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0:01
[Music]
0:13
all right you guys welcome back to another video lesson from ICU advantage and so this video is gonna be a lesson in a collection of lessons in which we're going to be talking about ICU drips and more specifically in this lesson we're going to be talking about our vasopressors but before we begin with this lesson if this is your first time to our channel and watching our videos and you'd be interested in more of this critical care educational content such as this video then please
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subscribe to our channel below make sure you hit that Bell icon that way you'll be notified as soon as the new lessons become available to you guys as always I really do value the the likes the comments and the subscriptions that you guys give us they really go a long way to help support this channel and for that I do want to thank you guys and for those of you who don't know me my name is Eddie Watson and this is ICU advantage alright so let's go ahead and start the lesson and talk about our
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vasopressors so you might be wondering what exactly are vasopressors you'll hear them commonly referred to as pressors and really this group of medications really represents one of the staples of critical care and so what these are is they're a subset of a larger group something that we call vasoactive medications which essentially means that they have an impact on blood pressure through action on blood vessels and so within this larger group is where we're going to find this group of
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pressors and so when we talk about these press or medications what they're really doing is they're primarily being used to activate the adrenergic receptors so if you think the sympathetic nervous system and the whole point is to work to increase the peripheral vasoconstriction now when we talk about our pressure's here it's important to note that there are a couple differences but for the most part the vast majority of them are working to activate these adrenergic
2:13
receptors and so by doing this really what we're looking to see is a drastic improvement in our patients systemic vascular resistance or the SVR and for reference are normal svr is going to be between 600 and 1200 this is the non-indexed version of the SVR and this is the one that typically most people we use and the SVR is really measuring our after load which is essentially how constricted our patient's blood vessels are and so in the case of the SVR the higher the
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number the tighter it is the more vasoconstriction you have now while our primary goal with these vasopressors is to increase our patient's SVR we are going to see other effects on things that ultimately impact our patient's cardiac output so I'm actually going to link up above to a previous lesson that I've done talking about this cardiac output calculation but just for a reference and to make sure that we're on the same page we have our patient's cardiac output is going to be equal to
3:14
our heart rate times our stroke volume and our patient stroke volume is really comprised of three different things one being their preload another being their contractility and the last one being their after load and like we just said the after load is essentially our SVR measurement and so primarily our pressors are working to increase our patient's blood pressure by impacting this after load but because a lot of these pressors are working on those adrenergic receptors sometimes we're
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going to see additional effects which may or may not help our patients cardiac output some of them can have effects on our patient's heart rate and actually increase our patient's heart rate as well as they can also have an impact on contractility and again possibly increasing contractility in our patients and even sometimes they can have a temporary impact on our patients preload and this temporary effect really comes from the increase in the venous constriction which is going to help to
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increase the preload for our patients so here you can really see that some of these pressors are are going to have an impact on a lot of the the different parts that go into determining our patient's cardiac output but the primary thing that we're looking for is the impact on our patients afterload or their SVR and our goal here is to increase that and so the patient population that you're going to be using these medications are the patients who are hypotensive and more importantly and
4:50
more primarily in patients who are in shock and so ultimately the end goal here is to increase the tissue perfusion especially in end organs who otherwise are not going to have enough perfusion to really function adequately so there's several different days oppressors out there and it's important that we understand the actions that these vasopressors have to help increase our patient's blood pressure all right and so to understand how these vasopressors have their action we need to understand
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something about our adrenergic receptors there's primarily two big groups of receptors that we're going to talk about here first and those are going to be our alpha receptors and our beta receptors and for our alpha receptors we can further divide this up into our alpha 1 and alpha 2 receptors and so in the case for our vasopressors we're really only going to focus on these alpha 1 receptors and the reason for this is these alpha 1 receptors are going to be responsible for smooth muscle
