Transcript for:
ICU Advantage: Dobutamine Lecture

all right you guys welcome back to another video lesson from icu advantage my name is eddie watson and make sure you guys subscribe to this channel to make sure you keep getting more critical care content such as this video here now in this lesson here we're going to be talking about a medication that i often find that a lot of people don't understand very well part of it may be the confusion that is often because of the look-alike sound-alike relationship with dopamine but it is a very different medication and used for different purposes which we are going to discuss in this lesson here so let's get into the lesson talking about debutane so dibutamine is a commonly used medication but it is also commonly misunderstood it can play an important role in the treatment of our critically ill patients thus it's important that you do understand how it works and why it is that we use it so let's start off and talk about what is domutamine and how does it work so dibutamine which also goes by the name dobutrex is classified as an inotropic agent what this means is that it increases cardiac output it has several different uses in those with heart failure and those in cardiogenic shock as well as potential benefits in other low cardiac output states now dibutamine is primarily a beta-1 agonist which means that it activates beta-1 adrenergic receptors so as a result of this activation we're going to see increased contractility of the ventricle this is ultimately going to lead to lower end systolic volume which leads to an increase in our stroke volume so if you remember our cardiac output equation cardiac output equals heart rate times stroke volume then you'll recognize that this increase in stroke volume is in turn going to increase cardiac output in our patients now one thing to keep in mind though is that beta blockers are going to work against the effects of dobutamine now dibnamine can also impact our patient's heart rate through this beta 1 activation although the effects of the elevation and heart rate is less pronounced than its inotropic effect this increase in heart rate though can also contribute to the increase in cardiac output from the equation that we just talked about above now in addition to the beta 1 activation it does also have some beta 2 and alpha 1 effects alpha 1 leads to vasoconstriction but the effect here is actually pretty minimal beta 2 which is more pronounced than our alpha 1 activation primarily here is going to lead to vasodilation now this is not always seen and sometimes just negates the alpha 1 activation but certainly can be seen in our patients and it is important to know about so you want to be on the lookout for potential decreases in your patient's blood pressure initially if your patient has low cardiac output though we'll often see this negated by the increase in contractility and in fact we can see improvements in their blood pressure as a result of that increased cardiac output now if this hypotension does present and persist in your patient then at this point you do want to stop the infusion and address their volume status now this vasodilation can help to decrease filling pressure as well as our afterload making it easier for the heart to contract again increasing stroke volume and thus our cardiac output so that's the essence of how it is that dibetamine actually benefits our patient now i actually want to talk about some of the misconceptions or confusions between dibutamine and dopamine now as i've mentioned these two medications are often confused for one another but they act in quite different ways it also doesn't help that the dose ranges are very similar which i am going to discuss here in a minute but if you remember about dopamine which i did cover in a previous lesson which i'm going to link to up above here dopamine is another beta 1 agonist but it has more chronotropic effect and thus we see more of an increased heart rate than we do contractility now dopamine also has more alpha-1 activation especially at the higher doses so instead of vasodilation like we see with dibutamine we're going to see vasoconstriction by increasing svr and afterload with the use of dopamine so i'm going to put up a quick chart here just to compare the effects of these two medications and hopefully help to drive this point home so we're going to be taking a look at our cardiac output our cvp our pulmonary artery occlusive pressure our svr our map and our heart rate and see how these two medications compare so first we have our tributamine and here we're going to see a strong increase in cardiac output we're actually going to see decreases in our cvp paop as well as our svr or our afterload and then for our patients blood pressure our map we're going to see increases here and this is going to be primarily driven by the increased cardiac output and then as far as their heart rate goes it's either going to be about the same or we might see an increase now when we talk about dopamine we're going to talk about two different doses we have our dose that's less than 10 micrograms per kilogram per minute and then our dose that's going to be greater than 10. so for our lower dose we're going to see that increase in cardiac output we definitely are going to see increases in our cvp and our paop and then as far as our afterload goes it's either going to be about the same or we might have at least initially some increase here and the same is also going to go for our patients map but like i said because of that chronotropic effect we are definitely going to see an increase in