Welcome back. Today, we are going to talk about SD elevation, myocardial infarction, or STEMI. So this is a high acuity issue that we've been managing, and I think we've gotten pretty good at managing these over the years. But let's just jump in. So a few statistics. Incidence of these is 750,000 per year, so quite a few of these. 2013, we had 116,000 or so patients actually died of these. Again, I think overall, we are getting better, although I don't have statistics here. 57% male, 43% female. The average age for males is 65, for females is 72. And 38% of patients who present with acute coronary syndrome have STEMI. And we differentiate this because the treatment is very different than a non-ST-elevated MI, and we're going to talk about that separate. So today, we're going to talk about ST-elevation. So what is ST-elevation? Well, basically, it's 100% inclusion of that coronary artery. As you can see in the third picture down, we've got, in this case, a plaque rupture with a clot formation that has completely occluded the artery. So the reason that that's important is because that goes on to develop a full transmural infarct. So the entire thickness of the myocardium is now jeopardized. And if we don't open that artery back up or get blood flow back to that area or reperfuse that area, a significant portion, typically, of myocardium will die. And so these can be devastating if they go untreated. Most of the time, and maybe all the time, these are ruptured plaques with thrombus formation. And so you've got that clot that you're kind of thinking about a couple different things when it comes to managing these things. So let's talk about brief history. The reason I say brief, because time is our friend. And the quicker we can get these patients to intervention, the faster. In fact, we've got guidelines and rules around how quickly we need to be able to manage these patients. But your job, when these patients hit the door, is to start with just your good old ACLS. So are they responsive? Do they have an airway? Are they breathing? And what's their hemodynamics? Do they have circulation? If they don't, these are the things you need to manage first. These patients can present as cardiac arrest. As you can imagine, significant amount of myocardium is in jeopardy. Ventricular rhythms are common. The second thing is if they're awake and talking, understanding their symptoms, onset, frequency, duration, severity, all of those things, pressure, burning, radiation, shortness of breath, nausea, vomiting, diaphoresis. Typically, these patients are sick. They look sick. I used to describe it, and we'll talk about physical exam here in a minute, but they had a color and you could see it. And it was kind of a gray, ashen color. And they also had this feeling of doom. They just knew whatever was happening was bad. And if they didn't get help shortly or soon, something bad was going to happen. And so it is this whole kind of set of symptoms that once you've seen a few, you'll start to kind of, there's just a stall. You don't even have to see the EKG. You know that there's something going on. Again, risk factors are the same as we talked about in the chest pain, hypertension, diabetes, hyperlipidemia, smoking, family history. I'm adding cocaine use here because that can cause several different things to happen that can be related to STEMI. And so understanding their drug history is important, too. Physical exam could be normal, but findings of heart failure, diaphoresis, that color, they have a color. And in some cases, they may have a gallop. And so it's variable, truly. But when patients are in the throes of it, they typically look pretty ill. EKG, I mentioned timing is important. Your goal for these is less than 10 minutes from presentation. The good news is many of us are in STEMI programs that have protocols. And even our EMS regs, our ambulances have 12 leads. And they can send those in from the field, and we can be ready. Some of my most exciting times were meeting those ambulances at the door in the bay there in the ED and taking them straight up to the cath lab and having everything ready to go and getting those patients intervened very quickly. It was exciting and high impact because those are the things that save lives. And so that was the fun part of the job. So for EKG interpretation, ST elevation does have some definitions. So there's a couple things for you to think about. Number one, it needs to be new. So if there's any potential issue or history of CAD where they may have a chronically abnormal EKG, you need to get your hands on the old EKG. It's really important. But that new ST segment elevation at the J point in two contiguous leads. So it can't be leads two and V2. It needs to be leads V2 and V3 or leads two and leads three because they represent two different areas of myocardium. So the concept behind this is that there's two leads that represent similar areas of myocardium so that you can see the extension. Any ST elevation that occurs in one lead is likely not to be real ST elevation. So two is the definition. In addition to that, you need a 0.1 millivolt elevation in all leads other