Cram The Pance - S1E23 Acute Coronary Syndrome (Unstable Angina, NSTEMI, STEMI)

Episode Date: May 22, 2021

Acute Coronary Syndrome (Unstable angina, NSTEMI, STEMI) review for your Pance, Panre and Eor’s.►Paypal Donation Link: https://bit.ly/3dxmTql (Thank you!)--- Support this podcast: https://anchor.fm/scott--shapiro/supportBecome a supporter of this podcast: https://www.spreaker.com/podcast/cram-the-pance--5520744/support.

Okay, so like the title says, today we're going to be going over acute coronary syndrome. This is definitely a big one for the pants, one that you should be very familiar with, because you'll definitely get some questions on it. I wanted to really quickly, like I always do, if you haven't checked out the YouTube channel, please do, it's under Cram the Pants on YouTube, so same name, and there's a lot of good visuals and things like that. To go along with the audio that I really feel helps solidify a lot of the topics that I go over and just help, especially with the mnemonics and different pictures I have and things like that. So check it out if you haven't already.

And thank you again, as always, for the comments, the likes, the new subscriptions on the podcast. I really appreciate that. So let's get started. Cute coronary syndrome. It's a term that's used to imply there's a suspicion or a confirmed acute myocardial ischemia or infarction. The is usually due to a plaque rupturing. And this forms a secondary artery thrombosis.

And this clot blocks the blood flow, either completely or sometimes there is some flow still going through and it's eschemic rather than a complete infarct. And we'll go over those types. So there's three types, I guess you could say severity levels, of acute coronary syndrome. There's unstable angina. There's non-ST elevation, myocardial infarction, and then a full-blown stemmy. So ST elevation, myocardial infarction. We'll go over those in a minute. Let's first start with the clinical manifestation. So I'll be pretty brief with these because most of these are going to be familiar with. The only thing I really want you to focus on is the atypical presentations. So most patients are going to have chest pain, obviously, but not all,

which I'll go over again in a minute with the atypical presentations. The key to the chest pain, though, in acute coronary syndrome, is that it's not relieved, typically with rest or with nitro, nitroglycerin. It's generally lasting over 30 minutes, and that's really what differentiates it from stable angina. Stable engine of these patients are going to take a nitro, they'll go back to feeling normal, they'll be exerting themselves, they'll sit down and get some rest, they'll start feeling better. But this is completely opposite than that. It's not getting better with rest. They've taken their normal amount of nitro. It hasn't gotten any better. And it's lasting much longer than it normally does, generally over 30 minutes. So that's what makes this different and obviously more

troublesome. The chest pain can radiate to the left arm, the lower jaw, the back. And there's a few keys to the type of chest pain that help you differentiate it from other things. So it's typically going to be non-positional. So it's not going to change with position. It's not going to get worse when they lay down. It's not going to be relieved sitting forward. And this helps you because you always need to be thinking of your differentials with your clinical presentation. So if they say there's no change in position, no improvement when the patient sits forward, what can you kind of rule out because of that, at least for the sake of a vignette? So paracarditis. Paracarditis is usually relieved on a patient sits forward. So if you see that, that pain is not getting better

when they're leading forward, you can kind of rule that out at least again for the sake of a vignette. So it's normally non-positional. It doesn't change the position. So that's one description of the chest pain. Pain's also going to be non-pluritic. So it doesn't get worse with inspiration. Again, think about your differentials. You can start to rule out some of the pulmonary causes like pneumonia, pneumothorax.

So it doesn't change in intensity with respiration. And then finally, the pain's going to be non-reproducible. So if you push on their sternum, you palpate the ribs, there's no change in the pain. Whereas a patient with costalcondritis, another differential, You push on their sternum, the pain is going to increase. And that's how you need to be thinking, not only for the boards, but when you're practicing, ruling out and ruling in certain different differentials that you have. So those are the descriptions of the type of chest pain, so normally non-pluritic,

non-positional, non-reproducible. And then finally be aware that due to the sympathetic activation in acute coronary syndrome, these patients are going to have tachycardia, they're going to be diaphoretic, they may have nausea, vomiting, all these extra symptoms due to the sympathetic activation. So those are the more common symptoms you're going to see in acute coronary symptoms. So what's the atypical presentation that you need to be aware of and who are you going to see it in? So atypical symptoms, patients are normally not going to have chest pain. That's what's so atypical about it.