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contraction 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're not going to talk about the beta 3 receptors but we are going to talk about beta 1 and beta 2 now these beta receptors are located in different parts of the body beta 1 receptors being located in the heart and beta 2 receptors are located in the lungs and if you ever have trouble remembering this just remember we have one heart and two lungs beta
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ones in the heart beta twos in the lungs and of these two receptor sites beta one is going to be the the main one that we want to focus on although we will talk about beta two a little bit and so what happens when our beta 1 receptors are activated is we're going to see an increase in our patient's heart rate which is a positive Crona tropic effect as well as we can also see an increase in our contractility which is going to be a positive ion AFET now for our beta 2 receptors the
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the primary thing to know here is that this is going to cause smooth muscle cell relaxation within the lungs and so these are our adrenergic receptor sites primarily the ones we want to worry about are the alpha 1 and the beta 1 receptors now in addition to these we do have a couple other receptors that are going to come into play the first of these is going to be our our v1 receptors and v1 is going to be activated by something called vasopressin and this is going to cause
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smooth muscle contraction and then finally one other receptor I want to talk about is called a t2 and this one is going to be activated by angiotensin 2 and is going to cause peripheral vessel constriction all right so these are the receptor sites that you guys need to know in order to understand the effect of different vasopressors the last thing i want to cover here are two different terms that are going to be important to know this is going to be to have an agonist versus an antagonist and
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so here essentially an agonist is something that fully activates the receptor to which it's binding to and an antagonist is going to be something that does not activate the receptor in fact can block the effects of the other agonist and so here in the case of our vasopressors that these are going to be agonist of these various different receptor sites that we just talked about alright so now I want to move on and talk about these different phase oppressors that we use and the first of
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these is going to be what we call Levophed which is also known as norepinephrine and you'll probably more commonly hear this one referred to as levo so Liva has been around for a while has actually discovered in 1946 and it was first approved to be used as a medication in the 1950s and Levophed is a direct acting vasopressor agent means it directly has an effect by directly impacting these receptor sites and Levophed is typically going to be the first-line pressor that we're gonna
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we're going to use and in fact in the surviving sepsis campaign guidelines Levophed is listed as the primary presser to be using first and so when we talk about the receptors that Levophed activates it's primarily an al for one receptor agonist what it does also have some agonizing effects on our beta 1 receptors as well and with Levophed it's going to have roughly equal vino and arterial constriction effects so one important thing to know about Levophed is that it can cause
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tissue necrosis and limb ischemia if you have any sort of extravasation so now let's move on and talk a little bit about the dosing of Levophed typically our concentration is going to be 4 milligrams and 250 MLS but you can see the lesser concentrations of two milligrams or a double concentrated at 8 or a high concentration of 16 milligrams as well now per the literature the standard effective dose of levo is going to be 1 to 12 micrograms per minute now I know for a lot of you out there that
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have used Levophed you realize that this is definitely not the case in which most hospitals operate in fact most hospitals usually have ranges of one to thirty or one to fifty or even more so definitely important to know your hospital's policy for the ranges of the medications that you're using now it does have a fast onset of just one minute and when it comes to making our dose changes with levo that we're gonna be doing this every three to five minutes for
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titration and so now let's move on and talk about Neos a nephron what's also known as phenol Efrain and this one you often will hear referred to as neo now in the case of neo this has actually been around for a while as first patented in 1927 and then used medically in 1938 and it has a lot of different medical uses it is another direct-acting vasopressor just like Levophed but in the case of neo this one is actually a pure alpha receptor agonist so unlike levo this is not going to have
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any effect on those other receptors now one thing to know though because of this is that actually can cause a baroreceptor mediated reflex bradycardia and so if this happens this can't lead to a mixed effect on our patients overall cardiac output and so if we do see this we do want to discontinue this infusion and really if you need to you could use a chrono trochaic medication as well now neo is not typically our first line of choice but this can certainly vary depending on provider
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preference but it is a good alternative in cases where we either have Levophed induced arrhythmias or really as a adjunct in Salvage therapy to try to add what we can to increase our patient's blood pressure once again this one's also going to have equal vino and arterial constriction and just like in the case of levo extravasation can lead to tissue necrosis and limb ischemia and so now moving on and talking about our dosing here our typical concentration is
