Increasing ventricular contractility – inotropic effect | NCLEX-RN | Khan Academy

November 11, 2019 0 By Kody Olson

I’m going to start
out by showing you the membrane potential
of a cardiac cell. And I know you’ve seen
this a few times now, so you might be getting
kind of tired of it. Or it might be seeming kind
of familiar, and that’s good. That’s good that you
know this by now. But let’s just go
over it just in case you need some refreshing. So if you have a
heart muscle cell, and let’s just make sure that
we’re totally on the same page, this is a heart muscle
cell, or a myocyte. If you have one of these cells
and you’re looking at it, usually it kind of hangs out in
a negative membrane potential. Meaning the cell is negative
relative to its environment. And it kind of hangs
out there for awhile. And then we know
that at some point, it’s going to get some positive
charge from a neighboring cell. It’s going to have
an action potential. It’s going to go
really positive, and then it’s going to
peter down a little bit as the potassium channels
let out potassium. And then it’s going to
go through this kind of interesting plateau
where calcium is rushing in, potassium is rushing out,
and finally, it kind of goes back down as
potassium wins the game. And potassium kind of
drives it back down to its kind of happy place
where it likes to be. Around negative 90 or so. So these are the phases
of an action potential. And we know that
they’re numbered off. This is phase 0, or
4 rather, phase 0, and this is 1, 2, and 3. So these are the
normal phases and how we count off what
it would look like. And what I want to do now
is draw your attention to the heart. And let’s not lose sight of
what the whole organ looks like. And this is our
four-chambered organ, this is our heart muscle. With the two ventricles down
here and our two atria up top. And this is our right atrium,
left atrium, right ventricle, and left ventricle. So this is what it
looks like, right? And there are actually
nerves that come and sit on different parts of this. So there’s a nerve that might
come and sit right there. And this might be a
parasympathetic nerve. I’ll write P for
parasympathetic. And actually,
parasympathetic nerves also come over to
the left atrium. They settle in on left
atrial tissue as well. And you also have sympathetic
nerves that come and settle in over here and on
the other side as well. Now as far as the ventricles
go, you really only have sympathetic
nerves down here. So that’s an
interesting thing, and I wanted to point that out to you. So you really only have
sympathetic nerve stimulation. You don’t really have much
parasympathetic activity down here. So I’m going to focus in now. The rest of this
video is actually going to just focus
in on the ventricles. I’m actually going to
just kind of ignore what happens in the atrium
because the main point I want to make is that sympathetic
activity on the ventricles is going to cause
increase contractility, meaning you’re going
to be able to cause increased force of contraction. And why do I not care
as much about the force of contraction of my atria? Well, it’s because
the atria are going to be used to help
fill up my ventricles. But my ventricles, the force
of contraction in my ventricles is really important
because that’s going to affect how the blood
gets to the rest of the body and to the lungs,
and so that’s why I want to focus in on
just the ventricles for the rest of this talk. Now, I’m going to draw
a ventricular cell. So this is a
ventricular muscle cell. Let’s say it’s right here. This is this little guy
over here where the x is. So this ventricular cell–
I’m actually also going to even be more
specific, I’m going to focus in on what happens
in phase 2 and 3 of this cell. So our ventricular cell,
it’s going to, in phase 2, have some channels. It’s going to have some
potassium channels. Voltage gated. Potassium leaving. It’s going to have
some calcium channels. Some voltage gated calcium
channels letting calcium in. And you remember, actually,
when that calcium comes in, we talked about the
fact that there’s this sarcoplasmic reticulum. This is our
sarcoplasmic reticulum. And this sarcoplasmic reticulum
is kind of a bag of calcium. And so the
sarcoplasmic reticulum is going to wait patiently
for a little calcium to come and bind to its channel. And the moment it
does, it’s going to start letting calcium out. So this thing is
full of calcium. And it’s going to start
shooting into the cell. Into the kind of
cytoplasm of the cell. So these are kind
of the changes that normally take place
in phase 2 and 3. You have calcium
rushing in, and you have the sarcoplasmic
reticulum dumping calcium out. And you also have–
