Hey folks, Scott Weigart here, and this is an MCRIT Podcast. Today on the podcast, we have a cardiovascular mcrit episode, which means you're going to be hearing from Trina Augustin, editor of cardiovascular mcrit. brilliant cardiac intensivist friend and i'm always so happy to do episodes with her In the podcasting world, sometimes you record episodes and after the recording's done, you're like, this is gold.
and you want to get it up as quickly as possible and then you look at your posting schedule and it's not going to come out for two months and you're like oh drat I wish I could share this today. Well, this is one of those episodes. It's a two-parter. This is part one in which we deal with the basics of inotropic agents. And then in part two we'll discuss some specific scenarios. It's great stuff. It is the companion to the Vasopressor Podcast, the Vasopressor Basics Podcast I did.
somewhere in the 200s i don't remember the exact number but that one also had an incredibly positive response and i think this will join that same litany of uh hemodynamic management basics so hopefully you like it if you do please put something in the comments let me know that you like these and you want them to keep going in this vein because I don't get a lot of feedback these days outside of the socials where I try not to traffic.
And so I would love to hear from you if you like this episode. Right before we jump in, I just want to mention a conference near and dear to my heart, and then we will join Trina Augustine to discuss inotrophies. Alright, here's what I want you to know. Reanimate 11 tickets are now for sale. Reanimate is our resuscitative ECMO conference with VA ECMO, ECPR, Crash VV ECMO. It is in San Diego every year. It is November 12th and 13th.
and it sells out rapidly every single year. Every single year, I keep doing these ads. People are like, I'll wait, I'll wait, I'll wait. And then they decide to buy their ticket two months beforehand, and we have none. And they're like, oh no, I wish I really wanted to come this year. I'm like, yeah, and you should have done it when I talked to you in January.
So if you want to come to reanimate, now is the time to buy your tickets. Go to reanimateconference.com. That's reanimateconference.com. Buy your ticket and then you will not miss it again this year. All right, let's get to the show. So who are you and what do you do?
Scott, it's wonderful being here again today. I am a cardiovascular intensivist and emergency medicine doctor at Mayo Clinic in Rochester and someone who is very passionate about cardiovascular critical care. And therefore very passionate about inotropes, the topic of today. 100% I think this is one time.
especially in medicine where you get to see how much it's an art, not just a science. So I'm super excited to talk about this topic today. Yeah, we've had basics of vasopressors I've already done. I figured I'd tag team with someone who this is their life is all things cardiac. resuscitation to discuss inotrophies. and you know i think this one is the one that is more black box for people in the ed they they
have vacillated from dopamine to norepinephrine, and they're pretty much throwing that on for any patient that needs a vasopressor. But... And inotropes, unless they're being told by another service or they're like, oh, I guess we got to do something. I don't think it really comes into the ED curriculum as strongly. And I think we're going to remedy that today.
So, Trina, I figured we'd discuss it from the perspective of agents first, and then we could talk about some specific conditions, if that's cool with you. Sounds wonderful. Let's do it. All right, let's start with a classic ED inotrope, dobutamine. Tell us a little bit about dobutamine. Fantastic. So I think dobutamine is...
Oftentimes one of the workhorses in the ED and part of that's because it's a drug that's fairly easily accessible and has a quick onset, which we know in the ED is something we really care about. So this is kind of your classic and catecholamine inotrope that's going to work on your adrenergic receptors. So it's going to primarily work on those beta receptors.
so beta 1 and beta 2 and as most of the listeners will know with working on those beta receptors with beta 1 you're going to see increased contractility so increased like force of contraction You're going to see some increased chronotropy, so increased rate of contraction or increased heart rate. And you can also see some increased lucitropy or relaxation. Now, its beta 2 effects can lead to some vasodontosis as well.
And what a lot of the listeners might not be aware of as much is that it can actually have a little bit of effect on alpha receptors too when it's used at a higher dose. And if you ever look at the literature on stress tests when they use dobutamine at really high dose, like 40 mics per kg per minute, you actually sometimes see more hypertension than hypotension, which tells me that we're getting a little more of the alpha effect.
