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Cardiac Labs – What and When to Use Them

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***Previously Recorded***

Do you need a troponin or a CK-MB? What about a CK-MM? BNP?! In this session, we will cover all those pesky labs that deal with your cardiac patients and what they ACTUALLY mean.

Video Transcript

I just want to kind of get this, uh, make sure everybody’s on the right track for today. If you are running a, this tutoring session in mobile, um, try turning the uh, your phone sideways cause that may allow you to see a little bit better. Um, ideally, sometimes this has done better on a desktop, but you can see the session. Uh, we are looking into, we noticed that this morning there was a little bit of an issue with maybe a couple of users and not being able to quite see everything in the middle. So I’m trying to turn the screen a little bit, make it a little bit better for everybody. Uh, anytime while everybody’s jumping on, just tell me where you’re at, where you’re from, uh, dropping names in the chat, you know how this is. Um, and then the sweet Chicago’s excellent. Who is here for, um, amorous back. Excellent. Who is here for in our city live? Anybody if you. Excellent. Did you like it? Did you enjoy it? Did you get everything you needed to out of it?
I’m gonna back this up. Oh yeah. Perfect. Cool. So you saw me do my crazy sock method, which, uh, I think I’m doing tomorrow. It should be good. That one tomorrow. So cool. Um,
one other bit of housekeeping. Oh, uh, how many of you I moved it. Oh No, here, let’s try that there. That’s probably a little bit better. Cool. Okay. Uh, another little bit of housekeeping who in here, we just launched a brand new course yesterday, medical terminology. And if you have not seen it, go check it out. I am selfishly pugging plugging my own lessons. Um, there was a lot of fun to create a love medical terminology. Um, I’m big on it and uh, it’s like, I forget how many lessons, but we go over all the systems and, and uh, prefixes, suffixes, basic chord structure, how you make words, how you break them down. It was Kinda my, my shameless plug. Um, so let’s get going. So cardiac labs, these are the labs that we’re looking at for this afternoon before we get going. Um, I know that some of you jumped out of the session this morning to go catch Nicole session and is, are there any other, uh, questions that I at can maybe answer from that one this morning if you wrote it down? Um, that way we can, the way I can answer them for you and if not, we’ll get going on this one.
yes, no, maybe so if not we’ll, we’ll go for it. Alright, cool. Cardiac clams. So with cardiac labs we’re doing a couple of things, obviously working at labs for the heart. Um, who can give me some examples of some cardiac labs that you would maybe check on a patient. I’ll give you guys just a second type than in tropes. Cool. There’s a couple of other ones that we’re looking at that we’ll go over today. Anything else? So we’re talking like all cardiac labs, so any labs associated with heart disease, heart failure, uh, in my B, B and p. Perfect. Yep. Cool. So cardiac labs, c, c, k something, read. We’re going to get into it. So there’s, there’s actually a C K, um, which is great. And kinase. So we’ll get into that here in a minute. But the first one I’m looking at is proponent. Search opponent is zero. Oh, okay. Before I, before I go over these, um, is anybody not in the United States? Because if you’re not, I have a really cool resource for you that I’ll give you at the end. Whereas in Maine, everybody’s in the United States. Everybody uses these. Okay, cool.
John John’s in the u s okay, perfect. All right. Majesty. I’m going to give you, um, at the end of this, we have a cheat sheet for international units and I know that this value is different and this is why I want to give it. Um, so the first thing I want to say before we go over any of these values today are that are that any of these values, um, they’re, you should always pay attention to your, uh, facility policy, right? So the first thing I want to do is, so this is kind of the generalized standard and there’s, there was a huge method in developing what true opponents actual like value is to determine if it’s, um, elevated. And this is kind of the general value. Most of the hospitals that I’ve worked in have been, uh, less than, uh, anything less than 0.1.
