Inotropic Agents (Nursing)

00:01 Okay, let's get into our inotropic agent. There's something I want you to pay attention to and to really remember. The effect of inotropes is greatly reduced when you're in the environment of acidosis, meaning if our blood pH is acidotic, the inotropes are not going to work as well. So just remember that. If you're running specific inotrope such as epinephrine or dopamine or dobutamine and then all of a sudden it seems like they're not working as well, get an ABG and see what your pH might be.

00:31 You might have gone acidotic and then we need to correct that.

00:36 Our main inotropic agent is epinephrine. This is going to activate both beta I and alpha I at different times. Okay. Now when you think about these medications, I want you to think about them in a way of what's the primary job and then what's the secondary job. Okay. So when we are going to start epinephrine, the primary job is to increase contractility. That's what we want. We want that left ventricle to contract harder. Okay. This is the most powerful inotropic medication that we have.

01:07 Now, think in your mind there is a secondary job to this.

01:11 The secondary job of epinephrine is vasoconstriction. When we get up to higher amounts of epinephrine, we're going to cause vasoconstriction on both the arterial and the venous side.

01:23 This is going to occur about 0.06 to 0.08 mcg/kg/min or around 6-8 mcg/min.

01:31 That's when we start really vasoconstricting and it can also increase heart rate as a secondary job. So because we're activating that beta which we're getting both chronotropic and inotropic, our secondary job could be that the heart rate is going to increase, but remember when we're starting epinephrine we're doing it because we want to increase contractility knowing that we will vasoconstrict and increase heart rate at a little bit higher amounts.

02:00 The adverse effects to epinephrine is increased risk of arrhythmias. Because you're activating beta and maybe the patient has cardiomyopathy or has just had a heart attack, that tissue is already irritated in the heart. So when you severely activate beta and add a lot of epinephrine to it, you're irritating an already inflamed heart which can cause arrhythmias. You're also going to decrease myocardial perfusion.

02:27 So some physicians do not like epinephrine following a bypass surgery or following a heart attack. And then you might have tachycardia because of that chronotropic effect.

02:40 Now, many institutions use 2 to 10 mcg/min as their range.

02:47 You can go all the way up to 20 mcg a min. Other institutions use mcg/kg/min so that range would be 0.01 to 0.2 mcg/kg/min. Now there is really no top or max to this medication but eventually you saturate all the beta receptors and you're not going to get a better effect with increasing contractility or causing more vasoconstriction. If you want more contractility, you may have to add or go to a different medication.

03:20 The second medication we have that increases inotropic support is dopamine.

03:27 It also activates beta I and alpha I at different levels.

03:32 Now, when you think of dopamine again, think of its primary job is "I wanna increase contractility.

03:38 I always think about dopamine as being epi's little brother.

03:41 It does the same thing but doesn't do it as harshly as epinephrine does. bodies Now, in our when we go on to fight or flight mode, our bodies naturally release dopamine to get our heart rates start to elevate and get higher contractility so our blood pressure is higher.

04:03 It naturally releases dopamine before epinephrine. Okay? So when I'm starting dopamine, I want to increase contractility, but I know there is a secondary job to dopamine. We're going to cause vasoconstriction at about 8 mcg/kg/min and above. Okay. So, about 0-7 mcg/kg/min there's not much vasoconstriction going on. Once I hit that 8-20 mcg/kg/min, I am activating alpha I and getting some vasoconstriction. So take note of that. Now, some adverse effects that you might have with dopamine are arrhythmias just like epinephrine.

04:43 You can also have an extravasation injury. So say the dopamine is not going into the vein but actually going into the tissue, that's going to vasoconstrict everything around it blocking blood flow and you may have an extravasation injury.

04:56 Also tachycardia because of that chronotropic effect. The range with dopamine is 2-20 mcg/kg/min.

05:04 Our next inotropic agent is dobutamine. With dobutamine, I want you to think of its primary job is again to increase contractility. When I start dobutamine, I want to increase the force of contraction. Understand that it has a secondary job where it's going to start vasodilating at greater than 5 mcg/kg/min.

05:25 In certain patient situations we want that to happen. In cardiogenic shock, when we have a low cardiac output but we have a very high SVR or afterload, we want to reduce that afterload. So this effect is warranted but it can cause hypertension in some situations. So an adverse effect of this medication is hypotension when we have a low cardiac output and a low CVP. Right? We want to fill the tank to an optimal level before starting in this medication because if we vasodilate and we remove the only compensatory mechanism that this patient has to maintain some semblance of blood pressure, we're going to drop their blood pressure before we even increase cardiac output. Another adverse effect of this is arrhythmias.

06:14 Okay, so because it activates beta I, it's got a risk of arrhythmias and in patients that are in atrial fibrillation, we can cause them to go into a rapid ventricular rate.

06:24 The range of dobutamine is 2-20 mcg/kg/min. You can go all the way up to 40 mcg/kg/min but you won't see much of an added benefit after 20 mcg/kg/min.

06:36 Our last inotropic agent is milrinone. Now, when you hear milrinone, I want you to think of the word ino dilator. That's because it has 2 primary jobs. First primary job is it's going to increase the contractility of that left ventricle. We want the left ventricle to start squeezing harder to increase cardiac output. The second primary job is we want it to vasodilate, but it's only going to vasodilate the arterial side.

07:02 That's what I really like about this medication is it does not affect the venous side, just the arterial side. So, with vasodilating the arterial side and increasing contractility, we really going to increase our overall cardiac output. But because it doesn't vasodilate the venous side, we don't drop our preload, meaning we don't decrease that pressure going back into the right ventricle. This is really good for patients that have RV failure as well because that right ventricle is not able to squeeze as much. If we drop the pressure going in there, we need that to help it go through the heart, through the lungs, and over to the left ventricle. So we want to maintain our preload or maintain our central venous pressure. This medication is really good because it does not drop that. Now, it does have an adverse effect of hypotension. We'll talk a little bit about that next in our special considerations. The range of this medication is 0.25-0.75 mcg/kg/min. Now, some special considerations when starting milrinone is that it has a long onset of action, about 15 minutes. So what does that mean? That means when we start milrinone, it's going to take about 15 minutes to see the full effect.

08:19 This is a lot longer than our other inotropes of epinephrine, dobutamine, or dopamine which is in just a few minutes. Right? So when we start this, just expect that it's going to take a long time for you to start seeing the effect. Now, the physician may order a bolus so that the onset of action is lower. But because it has such a long onset of action, we also titrate this slowly. Typically with milrinone, we don't titrate this ourselves within certain parameters. Usually we set it and then we leave it for a long time, meaning the physician may order it at 0.25 mcg/kg/min and then we wait a long time to see how it's affecting the patient and then after a few hours we may increase it or decrease it. So, the titration is really slow on this medication.

09:12 Also consider that this medication has a long half-life. So it's got a half life of upwards of about 3 hours. So what that means is when you shut this medication off, it's going to continue working for a long time. Why is that important? Well, this medication can cause hypotension in patients that already have a low SVR, meaning they're hypotensive and then because their SVR is already low, meaning they're vasodilated, we start this medication and we just further vasodilate their vasculature and that drops our blood pressure even more. Now, with that long half-life, you're going to be battling that low blood pressure for a long time. You may need to give some fluids or we may need to start a medication that causes vasoconstriction to counteract the effect, but just keep that in mind that that is going to last a long time. What I really like about this medication is that it's only selective to the inotropic part of beta I, meaning it doesn't really affect heart rate.

10:14 When you start it, you're not going to see an increase in heart rate, just an increase in contractility.