But clinically in the ED, what I find is that this is a nice inotrope and the fact that it's often fairly humidistable. You know, there's a lot of fear of it causing a lot of vasodilation from those beta effects and hypotension. I don't see that as much What I do see is that it has quite the affinity for beta-1 receptors and causes a lot of coronotropy.
So while we do sometimes like a little faster heart rate because, you know, your cardiac output is equal to your stroke volume times your heart rate, and an increased heart rate can help with that cardiac output. Sometimes it's maladaptive because it causes so much tachycardia or arrhythmias and so it can be problematic in some patients. But overall, great drug onset is quick. Offset is fairly quick.
And it's something that you can pull up and add nicely to norepinephrine if you need it in a setting for cardiogenic shock. Yeah, I think you've hit the major points on it. A lot of the vasodilation is dose-dependent, and I think people are expecting too much from this agent. And one of the themes that you'll hear with any of these catechols is if you just want the inotropic effects, you really have to stay in the low dose range.
So between 0 and 10 micrograms per kilogram per minute, you're probably getting mostly an inotropic effect with not much in the way of vasodilation. But past that dose range, That's when those beta 2 agents really are going to take some prominence in the effect and you're going to get vasodilation. The other thing with dopamine, you mentioned it's quick onset, but by virtue of that, it's also an agent with a quick off.
And that's really the key for making it an ED-friendly drug. And I know you talk about this in contradistinction to milleridone, which we'll get into in a second. So dose range I've seen in... textbooks is 0 to 20 but for me if I'm going beyond 10 I generally ask myself is this really a good idea is that similar to your practice
So you might laugh at this, but I'm even maybe a little more conservative. I tend to not go much above five. And part of the reason might be the population I work in, but part of it is it has such a chronotropic effect. So just for example, I used it this week in a patient that had cardiogenic shock that was actually secondary to a low heart rate. And even at doses of 2.5 micrograms per kg per minute, I had a heart rate increase of 15 beats per minute. So actually pretty significant.
And what I'll tell you is what you don't want to take is your patient cardiogenic shock and put them into AFib with RVR because that's super problematic. So frequently I find that you can actually get significant bang for your buck and significant increase in your cardiac index. with doses of even just 5 micrograms per kg per minute kind of max.
And above that rate, I start seeing so much chronotropic effects that oftentimes it becomes maladaptive for me. Now, different populations are different. And certain patients, you know, if you have that patient that is super bradycardic and that's driving their cardiogenic shock, higher doses might be okay.
Here again, this is all about targeting the drug to the patient's physiology. Absolutely. Now, let's say you had a patient you flipped into AFib due to over-exuberant dobutamine use. Have you found that when you turn it off, that AFib resolves, or do they stay in it? That's a little variable. I find that it gets Better? Definitely better. But there are times when you end up in a sticky situation where now you have this patient decompensating in front of you.
and you're reaching for electricity to actually cardiovert them. But then I do try to switch to an agent that is going to cause less chronotropy and less, you know, arrhythmias. I don't want to get myself in trouble here because clearly we had the DOOR MI trial. that looked at dibutamine versus milrinone and found no different in their composite outcomes, which was, you know, in hospital mortality, resuscitated cardiac arrest, non-fatal MI, TIA, stroke, renal replacement therapy.
And they also fall on no difference in arrhythmia. Now, they were powering the trier for, like, I think 11% difference, and maybe that was a little bit ambitious. I also think that there could have been effects that are clinically relevant that maybe didn't show up in the trial. But overall, I will tell you, as someone who works with this drug,
frequently and loves inotropes. This is one of the drugs that I've found causing the most chronotropy and arrhythmias. And I think if you look at it next to isoproteranol, it has some of the strongest beta-1 effects. Yeah, that's been my experience as well. You've also brought up a theme that we'll be running through our entire discussion, which is what we want is just a pure...
inotropic agent. We want something that is going to increase contractility and we keep getting the problems of chronotropy coming along for the ride. Trina, why has no one developed a drug that could just purely affect squeeze without affecting chronotropy? It seems like that would be the holy grail here.
