Okay, so today we're going to go over acute coronary syndrome that involves unstable angina and STEMI, STEMI, and then a couple other miscellaneous topics, which we'll go over at the end, like Dressler syndrome and cocaine-induced MI, so some other things that I feel are important for the pants. Just really quickly, I always want to say thank you so much for the comments, the likes. Every time you guys leave a comment, it just makes my day, so I really do appreciate it. If you haven't checked out the podcast yet, please do.
It's under Apple Podcasts and Spotify under the same name, Cram the Pants. I think it's good for on-the-go when you're driving to clinicals and things like that. Please, as always, if you're enjoying the podcast, you're liking it, go ahead and leave me a review. Like I said, it really does make my day and I really do appreciate it.
Let's go ahead and get started with acute coronary syndrome. Acute coronary syndrome is a term used to imply there's a suspicion or a confirmed acute myocardial ischemia or infarction. This is commonly due to plaque rupturing or breaking free of an artery, which forms the secondary artery thrombosis.
the clot blocks the blood flow so we can actually take a look at what that looks like here i got a couple different diagrams and you can see you have this plaque with a fibrous cap and this is all enclosed there's no issues here except for the fact that it is blocking a little bit of the blood flow but blood's still getting through patient's fine but then all of a sudden you have the the cap will rupture as we can see here as well and what happens then you have all these platelets coming in and it starts to form thrombus here and because of that you essentially either can completely block the flow which would be an infarct or enough so that the patient starts to have anginal symptoms and you have ischemia here. So as soon as that clot breaks, it ruptures, you have all this clot forming here, and that's when we start to have issues with acute coronary syndrome. So there's three types of acute coronary syndrome that you need to be aware of, that you need to know of.
The three types are unstable angina, NSTEMI, which is non-ST elevation MI, and then ST elevation MI, which is a STEMI. And I'll go over those in more detail in a few minutes. So let's first go over the clinical manifestations.
Most of these you're going to be pretty familiar with. They're not going to be anything new to you, but there are a few things that I want to make sure that you are aware of and that you're comfortable with for the clinical manifestations. So the first thing is that this pain, a couple things that you need to know, it's not going to be relieved with rest generally, and it's not going to be relieved with nitro.
And the key to that is because patients can have stable angina. They take nitro for, they know they exert themselves a little bit too much and they'll start to have these angina symptoms. But generally, as soon as they sit down, they take that nitro, they pop the sublingual nitro, they start feeling better.
But in this case, in acute coronary syndrome, it's not the case. It's generally not going to get better with rest. They've already popped three sublingual nitros, it's not getting any better, and that's why they're in the ER today seeing you.
So this is different than their normal clinical manifestations of stable angina. Generally, the pain is going to last over 30 minutes. With acute coronary syndrome, you'll see some differentiations with that 30, 45, 60, but generally over 30 minutes. And then of course, I'm sure we've all heard this it can radiate to the left arm It can radiate into the mandible there the lower jaw and into the back And then these are a few keys that I want you to be familiar with so it can be it's typically going to be Non-positional so aka it's not relieved by sitting forward doesn't get worse when they lay down and The reason why these things are important is you need to be thinking of your differentials So if you have a patient that says well, I have chest pain But when I sit forward it gets better and then when I lay down it gets worse Well, what differential would you be thinking of for something like that? You'd be thinking pericarditis.
So with acute coronary syndrome, that's not the case. It doesn't matter what position they get in, it's not getting better. And then the next one is it's non-pluritic.
So it doesn't get worse with inspiration. So you can start to rule out some of your pulmonary causes like pneumonia, pneumothorax, which will all generally get worse with inspiration as they breathe, as they take in a breath. So again, it's going to be non-pluritic. And then finally, it's going to be non-reproducible. So if you push on their sternum, you palpate on the ribs, there's no change in the pain.
Whereas the patient with the differential, one of the differentials you should be thinking of, especially in younger patients, is costochondritis. And generally with costochondritis, you push on their sternum and they'll start to have some pain that'll get worse. So again, these are things that you need to be thinking of when you have your differentials in line on the vignette or in real life, that patients with acute coronary syndrome, it's not going to matter the position, if they're taking in a breath and it's not going to matter.
If you're pushing on their sternum, the pain is not getting any different in intensity. So those are some things that you need to be aware of. Now, these patients are also going to have sympathetic activation due to the acute coronary syndrome. So they're going to be tachycardic. They're going to be diaphoretic.
