Septic Shock Part 2: Fluids, Vasopressors, Steroids & the Physiology Behind Sepsis Care

Septic shock treatment has evolved dramatically, but why do we give fluids, start vasopressors, and use steroids? In Part 2 of our septic shock series, Dr. Michael joins Banter at the Bedside to break down the physiology behind modern sepsis care.

Rather than memorizing guidelines, we explore the "why" behind them. From cytokines and nitric oxide to vascular leak, venous reservoirs, and vasopressor selection, this episode explains the science that drives evidence-based treatment.

We also discuss the evolution away from massive fluid resuscitation, the role of norepinephrine and vasopressin, septic cardiomyopathy, warm versus cold shock, and why septic shock can sometimes feel harder to treat than cardiogenic shock.

Whether you're a nurse, APP, physician, student, or simply love critical care physiology, this episode is packed with practical analogies and pearls that make sepsis easier to understand.

🎙 Topics include:

•  Cytokines and nitric oxide 
•  Why patients become vasodilated and "leaky" 
•  Fluids vs fixing the bucket 
•  Early vasopressors and venous reservoirs 
•  Norepinephrine vs dopamine (SOAP II Trial) 
•  Vasopressin and VASST Trial 
•  Steroids in septic shock 
•  Septic cardiomyopathy 
•  Warm vs cold sepsis 
•  Why septic shock remains one of the hardest forms of shock to treat

Transcript

SPEAKER_01 0:06

Hey everyone and welcome back to Banter at the Bedside. This week we are finishing up Septic Shock Part 2 with Dr. Michael. We're really going to be looking at physiology. Just to recap last week, we talked about all of the studies in the progression from 1989 until now on the septic shock guidelines, how they were discovered and how the changes were made, and where we're currently sitting at. It's worth a listen, but you don't have to listen to that one to be able to listen to this part. This is one of our education episodes that we have here at Banter at the Bedside, and it's really supposed to feel like you are being taught right at the workstation at 3 a.m. So there's some interjections and questions and laughs along the way. Make sure you send us in your questions to give to Dr. Michael because we are happy to have them. In this episode, we will have Dr. Michael. He is a physician of 17 years of practice. He has worked in cardiac ICUs, medical ICUs, and cardiovascular surgery ICUs in multiple major hospitals. He has been medical director and is currently a program director for a fellowship. So he's a wealth of knowledge here to educate us. We have Abby, that's me. I'm a nurse practitioner of eight years. I've been in healthcare 17 years to represent the advanced practice providers we have in our healthcare systems. And then we're joined by Kaylee, an ICU nurse of 18 years, to help the nurses be represented in this education session. We are all here gathered together to learn together. As always, this is for entertainment purposes only. This is not medical advice. Please seek the care of your own medical professional. We do not represent any entity at all. All of our thoughts and opinions are our own. So let's get into this episode.

SPEAKER_02 2:00

Oh, the evidence-based literature and the guidelines and like why we do what we do and blah, blah, blah. But to me, it's just memorizing a lot of stuff. I really like going into the physiology behind it and saying, like, why do we do the things that we do? And so I'll probably spend the next little time, if that's okay, to like go over the physiology about why this stuff is helpful.

SPEAKER_01 2:26

Yeah.