heart rate so now for our higher dose dopamine once again we're going to see that increase in cardiac output that good increase in our cvp and our paop but now because we're hitting those alpha 1 effects we're going to see marked increase in our patients svr and their map and then again we're going to see the increased effects on our patient's heart rate so hopefully kind of seeing these two side by side really shows you some of the big differences here really think about here debuting the main benefit that we're getting is the increase in cardiac output as well as the support for our patient's blood pressure by increasing that cardiac output whereas dopamine we're really looking at the increased heart rate and then at those higher doses the increase in our patients svr and map as well all right so let's actually talk about some of the side effects that we can see so some side effects that your patient could experience with dibutamine would be things like increased heart rate and blood pressure could lead to headache nausea vomiting palpitations ectopy chest pain and shortness of breath some potential adverse effects that we could see would be things like asthma attack if they are an afib that this can lead to a rapid ventricular rate we can also see ventricular ectopy although actually seeing vtac is rare in our patients we can also potentially see hypotension although again this is pretty rare and then finally anaphylaxis all right so let's move on and talk about the dosing for dibutamine so here we're going to give this as a continuous iv infusion and the typical concentrations that we find are going to be seen in a mixture of d5 water and those common pre-mixed bags are going to be 250 milligrams and 250 ml which gives us one milligram per milliliter and then we have 500 milligrams and 250 ml which gives us two milligrams per milliliter and then we can also see 500 milligrams in 500 ml again another one milligram per ml concentration now our dosing that we're going to give our patients is going to be in micrograms per kilogram per minute which is the same that we use for dopamine so again this is going to add to that confusion but our typical dose for this medication is going to range from 2 to 20 mics per kilogram per minute that said we can go up to 40 mics per kilogram but it's not often that we're going to be using it at this high dose now we're going to see this medication take effect as early as two minutes but it can take up to 10 minutes for its peak effect so we typically aren't titrating this medication but when we do we want to make sure that we're giving it at least 5 to 10 minutes between the titrations so that we can see those effects all right so let's talk about our use of this medication and critical care and there's really three primary uses that are only going to be seen in critical care the first of these is going to be cardiogenic shock and this is actually one of our main uses for this medication and the whole purpose here is that by increasing the stroke volume and as well as potentially our patient's heart rate while also reducing the afterload that we're going to help to increase our patients cardiac output which is going to preserve systemic blood flow this is obviously a problem in cardiogenic shock and definitely is going to be benefit for these patients now another potential use that we have in icu is going to be as a bridge to support for patients with late stage heart failure and so here we're using dibutamine for its inotropic support and again for patients with that late stage heart failure who really haven't responded to other directed therapies by using dibutamine here that this can help to bridge them to a longer-term solution such as mechanical circulatory support such as a vad or even heart transplant that said we can also use this medication long term for palliative support for those patients who really aren't going to be candidates for either of the above and then finally the last potential use in the icu is going to be in our patients with sepsis now there is support for its use and there are recommendations that do come from the surviving sepsis campaign in the use of dibutamine in patients who have sepsis and also have systolic dysfunction and our goal here is preserving and organ functioning decreases in mortality were seen in patients when dibutamine was given when our patient's scv02 was less than 70 so those are our potential uses for debutane uh what we often will find in the icu as well as an overall review of this medication again lots of confusion that comes up around this medication it's oftentimes confused with dopamine so hopefully this lesson helped to kind of clarify some of the differences between those two medications and why we actually would be using dibutamine so i really hope that you guys enjoyed this lesson if you did please leave me a like down below it really goes a long way to help support this channel and the eyes of the youtube algorithm as well as leave me some comments let me know what you thought of this lesson i love to read your comments and i try to respond to just about everybody if you haven't subscribed already make sure you do so as well as share this lesson with anybody else that you think might find it useful a special shout out to our awesome youtube and patreon members out there the support that you guys provide for this channel is truly appreciated make sure you guys stay tuned for the next lesson in this series otherwise check out a couple really awesome lessons i'm going to link to right here as always thank you guys so much for watching have a great day