I mean, they're working on it, and I have to say, you know, reportedly Leibus Amenden, which we don't have access to here in the U.S., is pretty good with that, and even Milrinone potentially has less heart rate effects, potentially. But, you know, so levosomendin, which is a calcium sensitizer, is supposed to be much better. And there are some trials that, well, maybe not considered positive, that there's trends towards better outcomes. There's the Survive trial, the Revive 2 trial.
think there's things coming and there's also newer agents being developed, but it's tough. And, you know, there are times when a little bit of increased heart rate's okay, because that's increasing your cardiac output. But you do hit on it, and it's really interesting, because if you look at what drives oxygen, you know, demand and requirements, that increased heart rate is...
huge. It can cause up to 50 to 70% increase in oxygen demand. And clearly on a failing heart that's struggling, that's not optimal. So yeah, we have a long ways to go in this field. This brings up another critical question in the discussion of inotropes, which is... What is your ideal heart rate for a critically ill patient? Now, you could absolutely answer. It's going to be different in different circumstances, like a cardiogenic shock patient may not be as tachycardic.
Take the tachycardia as well as someone who's in sepsis, for instance. But do you have general ideas, and I'm sure it varies by age as well, as to what is the ultimate goal for a patient that needs that increased cardiac output, what we don't want to do it at the expense of increasing myocardial oxygen demand?
Yeah, so I'm laughing because that is a tough question because so many things play into it. You know, does the patient have significant diastolic dysfunction? Is this a patient with RV failure? Patients with RV dysfunction, I tend to like their heart rates a little bit faster. And if you have diastolic dysfunction, you might not want it quite as fast so that you have adequate time for filling.
I think, you know, it's interesting. So for example, when you're working in the ED, you see these patients come in and cardiogenic shock. And I had one the other day when I threw the probe on. He had like a single digit EF. I think they've later formally called it like 9% LBEF.
And when he came in, his heart rate was 130. That was a little faster than I wanted, but realizing that's a patient that when his heart rate is below 110, I'm starting to get anxious. Because truly, he is augmenting his cardiac output by his heart rate.
You know, he's not, his stroke volume is not big enough to do this on its own. So I think these patients with cardiogenic shock, you know, we do need to expect them to have a little faster heart rate. And if they don't, you need to ask yourself why, because it's kind of the natural compensatory mechanism. But what I find is when you start getting much above 110 beats per minute, I find that oftentimes it becomes somewhat malandaptive and I'm starting to wash them pretty closely.
You know that brought up an interesting point. So if you have such a poor ejection fraction, then the requirements for your time for filling is going to be markedly less, and you tolerate a higher heart rate. Versus someone who has a better ejection fraction, it's going to take longer to fill, and you might tolerate a lower heart rate.
Are your actually varying based on your echo findings to some extent? Or is it just a general gestalt of a cardiogenic shock patient could take more tachycardia than someone without?
You know, I think part of that is general gestalt, because most of these patients, you know, this is the compensatory mechanism. Now, it also depends on what kind of cardiogenic shock. Like, clearly, if you have cardiogenic shock, With a patient with a whole gum who's having a dynamic LVOT obstruction, you want a slower heart rate.
So here again, this is all about targeting it to the physiology of the patient in front of you. And people who work with me know this. I mean, I literally walk into these patients room with an ultrasound in hand all the time. So I'm not listening to them with my stethoscope. I'm physically looking at their heart and figuring out what looks what's right for them.
If you had to put general numbers on it, the 110 was thrown out there, and I think that's my number as well. Generally, I don't want to see patients going beyond 110 from my interventions. I don't want to push them to that, except... As you say, you know, a patient who really needs to get to the lab for some form of mechanical circulatory support, I'll take that extra tachycardia that's going to keep them alive.
to get up there. But, you know, for septic patients, for instance, that's usually the number. Now, let's say you had an 85 year old with some degree of CHF in their history. Would you still push them to 110 or would that number be lower?
You know, not necessarily. Typically, I'm good at that 90 to 110 range is kind of where I'm eyeballing and feeling comfortable. Typically, if they're much slower than that, you know, I'm intrigued as to why. You know, is this a patient that was on beta blockers coming into this? Do they just have chronotropic incompetence? Because it's unusual to be in cardiogenic shock and have a heart rate of less than 90.
pretty rare for me and I mean it's occasional and especially some of these postcardiotomy patients I'll see at some times. So anything else on dobutamine before we move on? No, I mean, I think the biggest thing that I will say about dobutamine is just really, really remember that... Patients can have such an incredible chronotropic response, and it can cause some arrhythmias, even though dorami didn't really show that. I think practically for the people who are using this as a first-line drug,
Typically, if you pair this with a little bit of norepinephrine and stay at low doses, that will give you your bang for your buck. You might actually affirm yourself by going to super high doses. So I always recommend start at that 2.5 or 5 micrograms per kg per minute and see what that gets you first. Love it. All right, Miller now.