Like that was the actual marker. So anything greater than 0.01 nanograms per mil was considered critical. Now this is kind of generalized standards, so just make sure that anytime you’re looking at these, you, uh, that you pay attention to the facility policy. We’re covering the normal values. These are normal u s values. This is, we use, I think the Davis, um, or not Davis. Uh, there’s another line book that we use. Um, but for the most part, these are all standardized. So just make sure that you’re paying, are I have to, I can not drive this point home hard enough, right? So just make sure that you’re looking at the thing I want to get. The thing I want you guys to really get out of this session is what values we look at, why we look at them. And is there anything that’s really, um, blatantly obvious about changes. Like, if I have a patient who’s tropes are 0.9, regardless of whatever unit you’re in, those are really high. Okay. So yeah, that’d be terrible. So here’s the thing, I’m tropes. So tropes who can tell me why, um, give me a reason why your opponent would be elevated.
Am I, that’s Kinda the number one reason. So let’s look at it. And so am I in myocardial infarction also known as a heart attack. Um, here’s what happens inside the cardiac myocytes are, um, there’s a protein called proponent for an eye. And what happens is, is when the cell dies or there’s damage in the cell ruptures, deponent is released into the bloodstream and then it becomes detectable and it over. Um, and then once it’s detectable, then it tells us that there’s myocardial damage and it’s specific to the cardiac monocyte, which is why the other values we’re going to talk about later are important. But for the most part, this is what we use it for. Who here has said, um, just say, I, um, if you’ve heard of this term demand ischemia.
let me turn this a little bit more. So we get to see a little bit better that ring lights in my way today. I’m gonna turn this off. Let’s see if we can make this better. Alright, let’s try this. Perfect. I know you can’t see my face. Sorry. You guys were playing with lights today. Alright, cool. Demand Ischemia. Demand Ischemia is basically when the heart, okay, so let me back up. Um, in order for, and they might’ve happened, you have to have a lack of profusion with an m I that happens in the coronary arteries. That means the coronary arteries are blocked. That oxygen can’t be delivered to the cardiac monocytes. Therefore the myocytes aren’t getting profused and the die. Similarly with demand Ischemia, the same thing happens. However, there’s no blockage and that results in like an EKG or we’ve got to do something different.
So with domain dischemia basically you can have causes where the heart is worth being worked so hard that um, or that there’s not, I’m going to lose one more time. And the perfusion is lacking that you will actually have an increase in troponin without having a, uh, an emi. So there’s two types. There’s cardiogenic and non cardiogenic cardiogenic acute coronary syndrome, very standard stuff. These two are uh, acute. Uh, the cardiogenic demand, uh, demands scheme in Mia are closely related, but am I, it requires much further interventions and there’s other criteria for it. But with a non cardiogenic cause these are reasons why. So I remember sepsis leads to shock and shock is a lack of profusion to tissues. And so if we have septic shock, we can have non cardiogenic demand ischemia. Does that make sense?
Perfect. Okay. Renal failure, renal failure results in hypoperfusion, uh, in some patients. So you can actually have demand ischemia there. The other one is extreme exercise. All of your other organs are in vital need. And if you, if these are much rare cases, but it can happen basically marathoners, extreme marathon and extreme athletes, they’re going to go out and they just basically put so much work on their heart that eventually they deprive it of oxygen. It’s the last thing that becomes profused. And so you have this demand ischemia. So these are the things, these are the causes that you would need. So if you’re a patient as am I, you’re going to get tropes. You know what your values are on. The other thing is most cases they’re going to be sent in like a green top tube. That’s the, the other thing. But again, refer to your Po, your facility for those. Let’s look at the next one. Be In p Ryan Nature Attic Peptide. So this is a normal way. So B and p amber asks, is this tutoring session being recorded? It is, however, they are not available to be, uh, viewed currently. I’ll say it that way. Um, we are obviously we want to make these available to everybody. We’re figuring out how we do that. So we hear you. You guys are asking for that all the time. Um, so B and p, when in what case would you use BNP for
Nope, sounds weird. Brain nature. Etic Peptide. So never heard of demand Ischemia, the connection with sepsis and more, well a, so amber says, I’ve never heard of demand ischemia over the connection with sepsis and more. Um, hopefully I’ve been able to make that connection for you. Um, we can always come back to that at the end. Amber, if you want me to clarify that a little bit more. Perfect. Yeah, yeah, yeah. I remember, I’ll tell you about the first case I ever heard what they made us keep in. It tripped me out. So BNP, um, let’s come back to this one. Brain nature to pip died. So if we looked at the term nature ISAs nature, he says when you break it down, uh, in at t is sodium and your ISAs is, you’re in like the process of urinating, right? So basically it’s a, it’s a, um, it’s a short protein that helps to improve, um, the facilitation of mooning moving sodium and water out of the body.
