Our next hemodynamic concept and
value is Systemic Vascular Resistance.
We've kind of talked about
this a little bit more,
let's dive in a
little bit deeper.
Systemic vascular resistance
normal is 800-1200 dynes.
Remember that, 800 to 1200.
Basically, it's the resistance to blood
flow of coming out of that left ventricle.
What's the pressure that that
left ventricle has to overcome
to get the blood
flow to come out.
What affects systemic
the diameter of our arteries,
the length of our arteries,
and the viscosity of our blood affect
a systemic vascular resistance.
Now, like I said,
the normal is 800-1200.
If you have a systemic vascular
resistance more than 800,
that means your arteries
are more dilated.
And if you have a systemic vascular
resistance closer to 1200 or greater,
your more vasoconstricted.
We'll look at that with a little
bit of animation here later.
Now, increased afterload.
What increases the pressure that
your heart has to beat against
to get that blood flow out?
Hyperthermia, aortic stenosis,
cardiogenic shock and certain medications.
Anything that would cause your
vasculature to vasoconstrict
is going to increase that
systemic vascular resistance.
Hyperthermia, if you're cold,
you're shutting all
that blood to your core.
Aortic stenosis is actually that
aortic valve is really tight.
And in order to pop
that valve open,
that left ventricle has to contract
really hard to get the blood flow out.
So the SVR is
really high on that.
Cardiogenic shock causes extreme
vasoconstriction of your vasculature.
And there's specific medications
like Levophed, vasopressin,
phenylephrine and dopamine.
Well, they cause vasoconstriction
as well increasing that afterload.
So we talked about what
let's talk about what
Anything that causes
vasodilation of your arteries
would cause a
decrease in afterload.
So anaphylactic or neurogenic shock,
extremely vasodilates those arteries.
Hyperthermia, when you're running a
fever, you're going to vasodilate.
Sepsis causes vasodilation
and specific medications
such as nitroglycerin, nitroprusside,
nicardipine and cleviprex
causes vasodilation of those arteries
and decreasing that afterload.