All right, so I love this drug, and I think you and I might have slightly different feelings on this drug, but just full disclosure, this is one of my work courses. Now, I will tell you it's a work course in the ICU, but not a work course for me in the emergency department. So I want to clarify that up front.
So milrinone is a great drug that is an inotrope that's going to cause increased contractility. It's going to cause increased lucitropy so that myocardial relaxation and allowed time for filling. And it doesn't cause as much of a chronotropic response that we see clinically. It's not working on beta receptors, so instead...
It's a phosphodiesterase 3 inhibitor, and it's going to increase cyclic AMP and calcium cycling for you. It also works in vascular smooth muscles, so you end up with venodilation, arterial dilation, and a decrease in your pulmonary artery pressure. So...
I love this drug, but there are some downsides that come with it. And one of them is that it can cause significant vasodilation. So oftentimes this is a drug that can end up causing a little bit of hypotension. So it's something to be aware of. The other thing is... It takes a while to start working. Now, if you look at textbooks and things like UpToDate, they might say, oh, onset is in 15 minutes, but read a little closer. That's when you're bolusing Millernode.
I'll tell you, it takes a brave human to bolus milrinone. If you're going to do that, it better be a patient that has a very high systemic vascular resistance and has pretty decent blood pressure because you will cause hypotension. Now, most of us will just start milrinode at kind of, you know, a rate and, you know, whether it's going to be 0.25 micrograms per kg per minute.
higher or lower, and we're going to just wait for it to kick in. Typically what I'll tell you is textbooks will say around 30 minutes. I would say clinically, I see most of its effects starting to hit around 45 minutes, meaning I will start seeing cardiac index go up on my patients with a SWAN, but I'll also start seeing their SVRI drop pretty significant, so systemic vascular resistance goes down.
and their filling pressures go down. And if you think about it, a medication that causes venodilation is going to increase your venous capacitance. So decrease that stressed volume and your filling pressures will decrease.
So overall, I would say I see those effects around 45 minutes. And so if you're someone who works in the emergency department, you can see why this drug, I mean, one, until you order it, it gets to bedside, then you hang it, and your nurses probably aren't familiar with it, so you're trying to figure that out. It soon becomes you don't have assistants with their contractility for maybe an hour or greater after you want it, which is too long.
Yeah, we don't have different feelings about this agent. It's just we're practicing primarily in different venues. And as you know, I practice only ED critical care, and that's why it hasn't had a big part in my practice. When I was in the CT ICU, then yeah, same as you. I love this drug. I would have it in the background for many of our patients. All right, let's forget about the textbooks. Where do you start this agent on your page?
Yeah, so, you know, I tend to start at anywhere from 0.125 micrograms per kg per minute to 0.25 micrograms per kg per minute. Now, textbook will say you can go as high as 0.75 micrograms per kg per minute. I will tell you the amount of vasodilation and subsequent hypotension that can come with that is significant. This week I took a patient that was really sick.
and started them at 0.25 micrograms per kg per minute. Within four hours, I had refractory vasoplegia, was on norepinephrine at like 0.11 on low-dose epinephrine at like 0.04 micrograms per kg per minute and That went from being on almost nothing when I had started the malaria patient with a cardiac index of 1.4. So I'll tell you that frequently
I find that even just 0.125 micrograms per kg per minute works well. Now, it depends here on your patient population. I know the CICU will run it a lot higher, but I typically don't go much higher than 0.37 micrograms per kg per minute on any patient ever. And how rapidly do you titrate it? Is this over?
multiple hours like if you're not getting the effect now you have the benefit this is another reason why this agent is better for your neck of the woods of usually having invasive cardiac monitoring and getting hemodynamic pressures from it so you could actually see the results of your work because the problem with any of these inotropes in a condition like septic shock
in the ED is oftentimes you'll get the increased contractility, but it will have no effects on blood pressure because the patient will let off some of their endogenous. uh catecholamine tone and so you will get you know these salutary effects but you won't know it unless you're really monitoring with a cardiac probe as opposed to you you know okay i have knockout in the contractility i want so how rapidly are you titrating
Typically, I will titrate it not quicker than every 45 minutes to an hour, and that's just because it takes at least that long to even start seeing the effects of the drug. And you're right. You know, I am a huge advocate of swans. I float them myself all the time. And that's what I did this week on a patient that just decompensated in front of me because it does really help.