SPEAKER_02 2:27

And I can reverse engineer all these guidelines, like based on the physiology of how we ended up, where we ended up at. So the first thing that comes in that uh talk about is cytokines. I I really got into cytokines, which I know sounds super nerdy, but uh it was it was something that was I thought was really fascinating and really explained a lot about things that were going on. And the problem with it was not everybody was on board with it. Everyone, like we we looked at cytokines as like areas where we could try to do stuff to try to help block the whole SERS cascade, cytokine type stuff, but people weren't super into it. And then when COVID came, it became huge. Like everybody was talking about cytokine. Because it was such a big deal with this like excessive cytokine release with COVID, and people really started getting back into it. And we started actually like targeting certain things like IL6 and all these types of things that came with it, and so it became a bigger deal. But the idea of sepsis is it does two things it activates inducible nitric oxide synthase, which basically means it makes our body make nitric oxide, which is a very potent vasodilator. So it dilates out all of our vasculature because it dilates out all of our vasculature, that's whenever it drops like our afterload, it drops our resistance and it gives us that high output shock. I I equate it to if you we average about like four to six liters of blood in our body. So let's say you have four liters of blood in your body and you have a four-liter bucket. So you have four liters of blood in a four-liter bucket. When you become septic, all of a sudden your four-liter bucket becomes a six-liter bucket. So all of a sudden, you now don't have enough blood in your bucket because you only have four liters now in a six-liter bucket. So you're going to be hypotensive. You're going to need some fluid because you've now just dilated out your vascular system because of this nitric oxide because of your cytokines. Additionally, you also uh with the cytokines is that it actually will break down the cell bridges, like the between cells, and it makes your cells leaky. And you start leaking fluid from the intravascular space into the interstitial space. So if you think about that six-liter bucket, it's like you poked a bunch of holes into that six-liter bucket. So now instead of having a four-liter buck bucket with no holes, you now have a six-liter bucket with a bunch of holes in it that's leaking out. So yeah, you can absolutely give fluid and that will help. It'll help fill up that bucket. It'll help your blood pressure, it'll help your heart rate, but it's still leaking out the sides of it. And that's due to that inflammatory response. And so nitric oxide. From the yeah, from the nitric oxide.

SPEAKER_01 5:28

Yeah.

SPEAKER_02 5:28

Okay. So whenever you're targeting treatments, you're giving antibiotics to reduce the inflammation from the infection. Whenever you're doing source control, you're trying to get rid of the infection so that you help reduce inflammation. But it's also why steroids are so beneficial, is you want to decrease that inflammation so that you stop being so dilated, you stop being so leaky, so you don't have to keep giving all of that fluid. And then the fluids help fill up that bucket from like where you lost it. Now, to me, it just, I don't know why it took us so long. If you had a if you had a bucket with like six holes in it, and and I said, I need you to fill this bucket up. I feel like being like, what can we do to plug these holes would be way more efficient than being like, what if we just poured the fluid in faster than it leaped?

SPEAKER_00 6:20

You mean actually fix you mean actually fix the problem.

SPEAKER_02 6:23

Yeah. Like for I I feel like for like 20 years, we were like, we're just not pouring the fluid in fast enough. If we pour it in fast enough, the bucket will be full. And then if you go back to Manny Rivers with early gold-directed therapy, they were 10 liters of fluid in that 72-hour period. A liter of fluid weighs 2.2 pounds, right? One kilo. So it was like they gave them 22 pounds of fluid, and then they were like, How do you feel? And then we'll be like, they feel short of breath, you know, they don't feel great.

SPEAKER_00 6:56

That's why they had to go and intubate him.

SPEAKER_01 6:59

He was like, Yeah, just intubate early.

SPEAKER_00 7:02

Has anybody ever been so puffy because you ate so much salt or you drank so much? Like that, you feel like shit. Like, are you kidding me?

SPEAKER_01 7:10

Ten liters that would require me to drink water. I do have a funny ultrasound story, but I don't want to like divert us from the education.

SPEAKER_02 7:20

I I will say, like, a liter of normal saline, right, has nine grams of of salt, which if you went to the vending machine and got a snack-sized one ounce Lay's potato chip bag, and I said, I want you to buy as many as you want until you feel like you got enough salt. And think about how many you would eat, and then one liter of fluid has the equivalent of 26 bags of one ounce Lay's potato chips worth of salt. Just one liter of normal saline. So if you could imagine giving somebody 10 liters of normal saline and giving them 260 bags of lay's potato chips worth of salt, and then asking them, being like, they they seem puffy. And I was like, Yeah.

SPEAKER_00 8:06

Do you think?

SPEAKER_01 8:10

I think I think we'll just have you come back. We'll schedule you real quick. We'll have you come back and talk fluids.

