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
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.
You might have gone acidotic and then we need to correct
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
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.
Now, think in your mind there is a secondary job to this.
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.
This is going to occur about 0.06 to 0.08 mcg/kg/min or
around 6-8 mcg/min.
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
we're doing it because we want to increase contractility
knowing that we will
vasoconstrict and increase heart rate at a little bit higher
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
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.
Now, many institutions use 2 to 10 mcg/min as their range.
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.
The second medication we have that increases inotropic
support is dopamine.
It also activates beta I and alpha I at different levels.
Now, when you think of dopamine again, think of its primary
job is "I wanna increase contractility.
I always think about dopamine as being epi's little brother.
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.
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.
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
around it blocking blood flow and you may have an
Also tachycardia because of that chronotropic effect. The
range with dopamine is 2-20 mcg/kg/min.
Our next inotropic agent is dobutamine. With dobutamine, I
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.
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
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
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
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
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.
This is a lot longer than our other inotropes of
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.
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
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.
When you start it, you're not going to see an increase in
heart rate, just an
increase in contractility.