Cardiogenic Shock Explained: Preload, Afterload, Inotropes & Shock Teams at the Bedside Part 1

Cardiogenic shock remains a high-mortality emergency in critical care—but survival is improving as clinicians better understand shock physiology and adopt cardiogenic shock team models.

In this episode of Banter at the Bedside, Abby and Kaleigh are joined by returning guest Dr. Michael for a practical bedside breakdown of cardiogenic shock recognition and management. Together they explain:

•  How to differentiate cardiogenic vs distributive shock 
•  Why preload, contractility, and afterload matter clinically 
•  When to use diuretics, vasodilators, and inotropes 
•  Dobutamine vs milrinone vs epinephrine 
•  How cardiac power predicts outcomes 
•  Why cardiogenic shock teams are improving survival nationwide 
•  How hemodynamics translate into real treatment decisions 

This episode is designed for ICU nurses, nurse practitioners, physician assistants, residents, fellows, and physicians working in emergency medicine, cardiology, and critical care.

This podcast is for educational and entertainment purposes only and does not provide medical advice.

Transcript

SPEAKER_01 0:06

Hey everyone, it's Abby and welcome back to Banter at the Bedside. We are here today for a new type of education episode. We're really hoping that this feels like you are sitting down at the nurses station with us as Dr. Michael, our return one of our returning physicians, educates us on some cardiogenic shock management and potentially cardiogenic shock teams, which is popping up in the literature. As always, this is for entertainment purposes only. This is not medical advice. Please seek the care of your own medical professional. This is solely medical information. Again, for entertainment purposes, and we do not represent any employer. Everything said here is our own opinions. As always, I'm one of your main co-hosts, Abby, and I'm a nurse practitioner. We're joined by our other main co-host, Kaylee. Hi everybody, welcome back. And then we have, as I said, Dr. Michael returning. Thanks for coming back.

SPEAKER_00 1:03

Yeah, thank you. This is a topic that I'm really excited about. It's just something that I has been kind of my child in terms of trying to like grow it and make kind of get it to where it needs to be on stuff. It's a lot more complicated than than I think we realized. And so hopefully I can kind of get us to there about how we can we can talk about the management and why cardiogenic shock teams and cardiogenic shock initiatives have become have become such a big deal. The first thing to talk about with it is understanding that it is a problem. So if you look back, the mortality for cardiogenic shock nationally is probably around 50% mortality. So you're talking about people that are showing up where half of them don't make it out of the hospital. And this was true for 30 years. If you look at at papers that go back from it from through the mid 80s through like 2015s, into 20 2010s, 50% of the people survived, and that was it. And then since then we've had this big jump where we're we've gotten down to about 20 or 30% uh mortality. So you're having a huge improvement in survival. Uh, and a lot of that has to do with the cardiogenic shock teams, but you're only as good as what you understand from it. So just the first thing is understanding that it's a big deal and understanding like why it's important to understand all the different facets with it. So the first thing I want to talk about is the definition. So whenever we're talking about shock in general, there's four main types of shock, right? You have your cardiogenic, distributive, obstructive, hypovolemic. So it's about understanding how you can diagnose cardiogenic shock. With a swan.

SPEAKER_03 2:45

Yeah.

SPEAKER_00 2:47

So that becomes like a that becomes like a difficult thing because if you're talking about shock, that part's easy. Like you're just saying, like, oh, you have somebody that's hypotensive. They have a systolic less than 90, a map less than 65, um or with signs of like organ dysfunction, right? Like your kidneys, your liver, something's not doing what it needs to be doing, your lactics up. It means, okay, now you're in shock. How are you supposed to tell what it is? One of the things that's always been like a pet peeve for me is when somebody's like undifferentiated shock, and that's how they present. And it's like differentiate it. Like they're it's not like they're it's not they're polar opposites of each other.

SPEAKER_02 3:28

Just figure it out. Yeah, went to med school for a reason. Yeah, you went to med school.