SPEAKER_02 8:18

You're like, I'm not going to talk fluids, but uh but yeah, so it's like it's a whole thing of like when you're when you're talking about these types of things, it's like, yeah, if if you look at it like I said, like a four-liter bucket becoming a six-liter bucket, yeah, give them a liter or two of fluid. They'll probably benefit from it. But the main thing to focus on is how can we fix the holes in the bucket? How can we shrink the bucket, right? So you don't need six liters. So vasopressors do two things. So people and would think about vasopressors is you just squeeze the arteries harder, which is true. Like you squeeze down your arterial system, it raises your blood pressure. But but what people don't realize is that we have something called a venous reservoir. So we have a lot. If you think about a dam and you think about water flowing over that dam, all that all that water and the bottom of the dam isn't being used, right? It's just down there. It's not like the water's like like it's just like a reservoir of water that's not being used unless you need it. Your venous pressure has your venous system has the same thing. It has like a reservoir of blood that you're not really using. If you need to use it, you can, but whenever you get hypotensive from septic shock, you actually lose, you don't change the reservoir, but you lose the like active volume that you're returning to the heart. And so you're not returning as much blood to the heart. By starting a vasopressor, you're actually squeezing down your venous system as well. And you're taking that unused venous reservoir and making that blood usable. So you're sending more blood flow back to the heart. So it's not just like squeezing your arteries, it actually does improve preload by sending that unused venous reservoir blood back to the heart and be able to start using it. So early vasopressors works really well. And so, like, that's the benefit of it. It also, if you think about it, and my metaphor of like a six-liter bucket versus a four-liter bucket is you're gonna squeeze down that six-liter bucket back to like a five or four-liter bucket. So you don't need as much volume. You're not gonna be needing four, five, six liters of fluid. You're squeezing that back down so that you don't need as much fluid. Yeah. Now, I I did forget to mention, and I can bring it up now, is vasopressor choice in septic shock. I should have mentioned that when we were talking about like like literature-based stuffed with it.

SPEAKER_00 10:43

Uh mention it all.

SPEAKER_02 10:45

So it used to be back in the day that people used a lot of dopamine, and then people used a lot of LeviFed, and then it it was always a thing of which one's better, which one should you start on something. And so the SOAP 2 trial came out, and the SOAP 2 trial looked at just undifferentiated shock. Like just someone came in in shock, you don't even know what kind of shock it is, and they started people on dopamine and they started people on norepinephrine. And it actually showed no difference in terms of mortality, but significantly more arrhythmias in dopamine.

SPEAKER_00 11:17

Yeah.

SPEAKER_02 11:18

And so the SOAP 2 trial was the one that definitively said stop using dopamine for shock. Start using norepinephrine. They did a subset analysis, so it didn't reach statistical significance, but they looked at cardiogenic shock patients, and people were like, well, dopamine's, you know, heart-wise. There was there actually was a mortality benefit in with norepinephrine being better than dopamine in the subset analysis for cardiogenic shock, but they didn't like do the study to look at it. So yeah. Now, the part that I didn't like about that was is I've been at institutions where they said, oh, LeviFed's the drug of choice for cardiogenic shock. And I was like, that's actually not what that said at all. Uh that is not the drug of choice for cardiogenic shock. It is better than dopamine. That is the only thing that it showed in that study. It didn't say it's better than like doputamine or epinephrine or milrenone or whatever. It is better than dopamine. And then they did the vast trial. The vast trial was looking at norepinephrine versus norepinephrine and vasopressin. And again, there was no mortality benefit, but the people that were on vasopressin with norepinephrine got to use significantly less norepinephrine. And so that became the big trial that says you should add uh vasopressin to your norepinephrine and septic shock. And that's like that fixed dose, 0.03, 0.04, whatever you want to like do with it on the thing with it. But it's actually not considered a second line vasopressor, it's just called it's considered a uh an adjunct. So second line is actually epinephrine because they just consider vaso an adjunct. So you should do like norepinephrine, then add vaso, second line do epinephrine, and then you would consider actually phenolephrine, and then most of the people do all that before, or you could throw angiotensin too, like kind of in there on the thing with it. Which doesn't make sense to me because norepinephrine and epinephrine are not that far off, and phenylephrine is alpha, and epi has all the alpha. So if you want to look at the three receptors that like constrict your vasculature, you have your like your, you know, your alpha beta type stuff from your norepinephrine, and then you have vasopressin, and then angiotensin is the next big step. So it makes sense that that would be the next one, but it's still like it's still very expensive. It's still like there's a there's a not a great, it's hard to get people to jump on board with it, but physiologically that's what makes the most sense is kind of that next line with it. But technically, you're you're as per guidelines, you would do norepinephrine, then add vaso as an adjunct, and then you would add epinephrine. All right. So sorry for my little like side thing there. So vasopressors increase uh venous return just as much as they increase blood pressure. So I think that there is a benefit from that in terms of like a venous reservoir type of a thing with it. Uh, and then I've already talked about oncotic pressure is what helps keep that fluid intravascular so it's not leaking out into the interstitium. Osmolarity, you know, we give hypertonic saline in people where we want to decrease like brain edema. And it's the same type of thing. So I like to think of it as like adding syrup. Like if you want to keep things in inside that bucket, it's leaking. Is if you just make the fluid thicker, it's not gonna leak out as much of those holes. So adding things like 25% albumin, adding things like hypertonic bicarb, hypertonic saline, whatever you want to add, then that's what's gonna like make it less likely to leak out. It's like adding in that thicker fluid, that syrupy fluid to keep your fluid intravascular.