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going to be 40 milligrams and 250 MLS and here our standard effective dose is going to be anywhere from 50 to 200 mics per minute and our onset is quick just like Levophed in just 1 minute as well as just like with Levophed this one we're going to titrate every 3 to 5 minutes all right so now moving on let's go ahead and talk about vasopressin again another more common term that you're gonna hear for this one is going to be vaso and vasopressin and the medical sense has been around for a
12:32
while but it really was first started using and treating shock around 2001 it's oftentimes a second-line treatment to patients who are resistant to the catecholamine vasopressors and so the way vasopressin works is it actually impacts the organ invasor pressin system or AVS to increase our patient's blood pressure and so it's going to act as a v1 receptor site agonist it does also have some effects in the kidneys causing water reabsorption within the distal tubules and the collecting ducts which
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is going to synergistically work to help to increase our patients blood pressure but the primary effect that we're looking for is this agonizing impact on these v1 receptors to directly cause that smooth muscle contraction now for vaso we find this typically in the concentration of 20 units in a hundred MLS and our standard effective dose is going to be 0.001 2.0 four units per minute now the onset for vasopressin is not as quick as levo and neo and we're typically looking at anywhere
13:39
from 5 to 15 minutes and when it comes to vasopressin this is actually a medication that we don't titrate so it's either on or off this isn't necessarily always followed in practice and some providers may want to decrease this dose but typically they'll set a dose and we turn it on at that dose and when we would no longer need it we turn it off all right so now let's go ahead and move on to epinephrine more common terminology for this one is going to be epi and epinephrine was first
14:08
synthesized in 1904 so this medication has definitely been around for a long time as well and typically you're gonna see F be used in cases where everything else has failed in the treatment of shock although in some areas like the cardiac world you may see this used more liberally but typically this is our last line to go to when nothing else is working now the interesting thing about epinephrine is this is a non selective agonist of all the adrenergic receptors
14:36
so this is gonna be alpha 1 alpha 2 beta 1 beta 2 and even beta 3 but however as we get to larger doses it's typically going to have a more selective effect on our alpha receptors so this is important to know now the typical concentration we're gonna find this mixed up in is going to be one milligram and 250 MLS and the standard effective dose for epinephrine is going to be 1 to 10 micrograms per minute onset is pretty quick with this we're looking at 1 to 2 minutes and when it
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comes to titrating epi that we usually want to do this every 5 to 10 minutes alright moving on to the next presser that we're going to talk about and this is one that we call dopamine there is no common name for this we usually just call it dopamine once again this one's been around for a while since 1910 one of the interesting things about dopamine though is it's really dose dependent on the type of effect that we're going to see it can act as either a beta agonist
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or an alpha agonist really depending on the dose now our typical concentration for dopamine is going to be 400 milligrams and 250 MLS and when we talk about our dosing there's a couple different ranges that we're going to see now overall the standard effective dose is considered to 220 micrograms per kilogram per minute important to know that this one is going to be a weight based rate that you have going and while I did give a lot of the other medications and non weight based rates
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there are a lot of facilities that do used weight based rates for those drugs too so like I said we have a couple different ranges that really kind of impact the way in which dopamine is going to have its effect on our patients the first dose range is going to be from 0.5 to 2 and this is going to be what we call our renal dose a lot of the literature really doesn't support this but you will find some providers who do still use it this way the next range we're going to talk about is from 5 to
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10 and this is where it's really going to have an EIN atrophic effect and the reason for is at these doses this is where it's going to be acting more as a beta agonist now from there when we get to the range of 10 to 20 this is where we're gonna see it be more adrenergic and the reason for this being that it's gonna be acting more as an alpha agonist now onset for dopamine is usually about five minutes and for dopamine we usually want to be titrating this about every 10
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minutes alright and so now looking at the last presser that we're going to talk about is something that we call G oppressor this is also basically angiotensin 2 in an IV form it's a synthetic peptide that really is identical to the the normal hormone found in our body and really this one is fairly new in the world of treating shock in fact it was just approved to be used in 2017 and the way it works is it actually activates the renin-angiotensin-aldosterone system so