Here’s what happens. BMP is found in the ventricles and as I say, I did this last time. Cool. Hello. My little heart here. Okay. Found. Okay. See that? Cool found in dart. Yeah, the little tiny heart. It’s not actual size. This would be like a for a like a 12 year olds maybe. I don’t know. So ventricles they actually found in the ventricle so as cause the heart is a pump rate. So squeeze it, squeeze it, squeeze it, squeeze as well. Over time, as the heart starts to fail, what happens is that these ventricles stretch. And so what happens is BNP is released and says, oh we need to squeeze a little bit harder cause we need to pump fluid out and we need to try to diaries a little bit. What happens is in congestive heart failure or heart failure, the ventricles get so stretched that this BMP level stays high and it can’t quite recover. So B and P is actually a measurement for determining the severity of congestive heart failure. So if we look at this normal BMP values are a hundred picograms per per per milliliter. So it’s actually a
woo, oh
I can’t do it that way. I have to do it this way. I’m going to tilt this down just a second so you guys can see the bottom of the screen. Okay, cool. So a hundred to 300 is mile greater than 300 is moderate. As long as you don’t get to 900, once you get to 900, that’s severe. I think the highest that I’ve ever seen is like 4,200. I think John said that he seemed like 4,500 so there’s some pretty significant BMP. The thing about BMP, make sure my next slide. So like we said, the BMPS and the ventricles and when the, when you have increased volume in a weakened heart, that’s going to make that B and p go up in order to get a confirmation for, you can’t just use BNP as like, oh hey they’re having an exacerbation or um, they’re having some sort of, or where they are in like in stage congestive heart failure.
They actually use a combination of diagnostics to rate the CHF. So x-ray and then an echo. So BNP is a protein released in ventricles, distress out increased BNP is related to heart failure and CHF. Yes, that is correct. Amber, you are dead on the money. So that’s, so again, what we look on the front of the X-rays, we look for cardiomegaly. So that’s that enlarged heart. Um, so normally let me stand in front of her. So like normal heart is about like this, what happens with Cardiomegaly, you actually see it, it gets about to this size. So it actually you’ll see like this extension usually through past that. Um, probably the sixth intercostals so it’s like you’ll get really big hearts. I’ve seen boot boot chip. Um, yeah, you can see that because that, that lower left ventricle, um, I’ve never heard it put like that, but I could see where you could get that from the, from that increased x-ray echo or we’re looking for, with the echos, we’re looking for decreased ejection fraction or fractional shortening.
That’s the term basically. Um, there’s a percentage when the heart squeezes and the blood is kicked out. You’re looking for how much is actually left, which is the ejection fraction. Um, normal injection fraction is like 50%. So anything less than that is pretty significant. Um, when my father in law, he had a, a, um, basically what that means, let me back up. So when you have an a decreased the objection fraction, what happens is, is that saying that so the heart squeezes, right? So it’s the power. You have all this power of the heart squeezing the blood out and then when relaxes and it fills, it says this is how much is left over when it squeezes. Well what happens is because the like the hardest failing for a variety of reasons, what happens is the heart fills and then when it goes to squeeze, it only squeezes so much and that what it’s, what’s actually left is that ejection fraction.