They're going to have nausea, vomiting, all due to this. So those are also things that you need to be aware of. And then this is the thing that I feel like is really important for you to be familiar with it. Some patients, certain populations, are going to have this atypical presentation.
so they're not going to come in with chest pain radiating to the left arm it's going to be different and that's why you want to make sure your clinical skills are you know up to par and especially on these vignettes that you're aware that certain populations are not going to present the same way so Let's go over the presentation these patients may have. So some of these patients, especially elderly patients, may have a syncopal episode. It's from the acute coronary syndrome. They may have weakness, palpitations, dyspnea in the absence of angina, or even epigastric pain.
And the population that you need to be aware of that can present this way is women, elderly patients, and diabetics, especially diabetics. A lot of times they'll have no chest pain and they'll just coming in, they're a little bit diaphoretic maybe, maybe some epigastric pain. Same with elderly patients and even women, sometimes they'll just have that epigastric pain.
So be aware, women elderly diabetics may have this atypical presentation that you really need to be aware of. It's really important for when you're actually out there practicing to be aware of these things and know, okay, I need to get an EKG and treat this a little bit more seriously. So those are your clinical manifestations.
Again, most of this stuff is probably not anything new. So let's go over the three types of acute coronary syndrome and what you should be familiar with with each one. So the first one.
is unstable angina. So these patients have an occlusion, partial occlusion of one of the coronary arteries. It's not completely occluded.
Some blood's still getting through. But be aware if these patients are having symptoms at rest, which they often will with unstable angina, the arteries are likely at least 90% occluded. So blood's getting through, but not much.
And like I said, they're generally not going to be, the symptoms are going to be improved with rest. They're not going to be relieved with nitrates. That's what makes this unstable angina rather than stable, which gets better with rest, gets better with nitrates.
So that's unstable. Now on your EKG, you're going to have these nonspecific signs on the EKG. So you'll have some signs of ischemia. Generally they're transient, but you may see a new T-wave inversion, some ST segment depression.
You're not going to see ST elevation though. You're not going to see that on unstable angina. So be aware of that. And then your cardiac enzymes are going to be negative.
So unstable angina, this patient's going to have this. chest pain that's different than what they normally have, or if it's their first time having chest pain, that's unstable angina right there until you've defined what their stable angina is. So if it's a new chest pain, unstable right away.
So otherwise, negative cardiac enzymes and then their EKG will not have ST elevation, but it may have some of these other signs of ischemia on there. Now, this is what your normal ST segment looks like. And these are some signs of ischemia that you'll see in unstable angina.
and your NSTEMIs as well. So this is ST depression you can see here, and then this is your T-wave inversion. So these are some signs, these are some things you may see in an EKG with a patient who has unstable angina. Now let's move on to your NSTEMIs, your non-ST elevation myocardial infarction.
So the only difference between unstable angina and an NSTEMI is that the cardiac enzymes are positive. So these patients have positive troponins. positive cardiac enzymes meaning these patients have myocardial cell death so the compromised blood flow to the myocardium in these patients is severe enough that their subsequent myocardial injury and that's the difference between an end stemmy and unstable angina the unstable engine of patients have not yet had any myocardial injury that's why their enzymes are not positive but in nstemi you're going to have positive cardiac enzymes the ekg will still look similar to unstable angina They're not going to have any ST segment elevation on EKG. They will have signs of ischemia, like I showed you in unstable angina, but they will not have ST segment elevation. And like I said before, the only difference between this and unstable angina is those positive cardiac enzymes indicating that there has been some myocardial cell death.
So this is obviously a little bit more severe, and a lot of times it's irreversible, the damage that's caused. And then finally, we have a full-blown STEMI, ST elevation myocardial infarction. this is uh you know the clinical manifestations we discussed previously is going to be similar they may be a little bit more severe these patients are going to have positive cardiac enzymes and then this is what the st st segment elevation looks like here you have your j point and you can see that's higher up here so st segment elevation mi so like i said the st segment elevation of the ekg is present because this patient has a complete occlusion 100 of the coronary artery is blocked So again, this can present in the same way as an NSTEMI.
Generally, symptoms would be a little bit more severe, but it can be similar in presentation. But these patients are going to have ST segment elevation on the EKG due to the complete occlusion of the coronary vessel. And to classify it as a STEMI, the EKG must have a new ST 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 again, this is going to be positive cardiac enzymes. Of course, this may not always show up right away. These enzymes sometimes take about four hours to peak. So a patient may come in and the EKG is starting to show ST segment elevation, but the enzymes are not yet positive. That doesn't mean they're not having an MI.
Just like in an NSTEMI, the enzymes may not be positive yet. So keep that in mind. It does take a little while for them to peak.
So ST segment, elevation MI. You're going to have 100% occlusion of one of the coronary arteries. You're going to have ST segment elevation, positive cardiac enzymes once they do peak.
