Vasopressors (Part 1) - ICU Drips

Alright guys, welcome back to another ICU Advantage video lesson, so this video is going to be one lesson in a collection of lessons where we're going to talk about

drips

in the ICU and more specifically in this lesson we're going to I'll be talking about our

vasopressors

, but before we get into this lesson, if this is your first time visiting our channel and watching our videos and you would be interested in more critical care educational content, like this video, please subscribe to our channel below. Be sure to hit the Bell icon that way, you'll be notified as soon as new lessons are available to you, as always.

I really appreciate the likes, comments and subscriptions you give us, they really help a lot. to help support this channel and so I want to thank you and for those of you who don't know me, my name is Eddie Watson and this is the ICU advantage so let's go ahead and start the lesson and talk about our

vasopressors

. So, you may be wondering what exactly vasopressors are. You'll hear them commonly called pressors, and in reality, this group of medications really represents one of the building blocks of critical care, so they're a subset of a larger group. which we call vasoactive medications, which essentially means that they have an impact on blood pressure through action on blood vessels and therefore within this larger group is where we are going to find this group of pressors and therefore So, when we talk about these medications or press, what they really do is they are primarily used to activate adrenergic receptors, so if you think that the sympathetic nervous system and the goal is to work to increase peripheral vasoconstriction now that we talk Of our pressure here, it's important to note that there are a couple of differences, but for the most

part

the vast majority of them are working to activate these adrenergic receptors and by doing this really what we're looking for is a drastic improvement in stamina. systemic vascular or SVR of our patients and for The reference is that the normal SVR will be between 600 and 1200.

This is the non-indexed version of the SVR and this is the one that most of us normally use and the SVR actually measures our afterload , which is essentially how constricted our patient's blood is. are the blood vessels and therefore in the case of SVR, the higher the number, the tighter it is, the more vasoconstriction you will have now, while our main goal with these vasopressors is to increase our patient's SVR, we will look at other effects on things that ultimately impact our health. patient cardiac output, so I'm going to link above to a previous lesson I did talking about this cardiac output calculation, but just for reference and to make sure we're on the same page as we have our patient's cardiac output.

The output will be equal to our heart rate multiplied by our stroke volume and our patient's stroke volume is actually made up of three different things, one is their preload, one is their contractility and the last one is their afterload and as we just said , afterload. is essentially our measurement of SVR and so our pressors are primarily working to increase our patients' blood pressure by impacting this after loading, but because many of these pressors are working on those adrenergic receptors, sometimes We will see additional effects that may or may not help our patients' cardiac output, some of them may have effects on our patients' heart rate and actually increase our patients' heart rate, as well as they may have an impact on contractility and, again, possibly increase contractility in our patients and may even sometimes have a temporary effect. impact on the preload of our patients and this temporary effect really comes from the increase in venous constriction that will help increase the preload of our patients, so here you can really see that some of these pressors are going to have an impact on the preload of our patients. our patients.

Many of the different

part

s that go into determining the cardiac output of our patients, but the main thing we look for is the impact on our patients' afterload or their SVR and our goal here is to increase that and therefore the population of patients than you. The ones who are going to use these medications are patients who are hypotensive and, more importantly and primarily, patients who are in shock, so ultimately the end goal here is to increase tissue perfusion, especially in end organs that are otherwise not going to have enough perfusion to actually function properly, so there are several different vasopressors and it is important that we understand the actions that these vasopressors have to help increase the blood pressure of our patients, and to understand how these vasopressors have their action, we need to understand something about our adrenergic receptors there are mainly two large groups of receptors that we are going to talk about here first and those will be our alpha receptors and our beta receptors and for our alpha receptors we can divide them further into our alpha 1 and alpha 2 and in the case of our vasopressors we are really only going to focus on these alpha 1 receptors and the reason for this is that these alpha 1 receptors are going to be responsible for the contraction of the smooth muscle.