than V2 and V3. So V2 and V3, we need a greater than 0.2 in men older than 40 or 0.25 in men younger than 40 or greater than 0.15 in women. So some additional things to think about there. But it's leads V2 and V3. And then a new left bundle branch block. If you don't have an old EKG to compare to and the patient has no history, if it's a new left bundle branch block, it's a STEMI until proven otherwise. And those patients need to go to the lab. If it's a previous left bundle branch block and there's some changes, then we've got scarbosis criteria that we can evaluate those changes with. And I included that in the readings. So take a look at that. But there's some complexities there as far as if there's been, if this particular left bundle branch block has enough changes that would warrant it being indicative of a STEMI. So I wanted to give you some examples. So first EKG is a 12 lead that represents an anterior wall MI. So as you can see, there's significant ST elevation V2 through V6. We talk about tombstones and we talk about fireman's caps. And that's what you're going to see pretty significant V4 through V6 where you kind of get the peak from the R wave that goes straight up into the ST elevation and then back down to baseline. So this is a pretty classic presentation for an anterior wall MI. Here we have inferior wall. You have the same thing. You have those tombstones, if you will, in 2, 3 and AVF. And some changes in V1 and V2. But the 2, 3 and AVF is where the ST elevation is. And so this is indicative of an inferior wall MI. And then some lateral wall changes in leads 1 and AVL. And then you'll see some reciprocal changes in 2, 3 and AVF. But this one is indicative of a lateral wall MI. I will tell you when we start to get into lateral and then certainly in posterior, and I put on here, these are top. Posteriors are very top. What we see here is we've got some reciprocal changes in leads V1 through V3. Some would suggest if you flip these around, you actually see and look them upside down, you see some ST elevation. And that's kind of where that comes from. But, again, we're looking at the back wall of the heart. And so when we look at the electrical activity and the way that it's changed because of the ischemia, you're seeing it kind of come through to the front wall and through that front wall to your electrodes. And so that's why it isn't as a clear picture as the anterior or inferior walls are quite much, quite more indicative or easier to identify. So let's talk about initial support. So these patients present, certainly you need to get them on a cardiac monitor. They do have high risk for ventricular arrhythmias. And you want to know what's going on at all times when it comes to their rhythm. You need to get an IV, get fluids going. What's their oxygen? Get some oxygen on them if they're hypoxic. So less than 90% is what our guidelines tell us. STAT labs, seroponin, chemistry, CBC, coagulation studies. Typically, we're not waiting for these lab results before we get them to the lab. But get that blood drawn. A lot of times what we'll do is start the IV and grab the blood at the same time and get those running, get them run STAT so we can get those results back as quickly as possible. If there's anything that we need to manage. Hemodynamic support if warranted. So if they're hypotensive and we need to get them on some pressers, we'll do that. We need to manage that, as well as any issues with ventilation. And then relief of their ischemic pain through the use of nitroglycerin, again, as we get them stabilized. From a STEMI management perspective, and I'm going to talk more about medications in a couple minutes. But some of us work in revascularization PCI centers, and we're going to be taking those patients straight to the cath lab. The goal is a door to balloon in 90 minutes or less. If these are transfers from other places, or maybe they presented to another ED before they came to us, then you have 120 minutes. So they're not giving us a lot of time. Most of us have driven these numbers down significantly. So it's been really exciting to see the improvement over the years of our STEMI management. Now, others of us might work in a non-PCI center, so we don't have that option. But we do have a couple options. So if the symptom onset is within 12 hours for patients who cannot receive PCI in 120 minutes, then lytics, fibrinolytics is indicated. And we need to get that infusion going within 30 minutes of presentation. And then transfer them to the PCI center. If we can get them to the PCI center with a door to balloon within 120 minutes, then our option is to do that rather than give them lytics. So, again, these are big decisions that oftentimes we have protocols in place to manage them and best understand who gets what and what our transfer options are and that sort of thing. So if you're working in one of those non-PCI centers, just get a good understanding of what happens with these patients when they present and how to best manage them so that you can be ready. So let's talk about medical management. And when I say medical management, I don't mean instead of. I mean in