And they're going to have different things. They're going to have epigastric pain. They're going to have dyspnea in the absence of angina. They're going to have weakness, palpitations. They may even have syncope. So these patients normally aren't going to have chest pain, but they're going to have these other symptoms. So you need to be aware of that. And who are you normally going to have these atypical presentations?

Well, it's three classes of patients. It's going to be women, elderly patients, and diabetics. So be careful, not only, like I say always, not only on the boards, but in real life, if you have maybe an elderly patient who said they had a synchable episode, and you're thinking of all these different things, you also need to think of an MI. Same with potentially a woman coming in that has epigastric pain. You don't want to think just GI problems. You also need to be thinking the potential.

of an acute coronary syndrome. So atypical presentation, women, elderly patients, diabetics, be careful on those. So the three types of acute coronary syndrome, like I went over before is unstable angina, non-ST elevation myocardial infarction, and N-STEMI, and then Stemmy, and then Stemmy, unstable, angina, N-STEMI, and then Stemmy.

So let's briefly go over for the three types of acute, I'm sorry, acute coronary syndrome. So we'll start with unstable angina, I'll kind of work our way up severity. So unstable angina. These patients have an occlusion in one of the coronary arteries, but it's not completely occluded. Some blood's still getting through, but be aware that if these patients are having symptom at rest, which they likely will with unstable angina, the arteries are at least about 90% occluded. So it's pretty well blocked, but some blood's still getting through,

just not a lot. You need to consider this in patients with symptoms of eczemia, so chest pain, dyspnea, diaphoresis. And remember the reason why this is unstable and not stable angina is because it's not going to be relieved by rest or nitrates. So they're going to have an atypical presentation compared with their normal symptoms of stable angina. They're going to say, I normally walk a hundred feet and I start to have angina and then I sit down and it gets better. Well, now they're going to walk 20 feet and they're going to start having angina and it's not getting better. So it's different than the normal presentation. That's what makes it unstable angina. So they have these symptoms of ischemia. And then the other key to differentiating this from an N-STEMI or a stemmy is that their

EKG, while it may be abnormal, show symptoms of ischemia or show signs of aschemia like ST segment depression, new T-wave inversion. They're not going to have ST elevation. No ST-segment elevation on EKG, and they won't have positive cardiac enzymes. So negative troponins, no ST segment elevation on EKG. They will have the ischemic signs on EKG. but no SC segment elevation. So that's unstable angina. It's going to present like all of the rest, but the difference is the EKG is not going to have ST segment elevation,

and they're going to have negative cardiac enzymes. So that's basically the least severe of all of these. The next one is going to be a non-ST segment elevation, MI, an N-stemi. The only difference between unstable angina and an N-STEMI, or non-STE elevation myocardial infarction, is that the cardiac enzymes are now positive. So positive troponins, generally troponins.

There's some other cardiac enzymes, I'll go over in a minute, but normally it's going to be troponins. So everything else is the same. Clinical presentation can be exactly the same. EKG findings can be exactly the same. It's just these patients now have positive troponins. So that's the difference here between that and unstable angina. And the reason why in an N-STEMI that the cardiac enzymes are actually going to be positive

is because there's now enough myocardials, there's, now myocardial cell death. So the compromised blood flow to the myocardium and these patients is severe enough that there is subsequent myocardial injury. And that's the difference between an end stemming and unstable angina. There's now myocardial injury and death. And that's why you're starting to have these positive troponins. The unstable angina patients have not yet had any myocardial injury. It's completely reversible in unstable angina still. So again, the only difference here positive cardiac enzymes otherwise everything else is the same the EKG may have signs of aschemia but they're not going to have ST segment elevation so the last one full-blown stemmy everything's

positive here so ST elevation ST segment elevation myocardial infarction this patient's presenting with potentially the same clinical manifestations we discussed previously but they're going to have positive cardiac enzyme so positive troponin but that's the same of it as an N-stemi the difference here is that that this patient's also going to have ST segment elevation on the EKG and that's because this patient the the difference in this patient is that they have a complete occlusion 100% of the coronary artery is completely occluded nothing's getting through the tissues dying all the way through the heart it's transmural so it may present the same way as an N-stemi but the difference is the