Now, for these beta receptors, these can be further divided into three groups, our beta 1, beta 2 and beta 3 receptors, now again here we are not going to talk about the beta 3 receptors, but we are going to talk about the beta receptors 1 and beta 2, now these beta receptors are located in different parts. In the body the beta 1 receptors are located in the heart and the beta 2 receptors are located in the lungs and if you ever have trouble remembering this, remember that we have one heart and two lungs, the beta two in the heart, the beta two in the lungs and of these two beta receptor sites one will be the main one that we want to focus on, although we will talk a little bit about beta two and then what happens when our beta 1 receptors activate is that we will see an increase in heart rate from our patient, which is a positive Crona tropic effect, and we can also see an increase in our contractility, which will be a positive AFET ion now for our beta 2 receptors.

The main thing we need to know here is that this is going to cause relaxation of the smooth muscle cells within the lungs, so these are our adrenergic receptor sites, mainly the ones we want to worry about are the alpha 1 and beta 1 receptors. Now, in addition to these, we have a couple more receptors that go a They come into play, the first one will be our v1 receptors and v1 will be activated by something called vasopressin and this will cause smooth muscle contraction and finally another receptor that I want to talk about is called t2. and this will be activated by angiotensin 2 and will cause constriction of the peripheral vessels, so these are the receptor sites that you need to know to understand the effect of different vasopressors, the last thing I want to cover here.

There are two different terms that will be important to know which will be having an agonist versus an antagonist, so here essentially an agonist is something that fully activates the receptor it binds to and an antagonist will be something that does not activate the receptor, in fact it can block the effects of the other agonist and here, in the case of our vasopressors, these are going to be agonists of these different receptor sites that we just talked about. Okay, now I want to come in. Go ahead and talk about these different phase oppressors that we use and the first one is going to be what we call Levophed, which is also known as norepinephrine and you'll probably most commonly hear this one referred to as levo, so Liva has been around for De In fact, it was discovered a while ago in 1946 and was first approved for use as a medication in the 1950s.

Levophed is a direct-acting vasopressor agent, meaning it has a direct effect by directly impacting these receptor sites and Levophed will usually be first. -Line presser that we are going to use and in fact, in the sepsis survival campaign guidelines, Levophed is listed as the main presser that will be used first, so when we talk about the receptors that Levophed activates, it is mainly a to to. a receptor agonist, what it does also has some agonizing effects on our beta 1 receptors and with Levophed you will have approximately the same wine and arterial constriction effects, so one important thing to know about Levophed is that it can cause tissue necrosis and ischemia of the extremities.

If you have any type of extravasation, now let's go ahead and talk a little bit about the dosing of Levophed. Normally our concentration will be 4 milligrams and 250 MLS, but you can see lower concentrations of two milligrams or a double concentrate at 8. or a high concentration of 16 milligrams, according to the literature, the standard effective dose of levo will be 1 to 12 micrograms per minute. I know many of you who have used Levophed realize that this is definitely not the case. the case that most hospitals operate in, in fact, most hospitals generally have ranges of one to thirty or one to fifty or even more, so it is definitely important to know your hospital's policy for ranges of the medications that you are using, now you have a quick onset of just one minute and when it comes to doing our dose changes with levo, we will do it every three to five minutes for titration, so now let's go ahead and talk about Neos , a nephron that is also known as phenol, Ephraim and Este, which you will often hear referred to as neo, now in the case of neo, it has actually been around for a while, as it was first patented in 1927 and later It was used medically in 1938 and has many different medical uses.

It is another direct action. vasopressor like Levophed, but in the case of neo, this is actually a pure alpha receptor agonist, so unlike levo, this will have no effect on those other receptors. One thing we should know because of this is that it can actually cause a baroreceptor. reflex mediated bradycardia and so if this happens, this cannot cause a mixed effect on the overall cardiac output of our patients, so if we see this, we want to stop this infusion and really, if necessary, you could use a chronotrochaic medication. Also, now neo is not usually our first line of choice, but this can certainly vary depending on provider preference, but it is a good alternative in cases where we have Levophed-induced arrhythmias or really as an adjunct in rescue therapy to try to add what we can increase the blood pressure of our patient once again, this will also have the same wine and arterial constriction and, as in the case of extravasation of levo, it can cause tissue necrosis and ischemia of the extremities , so now let's continue talking about our dosage here, our typical concentration will be 40 milligrams and 250 MLS and here our standard effective dose will be 50 to 200 microns per minute and our onset is rapid just like Levophed in just 1 minute and just like with Levophed this one.