SPEAKER_00 15:06

That's a good way to like that's a good analogy of like for people to kind of visualize what's happening.

SPEAKER_02 15:11

Yeah. So that's that's something that I, whenever I'm resuscitating somebody, if you think about it from that physiological level with it, is that you want to really focus on shrinking that bucket, plugging up those holes by decreasing inflammation, that's treating the infection, starting the steroids, shrinking the bucket with vasopressors. It's all just buying you time while you're recovering from the infection.

SPEAKER_01 15:36

Yeah.

SPEAKER_02 15:37

The the next big thing to get into that I think is really important is that is outside the scope of this talk is going to be deresuscitation of you just gave them 20 pounds of fluid. How do you like when do you decide to get that fluid back off of them? And I think that that's uh a really, a really important topic to talk about because oftentimes you'll get people out of the ICU, but they're still super volume overloaded. They end up with like pleural effusions or just lower extremity edema or poor wound healing, poor all this stuff from like all the fluid that's on top of them with it. But that can be a talk for a different day. I think the the main thing that I want to talk about here is understanding where the guidelines come from, right? Like understanding you're super inflammatory, you're vasodilated, you're leaky, you you give them fluids, you try to start treating the infection to stop that inflammation, then you start them on vasopressors, then you start them on steroids, then you start thinking about other things if you need them. You can start thinking about those like hypertonic fluids or additional vasopressors or whatever you need to do to be able to like get everything taken care of. And then monitoring, I think is super important if we go all the way back to the very beginning, is is understanding who should get the fluids, understanding that it's designed only for people with a lactic greater than four, only people that are hypotensive. It's not, oh, this patient has a pneumonia, give them three liters of fluid. Be like, were they hypotensive? Were they, did they have a lactic? No. Then you don't need to give them all that fluid. This is only for people that are in septic shock or people that are that are asymptomatic from it on the thing with it. Yeah. And having a good system that's gonna identify who's sick, right? And that is it, is it gonna be Muse? Is it gonna be just using SERS and just screening more people? I think we can we you could use Q sofa outside the ICU as a way of identifying who's sicker than the next person, uh, but you are gonna miss a lot of people. And then using sofa in the ICU actually is beneficial, but it is a lot more extensive as you look at it with it.

SPEAKER_01 17:45

Yeah. But that's I feel like we're we're probably doing a lot of the sofa stuff anyways.

SPEAKER_02 17:52

Yeah, yeah. Uh I think that's probably all of my my things. But if you look through the guidelines, you'll see things like recommendations on hypertonic bicarb, you'll see recommendations on cap refill versus reduction in lactic. You'll see you like you should see as you look back through them, like all of these studies that we talked about, like how like all these things they they now have recommendations for peripheral vasopressors. Like all of these things are starting to to show up in the guidelines, which I think is it's good. I mean, I think we're heading in a positive direction. I mean, if you think about like 1989 was the first time we defined it, 2001 was the first time you really started trying to do something about it, is we've come a long way.