SPEAKER_00 3:36

But if you if you if you look at it, right, like cardiogenic shock has low cardiac output, distributive shock has high cardiac output. The next thing people look at is filling pressures, like your CBP and your wedge. Distributive shock has low filling pressures, cardiogenic shock has high filling pressures. If you want to look at mixed venous, mixed venous is low in cardiogenic shock, mixed venous is high in distributive shock. If you want to look at SVR, like resistance, they talk about it's low in distributive shock, it's high in cardiogenic shock. They're literally exact opposites when it comes to hemodynamics. And people are like, I don't know, could be could be both. And I was like, no, it can't be both. You can say it's mixed, you can say like they have a history of heart failure, and I think that they're also septic. But when people are like, I don't know, that's frustrating for me because like you can do the very like the bare minimum of things and should be able to say, well, at least I don't think it's these two since they're complete opposites of each other.

SPEAKER_02 4:34

Yeah. We're big fans of people doing at least the bare minimum. Thank you. Yeah, we love a bare minimum.

SPEAKER_00 4:40

So if you can at least kind of give me like a it could be this type of a thing, and this is why, it's helpful. Clinically, it can be tough though, right? Like if you're if you're hypotensive, being like, okay, I think they're in shock, if they have cold extremities and signs of organ dysfunction, then you're now you're thinking of a low flow state, which could still be like hypovolemic or cardiogenic or even obstructive, but less likely to be distributive versus if you have warm extremities and you're like, oh, that's more of like a septic picture or you know, like going down the distributive shock pathway. Um, but it's hard, right? I'm not gonna be able to tell you 100%. You could maybe start looking for JVD or look for signs that they're they're volume overloaded that would point you in the direction of cardiogenic. So there's the clinical diagnosis. You can add imaging to that, and that's a huge, huge uh like increase in in probability, right? Like I put a bedside echo on them and their heart was barely moving, or I looked at their echo from a month ago and they have a history of an EF of 20%. Um, that's going to be like a lot, I'd be like, that's more likely to be cardiogenic. If you want to be a purist about it, then yeah, like to really be a purist about it, then you have to say they have to have a cardiac index less than 2.2 and they have to have elevated filling pressures, like a CBP greater than 12, a PA wedge pressure greater than 15. Um, that's how you're going to like say that they have cardiogenic shock, like definitively for that. Because hypovolemic shock, you have low cardiac index, but you're not going to have high filling pressures because you're hypovolemic. So you'll have a low index, but you'll have like a CBP of zero or one or two or whatever, you'll have a low, a low wedge pressure. So yeah, so a swan will be your definitive definition. You can certainly try to get through it with without a swan. But yeah, so I think that's the important thing to say, like, do I think that this person is in cardiogenic shock? Um, and then the next thing to understand is like what it's doing from a physiological standpoint so that you can treat it medically. So if you think about it from a um a physiological standpoint, cardiac output is heart rate times stroke volume. And then stroke volume has three components you have your preload, your contractility, and your afterload. So, in order to pump blood around the body, you have to have like an appropriate preload and appropriate contractility and appropriate afterload. And people in cardiogenic shock typically are have too much preload. So they're overstretching their ventricles. They're on like the bad part of the starling curve. And so it makes it so that the heart can't contract like it wants to contract. And then when you're talking about contractility, they they typically have low contractility. Uh, when we often most of the time when we're referring to cardiogenic shock, we're talking about like systolic dysfunction, either left or right. I mean, there's other types that you can talk about, but for the for this conversation, it's going to be systolic dysfunction. And then the last thing is afterlifts. Yeah, just better.

SPEAKER_01 7:39

Basically, we're not getting into the deep weeds of RV failure, even though I know he's salivating too, because that's his own.

SPEAKER_00 7:46

Definitely, definitely. I mean, I'm definitely going to go into it, don't get me wrong, but uh we'll keep it on the other side of it. And then the last thing to understand from that hemodynamics is when your heart can't pump forward, you get less blood flow to your kidneys. When you get less blood flow to your kidneys, your kidneys don't know why it has less blood flow. So it's just saying, hey, I'm not getting good blood flow. I'm probably like dry. And so it activates the renin angiotensin aldosterone system. And then all of a sudden you start squeezing everything down, and then your afroload goes up very high. You increase your aldosterone, which increases your uptake of fluids and everything. So you end up fluid overloaded, you end up really clamped down, you have poor contractility. So if you're going to look at it from a hemodynamic standpoint, you have low cardiac output due to too much preload, not enough contractility, too much afterload. So everything we do from medical management is trying to fix that problem.