And I do think that swans are making a comeback now. I would like to preface that specifically in cardiogenic shock and in the hands of experienced operators who also know how to interpret the data. Clearly, putting a swan in is not going to decrease mortality unless you know how to use the numbers. and actually change patients' therapies and treatment off of them.
But yeah, it's one of those drugs that titrating it from an emergency medicine perspective is pretty challenging as well. So, you know, especially without a swan because then you're kind of stuck, you know, monitoring SCVO-2s, urine output, lactate. skin temperature and sure you can do that and do your bedside cardiac focus and look at their vti and see if there's changes but it's hey folks but you know we're not getting right to the show because
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Please consider joining and thank you. Thank you. Thank you for listening. Challenging, especially in a busy, crazy environment. So that's the other reason I kind of don't advocate for it in the ED. And to be frank, in the ED, I don't use it myself. I actually have found really good workarounds. And so I think that it's a drug that... If you're comfortable with, sure, it's not that it couldn't be sorted down there, but I don't think you're crippled if you can't use it in ED. Absolutely.
You had mentioned only a brave person will bolus it. I just want to make this clear for the listeners. If you're in emergency medicine, just don't bolus this agent, ever. Just don't do it. It's going to bite you in the ass. It's not worth it. Just don't do it. If you need something rapid, we've given you one choice already, and we're going to give you a second one in a moment. So just don't bolus. No or no. It's not a good look to call your ECMO team down for that. They don't love... and
Just as in dobutamine, its quick onset led to quick offset, that is not the case with melanin. So if you go too far, if you start this too high or you titrate too rapidly, you're going to be stuck with that for a while. And that's the reason that I think it's not. a friendly drug. You're not going to see its results because of its onset time, and you're not going to be able to get rid of it if it causes too much vasodilation.
They usually categorize both dobutamine and milrinone as inodilators, but in my mind, milrinone is the inodilator. And if you're getting significant vasodilation with the dobutamine, it's usually because you've gone too high. So if you restrict your dose range, then you have... a agent that is pretty reliable for not causing intractable decreases in blood pressure in dobutamine, you're going to get the vasodilation with milrinone. It just comes along for the ride. You just have to...
Actually have that budgeted into your hemodynamic profile when you're using this. Anything else we should talk about in terms of Miller? I think just to give your listeners an idea, you know, the typical half-life for melanoma is like two and a half hours. But if you have renal failure, and frankly, most of these patients that come in with severe cardiogenic shock are going to have a component of this.
it will at least double. And if you're dependent on renal replacement therapy, it can be as long as 20 hours. So that can tell you, you will suffer with... persistent hasoplegia for a while. And I'll tell you, I've spent many anxious hours standing beside a patient's bedside watching them and just wishing that I could get the malaria out of their system as much as I love the drug. Now, if you had a patient who comes in on beta block...
This seemingly is an attractive way of going about bypassing them as opposed to just upping the dose of your beta agonists and therefore overcoming that block. Are you doing that in the ED with milk? Yeah, so that's a great point. I will reach for that if it's a patient that came in that was on beta blockers.
And I'm not getting the effects I need by using low-dose epinephrine or doputamine. So it is something to think about. And that's something that if you need to reach for this, you know, reach out to your CICU, your CVICU, if you have questions, because they will be very happy.
If you grab one of us critical care consultants who work with this drug all the time, there is nothing that we would rather do than just either help you over the phone or run down to bedside and help because we want to make sure that the right medications are started early on. So yes, something to always think about.
All right. We briefly mentioned Leavis Mendon, a calcium sensitizer we don't have access to in the U.S. Neither of us have gotten to play with it, so we're not going to really discuss it very much here. Is there anything you want to say about it, Trina? No, I just wanted to have FDA approval so we can use it. It sounds like a fabulous drug. All right.