SD segment elevation on EKG due to the complete occlusion of the coronary vessel and remember to classify it as a stemmy the EKG must have have a new ST segment elevation in two or more contiguous anatomical leads of over one millimeter. And then, of course, the presence of reciprocal ST depression helps confirm the diagnosis. So remember that to be classified as a stemmy needs to be two or more contiguous anatomical leads over one millimeter. And then also another thing that you should know is that a new left bundle branch block is a semi equivalent. until proven otherwise. So that's another thing that you should know. So those are the three different classifications of acute coronary syndrome. And one thing that I want to review before we break down the

process of diagnosing and treating is a little bit more info on the different cardiac enzymes. So proponents are the big ones, of course. It's the most commonly used. But you should be familiar with the other ones as well because I was actually asked a couple questions on CKMB. I think I may have even had a question on myoglobin. So let's go from really quick so you don't get that question wrong. So there's three different cardiac enzymes you need to be familiar with, at least the basics of each, and that's, of course, troponin, myoglobin, and then creatin kinase, or more specifically, CKMB. So let's start with the most sensitive, the most specific cardiac enzyme. That's the one you'll actually see 99% of the time being used here in

the United States, at least, and that's troponin. So troponins are proteins that are found in both cardiac and skeletal muscle, and when the heart is damaged, it releases troponin into the bloodstream. There's a few different types of troponin. There's tropon C, T, T, and I, but the T and I are more specific to cardiac tissue and that's the ones you'll see being tested. So troponin levels are normally going to rise about two to three hours after the onset of an acute am I and then it can actually stay elevated for up to 10 days. So once they go up, they a lot of times don't come back down to the normal level for about 10 days. It's important and something I'll go over in a little bit. So to be considered positive in acute myocardial injury,

Traponin must be above the 99th percentile of the upper reference limit of normal by the assay being used. So it's just a little side note there. So Traponin is a great test, but there are some caveats. There's always caveats in most tests. It's not a perfect test. So some of the caveats are, is that troponin can actually be elevated in patients with chronic kidney disease, in patients with a pulmonary embolism, which is really important because that's going to be one of your big differentials of a patient comes in with chest pain. They may have a P.E.

And their troponins might be positive, but they're not having an M-I. They actually have a P.E. So it can be elevated in patients with pulmonary embolism. And it can even be raised in trauma, like cardiovascular, and cardiopulmonary resuscitation. And it's not 100% specific. So remember that it's a good test, but it's not perfect. There's some downfalls that you need to be aware of.

So let's move on to CK and CKMB. We'll make this one brief because this test is not really used very often anymore. Once troponins were introduced, CKMB kind of was like out the door. They didn't use it as much anymore. So CK is creatin kinase, and it's an enzyme that's found in the heart, brain, skeletal muscle, and when there's muscle damage of any kind, this enzyme is going to rise. So it's not that specific at all. But then they discovered CKMB, which was actually more specific to the heart, still not as specific as or sensitive as trouponins,

but it was a better test. And it was actually pretty good until triponins came out and knocked it out. So there's really only a couple times you're going to use CKMB. If you live in a country where cardiac troponin assays are still not used, obviously not in the U.S., you can use CKMB. It's the next best thing. Or, and this is an important one because I did get a question on this in my clinical medicine exam, if you're checking for an early re-infarction, that's because unlike troponins that don't return to a baseline for sometimes up to 10 days, is CCMB can actually return to baseline within as little as 72 hours.

So if you have a patient who came in, they were having an acute-m-eye, you keep them in the hospital for a few days to observe, they had a stent, whatever. And then on day three or four, they start having new symptoms. They start having new chest pain, dyspnea. You want to know, are they having another infarction? Well, you can't use proponents again because they're still going to be elevated for a few more days. But KMB can be used because it'll already have returned to baseline likely and a new elevation and the number could indicate a reinfarchion.