We're going to titrate every 3 to 5 minutes, so now let's go ahead and talk about vasopressin again. Another more common term you'll hear for this will be vaso and vasopressin and the medical sense has been around for a while, but it actually started being used and treating shock around 2001. It's often a second line treatment for patients who are resistant to catecholamine vasopressors and so the way vasopressin works is that it actually affects the organ invasive pressure system or AVS to increase the blood pressure of our patients and therefore it will act as an agonist of the v1 receptor site.

It also has some effects on the kidneys, causing water reabsorption within the distal tubules and collecting ducts, which will work synergistically to help increase our patients' blood. pressure, but the main effect we're looking for is this agonizing impact on these v1 receptors to directly cause smooth muscle contraction. Now for vaso, we find this typically at the concentration of 20 units in a hundred MLS and our standard effective dose goes now is 0.001 2.0 four units per minute, the onset of vasopressin is not as rapid as that of levo and neo and We're typically looking at 5 to 15 minutes and when it comes to vasopressin, this is actually a medication that we don't use. adjust to be on or off, this is not necessarily always followed in practice and some providers may want to lower this dose, but usually they set a dose and we turn it on at that dose and when we no longer need it, we turn it off well, so now Let's go ahead and move on to epinephrine.

The most common terminology for this will be epi and epinephrine was first synthesized in 1904, so this medication has definitely been around for a long time as well and usuallyyou. We will see F used in cases where everything else has failed in the treatment of shock, although in some areas such as the cardiac world you may see this used more liberally, but generally this is our last line to go to. turn to when nothing else works now. The interesting thing about epinephrine is that it is a non-selective agonist of all adrenergic receptors, so it will be alpha 1 alpha 2 beta 1 beta 2 and even beta 3, but as we get to larger doses, it will usually have a greater effect. selective. in our alpha receptors, so it's important to know now, the typical concentration that we will find this mixed in will be one milligram and 250 MLS and the standard effective dose of epinephrine will be 1 to 10 micrograms per minute of onset.

It's pretty quick with this, we're looking at 1 to 2 minutes and when it comes to titling epi, we generally want to do this every 5 to 10 minutes, okay, we move on to the next press that we're going to talk about and this is one that we call dopamine. There is no common name for this we generally just call it dopamine again this has been around for a while since 1910 however one of the interesting things about dopamine is it is really dose dependent depending on the type of effect we are going to have. See, it can act as a beta agonist or an alpha agonist, really depending on the dose.

Now our typical dopamine concentration will be 400 milligrams and 250 MLS and when we talk about our dosage. There are a couple of different ranges that we'll look at now. In general, the standard effective dose is considered to be 220 micrograms per kilogram per minute. It is important to know that this will be a rate based on the weight you have. and while I gave many other medications and non-weight based rates, there are many centers that also use weight based rates for those medications, so like I said, we have a couple different ranges that really impact how what dopamine will have its effect on our patients, the first dose range will be 0.5 to 2 and this will be what we will call our renal dose.

Much of the literature doesn't really support this but you will find some providers that still use it this way, the next range we will talk about is 5 to 10 and this is where you will really have an atrophic effect of the EIN and the reason is that in these doses, this is where it goes From there, when we get to the 10 to 20 range, this is where we will see that it is more adrenergic and the reason for this is that it will now act more like an alpha agonist. The onset of dopamine is usually about five minutes and we typically want to titrate this every 10 minutes, so now looking at the last presser that we're going to talk about, there's something we call the G oppressor, this is also basically Angiotensin 2 in intravenous form is a synthetic peptide that is actually identical to the normal hormone found in our body and this is actually quite new in the world of shock treatment;

In fact, its use was approved in 2017 and the form. What works is that it actually activates the renin-angiotensin-aldosterone system, so the RAAS system and more specifically, it will activate our eighty-two receptors and by activating these receptors and blood vessels, this will cause vasoconstriction. The interesting thing we should know about this is this will have an action primarily on arterial vasoconstriction and because it is a synthetic version of angiotensin medications, like their ARBs, are angiotensin receptor blockers, they can reduce the effects of this medication. . Now there are two typical concentrations: we find a high concentration and a standard concentration. the high concentration will be two point five milligrams and 250 MLS and the standard concentration will be the same two point five milligrams this time in 500 MLS.