SPEAKER_01 18:34

Yeah. I do have a question. Um, so we had someone on one of our videos from the cardiogenic shock talk about warm sepsis and comparing it in terms of like swan numbers. So I hadn't heard warm sepsis in a minute. Is that are those one terms we still use? And you want to dive into what that is. I'm guessing they mean hyperdynamic was my guess.

SPEAKER_02 19:02

They I don't like sepsis is like you do you are warm, like you would have they mean like hold sepsis?

SPEAKER_01 19:10

So you were it was a video and you were talking about uh just like the basics of cardiogenic shock. Um and that district and you were comparing it cardiogenic shock to distributive shock. And so you said cardiogenic shock is low output, distributive shock, cardiac output is high. And so the comment was so are we ignoring the fact there is warm sepsis and it progresses to cold sepsis? In the ICU, most of the septic admissions are in the more advanced state where cardiac output and index is lower, not increased. Initial distributive shock is high cardiac output, yes, but even without heart failure, it will drop along with SVO2. Important caveat to note.

SPEAKER_02 20:00

I mean, yeah, I mean, I think that's more of an idea of just saying, like, like certainly it's things aren't black and white. Like you're not gonna put a swan in and being like, this person is a like this person is distributive and they will be distributive throughout whatever. This person is cardiogenic and they'll be cardiogenic, whatever. I mean, I I there there are many people that like I have a this patient has a history of an EF of 10% and now they have a pneumonia, or now they have, you know, a a cholecystitis or whatever. Like you can have like a mixture, and I think that's important to know. You can have septic cardiomyopathy where you have a reduction in your cardiac function that's often hidden, right? So yeah, if your heart gets like a stunning effect from the septic shock, you have such low SVR, uh, such low afterload that it that you often don't recognize it because their EF will look normal. And then as your sepsis goes away, as that distributive shock goes away, it uncovers the fact that you have decreased LV function and then you'll like slip into that low, that low output state. Yeah. And we we see that the same thing when we see like a large MI as well have people that have like a huge, like proximal LAD and their EF will drop from like normal down to 20%. But if you put a swan in them, they'll actually have like an SVR of five, six hundred because they have so much cytokine release because their body's like reacting to having a huge MI. And those make me the most nervous, right? Because they look okay. Like if you look at their index, you can be like, oh, their index is 2.5 or 2.7, like they're doing great. And then you take the the pulmonary artery catheter out, and then three days later they look terrible. And then you go re-look at them, and now they've shifted into that low output cardiogenic shock because all of that cytokine and everything's gone away. So, yeah, absolutely. You can have people that are in septic shock and they have high filling pressure. You volume resessity and they don't have a lower filling pressure. You can have people that are in septic shock that have a low EF, that then, as that septic shock goes away, as that distributive low afterload goes away, it uncovers the other one. Or you could have the other one. You could have somebody that starts out with like a low index and then they get septic and then all of a sudden their index goes high. I mean, it's it's important to know that a patient isn't going to just follow a rule book and you put a you evaluate them and say, Oh, their index is three. This is definitely distributive done. We never need to check it again. We're good. Yeah. It's a matter of being like, hey, yeah, three days ago their index was three. We took their swan out. Now they're cold. Now their lactic's going back up again. Now their creatinine's going up. Now something's different. And being like, well, it was septic before, they're probably just still septic. You know, it's a matter of understanding that patients can slip back and forth. They're, they're, they're similar. Like, it's not like once a like a person's not just going to fit into it and always fit into those. It's just to help you, it's to help you target your treatment, right? Like if you if you get hemodynamics back that are consistent with distributive shock, start maybe looking for an infection. If you get hemodynamics that are consistent with cardiogenic shock, then maybe you need to start looking for why are they in cardiogenic shock? You know, it's just to help you like guide you understanding that that patients are going to change. So yeah, uh absolutely it is a continuum. You can flip back and forth multiple times during the stay. Um and it's important to keep that in mind is being fluid with the idea that your septic patient could now be a cardiogenic patient and vice versa.