So you want, you want it to be 50 or greater, it’s usually like 50 to 60. So I was saying it’s, it’s pumping out about half. Well what happened with the fraction reporting is, um, you are, the ejection fraction is like, it’s only like 15% is pretty significant. Like I think after my father, my father loves MRI, he was down to about 15. That basically is an indication of how weak the heart is. Um, but again, you, you see h you check out the BNP you should do to x-rays and you do your echos to determine the severity of, of, um, of heart failure. So hard. Is it only ejecting [inaudible] Yep.
Correct. So what’s happening is basically think about it. So every time, so it’s weakened. So instead of, instead of kicking out like 50%, like it’s supposed to, it’s only kicking out like 15. So then it’s like, ugh, it’s weak, it’s weak, it’s weak, it’s weak. And then you get this overload of volume, right? So what happens if, imagine what that magic filling like a water balloon, right? So you fill a water balloon and every time you squeeze a water balloon, you squeeze like half of it out. Right? Well, imagine that you get to the point and you’re only squeezing like 15%, but the volume is thing the same. It’s still filling every time. Well, that water balloon is going with this be discussed in a critical care type course. Uh, Donna, what do you mean the critical care type course? Like a, like a different tutoring session or like an a specific course, like a lesson. [inaudible]
I’ll give you a second to type it out. We take three master’s classes. Um, Nicole is doing a heart failure specific heart failure. Last one was critical care. Uh, we do not currently have any critical care like courses or lessons, but do have heart failure lessons. Um, in theory they’re all the same, right? Oh, no, no, no worries. Um, so in theory they’re all the same for some, uh, for some patients they need help in getting out, um, getting that heart to be more effective. So what you’re looking at with critical patients, so if you have a critical patient and you want to get them, the thing that’s making them critical is the fact that they can’t get out the, the fluid. So they have like fluid volume overload. Um, they’ve got edema, they’ve got a cascade of other issues, and now they’re running the risk of like, uh, an impaired airway because they may have some fluid accumulation in the lungs.
You have, um, the decreased ability to, um, you have like a lot of hemodynamic instability. That’s what makes those patients, that’s what makes those patients critical. So the difference between like let’s say you have a med surge patient who has an, uh, an elevated BNP of like 4,500 and a critical care patient who’s got an elevated, the, the NPO of 4,500 is you’re treating your management of the, of the care is actually changing because you’re not going to be able to improve that BMPS number rapidly. So we’re talking about managing blood pressure, managing fluid status, um, that’s where it gets a little bit diff. That’s where it gets more in depth. So we’re talking about things like you could do swan, which is like a monitoring of, um, like pulmonary wedge pressures and uh, the um, uh, the different types of pressures in the heart.
And so it’s a much tighter control for those patients. You’re doing things like, uh, managing their blood pressure more tightly. You were doing things like sometimes dialysis, uh, the patients should just require more care and it’s more fine tuned. Um, so think about it like that. It’s not that don’t become overwhelmed with the fact that a, um, the path though is different in a critical, um, like a critical patient versus a med surge patients. The big differences is that you’re now involving different organs. You’re now involving more organs that aren’t, uh, compensating and you’re having to kind of fix them all together. Really. Uh, it’s, it’s way more complicated. I’m talking about it and we can talk about it for day. Like I love talking shop about this stuff, but, um, the thing that you want, that you want to think about is that you’re really trying to fine tune and improve the patient’s symptoms and condition. Um, versus where a med surge patient with a BNP of 4,500 is going to be, you’re talking about management and longterm care. You’re talking about, hey, how are they gonna manage when I send them home? That’s what I’m thinking about right now. I’m, how do I get him off the vent? That’s the difference between critical fair care does that. Donna, does that make sense? I know I may have talked a little bit in circles, but like that’s kind of the, the big difference between the two.
Perfect. Okay, let’s go the next one. Great. And kinase c k who could tell me where suitcase found.