Now, this is my darling. I love, if you just gave me norepi and epi, I could get by with any patient out there. I might want some other drugs sometimes, but I would never stray from that little throuple. So, what are your feelings about epinephrine as an ion? Yeah, so I love epinephrine as well. And I don't think you can be a cardiovascular intensivist or emergency medicine doctor and not love epinephrine.
So the one thing that I really want to bring out with epinephrine is I think that there's all this dogma about epi being bad. And there's all these trials, and people will point to things like the Optima CC trial, the CAT trial, or even the CATS trial when they're looking at inodilator. Plus, presser versus, I'm a presser alone. And they'll say, epi's bad. And they'll say, you know, there's increased refractory shock. And when you look at it, they're looking at.
lactic acidosis, which you and I both know epi is going to work on those beta 2 receptors and lead to increased glycolysis and anaerobic. type b lactic acidosis but you and i both know too you know the heart likes lactate to a certain extent it uses it as a metabolic fuel
So one of the things I find interesting on so many of those trials is that many of those trials actually don't show an increased mortality with epi. They instead are showing this kind of refractory metabolic acidosis, but no difference in mortality outcomes. So that tells you in itself that potentially that's not hurtful. The other thing is, is these Trials are using epi in a way that I never use epi.
They're using epinephrine at massive doses, you know, doses of greater than 0.2 micrograms per kg per minute. To me, that's epi being used as a vasopressor. You know, I think you and I love epi, but we love epi as inotropic epi. You know, epi for doses of 0.01 micrograms per kg per minute to 0.08 micrograms per kg per minute. And for the listeners who might use it in just mics per minute, you know, if you have a hundred kilo patient, that's like one to eight.
micrograms per minute. So much lower doses. And one of the things that sometimes brings it home to people is if we think of dopamine as a drug that has very different effects based off of different doses, Epi is the same way. In fact, so epi is one of those drugs that works on beta-1, beta-2, and alpha-1 receptors. And everyone likes to think about all the alpha effects. But even if you look straight up to date, it will even say epinephrine used at low doses.
functions mostly as a beta agonist so beta 1 and beta 2 and can actually induce some vasodilation and then increase contractility and chronotropy. And so I really think it's important when we're talking about epi that we are referring to the fact that we are talking about inotropic levels of epi. So doses of 0.01 to maybe max. 0.1 micrograms per kg per minute
and not above there. If you're going above there, just realizing you're using it as a vasopressor. Yeah, no, I could not agree more with all of that. And it was eye-opening when I went back and did my second fellowship in the CTICU where I had not touched, you know, I went through my first critical care fellowship.
never doing cardiothoracic icu and this was one of the main things i took about it was just a love of low dose epi and in the past in the ed most people would start it started at 10 the patient's hypotensive it's like
No, no, you're not understanding. This is an agent. You've said the dose range in micrograms per kilogram per minute and gave people that one to eight. I would say just... remember one to five and that should be where you're actually sticking around and that'll be nice because it's the dobutamine range as well in terms of
you know, different units, but you get the idea of that is your dose range of this. And if you do that, you're going to be golden in terms of inotropic response. Now, why would you choose epi over W? And then I'll tell you my... Yes, I love this. So I think it's so great because it's truly a great inopressor. So it has inotropic effect. but it also isn't going to cause that vasodilation.
And I find that at really low doses, it's pretty hemodynamically neutral. You might see a slight increase in your blood pressure as your cardiac output goes up, maybe a slight increase in heart rate, but nothing huge on the increase in heart rate. So one of the reasons that so many people give it kind of a bad name is they're saying what's causing excessive tachycardia. What I'll tell you is
I don't find that in the low inotropic doses. And there was this interesting study that came out of the cardiac surgery literature a while back where they compared dobutamine and epinephrine, and they looked at dobutamine doses of 2.5. and five micrograms per kg per minute and compared that with epi 0.01 to 0.03 micrograms per kg per minute and what they found is that
Both of them increased the cardiac index. There wasn't a significant difference. But actually, dobutamine caused way more of a chronotropic or increased heart rate response. so you know i think that dogma of epi causing that much tachycardia it's not a thing when it's used at nice low doses Now, I reach for this drug on the Cicca subset. So I think it used to be that we thought about cardiogenic shock as these are patients with low cardiac index, high SVRI.