SPEAKER_01 8:43

I think it's really interesting first how like we learn about homeostasis. And me, one of the attending strokes, like we learn about homeostasis, and yet the body's like really bad sometimes at figuring out to do homeostasis. And that's like the premise of cardiogenic shock. Like it starts, and like those kidneys are like, I don't have enough blood, so I'm just going to make it harder for you. I'm going to activate the system to squeeze down, and it makes it harder for the heart to pump, which like continues the cycle of worsening cardiogenic shock. And it's like the body's so good in so many ways, but then in other ways it's like, no, you're hurting yourself.

unknown 9:21

Yeah.

SPEAKER_00 9:21

You're hurting yourself. No, no, no. Absolutely. Yeah. Like it, it, it, it, it can't just like look back on it and say, Oh, this is the heart causing this. All it says is there's not enough blood flow. Odds are I'm either bleeding to death or I'm dehydrated. I need to like hold on to everything I can.

SPEAKER_01 9:38

Yeah.

SPEAKER_00 9:39

Um, and it's just raw. Yeah.

SPEAKER_01 9:41

Can we just like briefly break down, uh, like make sure that like our listeners know what preload contractility and afterload are, just like super brief. And I'll make sure our website is live. So I'll make sure that there's more links to things in the show notes on our website that go into like more detail for that. If you're like, I really don't understand this.

SPEAKER_00 10:05

So, um, so it become there's the traditional definition, and then there's like the true definition. So I will try not to be like weird about it.

SPEAKER_02 10:15

So like going up with the true definition.

SPEAKER_00 10:19

So I so when we when people refer to preload, they typically are referring to volume. What's the volume loading of the ventricle? So, in order for your heart to squeeze, you have to stretch the ventricle open, which then allows it to kind of spring back and squeeze forward. So you're you're loading it with fluid to allow the the heart to then kind of stretch open so that when the valves open, it'll kind of go back and spring back and squeeze everything out. So we oftentimes when we're talking about what's the patient's preload, we're often talking about what's their volume status that's going to be able to be able to cause that to happen. If you don't have enough preload, like if you're dehydrated, the heart can't stretch because there's nothing to allow it to stretch. So you're not going to have good squeeze, or it's not going to be pumping out a lot of blood because it's not there to like squeeze it out. So you're not going to have a high pulse pressure. The difference between your systolic and your diastolic blood pressure is going to be low because you're just not loading the heart with a lot of blood. Versus if you're if you have too much preload, then that usually means you have too much volume and you've actually overstretched the ventricle. And it's like a it's like a spring when you've pulled the spring back too far, it's overstretched, it can't quite go back the way it was before. So it just doesn't work. You've kind of overstretched it. And so that's why when that's what we typically, when people are talking about preload, they're talking about the volume loading of the ventricle. Now, that's fine. I think we can talk about that. I think the true definition is the stretch of the of the myocytes at the end of diastole. So it's it's really more at the actual muscle level when we're being like a a purist about it.

SPEAKER_01 12:04

And you're nothing but a purist.

SPEAKER_00 12:07

Well, I think it just understands it better that you can have like a really thick ventricle and it's much harder to stretch it and that you could have less volume. Just there's it doesn't necessarily equate fully to be a, but it's a great way to think about it. It's just saying you're loading the ventricle with volume that allows that ventricle to stretch open so that when it's ready, it will squeeze it back. I think about it as loading a spring. The more you pull a spring back, the more it's going to shoot forward until you get to some critical point and then it's overstretched and then it's not going to squeeze back.

SPEAKER_01 12:40

Yeah, like the slingshots with water balloons as kids.