I think to a degree, but I’m looking forward. So Vanessa says the heart, uh, muscles. Okay. So there’s three types of CK. When we look at c k well, it’s creating kinase. What we’re looking at is you usually have damage to a muscle. So there’s three variants, it’s what we call it, or they’re called, um, isoenzymes and the differences you have c k m m which is skeletal muscle. If I’m driving my car and I get in a car accident and uh, I go to the hospital and they run a C K C K is going to be elevated. CK By itself is also allowed value. Uh, but there are various, m c k m m is skeletal muscle. So my c k n m may be elevated, but my CK MB, which is the one we’re going to talk about, maybe normal k a c KBB is specific to the brain unless you have some sort of brain and soul that’s going to be within normal limits.
Yeah. Crush injuries. Yup. Gas Seen, I’ve seen those things go up. It’s ridiculous. Alright, here is your normal range, man. You see, don’t let me forget going to give you that cheat sheet. Um, and for those of you who are interested in the cheat sheet, it also has us values as well. It just, it’s a nice little um, visual so that you can see the difference. The one oh 2.4 a lesson to perform nanograms per mil, it’s detectable in three to six hours. It’s peak is in 12 to 24 hours and the c k. Um, so here’s, here’s where it’s really important and this is why you want to know about the CK-MB is that in lieu of a troponin not being available, lab doesn’t do it. There’s some sort of limitation. What have you, you can do CK-MB instead. Just know that, that your opponent is specific more to those, remember those cardiac myocytes. And the other thing is that they’re going to be detectable, um, sooner versus your CKMV. Okay. So that’s the difference. That’s, that’s kind of the thing is we like, we go, okay, well what’s available. So when you say cardiac labs, we’re going to do CKC K and B and a trope typically.
Yeah. So they’ll start, they’ll peak in 20th, pick in 12 to 24 hours and then I’ll start to come down. But again, you want to kind of use these things all together. You want to say, um, uh, one of the things we talk about when we talk about, uh, liver enzymes, and I talk about this, I know in the, uh, the liver function test, the lesson is that you can’t ever take one specific enzyme, especially with cardiac labs, unless it’s trope tropes. Like the only one you get to pass on, um, and say, hey, this is the problem. You kind of take them all together. The other thing that I want to caution you is don’t treat numbers, never treat numbers. You always want to treat the patient, right? You always want to say, oh, hey, here’s c, K and B is 2.5, but he’s asymptomatic. Maybe he has a previous injury. That’s the other thing that you got to think about with these. Let’s see if I have one more slide. Nope. Okay. So you guys had questions about demand ischemia. Let me go back. Does that all make sense with the CK
I know Nicole not doesn’t have a session right after me, so I’m not trying to fly through this stuff today. All right. Demand Ischemia. So the patient I had, um, was a crotchety old man and um, he shows up to the Ed. I was working in the ICU, snoop shows up and uh, I’d never heard of it, never heard of it in nursing school, never heard of my icy residency, never heard of it at all. Um, we were a surgical trauma ICU and I’d never heard of, I had just never heard of demand ischemia. So I wasn’t, it wasn’t a CV ICU, I wasn’t in, wasn’t dealing with like Impellas and swans and all of these things that are really just for heart patients. But I get this hard patient and uh, he’s on the floor and he’s fine, but the thing, so apparently he had had some sort of infection, which is why it’s really important to know about the non cardiogenic, the main dischemia.
