Now that we've covered the
four parts of blood pressure,
let's look at shock in relation to
those four parts of blood pressure.
What shock is that we do not
have enough blood pressure
or mean arterial pressure
to perfuse the body,
we're not getting
enough oxygen somewhere.
So when you're trying to identify
the different classes of a shock,
we need to look at what is affected
in those four parts of blood pressure.
So if it's cardiogenic shock,
it's going to be your contractility
or your heart rate that is affected.
Hypovolemic is your preload,
there's not enough fluid volume status.
And if it's sepsis,
it might be vasodilation.
So let's look at these a
little bit more in depth.
When we're talking about cardiogenic
shock, what is affected?
Well, it's your left ventricle.
So which part of the four parts
of blood pressure is affected?
Well, we definitely know
if my left ventricle
can't contract hard enough
because it's damaged,
then it's going to
be our contractility,
that part of the four
parts are blood pressure.
Our blood pressure is low because
we don't have enough contractility.
Your heart rate can also
be affected depending on
if the right side of the
heart is affected as well.
So you might have a low cardiac output
because we don't have enough contractility
and we may not have
enough heart rate.
So how does the body
compensate for that?
When the blood
pressure gets low,
the body will always try to
compensate to increase it.
Well, can the body compensate
with increasing contractility?
It can't in cardiogenic shock,
because the LV is damaged.
Can it increase heart rate?
Possibly, but it may be that
mechanism may be affected as well.
Can it pool volume into
the vascular space?
So it's not going to it's
not going to change by that.
How will it compensate?
So you'll see your SVR being really
hard, you're trying to maintain a map.
In turn because the
SVR is really high,
you're going to see that your CVP and
your PAD is going to be elevated as well.
Now, with hypovolemic shock,
what is our issue here?
we don't have enough blood volume.
And so without
enough blood volume,
our CVP and our PAD or wedge
pressure is going to be too low.
We don't have enough preload
going into those ventricles
to maintain a mean
How will our cardiac
output be affected by that?
Well, we learned a little bit earlier
that if our CVP and our PAD are low,
we're not going to have blood
volume going into the ventricles.
So we're not going to have enough blood
volume going out of the ventricles.
So our cardiac output
and index will be low.
Now, how does the
body try to compensate
in relation to the four
parts of blood pressure?
can it increase heart rate?
Yes, it can increase heart rate
to try to maintain blood pressure,
because that's not affected.
So in hypovolemic shock,
you'll see a fast heart rate.
Now, will it try to increase your
SVR and your vasoconstriction?
Yes, it'll vasoconstrict so it'll
increase your systemic vascular resistance
to try to maintain
a blood pressure.
That's how in hypovolemic shock,
the body tries to compensate.
So let's move on to sepsis.
There's two parts
of septic shock,
state of septic shock,
and the hypodynamic
state of septic shock.
In the hyperdynamic
state of septic shock,
basically your vasculature
is vasodilating like crazy.
So your SVR drops, which then in turn
drops your mean arterial pressure.
Now, how does your body
try to compensate to that?
Can it pull more fluid into that bigger
tank that vasodilation of the arteries?
No, not quickly.
Well can it increase heart
rate and contractility quickly?
So you'll see your cardiac output and your
heart rate start to increase dramatically,
because just trying to compensate
for that low blood pressure
because your SVR is really low
plus there's no afterload it
gets to the left ventricle.
So your cardiac output is going
to come out really, really easy,
because there's no
resistance against it.
Your CVP and your PAD are
going to stay about the same.
If you've got a lot of vasodilation,
you may see your CVP start to drop.
Now, with hypodynamic state,
which is the last stage of septic shock,
you'll see again more extreme decrease
in systemic vascular resistance,
which is probably going to
cause your CVP to decrease
unless you've given
a lot of fluid
and it's going to cause your PAD
or your wedge pressure to decrease.
But what's more important is now the
heart is starting to get affected.