SPEAKER_01 23:50

Yeah. And I think if anything from the first part of this taught us in terms of like starting in 1989 all the way to our current guidelines, like I think one of the biggest things that it seems that changed is that there is not necessarily like a one size fits all. Like you really do have to understand the physiology behind some of this medicine and understand what that patient is presenting with. And I think that's that seems to me to be like the throughput of all of that learning is it's like, well, is it do all this stuff or do whatever you want? Well, do whatever you want is very different now because we we have so much science and we know what's good and what's bad and how to respond to different things. So I to me it was just one of the questions, and I was like, well, let's just clear it up for our viewer.

SPEAKER_02 24:42

No, absolutely.

SPEAKER_00 24:43

Yeah, I think that was a comment on just that one one clip. Yeah. And instead of like, you know, there's a whole hour at the zone. Yeah. Yeah.

SPEAKER_01 24:54

But you know. I do also uh I do frequently get questions from students that they think alactic acid is solely tied to sepsis. And so I do just want to put out there and is I because there is anatomy and physiology, like, but there is no greater campaign in medicine than the surviving sepsis campaign. I mean, like that thing stands the test of time.

SPEAKER_00 25:22

I mean, okay, I have a question for Michael. This doesn't have to be backed by like any statistics, but in your opinion, do you think it's harder to treat septic shock or cardiogenic shock?

SPEAKER_02 25:31

That's a good question. I would say with the right tools, you should be able to support somebody enough to get out of cardiogenic shock if you're willing to like put them on like ECMO or put them on like a big device. It and it should be able to do it unless there's some other component going on with it. But overall, you should be able to support them. Now, that's like treating the shock. Now, down the road of like, do they do we have an out? Like, are they gonna be a candidate for a bad or a transplant or recovery and all that? That's a whole separate thing. If you're talking about just the shock part of it, I would say it's it's probably harder to treat septic shock because you're we're limited on what we like. I can give anti prod spectros, I can give vasopressors, but like you can keep going up on vasopressors, but like the ones that are just like so sick that it doesn't matter. Like I've seen people with like a bad MERSA infection. I mean, they're on all the MRSA coverage, they're on all the, and it just doesn't matter. You pour fluid into them, you pour pressors into them, like it just nothing is bringing them back from it. And that's hard because it's just like, look, like I'm using all of my tools. I, you know, I thought to me, I there's this whole thing in like smaller hospitals where they'll be like, oh, we're we're on maxed norepinephrine, and it'll be like 30 mics or whatever. And I've had people on 200 mics of norepinephrine that have survived, like and and didn't like lose digits, didn't do anything, and they they lived. They would not have lived if I maxed it out at 30. Yeah. And so, like, uh, you know, like how I've had people, like I said, on maxed out angiotensin and and 200 of norepinephrine and 50 of epinephrine, and you know, this isn't in mics per kilo, this is just in mics per minute, but like and and vasopressin and all this, and it just doesn't matter. You know, they still have a map in the 40s and 50s, and and I can't, you can't put them on ECMO for septic shock. Like, you can't, there's no device that's going to get them out of it. Uh, you could consider, you know, some people like doing, we looked into doing like CRRT to help like reduce cytokines and like all this type of stuff that never really panned out much either. And I like I I've just seen people that despite max max stuff, it just doesn't matter. And whereas like in cardiogenic shock, unless they also had like gut ischemia or like livered something where they took a hit that they couldn't come back from, if you got it early, you should always be able to support them enough to like get them out of the shock, as long as there's not some other part to it.

SPEAKER_01 28:23

Yeah. Yeah. I I think I agree. I think for me, the other sometimes even when they are getting better with septic shock, is it can take so long and there's not a lot. Like once the things are started, like that's it. Like it's just time, and I have to explain that to families a lot. Like, like we we gave them everything that we can. The rest, like right now, we're just giving them time to see if their body responds to it. Cardiogenic shock has quicker not always. I mean, there's always an exception to everything, but a lot of the cardiogenic shocks, you can see some good improvement really quick. And it's a little bit more, I don't know, satisfying or gives you a little bit more like spark to like, okay, we can do this. Okay, we got this.

SPEAKER_02 29:17

Like we Oh, yeah, yeah, yeah. Yeah.