are high systemic vascular resistance. But we know more and more the sickest cardiogenic shock patients, you know, those that are sky stage E, that are in extremis, there is this point where they end up with inappropriate vasodilation. And they actually can have a low SVR. These are the very sick patients that when you add milrinone or maybe even dobutamine, that they can just decompensate further and suddenly they're hypotensive and even more hypotensive.
and now you no longer have adequate coronary perfusion pressure, and you have just precipitated worsening cardiogenic shock. So I find epi is great for the sick patients and I think it's an important drug especially first line in the ED because you really kind of can have something that if anything might increase your blood pressure nicely.
and not give you breezy tachycardia and also not give you hypotension. Yeah, you've put your finger on exactly my feelings as well. If you have a patient who is hypotensive, then it makes a lot more sense for me to reach for epi in the ED because I know if the nurses turn it up, I'm going to get... rewarded rather than punished like I will with these other agents.
So that just makes it so friendly to an ED environment where they might not have as much familiarity with the titration of these meds. Oh, the patient's hypotensive. I'll turn up. Probably shouldn't be turning up the nor-epi, but they turn up the epi instead, and everything still works out, as opposed to some of these other agents. The thing you've mentioned that is a downside of epi, and I think I've seen this more with epi than dobutamine, though dobutamine could do it as well.
is the lactate going up does not represent metabolic badness, but you do lose lactate as a good marker of what's going on with that patient's tissue perfusion. Though this is far more problem of the higher doses of epinephrine, like the true presser dose is not really an issue. in the low dose inotropic range we're talking about. Yes, I would say that at inotrope dosing of epi, you can have a significant beta, you know, to lactic acidosis.
Oftentimes, I don't see anything crazy. You know that patient that came in the other day with single-digit EF? His heart rate was 130. I started Epi, and everyone's like, you sure you want to do that? Like, his heart rate's 130. And I said, watch this. I started it. his heart rate went from 130 to 110 lactate dropped from five to three just like that i mean the increased contractility that i got at fe.03 amazing the difference that it could make.
So, you know, yes, you might have it, but what I would tell, you know, the listeners is don't just assume that you're, you know, increasing lactate is secondary to the epi, like keep that in the back of your mind, but also make sure that you are adequately treating their cardiogenic shock. And, you know, looking at other markers to make sure that they're improving. Yeah, absolutely. And at the low dose range, the lactate effects are marked.
So again, stay low and you're going to be okay. All right. I guess we have to talk about this one just because some people are still thinking this is an inotropic choice. Dopamine. An agent I think should just be
taken out of the Pyxis from every ED in the country. But, you know, are you guys still using this in the CTICU for anything? I know there are cardiac surgeons that are like, no, if you give dopamine, it's much better for the right heart. And I'm like, show me the literature for that because I haven't seen it, but there is still some belief that this agent has uses. I don't see them. What's your feelings?
Oh, I hate this drug so much. Am I using it? Question one. I am only using it when it is dictated by one of my cardiac surgeons. I only have one surgeon anymore who uses it. I'm still trying to figure out if it's this insistent belief on increased renal perfusion because that's been pretty debunked. Any more, then their kidneys are better, right, Trina? There you go, exactly.
But what I will tell you is, you know, because so many people say, well, at low dose, you know, just like less than three mics per kg per minute. You're really not getting that much beta effects. You're not getting the alpha effects. It's fine.
I don't see that clinically. I will tell you, I had a patient here recently that the surgeon really wanted it on. And when I would go from dopamine of one to two, because they wanted them at three, the amount of heart rate increase and flipping them into afib, it just happened. You know, I find that this drug is just a messy drug. It has such a chronotropic effect. I really don't see that much of it in this drug. Maybe the one remaining use for it is since it...
stable in a code cart. You know, for EMS, if they have a patient that is super bradycardic and in cardiogenic shock, It could be something to consider then, you know, on transport into the hospital. Once we get to the hospital, I think we have much better drugs like isoproteranol, or frankly, I even use dobutamine all the time to drive up a heart rate on those patients.