And then generally, the symptoms are going to be more severe in these patients. So those are the three classifications of acute coronary syndrome that you need to know. Now let's actually go over those cardiac enzymes that I was just talking about.
So there's really... three that you need to be familiar with. There's going to be troponin, there's CK and CKMB, and then there's myoglobin. So those are the three that you need to be familiar with.
And I want to go over a little bit about each one. So let's start with the most sensitive and specific cardiac enzyme, the one that you'll see 99% of the time being used, and that's troponin. So troponins are proteins that are found in both cardiac and skeletal muscle.
And when the heart's damaged, the... releases troponin into the blood. There's a few different types of troponin.
You may hear of troponin T and I, even troponin C, but generally it's just troponin T and I that are used because they're more specific to cardiac tissue. So those are the ones you'll see, troponin T and I. Troponin levels will usually rise around anywhere around four hours after the onset of an acute MI, but they can stay elevated for up to 10 days, which will be important. It's something I'm going to go over in a minute.
So there's a few... caveats that you need to know about troponins. So troponins is a great test, but there's no perfect test normally.
There's always some kind of caveat. So troponins can be elevated in patients with chronic kidney disease. They can be elevated in patients with a pulmonary embolism, which is really important because if you have a patient coming in with chest pain, it could be a PE as well. It doesn't necessarily have to be an MI. And they can even be positive in trauma, like after cardioversion, after cardiopulmonary resuscitation.
So It's not 100% specific, which you need to keep in mind, but it is a pretty good test, and it's really the best test we have as far as lab tests to check for acute coronary syndrome. And this is just a general idea of what troponin is and where it actually is in the body. This is your myofibrillar troponins, and you can see they're actually released here when you have some type of ischemia or infarct in the heart within the cardiomyocytes, which gets into the blood, and this is what we're testing for here.
So remember, troponin, it's our... best test, but it's not perfect. There are some caveats that you need to be familiar with.
So let's work our way down the line to the less commonly used tests, but you still need to know them for the exam because I certainly did get questions on some of these. So next one is going to be CK and CKMB. CK stands for creatinine kinase.
It's an enzyme found in the heart, the brain, the skeletal muscle. And when there's muscle damage, this enzyme rises. It's not specific at all, but then they discovered CKMB. which was a more specific variation of the enzyme.
And this one's found primarily in cardiac tissue, not 100% specific, but more commonly in cardiac tissue. This test is not as common, or it's not as sensitive or specific as troponin levels. And there's really only two times that you're going to use CKMB.
So the two times you're going to use it is if you're in a country, because there are some countries that don't yet use troponin yet. USA, obviously, we use troponins. That's going to be our number one test.
But If you happen to live in a country where it's not available, CKMB is your next best test. It was a great test before troponin came along, but as soon as troponin came, CKMB was out the door. It just wasn't as good. So if you live in a country where it's not available, you can use CKMB.
And then this is the important one because this is what I was tested on and this is what I remember. So if you have a patient who has a reinfarction, so they come into the hospital. They had an acute MI, you treated them, you gave them a stent, whatever. And then a few days later, they start to have chest pain again. But you can't use your troponins again because remember, troponins are going to be elevated for sometimes up to 10 days.
So there'd be no point in doing it. But the good thing about CKMB is that it returns to baseline in as little as 72 hours. So you can check your CKMB for reinfarction. So that's really going to be your other use for this enzyme.
Otherwise, there's not a lot of times you're going to use it. And even with that being said, it's still not even commonly used for reinfarction. But that is one indication. And again, like I said, I was tested on that.
So just be aware of that. And then finally, our least commonly used, the one that's barely ever used anymore, is myoglobin. So the only benefit to this cardiac biomarker is that it peaks really fast, the fastest of all the biomarkers. And it used to be suggested to use as an adjunct to troponins to pick it up in MI. That may be the...
opponents hadn't detected yet but there was so many inaccuracies that it's just no longer suggested and overall the general consensus is that myoglobin just really shouldn't be used anymore for screening for acute coronary syndrome but remember it peaks really fast in as little as two hours the way i always remember that was my oh my It's fast. So it's just one of those dumb ways I used to remember this, but I did not forget that. So you remember myoglobin because again, another one that I got a question on, which one of the cardiac enzymes peaks the fastest, that's myoglobin, myomy, it's fast. So myoglobin is going to be your fastest cardiac enzyme. Outside of that, there's really not much other reason to use that.
So let's move on to the actual diagnosis. So when a patient comes in to the ER, the first thing you want to do before anything else, is get those EKG leads on the patient. You want to 12 lead EKG before anything else.