Now the standard effective dose for this is going to be 20 to 80 nanograms per kilogram per minute, this is essentially the same as point zero to two point zero eight micrograms now on the set for this is going to be about five minutes and our angiotensin titration we're going to want do this about every five minutes, so That's the last of the vasopressors we're going to talk about here, as you can see we have quite a few to choose from and they all have slightly different actions, so it's important to know some of the differences between these medications. because it's going to change some of the effects that you'll see, as well as the circumstances in which you might want to choose one presser foot over another, so I just want to do a quick review with a chart here that looks at some of these. differences all in one place so you can compare them side by side so first we'll talk about levophed or norepinephrine and we know this is a strong alpha agonist but it also has some agonizing beta one effects. very strong when it comes to increasing our patient's SVR, it has a small effect on our heart rate and our contractility.

Now Gneo in Ephraim, as we talked about, is a pure alpha agonist and it is a strong alpha agonist, but we are not going to see any effect on our beta receptors, this will also be very strong to increase the SVR of our patient, but we will not see any impact on contractility and if anything you might see a slight decrease in heart rate if they have that. reflex bradycardia now, if you remember, with vasopressin, it actually agonizes the v1 receptor, so you won't have any activation of the alpha beta receptor. Vasopressin is also quite strong at increasing our patients' SVR, but we will not see any impact on our heart rate. or contractility, and then for epinephrine, remember that this is a non-selective adrenergic agonist, although at higher doses it will have very strong agonizing effects on the alpha receptors, but we will also see effects on the beta 1 and beta 2 receptors.

The receptors epi are another one that is quite strong in increasing the SVR of our patients, but we will also see very strong impacts on the heart rate of our patients, as well as their contractility. Now, when we looked at dopamine, I like that we said it will depend on the dose. about the effects that you'll see from this, but generally it's going to be a pretty strong alpha agonist and it's definitely going to be a strong beta 1 agonist and you're going to see some impact on your beta 2 receptor sites right now. Again, this has a pretty good impact on our patients' SVR, as well as their heart rate and contractility.

Now finally, for our G oppressor, remember that this is an 82 agonist, so we will have no effects on the alpha or beta receptors. and this is going to have a pretty decent effect on our patients' SVR, but it's not going to have any impact on their heart rate and contractility, so I hope this puts it into perspective and shows you some of the differences with these vasopressors, the receptors that they are activating. as well as the effects you would expect to see when using them on your patient, so the important takeaway from all of this is to know that we have several different phase oppressors at our disposal.

Vasopressors will work to restrict our patients' blood. The vessels that work to increase blood pressure and ultimately end-organ tissue perfusion all have slightly different mechanisms of action, as well as the receptors they impact, and it will be very important for you not to know these concentrations, as well as the doses and range. of dosages that you can use on your patients because that will really come into play when it comes to managing your patients on these medications and so we'll go ahead and conclude this lesson here. I'm going to do another lesson related to vasopressors and just talk. about some of the information that is good to know when it comes to patients taking vasopressors, but I don't think that that content necessarily belongs in this lesson, so I'll put it out in a separate lesson and so on with that.

I said: I want to thank you very much for watching. I really hope you found this lesson useful. If so, go below and hit like. Leave us a like and a comment. It really is of great help. Please support our channel and we would love to hear the comments you leave us, like I said. Stay tuned for another lesson in this collection where I'll continue the lesson on vasopressors and talk about some of those interesting facts. In the meantime, feel free to check out the last series of lessons I did where we looked at the endocrine system and a lot of different disorders that you'll encounter in your patients, as always, thank you so much for watching and have a great day