SPEAKER_00 12:44

Yeah, yeah, yeah. Um now, contractility, I have the same problem. So technically, when we talk about how well the heart squeezes, there's technically there's contractility, there's function, and there's performance. And they're all three kind of different. So whenever we talk about contractility, the strict definition is the squeeze of the myocytes themselves. And but whenever we're measuring contractility, oftentimes we're referring to EF, right? If I ask you and I say, hey, how's the person's heart? Like, how how well does it squeeze? You're typically going to go to their last echo and be like, oh, their EF is 50% or their EF is 20%, which is a it's a reliable, reproducible way to measure contractility. It's technically not contractility, it's technically function because it can change with preload and afterload. I always had this like tongue-in-cheek thing that says the best way to treat heart failure is to give them like a little bit of sepsis because it will make their heart look way better. Your heart, your heart has to squeeze against a bunch of afterload. And if you get vasodilated out because you're septic, all of a sudden your EF's going to look like 40, 50%. And you'll be like, oh wow, their heart's doing great. And it's like, no, it just has nothing to push against. It's pushing against nothing. So it's going to empty out more blood because it doesn't have to push against any resistance. And so if if somebody, and the same thing as if you add a whole bunch of afterload or you squeeze everything down, their EF's going to look a lot worse. Or with preload. If you if you don't have enough preload or too much afterload, your EF can look worse. So your EF can change within the context of of preload and afterload, whereas contractility just has no bearing on it with it. Um, but I think EF is a great way. When we're talking about contractility, we we typically are thinking about it in terms of EF. And then the last thing when we're talking about resistance is we we typically are thinking about how how clamped down is the vasculature. So we we typically talk about systemic vascular resistance. And I think that's a fine way to think about it. It's a calculation map minus CBP divided by cardiac output times 80. So your cardiac output's in the denominator. If you have a high cardiac output, you'll have a low SVR. If you have a low cardiac output, you'll have a high SVR. Again, it's not technically the best way to measure afterload. The best way to measure afterload actually has to do more with Laplace's law that has to deal with wall tension. And that has that the technical definition of afterload is the like the wall stress or wall tension of the ventricle during systole. You can tell I love math. So I like it's a lot of equations that get kind of like thrown in there. But Laplace's law is delta pressure times radius divided by twice the wall thickness. So if you have a super dilated heart that's really thin, uh, you're gonna have a lot of afterload even if you don't have a lot of pressure. So if you think about someone that has really bad heart failure, typically they'll have like a blood pressure of what, 90 over 70, 90 over 60. They don't have like a 180 systolic, but they still have a lot of afterload problems. And the reason they have a lot of afterload problems is because they have a very dilated heart. So they have a big radius, they have a thinned out heart, so they have low wall thickness, uh, which leads to high wall tension or wall stress. That is a better measurement of afterload.

SPEAKER_01 16:14

Just Le Pass, Le Paz's Le Pass La Paz's law. Yeah, yeah.

SPEAKER_00 16:20

So very easy to consider with all that stuff. Um easy.

SPEAKER_01 16:27

So those that's sounded easy. You doing all this math all the time?

SPEAKER_00 16:32

I do, yeah. I mean, I'm not like I'm not like doing that equation at the bedside, but like whenever I think about somebody, I'm saying like I, you know, you can think about what's their volume status for in terms of volume loading from a preload. How well do you think the heart's squeezing and then how much resistance does it have to push against? I think the the other thing that if you want to get into the this will become more important later, but EF is also, I think, a little bit misleading, right? It becomes misleading in two ways. One, if you have severe mitral regurge and you have an EF of 40%, you don't know which direction that that it's going, right? Like it could be 40%, there's 40% less blood in the ventricle. It doesn't tell you that 40% of that blood went forward. The 40% less blood, it could be going a lot of it's gonna go be going back up the mitral regurge. So it's not truly a 40% EF. If you closed off the mitral valve, the heart's gonna be a lot sicker and it may only be like 20%.

SPEAKER_02 17:31

And then that's what makes it heart, even if you have a swan, if they have like mitral valve problems.

SPEAKER_00 17:35

Yeah, yeah, yeah. Mitral valve problems, tricuspid valve problems. There's all sorts of things that can make it more difficult. And then the other thing is that 40% is a percentage, but it doesn't tell you a percentage of what, right? So it's a percentage of in-diastolic volume, and everybody has a different amount of volume in their ventricle at the end of diastole. So the normal amount of blood in a heart is 100 mls at the end of diastole, but some people with like chronic heart failure have 250 milliliters. So if someone, if someone has an EF of 20% with a normal size heart, they're only pumping 20 mls of fluid out with a 20% EF. If you have a big old dilated heart with an EF of 20%, you're pumping 50 milliliters out per beat. So that person has significantly better cardiac output, even though they have a much bigger dilated heart because they they have 20% of a much larger volume. So you have to take a lot more into consideration. If two people are beside each other with a 30% EF, they could be wildly different depending on what their mitral regurge is or how dilated their heart is, is is the the reason for that. Yeah. So that that's how I think about preload contractility and afterload. Not a simplified way, I apologize.