So keep that in mind because, again, I did get a question on it. In clinical practice, it's still not really used that often, even for reinfarctions, but just be aware that that could potentially be asked. All right, so let's go over the last cardiac biomarker, which is myoglobin. That's really not used anymore. The only benefit to this cardio biomarker is that you should be aware of is that it peaks really fast. It's actually the fastest of all the biomarkers. The way the dumb way that I used to remember it was it's myoglobin.

I used to remember myomai, you are fast. I know that's really, really corny, but I still remember it today. So myomai, you are so fast because you're going to get, you might get a question like I did, and they're going to ask which cardiac biomarker is going to be the first to peak. And I remembered my omai, myoglobin. So it used to be suggested to be used as an adjuncted troponans to pick up an MI that maybe the troponans hadn't detected yet because it didn't peak yet with troponants. But there's so many inaccuracies that it's really not suggested anymore.

And overall, the general consensus is that myoglobin just shouldn't really be used anymore for screening for Hugh Cornynery syndrome. But that doesn't matter, they still might ask you a question on the boards. Remember, my oh my, myoglobin is the fastest one. So as far as cardio biomarkers, troponin is your absolute best. It's your most sensitive, specific. It's the one you'll likely see being used. KMB, only if troponins aren't available.

or maybe if you're assessing for re-infarction, and then myoglobin, you're not really going to use it unless you get some weird question about which one peaks the first. And then, yeah, myoglobin. All right, so let's move on to the diagnosis. So let's picture this. You have somebody coming into the ER, wherever you're practicing, and they have this crushing chest pain,

radiating into the left arm, nausea, diaphoretic. How do we start the workup? What do we need to do to diagnose these patients? So the first thing you want to do before anything else is get those EKG leads on the patient. You want to get a 12 lead EKG before any. anything else. I'm referring to diagnosis here. So obviously you want to give them aspirin O2, but I'm focusing on diagnosis. So as far as diagnosis, EKG as soon as they enter the facility.

Remember, ST segment elevation will present prior to your troponans being elevated. So that's why EKG early on is so important. And the general rule is to have door to EKG time in under 10 minutes. So within 10 minutes of somebody coming in with chest pain, you should have an EKG back so you can assess for that. Okay. So within the first 10 minutes of the entering the facility, complaining of chest pain, they have an EKG done. All right, now let's quickly review the leads that are going to be involved in each type of MI. And one thing that you need to note about ST segment elevation on EKG is that even though you're looking for ST segment elevation, you need to know that early on before the EKG progresses to a full-blown stemmy,

you may not yet see ST segment elevation. What you may see instead, and you need to be aware of this, it's typically the earliest sign of an acute MI on EKG is the subtle increase. T-wave amplitudes over the affected area. So you'll see the T-waves becoming more prominent, symmetrical, pointed. They're known as hyper-acute T-waves. So you need to know that this may be an early progression to SD-segment elevation. All right. So which leads are involved in each type of infarction and where are you going to see, like which ST-segment elevation? So the one you'll likely see on an exam, the one I always got asked was inferior wall and

I know this one very well because this is likely for whatever reason the one they always seem to ask an inferior wall in my it's going to be leads to three and a vf two three and a vf inferior wall usually involving the right coronary artery and if you're only going to remember one remember this one inferior wall leads to three and a vf next anterior wall am i this is generally leads v3 and v4 and commonly affects the the left anterior descending artery septal wall i is going to be v1 and v2 that's normally your proximal l-a-d lateral wall is going to be one a vl v5 and v6 that's normally your circumflex and then posterior wall this one's a little weird but um posterior wall on v1 and v2 you're going to see an st depression and this is actually a reciprocal depression so think