SPEAKER_01 29:19

Like we had an impella as soon as this patient got the impella put in, much more awake. I mean, the next day sitting up in the chair with their impella, and it's just like it, I don't know, it's so much more satisfying as opposed to No, I I agree a hundred percent.

SPEAKER_02 29:35

Like, yeah, whenever we have our critical care fellows or our palm critical care fellows like showing them the pace of cardiac critical care versus like the medical ICU, is it is one of those things. It's like we gave them the steroids, we gave them the antibiotics, we gave them the fluids, like they're either gonna get better or they're not. And so much of it is like, let's check back tomorrow. Like, how do they look in 24 hours? How do they look in 48 hours, as opposed to like cardiogenic shock and some of these things? It's like, how do they look in two hours? How do they look in, you know, like immediately and frequently going back to the bedside and seeing people improve that quickly versus those like slow, slow improvements is the pace of the pace of treating septic shock versus the pace of treating cardiogenic shock is wildly different.

SPEAKER_00 30:25

Yeah. As a nurse, I think it's quote unquote easier to take care of a patient in septic shock. It's like a bum rush at the beginning, and then well, we've done everything. Yeah. Versus cardiogenic shock, where it's like, okay, well, this isn't working. Now they can't breathe. Now they need to be on bipass, now they need to be intubated. Well, shoot, we can't get the volume off. So now we need to put a bass cap in. Now it's CRT. Turn up your melanin, get your swan numbers, send them X Venus.

SPEAKER_01 30:49

You know, turn it down, turn that down, turn that is like it literally is like hour to hour sometimes.

SPEAKER_00 30:56

Yeah, so I do feel like there can be a little bit more work with that. Like you said, you see improvements quickly, but if they're not improving, it's like you do so much, and it can get to so many different things.

SPEAKER_02 31:07

So I also see I've also seen things where like somebody didn't look that great on Mel Morning, and then I tried debutamine and they looked great, like they just responded way better to it. And I and I feel like you can go in the room and and make changes, whereas like you're on broad spectrum, like there's you're not really like extra broad spectrum. You can't be like, let's try like this broad spectrum. You know, like there's not a lot of like things that you can tinker with in septic shock versus you can make small changes in cardiogenic shock that can make a difference, I feel like. And it and that's uh and I so I find myself in the room way more often in in cardiogenic shock to say, like, could I optimize? Could I do something different?

SPEAKER_01 31:51

Do you know for those that survive septic shock and make it out of the hospital? Do you know the six-month mortality for those patients? Because I know for cardiogenic shock it's still decently high.

SPEAKER_02 32:04

Yeah. Uh I don't, I don't, I mean, I don't think it's that bad on on a lot of stuff with it. I mean, unl unless it's from like other issues, you know, like critical care biopathy or like whatever. But I think overall, like it's not tremendously different unless that sepsis is like the beginning to an end, you know, like a yeah, they have cancer, they you know, like if it's like a a presenting thing of like they have some sort of immunodeficiency, but just for like that, I don't think it's terrible. But I I don't know enough about it. I stay in my ICU bubble and just assume everybody does great whenever they leave.

SPEAKER_01 32:41

Yeah. It's uh it's we gotta hang on to the things that we can, right? That you make it out of the ICU and you don't bounce back. You're out there living life. That's the best way. Well, any other questions, Kaylee?

SPEAKER_00 32:55

No.

SPEAKER_01 32:56

Well, this has been fun. Thank you so much, Dr. Michael. Make sure you send us your comments. We'll post more clips on social media. Our website is live, banter at thebedside.com. You can always send in a comment. We'll make sure to bring Dr. Michael back for his fluid talk since we hinted at it so heavily in this one. Uh it is a good, it is actually a really, really good talk. And I do have like clips of him throwing Lay's potato chips on a table that we could clip into the show. So um, it is actually a really good talk, even though we we continually poke fun at him about it. But make sure you hit the like, the follow button. And from all of us shift talkers here, until next time. Bye.

SPEAKER_02 33:40

Bye. Thank you.

SPEAKER_01 33:41

If this felt your kind of conversation, make sure you're following, leave us a review, and we'll see you back here soon. Bye. Step into the light where the stories come.