SPEAKER_01 18:51

But uh blood going in, blood going out, and the squeeze.

SPEAKER_00 18:55

Sure. We could do that one too.

SPEAKER_01 18:57

You love that, I'm sure. You're like, oh God, what did I teach you?

SPEAKER_00 19:02

But no, I mean I think it's I think it's important to just be if you you just have to identify when there's a problem with it. I think that's the biggest thing. Is there a problem with their preload? Is there a problem with their contractility? Is there a problem with their afload? Because then that's how you're going to uh take the management of it and say, like, this is why I'm doing the management that I'm doing. So it's it becomes much easier when you think about somebody with decompensated heart failure or cardiogenic shock, is if they have too much preload, you need to just get rid of preload. So if their preload is too much volume, get rid of that volume. So diuretics play a huge part in that. Get them to more out than in, then they'll have a negative fluid balance. And then you're helping get rid of that preload. If you can't do it diuretics, then you start thinking about doing it with uh dialysis, like CRRT or or intermittent HD. But like you're you're at least getting that preload down. That's gonna help, like, so you're not overstretched, and then the heart's actually gonna work a lot better when it's not overstretched. So you're trying to get them down to a normal uh preload. I think the easiest thing for me, if you have a swan in, it's try to get their CBP down to less than 10, try to get their uh wedge down to less than 20. Those are nice, easy round numbers to think about uh as kind of a goal. Now, there's more subtleties than that, but that's a pretty easy goal. Just I'm gonna keep doing this until they have a CBP less than 10 and a and a wedge less than 20. So diuretic split. And just put it in. Now, I actually do agree with it with right heart failure, they're actually way more likely to go on CRT than left heart failure.

SPEAKER_03 20:44

Yeah.

SPEAKER_00 20:46

So I'm I have a way quicker trigger to to to put in for CRT if it's if it's right-sided cardiogenic shock. And then the next thing is to think about is contractility versus afterload. I'll probably talk about afterload first. I think afterload is the most important because if you can get them to have a better afterload, it just takes the stress off the heart and their EF will improve. And and sometimes you don't need to improve the contractility if you can just kind of relax the afterload. And and there's actually a ton of papers out there that say if you can use afterload reduction with like nitropresside or nitroglycerin, they actually have better outcomes than if you try to use inotropes to like increase contractilities. If you can, after load should be your go-to. Now, you know, if your MAP 60 or 55 or whatever lower, then it's harder. If you're on vasopressors to try to just get a perfusible blood pressure, then yeah, you you can't be like, well, let me put them on nitroglycerin or nitropresside and let me do something. But if you're like, you've probably taken care of that cardiogenic shock patient where their blood pressure is like 95 over 85, like they have no pulse pressure, but they're diastolic. Crazy high, they're just like so clamped down. That's like a perfect patient to put nitroprusside on and really just like afterload reduce them. And typically you don't even need an anotropic agent because once you can just allow the heart to squeeze and like actually unload, uh it does considerably better. So uh my kind of like overall rule is if your diastolic blood pressure is higher than your map goal, you can tolerate afterload reduction. So if your map goal is 65 for perfusion and your diastolic 75, then I'm more likely to be like, let's just start with afterload reduction, versus if they're 90 over 60 or whatever, 89 over 60, I don't feel as comfortable saying like they're gonna tolerate afterload reduction.

SPEAKER_01 22:46

Yeah. I make sure you got some room.

SPEAKER_00 22:49

Yeah, you have some room to do some stuff with it. Which we can go ahead and start talking about. It becomes huge in cardiac cardiogenic shock initiative, but cardiac power, do y'all use that a lot on the things with it? Mm-hmm. Well so we use it when we have the pillows, basically. Sure. It's on it's on the screen.

unknown 23:08

Yeah.

SPEAKER_02 23:08

That's really the only time even though.

SPEAKER_01 23:11

Mm-mm. No, you are correct. We we've talked about I've been in conversations with cardiac people where it's like it really needs to become more standard talked about. So I think it's good.

SPEAKER_02 23:23

Driving their mortality rates up, like knowing that number.