about it since it's the back side of the heart you're actually seeing the opposite of what it's actually doing so there's actually st segment elevation but you're looking for the wrong you're looking from the wrong side. So at the posterior wall in my, normally what you do is you actually put leads on the back of the patient, normally around the scapula, and they're called leads V7, V8, and V9. And when you do these leads on the back of the patient, you'll actually see ST segment elevation on 789, V7V8, and V9, and that's your posterior wall. But on a regular EKG, if you didn't add those extra leads, on a posterior, you're going to see V1 and V2 ST segment depression, reciprocal depression. So remember that one. Especially if you ever suspect that a patient is having a posterior wall in I, make sure you ask the tech or whoever is doing it to put on those extra leads on the back. All right. So that's the EKG. You get that done right when they come through the doors right away. Next diagnostic test you want to do within those first 10 minutes is obtaining your cardiac biomarkers. So your troponin levels generally.

As far as diagnosis and the things you have that you really have to do and to differentiate, it's really EKG and troponants. You're going to get a chest x-ray, of course. you're going to be obtaining other labs, your electrolytes, your H&H, your H&H, your HMoglobinocrit. You know, but the things you need to focus on for the exam and the most important things in real life, your EKG and troponins. I know it sounds so simple, but the results of these two tests are going to guide the treatment plan for these patients. So don't waste too much time, at least for the sake of the exam, worrying about the little

details. Most important thing for diagnosing ACS, Q coronary syndrome, EKG troponins. Keep it simple. And if you look at any ACS algorithm, these are the two things that are going to guide your treatments the EKG and proponents so focus on those don't overcomplicate it let's make this simple you got too many other things to remember so focus on your EKG and your troponance all right so let's move on to two treatment now this one there's a mnemonic that we can use to help us remember what we need to know so you may have heard that of the mnemonic mona bash mona bash bash i altered it a

little bit because i felt like Mona bash doesn't create a good visual for you in your head So what I use instead is I use moan and bash because I think about a patient coming into the ER is having an MI. They're moaning in pain. They're bashing their chest, bashing the table. So I think of moan and bash. And to me, if I have a visual, I remember mnemonics much better. So moan and bash to me was much better than mona bash. You can remember either one. But for this, for the sake of this podcast, we're going to do moan and bash because that's what the patient is doing. They're moaning. They're bashing on their chest. So it's a good mnemonic but it does have some FYIs that I'm going to go over so moan most patients coming with chest pain are going to get moan initially or at least part of it we're going to go over

the caveats now so what does moan stand for moan stands for morphine oxygen aspirin and nitrates moan so they come in you treat them with moan let's start with the uh the the FYIs though so let's start with m which is really the most controversial so m stands for morphine morphine used to be used a lot for MIs, decreases chest pain, decreases anxiety, decreases cardiac workload. So these patients felt much better as soon as he gave morphine. But it turns out that studies over time showed that morphine actually had an adverse outcome on patients who were having an MI. And studies actually showed patients treated with morphine had a higher rate of mortality than those not treated with morphine. And one of the main reasons is there's a couple things, but there's an interference

with the absorption of antiplatelets that you're using, which are going to help in these patients like Lopidogrill. And overall, the general rule is that you're only going to use morphine if the patient has an unacceptable level of pain. They're just, you know, screaming in pain, nitrates aren't doing anything. It's not getting any better. Then you use morphine. You don't want to torture these patients, but you're not going to use it in every patient. Remember that morphine you'll only use if they have this unacceptable level of pain, not relieved by nitrates or other methods. Okay. So let's move on to the O and moan. And that's going to be oxygen.

Oxygen is another one that you don't always use. So supplemental oxygen should be given as necessary to maintain oxygen saturation above 90%. So supplemental O2 in patients without hypoxia has not been shown any benefit. So it's not necessary. So only if they're hypoxic are you going to give them oxygen, 90% or less. You want to keep the O2 saturation above 90%. So if they're any less than that, they're hypoxic. You give them oxygen.

If not, there's really no reason. And it's not going to make anything change. It's not going to have any benefit. So morphine and oxygen are the ones you're not really going to give in every patient. The next two that we're going to go over, there's pretty much you're going to use them in every patient unless they have any absolute contraindication. So let's move on to the A in Moan. That stands for aspirin. You're going to give almost everybody aspirin.