But maybe for pre-hospital providers, if you're someone here saying that that's all I have, okay, it might be a reasonable use. They have EPI as well, which will temporize that situation pretty nicely. So yeah, I'd love this to just be gone from medicine. All right, last agent, and then we can talk about some conditions. Good job. So, I do like this drug. You know, I think it's an oldie and a goodie, meaning it was a drug that was used a lot and kind of, I think, fell out of vogue.
I am bringing it back in just a little bit and in very specific situations. So it works on those sodium potassium ATPase channels. It's going to increase your contractility. It also has kind of that increased parasympathetic effects where it's going to cause a decrease in your heart rate.
So I find that this drug is the most useful on those patients that have a decreased EF. You know, they come in and they're in AFib with RVR. You throw the probe on and you're like, great. You know, their EF is like 15%. You know, you don't want to definitely give any beta blockers
or any, you know, calcium channel blockers. Sure, you can do amyodorone, but amyodorone also has a fair amount of beta blocker effect when given IV. And so digoxin can be kind of a great drug for that. It can help to slow the heart rate down and increase your contractility. You know, the things to be aware of is it does take a little bit of time for it to take effect, although you can bolus it, and so, you know, it...
I would say typically I find that it still takes 30 to 45 minutes to see clinical effects. Textbooks might tell you a little different. And also, you have to be careful with this with patients with renal dysfunction because it can also build up, and this is something that you want to make sure that they don't get digitoxic.
So I find that it's not quite as easy to titrate and work with and it's not as friendly for most people, but I do think that it has some utility. How are you giving it? Just really practice. So really practically, I tend to do boluses. A lot of these patients for me are patients that are also having some renal dysfunction because they came in in cardiogenic shock. so i like do 125 microgram bolus times two some people will be more bold and they'll do 250 micrograms times two
And then they're scheduling it. But if you're working in the eMERGE, you know, the bolus is all that you're really going to have to do initially. What I would do is tag in your pharmacist. Say, look. This is what their kidney function is. This is their GFR. What should I start with? and go from there. Realizing you're not going to cause dig toxicity if you give them a bolus of 250 micrograms times two and you stop and you're not continuing to give them the drug, you should be fine.
But I would recommend Paul to your quick ED pharmacist when you're doing this. And what's the spacing between those two boluses of either 125 or 250? You can do it pretty quick. Typically though, I'm not doing it closer than I think a couple of hours, so you might just be giving the first dose and then sending them upstairs.
and then subsequent doses might only be once a day it might be every other day based on their renal function and so from an ed perspective There's really no patient you couldn't get away with giving 125 or 250 bolus because even with renal failure, the first dose is a freebie because it's going to give the same blood effect.
and anyone else is just going to stick around for a lot longer. So really it's the second dose, much like antibiotics. I tell people don't adjust for renal failure for the first dose. You actually want to get maximal effect, and then you have to start worrying about it. All right, so you mentioned the AFib patient. Is there anyone else you'd be giving the job?
I think those are the primary patients that I find myself giving it to, and part of that's just because ease of dosing. You know, if I'm really wanting to have a consistent inotrope, I'm reaching for something that I can titrate easier. I tend to like drips for that. So it's typically those patients that I can think about right now that I would use it for.
And this agent does. It is that holy grail if it didn't have all the other problems attached to it because it really does give you contractility. And it not only doesn't increase the heart rate, it actually decreases the heart rate. So this agent would be great. It's just a shame.
that it has all these other side effects and problems and toxicities. And, you know, what we really need is a digoxin analog that eliminates a lot of that stuff and just gives us what we want, which is lower the heart rate, increase contractility. And then we just... Alright, anything else on the agent's side before we talk about conditions? Well, let's do it.
All right, you'll have to wait a couple of weeks for conditions. We're going to do that as a part two. But since I have not finalized that episode yet, if you have questions and you put them in the comments, I will get them answered by either myself or by Trina. before posting part two. So please, please, please put any questions, disagreements, comments, etc.
in the comments section for this episode, and then I will be able to respond in part two. Scott Weingart for the MCRIT Podcast, saying bye-bye. You hate that sound. I hate that sound. Why are you hearing that sound? You're hearing that sound because You are a... unpaid listener to mcrit and yet this is one of those episodes where only the team members the mcrit members get the full episode which means you are missing out on tons of resuscitative goodness
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