when I say out, out into the cell–
and then you also have potassium actually
leaving the cell entirely. Now, if you have
sympathetic nerves. Let’s say this is my
sympathetic nerve. I’m going to write
S for sympathetic. Well, maybe I’ll just
write it out just to make sure that we
don’t have any confusion. This my sympathetic nerve. My sympathetic nerve
is going to have– let me make a
little bit of space here– is going to have
some neurotransmitter in this kind of space in here. And that’s going to
bind to a receptor. Now a receptor is
going to send a message into the rest of the cell. And this neurotransmitter
that’s doing the messaging, and we actually– I
almost switched it. I was going to
write acetylcholine, but what I mean to
write is norepinephrine. And acetylcholine, just
as a point of reference, is the neurotransmitter that
the parasympathetic nerves use. So I want to make sure
I don’t screw that up. So norepinephrine goes into
the cell, and what does it do? Well, it’s going to
cause an effect here. It’s going to make the calcium
rush in even more forcefully. It’s going to activate these
channels so that they let out more calcium when they get
a chance to do that as well. And so these are two
major changes, right? It’s going to activate
more calcium coming in or basically activate
these channels so more calcium can rush in. And it’s going to
let more calcium out of the sarcoplasmic reticulum. So my curve is going to
start looking like this. Calcium is going
to make this rise. It’s going to rise
because remember, calcium wants the membrane
potential to go up. And the reason
that it goes down, eventually, is
because of potassium. So if you have more
calcium rushing, it’s going to quietly
start winning the battle. So it won’t be a
plateau anymore. It’ll start kind of looking
like I just drew it. Now a second thing that
happens with sympathetics, and this is actually
very interesting, is that you have these
ATP controlled channels or proteins, really, that
allow calcium back in. So these are
transporters that are going to get calcium
to come back in. And of course, this
is going to happen when the sarcoplasmic reticulum
is ready to kind of mop up all the calcium
and let it reenter the SR, the
sarcoplasmic reticulum. So when that’s
happening, usually you get a decline like what
I’ve drawn in phase 3. But if you’re going
to stimulate that, and that’s exactly what
happens, the sympathetics kind of stimulate that, well, all
of a sudden now the calcium can get quickly put back into
the sarcoplasmic reticulum. And if it quickly
goes back inside, then the calcium current
falls more rapidly. And the potassium
current dominates even more than it usually does. So basically, what
happens is instead of having kind of a slower phase
3, you have a rapid phase 3. And that is because of
the fact that you’re able to get the calcium more
quickly and more efficiently tucked into the
sarcoplasmic reticulum. So at the end of the day, you
see some interesting things, right? You see that you’re able to
quickly get back to baseline. And as a result, this
distance goes down. So you actually have
a smaller contraction in the sense that–
let me rephrase that completely so I
don’t confuse you– you don’t have a
smaller contraction, you have a shorter, in
terms of time, contraction. But you have more calcium that’s
actually coming into the cell. So these are two key changes
I want to point out to you. The fact that you have
more calcium coming in, but it’s a shorter
period of time. So those are the effects
of the sympathetic nerves on the ventricular muscle cells. So you can see now
that you’re going to have a change in inotropy. And inotropy just
means a change in force of contraction or affecting
the force of contraction. And here we’re
talking specifically about the ventricles, but
those are the chambers I said that we care more
about in this scenario. And so inotropy is really shown
to be affected right there. So you can see right there,
you have more calcium, and more calcium
means more force. So more force of contraction. And that’s because calcium
actually directly affects the mechanism that a
cell uses to contract. And we’ll talk about that
in future videos, exactly what that mechanism
might look like. But really, that
increase in calcium is a demonstration of
the inotropic effect of a sympathetic nerve. And this effect is
actually showing you that the ventricles can
repolarize more quickly. So this is more, let’s
say, rapid ventricular repolarization. So that the ventricles
are actually kind of reset and ready to
fire again more rapidly. Rapid repolarization. So these are the two major
sympathetic nerve effects on the ventricular muscle cells.