And of course, I'm referring to diagnosis here. Obviously, you want to give them aspirin O2, but strictly focusing on diagnosis, EKG as soon as they enter the facility. And remember, ST segment elevation will present prior to troponins being elevated. So that's another reason why EKG is so important early on. The general rule for an EKG is to have it done within 10 minutes of the patient's arrival.
Now let's... quickly go over the leads that are involved in each type of mi and before i do that i just want to give you a quick idea here i know we're talking about st segment elevation but we need to be aware of is like i said st segment elevation doesn't always happen right away what can happen before this is of course a normal ekg tracing what can happen before you have st segment elevation is actually start to develop these hyper acute t waves so that's one of the first things you'll see before st segment elevation so You just have these subtle increased T wave amplitudes over the affected area, and you'll see these T waves becoming more prominent, symmetrical, and pointed, and these are known as hyperacute T waves. So if you see these, suspect that the patient may be having an MI yet, it just hasn't progressed to ST elevation.
Once you have ST elevation, the next change here, you'll start to see some T wave inversion, which you also may see in some of these stages in between, but Q waves are the next big thing. So Q waves will develop after ST elevation. And unless you get the patient to the cath lab or you get the infarction solved very quickly, there's going to be permanent damage to the muscle of the heart.
And these Q waves are going to persist pretty much for the rest of the patient's life. So anytime they have an EKG done, they're going to have these Q waves. And that's an indication that there was damage and death to the cell walls of the heart. So you can have a patient a few years later, you do an EKG on, you ask them, oh, did you have an MI at some point in the past?
And they'll tell you, yes, I did. And that's why you'll see these Q waves. So initially, obviously, this is a normal EKG. You're going to see the hyper acute T waves, then ST segment elevation. And then later on, you'll see the Q waves that are going to persist pretty much for the rest of the patient's life.
Normally develops a few hours after the MI, but then again, it'll normally persist for the rest of their life. So I just wanted to go over that really quickly before we go into the actual EKG tracings. and what you're going to see so let's go over the first and probably the most important one the one that always seems to be tested for whatever reason but if you have an inferior wall mi this is going to be leads 2 3 and avf this is going to be your right coronary artery involving and if you're only going to remember one just remember this one because this is the one that always seems to come up so inferior wall mi you can see here leads 2 3 and avf you see that st segment elevation you see the j point there and then boom this big old st segment elevation here and two three avf and you can see the reciprocal depression in avl and lead one so you see right here two three and avf and then the reciprocal depression in uh one and avl so that's your inferior wall mi next one is going to be your anterior wall in mind so this one's kind of sometimes they'll say like v2 through v4 v3 or v4 but generally it's v2 to v5 and that's going to be your your left um i'm sorry your left anterior descending artery, so V2 through V5. And we can see here an anterior wall MI.
So you see some progressive ST elevation and even Q wave formation of V2 through V5. Here you can see these nice big peaked ST elevation here. You can start to see some of these big old Q waves here. And there's even some ST segment elevation in 1 and AVL. But you can see this is an anterior wall MI here.
You see 2, 3, and 4, that big old ST elevation. starting to see the Q waves as well. So that would be an anterior wall MI, V2 through V5, left anterior descending. Then we have our septal wall MI, which is generally going to be V1 and V2, which is your proximal LAD.
And we can take a look at what that looks like on EKG. So there's going to be, you can start to see the ST elevation in V1 and V2, even extending it to V3 here. You can see V1, 2, 3. You can see the ST elevation. So this is a septal wall MI here.
there's even a right bundle branch block here you can start to see some of the bifascicular block and left anterior so there's a lot going on here but your septal wall here v1 and v2 even say v3 That would be a septal wall MI there. And then we have our lateral wall MI. So in a lateral wall MI, it's going to be one AVL V5 and V6, which is going to be your circumflex artery. And then we can take a look at that on the EKG. So this is going to be an anterior lateral septal, I'm sorry, an anterior lateral STEMI.
So you can see ST elevation in V2 through V4. So that's your anterior portion here, V2, V3, V4. and then you can see your lateral leads so we see in one we can see in avl and then we can see in v5 and v6 so that's your lateral leads so one avl v5 and v6 we see st elevation and then we also see the anterior portion in v2 3 4 so that's an anterior lateral wall mi and then finally this one's a little bit different this is your posterior wall mi so this is going to be Not ST elevation on a regular EKG. What you're going to see, because you're seeing the backside of the heart, you're seeing the opposite. So if you ever see on V1 and V2, you see ST depression, you should know that you need to get leads V7, V8, and V9, which are placed on the back of the patient to see the true ST elevation.
So we can see here on V1 and V2 here, even into V3, we see this ST depression. So what they did was they realized that this, so they said V1 and V2 has ST depression. Let's see if this patient has a posterior wall MI.