But basically what happened was that he got sick and basically the perfusion, the lack of profusion to those cardiac myocytes cause the cells to die and to rupture. And because it was an overall, um, so let me pull this guy up. So I wanna I want to show you the difference. So if I have, let’s see, see if I can find the widowmaker on here. Left, right circumflex. Okay, cool. So see if I can do this. I’m doing, this is very backwards for me. So hang tight. Okay, here we go. Cool. Right in front of the camera. Um, this is the left a l the OBD [inaudible]. Um, this is one, I’ll just say it this way. This is one of the, uh, major arteries that that supplies blood to the left ventricle down here. Okay. Now, if there’s an occlusion that happens basically because of like a coronary artery disease, let’s say there’s a promise here and all of the profusion as it comes down gets stopped. So because there’s no profusion, all of the cardiac monocytes on the left ventricle don’t get perfused. And that your ponens go up. That isn’t in mind with demand ischemia. All of the cardiac myocytes because the overworking of the heart, like with Sepsis, it’s that lack of profusion. All of the cardiac myocytes are impaired. And what happens with that, that causes a Troponin to go up. So just like with, uh, maybe, um, I know. Yeah. So there’s no obstruction.
And without, without that obstruction, it’s just him.
What does concierge mean? Oh, concierge. Yeah. So there’s like an over amber, there’s a amber ass. So is it from like a, an overworking guest? So basically there’s this just lack of profusion overall. So like, I know that, um, sometimes we ask a question on a d dimer. Well with a d dimer, we can’t tell if it’s um, a VTE, a p e or a, um, or DVT. It just tells us that there’s a clot somewhere. Same thing with demand ischemia. Demand Ischemia says, Hey, there’s ischemia from the overworking demand, right? Lack of oxygen to those mind out with the blood pote. Correct. Whereas the MIA or results from an obstruction, which is why patients need to go to the cath lab to either get a stent or the PCI done, which is the big difference. Does that make sense? Perfect. Now you can go on and bragged all your friends. You’re like, I know what demand. Just give me this for sure.
Even vote those three.
Okay. If we built, I’m being prompted. Here you go. I have a teleprompter. A cute card. Okay. If we built a done for you program. Oh, okay. Okay. Got It. Okay. It took me a second. Okay. If we build a program done for you, sorry, I’m so used to that camera. Be in there. Okay. If we both like a like a program that was done for you. Tell me in the chat which term you like best. Number one and vote. This is number one. Concierge fancy number two. VIP number three was the last one. Oh, white glove. Also, none of these have anything to do with cardiac labs. This is strictly an NRSNG thing.
I need votes. Peeps. Go on for that lip.
Amber, you only get one vote and we voted twice. No, that’s cool dude. VIP Is this the, that’s it. VIP. Yeah, for sure. Wow. Alright, cool. Thanks. Groovy that we can help it out. That’s awesome. Hey, they all said hi. So, Hi Dawn. Sorry. Camera’s right there. Hey guys. Amber Peng. I don’t think anybody knew about midterms online yesterday. I forgot to and that was on my list to do. I asked people about it. Mid term is live, guys, go check it out. I’m supposed to be sending out a notification on that. [inaudible] all right, cool. So yeah, I know God, I’ve got to keep tabs on him. All right. So are these, are there any of these, I’m going to move this, this camera killing me today cause I’m trying to look here and here we go. Sorry. Are there any of these that you guys want me to go back over or that you have questions on? Yeah, demand scheming is one no one ever knows about. You say demand ischemia. Like why is this trope up? Well and it’s usually mildly elevated. It’s not a lot. So you’ll get like a critical lab back and there’ll be like critical lab of like 0.04. You’re like, why? So look at the patient’s presentation. Is he septic? Um, did he have some sort of renal issue? Does he have some sort of extreme like fatigue? Um, maybe Rhabdo,
g e P.
Yup. Now you know, now you know, I need a little rainbow and star the more, you know, um, and that’s right. So yeah, that’s, that’s one of the big things. So, and you can also have from acute coronary syndrome, um, atherosclerosis, like all those things. If there is a, an overwork and a higher demand because of more fatigue, you can get it. So think lack of perfusion. So the way I want you to differentiate it is, okay, trope is going up, trope is going up because the cardiac monocytes are dying. Okay. Why? We know it comes from a lack of provision. Why are we not getting perfused? Is there an obstruction or is there an overall lack of profusion? If it’s instruction, thank EKG, PCI, m I if it’s a lack of, if it’s Sepsis, lack of profusion, shock, hypovolemia, all of these things are going to potentially cause um, those are going to cause your non cardiogenic, um, demand. Dischemia so am I um, no, the classification. So, uh, let’s see. Am I can come from both. So the myocardial infarction is a specific infarction due to an obstruction. That’s the easiest way to remember it. Um, but the obstruction comes at different levels.