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the RAAS system and more specifically it's going to activate our eighty two receptors and by activating these receptors and blood vessels that this is going to cause vasoconstriction interesting thing to know about this is this is going to have primarily an action on arterial vasoconstriction and because this is a synthetic version of angiotensin medications like her ARBs are angiotensin receptor blockers can reduce the effects of this medication now there's two typical concentrations
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that we find a high concentration and a standard concentration high concentration is going to be two point five milligrams and 250 MLS and the standard concentration is going to 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 thing as point zero to two point zero eight micrograms now on set for this one is going to be about five minutes and
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our titration for angiotensin we're going to want to do this about every five minutes all right so that's the the last of the vasopressors that we're going to talk about here as you can see we have quite a few of them to choose from and they all have slightly different actions so it is important to know some of the differences in these medications because it's going to change some of the effects that you're gonna see as well as the circumstances in which you might want to choose one
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presser 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 that this one is a strong alpha agonist but it does also have some beta one agonizing effects it's going to be very strong when it comes to increasing our patient's SVR has a little bit of an effect on our heart rate and our contractility now Gnaeus in Efrain like
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we talked about is a pure alpha agonist and it is a strong alpha agonist but we're not going to see any effects on our beta receptors this one is also going to be very strong at increasing our patient's SVR but we're not going to see any impact on contractility and if anything you might see a slight decrease in heart rate if they have that reflexive bradycardia now if you remember with vasopressin this one actually agonizes the v1 receptor so it's not going to
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have any alpha beta receptor activation vasopressin is also though pretty strong at increasing our patients SVR but we're not gonna see any impact on our heart rate or contractility all right and then for epinephrine remember this one's a non-selective adrenergic agonist although in higher doses it's going to have very strong alpha receptor agonizing effects but we are also going to see effects on the beta 1 receptors as well as the beta 2 receptors epi is another one that's pretty strong at
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increasing our patient's SVR but you're also going to see very strong impacts on our patient's heart rate as well as their contractility now when we look at dopamine I like we said it's going to be dose dependent on the effects that you're going to see from this but it's typically going to be a pretty strong alpha agonist and it's definitely going to be a strong beta 1 agonist as well as you will see some impact on your beta 2 receptor sites now once again this one
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does have a pretty good impact on our patients SVR as well as their heart rate and contractility now finally for our G oppressor now remember that this one is an 82 agonist therefore we're not going to have effects on alpha or beta receptors and this one's going to have a pretty decent effect on our patients SVR but have no impact on their heart rate and contractility so hopefully this kind of puts it in perspective shows you some of the differences with these vasopressors the
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receptors that they're activating as well as the effects that you would expect to see when using these in your patient so the important takeaway from all of this is to know that we have several different phase opressors at our disposal again vasopressors they're going to work to constrict our patients blood vessels working to increase their blood pressure and ultimately their end organ tissue perfusion they all have slightly different mechanisms of action as well
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as the receptors that they impact and it's going to be really important that you no these concentrations as well as the dosages and the range of dosages that you can use on your patients because that's really gonna come into play when it comes to managing your patients with these medications and so that's gonna go ahead and wrap up this lesson here I am gonna do another lesson related to vasopressors and just talk about some of the good to know information when
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dealing with your patients who are on vasopressors but I don't feel that that content necessarily belongs within this lesson here so I'm gonna pull that out into a separate lesson itself and so with all that said I do want to thank you guys so much for watching I really hope that you found this lesson useful if you did please go down below and hit a like leave us a like as well as leave us a comment it really goes a long way to support our channel and we'd love to
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hear the feedback that you guys leave for us like I said stay tuned for another lesson in this collection where I'm going to continue the lesson on vasopressors and talk about some of those good to know tidbits of information in the meantime feel free to check out the last series of lessons that I did in which we took a look at the endocrine system and a whole host of different disorders that you're gonna find in your patients as always thanks so much for watching and you guys have a great day
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