So they switched out these leads, put it on the back of the patient, which I'll show you in a second. It's the back right under the left scapula. And then you can see here V7, V8, and V9 has this nice little big ST elevation. So again, because it's the posterior side of the wall, you're seeing the opposite.
So you see depression in V1 and V2. But if you put it on the back of the patient, which I'll show you here, you put leads v7 8 and 9 you can see the back side of the wall so then you see this st elevation on v7 v8 and v9 so be aware of that for your posterior wall and eyes and be aware in real life if you ever see st depression in v1 v2 even as a v3 you should be thinking this patient may be having a posterior wall my ask the tech to put those leads on the back of the patient okay so that's your ekg that's the big thing that these patients need that's the diagnostic test you want within 10 minutes of these patients coming through the door. And then the other thing that you want, of course, is their cardiac biomarkers.
That's another one you want within 10 minutes for diagnosis. And these are going to be the things that are going to guide your treatment and decide what these patients need next. Of course, that's your troponin, your CKMB, your myoglobin. Of course, these two probably not going to be used.
Just be aware they exist. It's most likely just going to be your troponin. So those are your cardiac biomarkers. Then, of course, you're going to want to get a focus history and exam. I'm not going to go over the...
All of the other things that you're going to be doing. So, I mean, Pacer's going to come up with chest pain. You're going to get a chest x-ray.
You're going to get your electrolytes, your H&H. You know, you're going to get a bunch of other things. But are those really important for you to know for the exam? Do you need to know that you're getting a chest x-ray? No, they're not going to ask you that.
They're going to ask you about the URKG, and they're going to ask you about your troponins. That's all they're going to ask you. So, it's not overcomplicated. I don't need to go over all of your electrolytes and all of your other labs and everything like that. Those are the common sense things that you don't need to waste your time on when you have so many other things to focus on.
diagnosis ekg troponins any algorithm that you see for acute coronary syndrome is going to follow those two findings and that's what you really need to know so that's all you need to know for diagnosis make sure you get your biomarkers and make sure you get your ekg of course you want to get a focus history and exam you know find out what's going on with the patient as best you can so let's move on to treatment so you may have heard of the mnemonic monobash but i don't like monobash because i don't feel it creates a good visual monobash doesn't really mean anything So what I did instead, instead of moan and bash, is I came up with moan and bash. Because when you think of a patient that comes in with chest pain, what are they doing? They're moaning in pain.
They're groaning, moaning. They're bashing their chest. They're hitting the stretcher.
They're in so much pain. They're moaning and bashing. So moan and bash. That's what I remember because I think of that person coming in. See this guy here?
He's moaning. He's grabbing his chest. He's bashing his chest.
That's what I remember, MOAN and BASH. And MOAN and BASH stands for morphine, oxygen, aspirin, nitrate, beta blockers, ACE inhibitors, statins, and heparin. So I'm going to go over all of those and all of the little caveats and FYIs because there's a lot for a lot of these. So what you should know is that when a patient first comes in to the ER, you want to start with MOAN with the caveats that I'm going to go over.
But this is generally what you want to start with your initial treatment when a patient first comes in. The first one of that is morphine, and this is probably your most controversial here. The one that you're going to hear is not really used anymore, so let me go over why that is. Okay, so morphine was previously used very frequently in acute coronary syndrome.
It decreases chest pain, decreases anxiety, decreases cardiac workload, but it turned out that study showed it actually had an adverse effect on outcomes. Study showed patients that were treated with morphine compared to those who were not at a higher rate of mortality than those not treated with morphine. And one of the main reasons is its interference with absorption of antiplatelets like clopidogrel, which is obviously a big helpful agent in acute coronary syndrome.
So overall... Morphine you're not going to really use often at all anymore. The only time you're going to use morphine is if this patient has an unacceptable level of pain that's not relieved by nitrates or other methods. Otherwise, you avoid morphine. Morphine is basically used as a last line.
These patients are screaming in pain. Nothing else is helping them. You don't want to torture them, so you're going to use morphine. But otherwise, it's not going to be commonly used anymore. So it's part of the mnemonic and it helps the mnemonic work.
But remember, morphine is just not used very often anymore. now we're going to go on to another one that isn't used often but it does have a place so oxygen is the o in moan and oxygen should be given as necessary to maintain oxygen saturation above 90 percent but supplemental o2 in patients without hypoxia that patients that are above 90 has not been shown to offer any benefit so it's really not necessarily so only if they're hypoxic are you going to give oxygen so morphine and oxygen oxygen you're not going to give to every patient next to you generally are these are These are ones that you're going to be using almost every patient. So the A stands for aspirin.