Just the, the easiest way to remember it. Is there a Cli? Is there like a got here late? Did you mention how to treat demand ischemia? So you would, uh, improve the profusion?
So think so, think backwards. Right? So Kathy, Kathy says it got here, got here late. Not a problem. We’ve got she covered. Uh, did you mention how, sorry, I’m just reading out of habit. I just read it. Uh, did you mention how to treat demand ischemia? So when you’re treating domain ischemia, what I was explaining is that the trope the troponins go up because there is either, um, Yup. So there’s either a blockage because the myocytes are dying like an MRI or there’s an overworking of the heart because of lack of perfusion, which is the second, which is when you fall into domain ischemia. So you could theoretically create an algorithm that goes down and says, okay, a trucks are up. If I go this way, is it, it’s like a profusion because of, uh, uh, an obstruction. Think, am I? If you go no obstruction, then go, OK, demand ischemia. Is it cardiogenic? So is it acs or if we go the other way, is there some other cause of the lack of profusion? Cathy, does that make sense? So you have to treat the profusion. So if it’s sepsis or hypovolemia, give them volume and prove the profusion.
Cool. Uh, let’s see. [inaudible] amber says blockage. Jakarta and MIA is evaluated with trope in demand. Ischemia is non cardiogenic demanded scheme. You can be cardiogenic if it’s related to acute coronary syndrome.
okay. Am I? No, you’re good. Um, so here we go. Demand Ischemia. Uh, let’s see, am I is evaluated with trope and demand ischemia? Non cardiogenic is evaluated. EKG, c,K and B. I’m trying to read your question and make sure I understand that my is evaluated with the troop. Anytime there’s a suspicion of cardiac injury, it’s true. So your demand, ischemia patients can still have chest pain, but the difference is differentiating. Is the chest pain related to an obstruction or is it related to
you know, some other unrelated like a demand, like, oh, my chest feels tight because I have zero profusion in my heart versus like an isolated area that’s being infarcted. Um, demand ischemia. So anytime there’s a suspicion for elevated proponents, you’re almost always going to get an EKG. You’re almost always going to get a CK MB cause I want to trend those all together. Um, but again, more information that you have, uh, the, the better. Um, you can evaluate it. So I’ll use another example. Um, liver function tests, liver function tests or Alk phos AST, uh, alt, if your AST is elevated by itself, that is not an indication of liver damage. If your alt is elevated by itself, it is not specifically an indication for liver damage. Same thing with alkaline phosphatase. The reason is is because these, um, these enzymes are found also in other areas of the body.
For instance, AST is found in muscle. So if some sort of somebody goes, works out, goes to the doctor and gets blood work and they’re l, they’re AST is elevated, then that can be the cause of it. You have to look at them altogether. So you have to actually look at all three values and see if you have trends along those. Let’s say, oh, alt is elevated, AST is elevated, our process is elevated, and that Bilirubin is high, probably liver. Okay. That’s, yeah, so better. Yep. So the more information you have, the better you can treat it. So the difference too is that if you can evaluate stemi versus non-stemi versus stemi and non-stemi, s t elevated Myo Cardio Myocardial Infarction, non-stemi, non St segment, elevated myocardial infarction. That’s how they’re differentiated on EKG. That’s so both of those silvercar a PCI but some, but the non estimates are typically, um,
I don’t want to say they’re more treatable. They’re the less life-threatening, they don’t require as soon soon-ish in interventions. Whereas like you got to go 90 minutes to door with a stemi or at 90 cents, 90 minutes from like a Florida door is what they call it. So when you actually from the time it’s evaluated and diagnosed to being in the cath lab. Cool. Does anybody have any questions about this or from the, from the session earlier? I know that we got off kind of quick earlier and I wanted to make sure that if anybody had any questions about those. So in the first session earlier we covered basic metabolic panel, comprehensive metabolic panel cvcs, liver function panel, renal panel lipids. So if you have any quick questions over those, I can answer them for you. Glad to help. Um, as we do with all of our sessions, just wanting to get a little bit of feedback. Let me find that. Oh, uh, majesty. Are you still hanging with me in here? Cause I gonna make sure I get that for you.