addition to revascularization. So certainly antiplatelet therapy, typically aspirin and a P2Y medication, especially for primary PCI, or you'll see a couple different options there if you're going to use lytics. But this is what the current guidelines tell us. From an anti-coagulation standpoint, remember we talked about most of the time this is a plaque rupture with thrombus. We want to really fight against that and hit that hard. So heparin, either unfractionated or low molecular weight or by the route for PCI or lytics is indicated. Again, this is all in your readings. Nitrate, sublingual nitro times three with a nitroglycerin drip if the pain continues and the blood pressure stable and can tolerate it. Morphine only in severe pain exists. So if we can't get them pain free and they're on all the nitro we can get them on, then you might want to think about morphine. But it's not as standard as what it was, you know, quite a few years ago. Beta blockers on board unless they're hypotensive or bradycardic. These can help kind of stabilize things from an adrenergic response. And then statin therapy, high dose statin provided as early as possible helps with some of that plaque stabilization. So again, lots of things to think about in that short term management. Once we've got them revascularized, what are the things we think about for longer term management from a medication standpoint? So certainly their aspirin, so dual anti-platelet therapy or DAPT. Low dose aspirin along with one of the P2Y medications. Beta blockers are important unless they're hypotensive or bradycardic. Statins, they maintain that high dose statin. ACE inhibitors if blood pressures can tolerate. And then nitroglycerin PRN with instructions gets sent home with the patient. So what I want you to see here is most patients end up on four or five new medicines after an event like this. That is a lot of education and a lot of engagement with the patient to understand why. And every one of these has a very distinct mechanism of action that decreases risk of issues, comorbidities and early deaths after they go home. So really important. But we don't just hand patients prescriptions and walk out the door. They need to understand why they're on these and why they're important. For some of our patients, this is a significant financial investment. So they need to understand why these are life saving and why this is so important for their long term management. Our follow up medication adherence is abysmal, in my opinion. We've got some studies out there that say as many as 60 percent of our acute MI patients six months after their event are not on the medicines that they should be on. And so I think we need to do a better job at the time of the event and really helping them understand why long term management is so important. Additional considerations, anti-inflammatories, we need to discontinue those and discourage their use. And I would be very prescriptive with the patients about no more ibuprofen or Motrin, that kind of thing. For several reasons, part of it's related to the anti-platelet meds that they're on, but then also the post-MI management. Systolic dysfunction. Some of these patients will end up with a drop in their ejection fraction if we didn't get to them in time or they didn't present in time. And so we need to make sure that we're managing that as well. So appropriate medical therapy and follow up for need of a possible defibrillator. Again, these patients now are not only post follow up for their coronary disease, but they're post follow up for their cardiomyopathy. And they need to be managed closely and monitored closely to make sure that their EF either improves or if it doesn't, then it's managed appropriately. Cardiac rehab, all these patients, it's a level 1A recommendation. Cardiac rehab referrals are important and they need to be educated on why maintaining that appointment and program is important for their long term management. Patient education, I just talked about. I can't talk about it enough. This is so extremely important for their event, understanding it, for the medications that they're on, for secondary prevention and for who to call and when. What symptoms do they need to worry about? Which symptoms don't they? I mentioned under the chest pain talk that we will oftentimes get these patients back because they're nervous and you can't blame them. They had a life threatening event. So every twinge and every feeling in that chest that they're going to get, what is that? And do I need to worry about this again? So lots of education and support. Site management is important. So what happens to that either femoral or radial site if they have concerns? And then I typically recommend we follow these patients up within that first week because there's so many new pieces of information, making sure they got their meds and they're following up appropriately. So, again, if you have any questions, please let us know. Reach out to the Academy. But we appreciate your time today and look forward to any feedback that you may have. Thank you.

STEMI

coronary artery

transmural infarct

EKG patterns

cardiac rehab