SPEAKER_00 23:26

It it was the it was the they they re-looked at all the shock trials that they did for cardiogenic shock, and they were like, doctors love objective things, right? If you can give me like some objective number that I can make a decision on, that is much like that's super helpful. And so they went through all that data and they said the best indicator of outcomes was actually cardiac power, which is cardiac output times map divided by 451. And uh, with that, if you have a cardiac power less than 0.6, there was a really sharp kind of downward trajectory that said you just weren't going to do well. So, like spoilers for as we get into the cardiogenic shock initiative, the recommendations are if you have a cardiac power less than 0.6, they recommend mechanical circulatory support. They recommend putting in some sort of device as kind of your, your, your breakpoint with that. And it makes sense. If you have, if you have a low cardiac output but a high map, then you have some room, like we were talking about. We have some room to do some stuff. Whereas if you have both a low cardiac output and a low map, you're you don't have a lot of room to do stuff. Um so when it comes to afterload, I'm always looking at the diastolic blood pressure and saying, okay, where is it? Do I have the ability to give afroload? If I do, I really like to do it, especially if you have a lot of valvular dysfunction. If you have severe mitral regurge, you're gonna really like afroload reduction. If you have aortic regurge, you're gonna really like afroid reduction. So those are those are the reasons I really like to focus on afroloid reduction first, if possible. But if you're if you're already hypotensive in shock, low blood pressure, then you can't, you just can't do it at that time. So now you're talking about contractility. Um, and these days, when it comes to inotropes, there's really only three that we use. We use milmerone, dobutamine, and then epi is often considered an inotrope. The previous job I was actually I was not allowed to call it a vasopressor.

SPEAKER_02 25:27

We're not using it for that.

SPEAKER_00 25:29

Sure. So, like at low doses, like less than five, it has a a really nice, like almost pure inotropic effect. As you get to higher doses, that's when it gets much more of a vasopressor effect.

SPEAKER_01 25:41

Um so you weren't allowed to call it a vasopressor, right?

SPEAKER_00 25:44

Right. If we had it on, it was for inotropy. Now, I like to call what yeah.

SPEAKER_01 25:51

Well, I had one doctor and a travel doctor that came and was like, You guys doing debutamine and levo together, you're just doing epi. He's like, That's all you're doing is Epi. He's like, You're just giving it into two different ways, two different drugs doing what Epi did. So I did Sure. I mean, I mean, Let us Leva. He was from like the CT surgery world doing travel. And um I I did try Epi. I will say I didn't hate it all the time. And there's times now that I'm like, you know, maybe low dose epi is all we need.

SPEAKER_00 26:25

Not my first one, but yeah, and uh, you know, what he's referring to is that both debutamine and milmorone are inotropes, but they vasodilate. So we we usually refer to them as inodilators, where we usually refer to epi as an ino pressor. So it like it gives you an idea. Like if if you're hypotensive and you need contractility, then maybe epi will be able to help you out. Versus if you're if you if you have some ability to tolerate some afrood reduction, the best way, like if we talked about when we talked about it, for people in cardiogenic shock, they have low contractility and high afterload. So if you can get them to tolerate melranone or debutamine only, that's the ideal scenario because you're you're fixing the aflode part and you're fixing the contractility part. But sometimes they get hypotensive, especially on melranone, which is a little bit more potent of a vasodilator. And then you're like, well, I started melrenone, their index is better, but now they're on five of Levo. And I I don't disagree. I will say in RV failure, milrenone and vasopressin both lower PVR, pulmonary vasistance. So they're both fix the afterload of the right side. So if you're on melranone and vaso RV failure, I would say that is still superior to epi. So while while while while melanone is an ionodilator, vasopressin is a vasopressor, you're kind of one's dilating, one's constricting on the arterial side, they're both dilating the pulmonary vascular bed. So you're getting that benefit from both of them. So I would say that is not equal to saying, like, well, if you're going to do melmenone and vaso, why not just do epi? That would not be equal, especially an RV dysfunction. So some subtleties. But I think it's important to understand the biggest thing for me is when dealing with inotropes is dobutamine works in five minutes. Milmernone reaches a steady state in like four to six hours. You'll see it start to work, but it takes a while. So if you need something fast, don't go like reaching for Milmerone because it's not going to be fast. It's good. It works very well, but you're you're going to need some time. Or if you're unsure, if you're like, well, maybe they'll like like ionotropy, maybe they won't. Dobutamine's so fast on and fast off that if you put it on and don't like it, then uh you're gonna have a lot more benefit to turn it off. Versus if you start Milmarino and you're four hours in, you're like, let's not do that. You got another four hours to like get it back off. Um, you know, if I if I was giving advice to someone and saying, like, what would you reach for in somebody in cardiogenic shock from an ionotrope? I would probably reach for dobutamine. If they were profoundly in shock, I'm not against reaching for epi, but dobutamine is a really nice uh a way to see if you need contractility. I like it in patients who are inappropriately uh have a normal heart rate, right? If you're in, if you're in, you've taken care of heart of cardiogenic shock patients and like their heart rate's like 105, 115, they're super tachardic. And then you'll take care of these cardiogenic shock patients and their heart rate's like 75. And they're like, why is your heart rate 75? Like your heart's barely moving. It it really needs to be beating faster than this. And you're like, I'm on, I'm on all this stuff, like beat faster. And I like dobutamine and that that side of it because it does have a little bit of like chronotropy that kind of helps the heart rate out that I that I like a little bit more with it. So I find myself reaching for du dobutamine in that situation. Yeah.

