Vasoconstrictors and Hemodynamics (Nursing)

00:01 Okay, now we're going to move on into vasoconstrictors. Our main vasoconstrictor is norepinephrine.

00:08 This is going to activate both alpha I and beta I. Okay.

00:12 Now, when you think about this medication, I want you to think of the opposite of epinephrine.

00:17 Its primary job is to vasoconstrict. When I'm starting norepinephrine, I know I'm starting it because I want to cause vasoconstriction in order to increase blood pressure, but know that it has a secondary job where it will increase contractility at higher amounts, about 0.08 mcg/kg/min or 8 mcg/min but this does have some adverse effects. It does cause small vessel injuries at higher amounts.

00:45 So you will see your fingers and your toes of the patient starting to turn purple because we're causing small vessel injury. Just know at high amounts those vessels are really going to clamp down, but think about it if your fingertips on your toes are turning purple, imagine what the small vasculature in the patient's brain is causing.

01:05 There's not a lot we can do about it if we need to keep blood pressure, but just keep that in mind.

01:10 You're also going to have decreased organ perfusion because we're really vasoconstricting everything down, we might decrease the perfusion to our gut to our liver and to some other of the main organs, like I had said the brain earlier. Because of that, we're going to see an increase in lactic acid.

01:31 Now, if we've got levophed or norepinephrine on for a long time, you may see your lactic acid starts to increase. That's an indication that we do not have good organ perfusion.

01:43 Our last adverse effect is extravasation injury. Right? Just like with dopamine.

01:49 If this medication goes into the tissue of wherever the IV is located, this could really cause vasoconstriction around that area like a local vasoconstriction and that can be a big issue because that tissue can actually die.

02:06 The range of norepinephrine is 0.01–0.2 mcg/kg/min or in some institutions 1–10 mcg/min.

02:17 Okay. Now you can go all the way up to 20 mcg/kg/min and there is really no top to this but at some point you're saturating the alpha I and beta I receptors and you're not going to get much more vasoconstriction from it so you need to go and do another medication to help vasoconstrict. That leads us into our next medication.

02:40 Vasopressin. Vasopressin is a powerful vasoconstrictor. Okay.

02:45 It only has 1 primary job which is vasoconstriction. It does not have a secondary job.

02:51 Vasopressin is actually natural in our body and is called antidiuretic hormone.

02:57 Now, when I think of antidiuretic hormone, that means it's going to stop our body or reduce the amount of urine that we are going to make. Okay.

03:06 So expect, if I'm starting vasopressin I may have a decrease in urine output. Other effects again is small vessel injury like we talked about with levophed, decreased organ perfusion which causes increase in lactic acid and a decrease cardiac output because we're really vasoconstricting that aorta and not allowing as much blood coming out of that left ventricle.

03:28 Now, this also has a delayed onset of action so it's going to take a little bit longer to work.

03:33 This medication, just like milrinone, we're going to start at a certain amount and leave it for a long time. So we may start it at a range of 0.03 and then allow it to do its thing and hopefully it increases the blood pressure by vasoconstriction. We have a range of 0.01 to 0.04 units/min.

03:55 Our next vasoconstrictor is phenylephrine or neosynephrine. Okay. It's known mostly by phenylephrine.

04:04 Now, this is going to activate only alpha-1. It has 1 primary job and only 1 job and that is to vasoconstrict. And what I really like about phenylephrine is it only vasoconstricts the arterial side so it doesn't mess with the venous side at all.

04:19 You'll see a lot of anesthesia physicians using this during surgery. So, again, no secondary job but we can have some adverse reactions. We can have small vessel injury, decreased organ perfusion, again a decreased cardiac output because we're increasing that afterload. You can see reflex bradycardia from this. It doesn't have an effect on contractility, meaning it doesn't increase the contractility by activating beta I, which is a great choice for patients that are in tachycardia or arrhythmia because it really doesn't affect the heart rate and the ECG of that patient.

05:00 Now, the range of this medication is 5–180 mcg/min. So a lot of times, going back, levophed is our primary vasoconstrictor. If that's not working enough, we do vasopressin is what we start. And then naturally or normally we start phenylephrine if we need a 3rd vasoconstrictor, but the issue is is that phenylephrine is acting on alpha I. Alpha I should be already fully saturated with our norepinephrine.

05:32 So instead of going to a medication that maybe will not have any effect, there is a new medication we can try and that new medication is angiotensin II.

05:44 Angiotensin II, again its primary job is vasoconstriction but it does it in a different way.

05:50 Our body naturally produces angiotensin from the renin aldosterone system.

05:55 Okay. Angiotensin I is produced then it goes to the lungs and then the lungs change angiotensin I into angiotensin II and then that causes vasoconstriction.

06:05 Okay. We just bypass all of that and put angiotensin II directly in the blood and it causes vasoconstriction. So now, facilities are starting to use angiotensin II as a 3rd line vasoconstrictor instead of phenylephrine.

06:21 We still have adverse effects of small vessel injury, decreased organ perfusion but also angiotensin II can cause deep vein thrombosis so they need to be on a prophylactic.

06:34 The range for angiotensin II is 1.5 to 80 ng/kg/min. This medication is also one that we start and let it go for a long time and we will titrate it slowly.