sweet. Um, oh my goodness. I’m operating like three screens right now. I feel like Hugh Jackman and swordfish. Hold on one second. Majesty. I want to get that cheat sheet for you and I want to get the cheat sheet for everybody else and I’m also going to drop some links in here for, um, let’s see. Let’s do labs. Cool. First one I’m going to drop is the direct lesson two, um, critical labs. I find it. Okay. So here is, this is the one I need someone to type messages back and highlight super important comments. What do you mean? Oh, you mean just like in the chat?
oh, it sounds good. Thanks amber. Um, let’s see.
oh, there you go. There you go. Cool. Okay. Somebody dropping a few. Just a quick question, kind of off topic, what in your opinion, if the doctors [inaudible],
uh, paying asks, uh, just a quick question, kind of a out of the top. No, you’re right on topic. Um, in your opinion, if the doctor orders a trope, do they need to order a CK-MB? Sometimes it’s not a bad idea. A you can get, you can glean some information from it. Um, it’s not, you can get some sort of insight into it. And I don’t want to say no because every provider will have their own like, hey, this is why we do it and that’s totally okay. Um, just follow with the, you know, like you’re not going to do any harm to the patient. So the question is, I guess, let me think of it. Let me rephrase it. It could you potentially make the problem worse or harm the patient by doing a CK MB in addition to, or instead of a trope. And the answer is no. Low cost to the patient. The worst you’re going to do is have to stick them again,
um, [inaudible]
and you get more information. So I would say, I would say that one trope is obviously going to be more specific, but what I, what I would want to say is, uh, to do one or the other to do CK-MB.
or to not do this gay and B, if that makes sense. I feel like I just talked to him in a circle, which would probably been um, oh, they find this one international. So it’s one of my favorite cheat sheets. Here we go. Cool. Cool. Fat Majesty. That is the one perfect. Um, uh, majesty that is the one that cheats you ever talking about you with the International. I think if I remember right, I think a tropes are actually evaluated in milligrams per mil
in not the United States. No micrograms. Sorry. So if I’ve got a trip back on a patient and it was 0.35 and I am not in the United States, I probably should not jump too quickly because it’s a different unit. It’s 0.35. This is why the joke is decimal points kill, right? So this is why we always pay attention to the units. So that’s that one. All right. Last thing I’m going to throw in your before a piece out for the day is this user feedback form. This thing gives us a lot of information. Takes like 30 seconds to do. Just tell us, uh, you know, let us know how the session went. And, um, you know, if we’ve been helpful at all cause we want to make sure that we give you guys the right content, make sure that we’re giving you what you need. If I’m doing restraint tutoring sessions and you’re not getting a lot of,
you know, there’s not a need for it. Um, or if I do, you know, fire and fire safety, it’s important. It’s a fundamental concept. But what I don’t want to do is, um, when I could be teaching you about pain, pain management for medications, you know what I mean? So, uh, just in that form real quick, you know, let us know if you’d like to session what we can do, uh, to make it better. Um, cause we always like to know. And then what are the concepts you’re looking for? So guys, I’m going to peace out for today. Um, we love you guys. Go check out med term medical terminology, Super Fun to do. Um, go check out those courses I put in there. Uh, check out those cheat sheets and, um, let us know what else we can do to help you guys. So like we always say, go out and be your best selves today. And as always, happy nursing.