Okay, now we're going to move on into vasoconstrictors. Our
main vasoconstrictor is norepinephrine.
This is going to activate both alpha I and beta I. Okay.
Now, when you think about this medication, I want you to
think of the opposite of epinephrine.
Its primary job is to vasoconstrict. When I'm starting
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
but this does have some adverse effects. It does cause small
vessel injuries at higher amounts.
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.
There's not a lot we can do about it if we need to keep
blood pressure, but just keep that in mind.
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.
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.
Our last adverse effect is extravasation injury. Right? Just
like with dopamine.
If this medication goes into the tissue of wherever the IV
is located, this
could really cause vasoconstriction around that area like a
and that can be a big issue because that tissue can actually
The range of norepinephrine is 0.01–0.2 mcg/kg/min or in
some institutions 1–10 mcg/min.
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.
Vasopressin. Vasopressin is a powerful vasoconstrictor.
It only has 1 primary job which is vasoconstriction. It does
not have a secondary job.
Vasopressin is actually natural in our body and is called
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.
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.
Now, this also has a delayed onset of action so it's going
to take a little bit longer to work.
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
Our next vasoconstrictor is phenylephrine or neosynephrine.
Okay. It's known mostly by phenylephrine.
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.
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.
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
is acting on alpha I. Alpha I should be already fully
saturated with our norepinephrine.
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.
Angiotensin II, again its primary job is vasoconstriction
but it does it in a different way.
Our body naturally produces angiotensin from the renin
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.
Okay. We just bypass all of that and put angiotensin II
in the blood and it causes vasoconstriction. So now,
facilities are starting to use
angiotensin II as a 3rd line vasoconstrictor instead of
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.
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.