comes in, maybe had a MI a few years ago, another one last year, and now they're coming in, they're saying, well, I don't feel as good, I can still do my independent activities of daily living, I can walk around, but not as much. And they're actually coming in with early signs of shock. That's becoming more 40 to 50% of the patients in tertiary ICUs in this country. Why does that matter? Because those patients are at high risk of death, and they're under-recognized and they're not thought to be in shock. If you suspect a patient to be in cardiogenic shock, you want to also stage the cardiogenic shock. This is something that was developed in 2017, and now is being used more often in our world. It's basically grading the severity of cardiogenic shock. So stage A would be, it's called Sky Stage, so Sky Stage A would be at risk for cardiogenic shock. We don't care about those patients. So B, we do care about them. These are patients who have beginning signs of shock, maybe they have clinical signs of hemodynamic instability, but they're somewhat warm on exam, their lactate's not elevated. Basically a pre-shock state, and if you don't aggressively treat the patient, they will then become stage C, who has signs of hyperperfusion, their lactate's elevated more than two, and they need pharmacologic or mechanical support to maintain a decent circulatory status. D is once you start becoming on two to five vasopressors or inotropes, or needing more than one device and one medicine, and then E, basically you're about to code. So I don't know if you use this in your ISUs, but this is becoming more the common nomenclature that we use for grading the severity of cardiogenic shock. Would Sky B be like A, B, if you're a chronically competent heart failure patient? If they have a low cardiac output. So that's the difference. Most patients who come in with acute or chronic heart failure, they're not an ICU patient. They're managed on the floor somewhere. But if they're having signs of hemodynamic instability, respiratory failure, those kind of patients, they're at least B. If their lactate's above two, they're C. So how do you manage cardiogenic shock? Again, these are stuff that you know just from managing shock, but I want to just point out that the ABCs still take precedence. Control their airway, their breathing, and their circulation. A common thing that I've seen is that somebody wants to give diuretics right away because they're cold and wet. Diuretics don't work if you don't have perfusion. If there's no blood being delivered to the kidney, it's not going to be able to, diuretics can't work. So you really need to use vasoactive medications. And that's for any type of cardiogenic shock, whether it's cold and wet or cold and dry. And the first-line therapy, and the most evidence-based therapy, is norepinephrine. The SOAP-TRUT trial suggested that, right? And for any patient with cardiogenic shock, actually any patient with shock, one of the best tests to assess their cardiovascular status is by doing a bedside focus, right? And if you suspect it's due to MI, which some patients are, then you need emergent cardiac catheterization. There's a trial called the SHOCK trial, which shows benefit to emergent cardiac cath for patients with cardiogenic shock. We've been using pulmonary catheters more often now, and the cardiology world is becoming more popular again. It had a fad. In the 1980s, 1990s, it was used a lot, and then it died out in whatever the first decade of the 2000s is. And then now it's slowly coming back because you can get objective data to guide your cardiovascular management. And then, nowadays, they're starting to become evidence-based therapies for treating patients in refractory shock. This will be talked about tomorrow, but I'm just foreshadowing it for you. There's balloon pumps. There's microaxial devices. The brand name is Impella. It's the only one out there. And there's ECMO to help support cardiovascular status. Not one of them is evidence-based. We still use it anyway, but there's no randomized trial showing benefit except for in March of 2024. The Danger Shock trial was published in the New England Journal, showed benefit to Impella therapy. This will be discussed later, but I want you to know this because this device is very, very expensive. In the United States, it costs at least $30,000 for each one of these devices. But it'll save some lives at the cost of taking out the kidneys. I'm just going to skip this because we just discussed this, and I'm going to skip this because we already talked about this as well. So that's basically an overview in 29 minutes about acute coronary syndromes, both NSTEMIs and NSTEMIs, and then cardiogenic shock, and also about mechanical complications of MI. I'm free to stay for questions or things.

acute coronary syndrome

troponin levels

STEMI

NSTEMI

atherosclerosis

cardiogenic shock