Generally between 162 to 325 milligrams, chew and swallow, most of the time it's going to be 325. The only reason you're not going to give somebody aspirin, with acute coronary syndrome. Really the only contraindications is if they had some rare anaphylactic reaction aspirin, or if they already took it on the way there. They were at home. They started having chest pain. They threw some aspirin down.

They chewed it up and they ate it. Or on the way over, the paramedics gave them on the drive over. That's the only time you're not going to give aspirin. Otherwise, everybody's getting aspirin in acute coronary syndrome. And the other one, the N in moan, which is nitrate. So nitroglycerin are going to be given to patients with the schema chest pain. typically you're going to start with your sublingual nitro, and then that's going to be followed by IV nitroglycerin if the patients are still having persistent pain after you give them three sublingual nitroglycerin, which a lot of times patients who have a history of stable angina are already going to have taken those three, and that's why they're coming into the ER because they're not getting any better. So nitrates work great.

They make patients feel much better. They decrease angina. They increase the myocardial blood flow. They decrease cardiac demand by decreasing blood. both preload and afterload. But you have to be careful because these medications, there's some contraindications because it's mainly because of their effect on preload. So they decrease preload.

And decrease preload, what does that do? Decreases blood pressure. So you don't want to give these patients that are hypotensive. Generally, you're looking at a systolic less than 90. You would avoid nitrates in. And then also another reason related to the preload. They decrease preload. So you don't want to give these patients.

This one's really important. because you'll probably get a question on this. Because they decrease preload, you don't give them to patients with an inferior MI with right ventricular involvement. Because this type of MI in this part of the heart, right ventricular involvement, inferior MI is dependent on preload. So you don't give nitrates in these patients. Same goes for morphine as well.

A patient with an inferior MI with right ventricular involvement, no nitrates, no morphine. You can't decrease the preload. They're preload dependent in this type of MRI. So you don't use either one of those. those, they're in an inferior or posterior wall in my. As we discussed anyways, morphine, you're not going to use very often anyways, but keep that in mind. So nitrates and morphine and avoid in those types of MI. And then finally, the last one, the one you're probably familiar with because of all the infomercials about this, all the commercials,

you're not going to use your phosphodiasterase 5 inhibitors. Patient was taken at phosphodiasis 5 inhibitor for rectile dysfunction in the last 24 hours. So your P.85s like Cialis, Viagra, last 24 hours, you can't give them a nitrate because they both vasodilate. You give them together. They have the synergistic effect and the patient can become extremely hypotensive. So those are the three contraindications for nitrates. It's going to be hypotensive patients, patients with an inferior MRI with right ventricular involvement, and then patients taking PDE5 inhibitors in the last 24 hours.

Otherwise, give them nitrates. They work great for a number of reasons. Okay, so that's Mone. Let's move on to the second part of the treatment plan, which is Bash. So Bash stands for beta blockers, ACE inhibitors, statins, and heparin. So beta blockers. Beta blockers are going to be administered almost universally to all patients with acute coronary syndrome. Of course, who don't have contraindications, which I'll go over in a second.

So why do we give beta blockers in acute coronary syndrome? Well, beta blockers do a number of really good things. So they decrease the oxygen demand of the heart. They decrease the blood pressure. They decrease remodeling, which is really important. The heart is potentially dying and it's starting to remodel, which can lead to heart failure. They improve left ventricular hemodynamic function. And overall, they reduce the infarct size, which is extremely important. And they can reduce mortality when they're given

early on. So everybody's going to get beta blockers unless they have a few of these things I'm going to go over now. So if they're extremely bradycardic, you don't use it. Obviously, you don't want to make their heart rate any slower if they're already bradycardic. If they have a heart block, it's contraindicated. Normally your second and third degree heart blocks. If they have a reactive airway disease, this one's kind of not an absolute contraindication, but it is one that you need to be aware of. And then patients who are high risk for cardiogenic shock, otherwise, beta blockers, almost everybody you want to use. One other reason why beta blockers are really important, I forgot to tell you about in a patient with a ACS is because one of the biggest killers in a patient