So you'll still see
a fast heart rate
because that's the last
that the body has to
try to maintain a map
but your cardiac output is
decreasing because the contractility
is just not able to contract hard
enough in the last stage of sepsis.
So now that we know the four
parts of blood pressure,
we know how they
relate with one another
and we know how they are
affected during shock.
We need to start learning
what can we do about it.
What intervention can
we do that will start
affecting these four
parts of blood pressure
and allow them to compensate so that we
can increase our main arterial pressure.
So starting with our heart rate.
If our heart rate is too low, that's
decreasing our mean arterial pressure,
what can we do to increase it?
Well, the first thing that
we can do is atropine.
increases the heart rate
because it works on the
parasympathetic nervous system.
It doesn't really actually
increase the heart rate,
what it does is it prevents
the body's parasympathetic
nervous system from
decreasing the heart rate.
So it really allows that SA node
to start beating a lot faster.
Now, atropine may not work
in a complete heart block
because there is complete
separation from that SA and AV node
to the Purkinje fibers
of the of the ventricles.
So if you're in a complete heart block,
and you need to increase heart rate,
atropine probably is
not going to work.
The next thing that we can do for
heart rate if we need to increase it
to increase blood
pressure is a pacemaker,
we can transcutaneously pace with
patches to increase that heart rate.
Also, the patient could be taken to the
cath lab to get a temporary pacemaker,
and then eventually a permanent
pacemaker to increase that heart rate.
Now, if the heart rate is too
high, and we need to decrease it,
what can we do to
decrease that heart rate?
Well, we can use a beta-blocker,
most commonly metoprolol or labetalol,
or some of these beta-blockers,
which the goal of that is
to decrease heart rate.
Just know that a beta-blocker
will also decrease contractility.
So you'll see cardiac output
start to drop with that.
We can also use a calcium channel blocker
that is selective with with the heart,
Diltiazem will decrease heart rate
because it's selective with the heart.
Now, calcium channel
blocker like Nicardipine
is more selective
with smooth muscle,
and that causes vasodilation.
So you need to use a
calcium channel blocker
that is selective to the
heart to decrease heart rate.
Going on to contractility.
If we've identified that the
reason our blood pressure is low
is because we do not have
How do we increase
Well, we can increase
contractility by an Inotrope.
The goal of an inotropic medication
is to increase that contractility
that squeezed power
of the left ventricle.
The inotropes that we have are epinephrine,
dopamine, dobutamine and milrinone.
Now don't worry about
we're going to go over them more
in depth later on in the series.
So just know if I want to
increase my contractility,
I need a medication
that is an inotrope.
But what if our
contractility is too high?
What if the cardiac
output is above 8?
that's an hyperdynamic left ventricle,
and we need to give fluids to
help lower that cardiac output
to help just relax
that left ventricle,
stretch it out a little bit
and and bring that hyperdynamic
left ventricle back to
a normal dynamic state.
Alright, moving on to
our vascular resistance.
What if we noticed that our blood pressure
is too low because we're vasodilated?
Our SVR is 600 and we are vasodilated
causing our map to be too low.
Well, we can use medications
Those medications we have are
Those medication's jobs,
the primary jobs are to vasoconstrict.
Well, if our blood
pressure is way too high,
and we find that our SVR is 2000
that means we're too vasoconstricted.
So how do we vasodilate?
How do we expand the aorta and the
arterioles to decrease our blood pressure?
In order to do that,
you need vasodilators,
you need medications that would
vasodilate the aorta and the arterioles.
Those medications are nitroglycerin,
nicardipine, Cleviprex and hydralazine.
Now, our last part is
fluid volume status.
If we've identified that our
blood pressure is too low,
because we don't have enough blood
volume, our tank is empty.
What can we do?
We can administer
we can administer albumin and
we can administer crystalloids.
Crystalloids are normal saline so we
can administer those to get more volume.
Now, what happens if
we're too hypervolemic,
we've got too much volume
on in our vasculature?
We can administer administer diuretics
to help us pee out some of that fluid
and if that's not working we can go to
dialysis to remove some of that fluid.