You're going to give them around 162 more often 325 milligrams chew and swallow and they're getting this as soon as they come through those doors The only reason you're not going to give somebody Aspirin in acute coronary syndrome the only real contraindications here is if they had some anaphylactic reaction aspirin Which is not common or if they had already taken it at home which obviously happens a lot or you know, the paramex had them take some in the on the ride over otherwise everybody's getting aspirin normally around 325 milligrams and the last one this one's used very commonly as well this is nitrates so nitroglycerin is given to patients with ischemic chest pain typically you'll start with sublingual nitro and then this is followed by iv nitro the patients are still having persistent pain after three sublingual nitroglycerin so nitrates work great they make patients feel much better they decrease angina They increase myocardial blood flow. They decrease cardiac demand by decreasing both preload and afterload. But you have to be careful who you give these medications to, mainly because of their effect on preload. They decrease preload.
And decreased preload decreases blood pressure. So a few contraindications. First one, you don't want to give these to patients that are hypotensive. So normally the number you're looking at is a systolic less than 90. And again, they decrease preload.
So you don't want to give it to anybody with an inferior MI with right ventricular involvement because this type of MI, the heart is dependent on preload. So you don't want to give them something that decreases preload. Same reason you wouldn't give somebody morphine that had an inferior MI with right ventricular involvement because morphine also lowers the preload and you don't want to lower preload in somebody that has a preload dependent type of MI.
So no morphine, no nitrates in patients with that type of MI. And then finally, the one that you probably are already aware of because of all the commercials with all the warnings, anybody who's taken a phosphodiesterase 5 inhibitor for erectile dysfunction in the previous 24 hours. So PED5s like Cialis, Viagra, both nitrates and PDE5 inhibitors are both vasodilators.
So if you take both of them together, they have the synergistic effect and the patient can become extremely hypotensive. So contraindications again for nitrates, most patients are going to get them. unless they're extremely hypotensive, generally blood pressure less than 90 systolic. Patients with an inferior MI with right ventricular involvement, and then patients taking PDE5 inhibitors in the last 24 hours.
So that's MOAN. Now let's move on to the second part of the treatment plan, which is BASH. Remember, they're moaning in pain, they're bashing their chest.
So what does BASH stand for? BASH stands for beta blockers, ACE inhibitors, statins, and heparin. So let's start with beta blockers.
Beta blockers are administered, this is another one you're getting up to almost... every patient, universally to all patients with acute coronary syndrome who don't have contraindications, which I'll go over in a second. So why are beta blockers so important in acute coronary syndrome?
Well, beta blockers decrease the oxygen demand of the heart, they decrease blood pressure, they decrease remodeling, which is really important, they improve left ventricular hemodynamic function, and they can reduce the infarct size, which is extremely important, and they generally just reduce mortality when they're given early on. And then another really big thing about beta blockers is most patients, the thing that will kill most patients with acute coronary syndrome is going to be a ventricular arrhythmia. A lot of patients with MIs develop these ventricular arrhythmias, which can be fatal, and beta blockers significantly reduce the occurrence of these arrhythmias.
So unless the patient has an absolute contraindication, use beta blockers. It's a no-brainer. Some of the reasons you wouldn't use beta blockers... You're going to be a patient with a second and third degree heart block, bradycardic patients, patients who are at high risk for cardiogenic shock, and then, of course, any reactive airway disease is also important to avoid beta blockers in.
So that's beta blockers give to almost everybody unless they have one of those absolute contra indications. Next one is going to be ACE inhibitors. So that's the AN-BASH.
It's really more for long-term use rather than in the initial treatment regimen. They're normally started anywhere from 24 hours to 16 days following an acute MI, and they improve left ventricular ejection fraction, they decrease remodeling, and overall improve mortality rates. It's another great med to use in acute coronary syndrome.
S is going to be for statins. so it's pretty obvious you have a patient with coronary artery disease they need to be on statin therapy so for all patients with acute coronary syndrome high intensity statin therapy like a tour of a statin 80 milligrams rosuvastatin 20 or 40 milligrams daily will be started and generally pretty early on it's actually suggested before you take these patients to the cath lab to get them started on high dose statins like 80 milligrams of tour of a statin and then finally uh the h in bash stands for heparin so it doesn't have to be heparin but these patients need some form of antithrombotic therapy and the goal of this therapy is to impede the progression of the thrombus that's formed in the coronary artery and thus prevent myocardial infarction and ultimately death so just remember antithrombotic drugs like heparin impede formation of new clots so they're not going to take away that clot but they're going to make sure it doesn't get any worse they're also going to make sure that no new clots are formed And then thrombolytic drugs like TPA actually break up and dissolve that existing clot. So just remember that because sometimes you can get them mixed up in your head. So that's BASH.