SPEAKER_02 30:00

Well, that's what I was thinking. A lot of the patients' heart rates are high already, and then yeah, yeah, yeah, yeah, yeah.

SPEAKER_00 30:05

I mean, if they're already super high, or if they've been prone to go into arrhythmias like AFib and AFRBR, of course.

SPEAKER_01 30:12

Yeah, of course they have. I did have one doctor, uh, another travel doctor, and never wouldn't use debutamine, only used millrenone, and he called it the mill. And it's nails on a chalkboard to me. And he'd be I'd be like, they're crashing, you want to start debutamine. The mill's fine. The mill. And I'm like, Okay.

SPEAKER_00 30:37

I think I think the interesting ther thing for me with Mill Renone is I rarely go above like 0.25. I have on very rare occasion gone to like 0.375. It's just not something that I typically go up on. If I if I'm needing that much Milrenone, then I'm already deciding on either they need mechanical support or we need to be thinking about a different agent. Milwren, if you look at its max dose, it's like 0.75. So it's got like this huge range of like being able to give it. And oftentimes people are like, well, you can't give Mil Renone. They have renal dysfunction. At those low doses, it really doesn't matter. You know, if you're sticking to like 0.25, then it's really not a big deal. The bigger issues is when you go to super high doses. And so I've I've come in sometimes and people have been on like 0.5 or like I've seen once I saw higher than that of Mel Ron. And it's just not something that I typically do. I just don't see the benefit of it. Like, like I said, I at this point I'm saying, look, this is clearly like not what they need more than what we can offer them. We need to start thinking about doing something different if if we're at those high doses. So I don't worry about the kidneys at the doses that I'm doing Mel Renone, but it does come up. You'll hear people say, well, we can't use it. They're they're in-stage renal or they have CKD or they have whatever. And it's fine at those those lower doses.

SPEAKER_01 31:57

Yeah.

SPEAKER_00 31:58

I think that's typically where I would do those things is I'm looking at uh I'm looking at diuretics. I'm looking ideally at an iodilator, but I also have to pay attention to in and looking back at cardiac power is I I need flow, I need cardiac output, but I also have to have perfusion. So I need to have that map like 65 and above. If if I have to, then I would I would be adding vasopressors to try to get the map up with it. So that's like the medical management that you're wanting to do to get them going. There's there's other things that are kind of like person by person, right? If they if they have a permanent pacer and they are at a paced rhythm and their paced rhythm is 60, then go ask the rep to turn it up to 80 or 90, right? Then you get a big uh jump in cardiac output. So there's all like subtle things or some little things, but like overall medical management-wise, diuretics to decrease preload, ionotropes to increase uh contractility, and then you're looking at vasodilators if you can tolerate it to decrease afterlife.

SPEAKER_01 33:01

Yeah, makes sense. Hey everyone, part two of cardiogenic shock management is going to be coming to you next week. Please make sure you leave a comment, like, follow, send us any questions, and we will get Dr. Michael to answer it for you. Until next time. Bye.

SPEAKER_04 33:24

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