with an MI is ventricular arrhythmias. And beta blockers significantly reduce the occurrence of these arrhythmias. So let's patient has an absolute contradiction. medication beta blockers is a no-brainer. You want to use that. So that's your B in Bash. Now A in Bash is stands for ACE inhibitors. So it's really more for long-term use rather than initial treatment regimen, but normally they're started within 24 hours, up to 16 days following into Q&MI. They improve left ventricular ejection fraction. They decrease remodeling and improve the mortality rate. So A in Bash is going to be ACE inhibitors. The S in Bash stands for statins. This one's pretty obvious you have a patient with coronary artery disease likely they need to be on statin therapy so for

all patients with acute coronary syndrome aces high intensity statin therapy like atorvastatin 80 milligrams or suvastatin 20 to 40 milligrams daily will be started and generally it's early on it's suggested actually before they go to the cath lab to start them on a high dose of statins like 80 milligrams of a torvastatin so that's the s in bash that stands for statins and then finally h which stands for heparin doesn't have to Heparin, but they do need some form of antithrombotic therapy. And the goal of this therapy is to impede the progression of that thrombus that's formed in the coronary artery that's preventing blood from flowing through and getting worse. So it's going to prevent the myocardial infarction and ultimately death. And remember, your antithrombotic drugs like heparin impede the formation of

new clots. So they're not going to get rid of existing, but they're going to make sure that that new clot doesn't get any worse. And they're going to make sure that no new clots form. And they're and then thrombolytic drugs like TPA are going to break up and dissolve existing clots so they can break up that clot that's already formed. So just remember that. Sometimes they can get confusing between the two. So that's bash. That's going to be your beta blockers, ACE inhibitors, statins, and then heparin.

One other adjunct med that you should be aware of is clopidogrel, which is Plavix, and then also glycoprotein 2B and 3A inhibitors like integerlin and epsimab, which can also be used. Those are kind of like adjunct meds, but mainly it's moan and bash. Those are the ones you really need to know with all of the exceptions I went over. Those are the basics to treating a patient with acute coronary syndrome. The final treatment options I want to go over, really it's just one thing, is reperfusion therapy. So this is the ultimate treatment option for a patient who's having an acute MI.

So reperfusion therapy can be a number of different therapies. It's basically just getting the blood flowing again. So it can be either with PCI, which is percutaneous, coronary intervention. So that's the cath lab. It's going to be a stent or angioplasty opening up that stenose valve that, you know, that's filled with the new clot and all of the atherosclerosis. If the facility doesn't have a cath lab or they can't be transferred a facility that has a catholic lab within 90 minutes, that's cut off time. The other option that you have is fibrogynalysis or thrombolytic therapy. So that's medications like TPA. So these are the clot busters that break

the clot that's causing the occlusion. So again, moan and bash, those are the ones you're going to use initially. So that's morphine, oxygen, aspirin, nitrates, plus your beta blockers, ACE inhibitor, statins, heparin, and then finally, in an acute am I, you need some form of repurpusion therapy. So that's either going to be your cath lab or your thrombolytic therapy if you can't get them to a cath lab within 90 minutes. Okay. So before we wrap up acute coronary syndrome, I want to review a few miscellaneous topics that I think are pretty high use. you may likely get a question on. So the first one is cocaine-induced myocardial infarction.

So these patients are going to present, just like an MI in many cases. They're going to have ischemic chest pain symptoms. They're going to have diapheresis. They can even have ST segment elevation on EKG due to the coronary artery vaso spasms. That's causing ischemia, potentially an infarct of the artery. That's why it's really important to get a good history on your patient and question about drug use. So there's four things that I think you need to know about cocaine-induced myocardial infarction. Four things I think it's enough to get the question right. So as I mentioned before,

cocaine use can cause coronary artery vaso spasm. So the coronary arteries are going to be vaso-constricted, either decreasing or completely occluding blood flow for a period of time. So remember that vasospasm of the coronary arteries. Second, this is probably the most important thing. Your EKG is going to show transient ST segment elevations. That's the key to diagnosis. Transient, most important word, ST segment elevation. That's the key. Your treatment, calcium channel blockers, first line, nitrates is like a close second, but both are going to stop the vaso spasm. So really important calcium channel blockers, your main treatment, nitrates is another option. Then the final thing you should know is basically not treatment, but something that you're going to avoid.