And then the last thing that I want you to be aware of is there are some adjunct agents like clopidogrel, glycoprotein 2B and 3A inhibitors. Those are your antiplatelets like integralin, epsiximab. So those are some other medications that you may use as an adjunct agent to the ones we went over. But really know MONE and BASH really well because those are going to be your antiplatelets. your main medications that you're going to use in a patient with acute coronary syndrome.
So the last thing that I wanted to go over as far as treatment is the biggest thing of all, and that's going to be your reperfusion therapy. So reperfusion therapy, it's the ultimate treatment option for a patient having an acute MI. So reperfusion therapy can be a number of different interventions.
So it can be percutaneous coronary intervention, which is going to be your angioplasty, your stenting, and then your thrombolytics like TPA. So those are the two options you have for reperfusion therapy in a patient that has an acute MI and you need to gain blood flow again through that coronary artery to avoid any further death of the cardiac muscle. So that's what you're going to use in these patients.
So let's just quickly go over each one. So first, PCI, percutaneous coronary intervention, you want to get this done within 90 minutes. If you cannot get PCI done you can't get them to the cath lab within 90 minutes you're gonna use TPA which is going to be your thrombolytics but if you can that's the the best treatment it's better than thrombolytics less risk you want to try to do PCI within 90 minutes so that's going to be like I said your angioplasty your stenting I'm sure we're all pretty familiar with this you just put the stent in blow up the balloon and then you put this is this the actual stent here just to regain perfusion through that infarcted artery and that's the the main goal for treatment is going to be PCI. And then of course you have your thrombolytic therapy or your fibroanalytic therapy.
So this is going to be the main medication you'll hear of most is going to be TPA that's at place. There's some other ones like streptokinase and some other ones that are less commonly used. But these are the clot busters. They break up the clot that causes the occlusion. And we can take a look here.
So what they do is they activate tissue plasminogen. And that produces something called plasmin. And what plasmin does is it breaks down and degrades fibrin.
So we can see fibrin strands are in here, which is actually forming the clot, stopping the blood from flowing. So you have something that breaks that down. You can see the plasmin dissolve these fibrin strands, and they can actually get blood flowing again.
So this is going to be your other option if you don't have a cath lab available to this patient within 90 minutes. So those are your couple options. Like I said, and again, like I said, TPA is going to be the one you're going to hear of used most commonly.
Like I said, there's also streptokinase. Really the only reason you use streptokinase, it is cheaper, but it's less effective than TPA, so it's not used as often. And really the only reason is if the patient's at a high risk for an intracerebral bleed, the risk in streptokinase is less than in TPA. So that might be one of the only reasons that you'd use it. so let's go over a few miscellaneous things related to acute coronary syndrome that i feel you might be asked the question on and i think it's beneficial for us to at least go over real quick so first it's cocaine induced myocardial infarction So I'm going to go over a couple, they're called vasospastic disorders.
And I feel like these are really important to know, not just for the boards, but in real life is because they can present very similarly to an acute MI. So you need to know to be able to differentiate because the treatment's very different for them. So let's start with cocaine-induced myocardial infarction.
So these patients are going to present just like an MI in many cases. They're going to have ischemic symptoms like chest pain, diaphoresis. They can even have ST segment elevation on EKG.
due to the coronary artery vasospasm which causes ischemia and potentially an infarct of the artery and that's why you want to make sure you get a good history on your patient questioning about drug use which is really important so really there's only four things that i feel like you need to know about this cocaine induced mi to get the question right so the first one is that like i already went over cocaine can induce coronary artery vasospasm so we can take a look here when the artery actually spasms it can clamp down so tight that you can actually have an infarct Normally this is transient and it will release again, but if it's long enough you can have some damage here. And sometimes it won't spasm enough or you'll just have some ischemia. But either way, you can have some trouble here.
These patients are obviously going to be in pain because of this. So two, this is your key. Because on the question they're going to say transient ST elevation. And that's your key to knowing that this isn't an MI, that this is some other vasospastic disorder.
So EKG will show transient ST elevation. That's really important, probably the most important. thing in this. Third one, you need to know that calcium channel blockers is going to be your first line.
Nitrates is a close second. Remember, anytime you basically have anything where there's spasm going on in the body, like esophageal spasms, remember calcium channel blockers is normally going to be your first line treatment. So again, like this, same with this one, no difference.
Calcium channel blockers is your first line. Nitrates are a close second. And then the fourth thing that I feel like is really important is to know that you cannot use non-selective beta blockers in these patients.
It can exacerbate the condition. It can lead to the vasospasm getting worse due to unopposed alpha-1 blockade. So no non-selective beta blockers in these patients. Okay, so the next vasospastic disorder that you should be familiar with is vasospastic angina, which used to be known as Prinz metal angina. You may still hear it being called that, so just be familiar with that name as well.