You want to avoid non-selective beta blockers in these patients. It can exacerbate the condition. It can lead to the vasospasm getting worse. due to unopposed alpha one blockade. So no non-selective beta blockers in patients with cocaine-induced MI. They want to give them calcium channel blockers. All right. So last miscellaneous thing I want to go over. Or actually, two more things.

I want to go over, uh, Dressler syndrome. It's very simple to learn. There's not really much to know about it, but you could likely get a question on it. So Dressler syndrome, all it is is a post-MI paracarditis. So in the days after a patient presents with an MI, they're recovering. All of a sudden, they have this new onset of chest pain. They may have a fever, pulmonary infiltrates, paracardiocardial friction rub, and this is a post-MI paracarditis known as Dressler syndrome. So treatment, once you rule out that they're not having a new infarction, treatment is going to be with either aspirin or colchicine.

Generally, we want to avoid other n-seds because they can thin the infarction zone from the MI and interfere with a scar formation in the area of the infarct. So treatment, again, is going to be aspirin or colchicine, and that's Dressler syndrome post-Mi paracarditis. thing that I want to review and then we'll be done. We'll just do a few questions is the triad of right ventricular infarction. So you definitely may get a question on this. And due to the right ventricular infarction and it's the right ventricle infarcting and essentially failing, you have this unique clinical presentation that you won't likely see in the other MIs and has this triad that you need to be aware of for the exam. The exam is always like triad. So definitely know this one. So this is the triad of right ventricular infarction. The three things that you'll see in a patient with a right

ventricular infarction, at least for the sake of the boards, increased JVP, increase the right side of the heart backing up into the jugular vein. So these patients are going to have increased JVP. You look at the neck and you see the jugular vein bulging out there. They're going to have clear lungs. It's really important. This is going to rule out left-sided failure or other pulmonary differential. So clear lungs, increase JVP. And then the last one is going to be a positive Kuzmol sign. So that's the paradoxical rise. in JVP on inspiration. So normally, I've gone over this before, but normally on inspiration, the appropriate response

is a decrease of JVP with inspiration, but because of the right ventricle failing, fluid backing up into the right ventricle, right atrium, moving up into the jugular vein. Now when they take in a deep breath, the fluid's actually going to back up and you're going to have this positive QSMal sign. So increase in JVP on inspiration. So those are the triad, increased JVP, clear lungs, and a positive QSmal sign. Okay, so that is acute coronary syndrome. Let's do five quick questions.

So number one. What population commonly has atypical symptoms in an acute MI? Three specific populations that have atypical symptoms of an acute in mind. It's going to be women, elderly patients, and diabetics. What medications should be avoided in an inferior or posterior wall, MI? Medications to be avoided in an inferior or posterior wall, am I? Morphine and nitroglycerin.

What is the treatment of choice in a patient with cocaine induced MI? Treatment of choice in a patient with cocaine induced MI. It's going to be calcium channel blockers and nitrates. Of course, calcium channel blockers really is your first line. Nitrates is close second. Question number four. An inferior MI involves ST segment elevation and which leads. Inferior MI, the one that they're probably going to ask you,

involves which leads, ST segment elevations, and 2, 3, and AVF. Inferior MI, 2, 3, and EVF. AVF. Then finally, which cardiac biomarkers peak the fastest, which are the fastest cardiac biomarkers to peak? Myomai, you are so fast, myoglobin. That is your fastest peaking cardiac biomarker. All right. So that is acute coronary syndrome. Thank you so much, as always, for listening to my podcast. Please, if you haven't subscribed yet or checked out my YouTube channel, please do. I really think it can be helpful. And thank you so much, as always, for the the comments, the subscriptions, the likes, the five-star reviews.

I really appreciate it. And good luck on your pants, your panery, your EORs, and good luck in PA school.