So there's a couple things that I feel like you should know. So again, the severity of chest pain with this can be indistinguishable from classic angina. pectoris which is associated with coronary artery disease but the difference is in the context in which it occurs so this is really important especially for your vignette they're going to say the patient is having chest pain but it was the middle of the night they were sleeping which is not going to be normal for your normal coronary artery disease normally that's from like some form of exertion normally it's not going to wake them up in the middle of the night but with vasospastic angina it typically occurs at rest So that's really important for your vignette to know that. Again, just like in cocaine-induced MI, the EKG is going to show transient ST elevation.
And then another way you can diagnose is with angiography. And you're actually going to provoke these vasospasms because they may not have it at the time that you're diagnosing it. But you'll have them, you'll perform angiography. And then you actually give them acetylcholine. There's a couple other ones, but the ones we use here are govamine, I believe it's caused.
CALD is not used here in the United States, but that's another one you may hear of. But acetylcholine is the one we most commonly use that can actually provoke the coronary artery vasospasm so we can visualize it on angiography to make the diagnosis. And then again, treatment's going to be the same, calcium channel blockers, same reason you want to avoid the beta blockers in these patients. Okay, so a couple of things I don't want to go over.
This one's really easy, Dressler syndrome. It's really just a few things that you need to know about this one. So Dressler syndrome, all it is, it's post-MI pericarditis.
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 fever pulmonary infiltrates pericardial friction rub but you want to make sure after you rule that out reinfarction that you consider dresler syndrome and the treatment for these patients is going to be with aspirin or colchicine generally want to avoid other NSAIDs because they can thin the infarction zone and interfere with the scar formation in the area of infarction. That's really all you need to know about Dressler syndrome. Post-MI pericarditis, they're going to present with the normal pericarditis symptoms, pericardial friction rub, chest pain, fever, and then treatment with aspirin or colchicine.
Last thing I want to go over is your right ventricular infarction. There's just a couple things that I feel like you should know with this. The clinical presentation is unique with right ventricular infarction.
They're going to have this triad that you need to know. This unique clinical presentation, like I said, is much different than you'll see in left ventricular wall and my soap. These patients are going to have increased JVP, again, because it's the right side of the heart, so it's backing up into the jugular vein. They're going to have clear lungs.
That's really important because that rules out left-sided failure or other pulmonary differentials. And these are in contrast to those found with left ventricular infarction, pulmonary congestion. You're not going to hear your third or fourth heart sounds.
So it's much different. Clear lungs, that's really important. And then finally, Kussmaul sign, which is paradoxical rise in jugular venous pressure on inspiration so normally I've gone over this before in some of the other videos but normally on inspiration the appropriate response is a decrease in JVP with inspiration but because in these patients the right ventricles failing because of the MI fluids backing up and you have the opposite response so you have this paradoxical rise in JVP on inspiration so that's the triad you need to know for right ventricular infarction that's the unique presentation of increased JVP clear lungs and Kussmaul sign And then finally, in a patient with a right ventricular infarction, you want to avoid nitrates and morphine.
Really important, no nitrates, no morphine in these patients, as well as in an inferior or posterior MI due to the decrease in preload. Again, this side of the heart is preload dependent. So you give them a medication that decreases preload, like a nitrate or a morphine, you're going to make the failure much worse.
And it could potentially be fatal for these patients. So be aware of those few things. with a right ventricular infarct those are some important things that you need to know all right so that's it let's really quickly test what you learned from today do five quick questions and then wrap it up so which population will commonly have an atypical presentation during an acute mi so what are the three types uh what are the three populations that will have an atypical presentation it's going to be women elderly and diabetics women elderly and diabetics what is the treatment of choice in a patient with cocaine induced mi Cocaine induced MI they're gonna get calcium channel blockers remember nitrates is a close second An inferior wall and my will be seen on what leads on an EKG This one's really important because this is the one they always seem to ask it's gonna be two three and AVF Remember that one remember that concrete that in your head. That's probably the one you'll be asked which cardiac biomarker peaks the fastest That path the fastest one to peak my oh my you're fast.
That's myoglobin and then finally Post-MI pericarditis is known as Dressler syndrome. Okay, so that's the five questions. Thank you so much as always.
That ran longer than I thought it was going to, but I think there was some good stuff in there. Hopefully it'll help you for your exams. Please leave me a comment if this is helping. You know, give it a thumbs up and subscribe to the channel. I'm releasing new videos every week about now, maybe seven to ten days.
And thank you so much for everything, all the comments. Good luck on your pants, your pantyhose, your EORs, and good luck in PA school.