What is contractility? | Circulatory system physiology | NCLEX-RN | Khan Academy
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What is contractility? | Circulatory system physiology | NCLEX-RN | Khan Academy


Something that I really,
really enjoy doing– and I’ve done it a
lot– is camping. And so I’m going to
start by telling you a little story of a
recent camping trip. And I like to, in the morning–
let’s say around 9:00 AM– head down to the river. It’s always kind of
a fun thing to do. And so this day
was no different. I went down to the
river feeling good and had a big smile on my face. And what I want to do is
think about that moment. In fact, if we had stopped
time around 9:00 AM as I was down by the river,
what would you see in my heart? What would you have
actually noticed? Now, the heart has, of course
nerves, leading up to it, so we’ve got sympathetic nerves. And these sympathetic
nerves at all times are releasing some amount
of their neurotransmitter. And the neurotransmitter’s,
of course, just some chemical that
helps communicate a message. So this is my
neurotransmitter, and I’m going to name it
norepinephrine, which is the one that this particular
one will be releasing. And so the norepinephrine
is headed from the nerve. And it’s headed over
to my heart cell. And so, of course,
my heart cell, it has little receptors
on the surface. And let’s say that of these
three receptors, one of them gets the signal. And this guy right
here releases now the signal in this heart cell. And of course, calcium is going
to come into the heart cell. And we’ve talked previously
about exactly how that happens, but you know that that happens. And if that calcium gets into
the heart cell, which here it does, where is it going to go? Well, you have, of course,
muscle proteins– myosin, actin– in that heart cell. And those muscle proteins are
going to basically require a little bit of calcium
in order to work properly. So this is my myosin. And let me now draw some actin. This is actin protein. And this actin I’m showing in
kind of a crunched situation. This actin is kind
of crunched together. And when I say
crunched, I basically mean that there’s
very little room, because this is going to
be the end of systole. Let’s just assume that we’re
at the end of systole here. I’ll write that here. End systole. So it turns out that, I guess,
when I froze time at 9:00 AM, it happened that I caught this
magical little time point– end systole. And some of that calcium is, of
course, binding to troponin C. And I’m just going to scatter
some calcium randomly, so I really am not
putting too much thought into exactly where it goes. But it’s kind of
throwing it out there. And now our question
is going to be how many myosin heads
are actually working. And I’m going to circle the
ones that are working in red. So this one is working
because it’s close to actin. And there’s calcium on there,
and it’s the right polarity. But the next one
over, this one, I’m not going to circle because
it’s the wrong polarity. This one has calcium
that’s too far. It’s on the wrong side. And this guy– well,
this guy actually would be circled
because he’s got calcium on the right-polarity actin. This guy I would circle as
well for the same reason. And these two I cannot circle
because they’re the wrong polarity. But this one I will circle. So we’ve got about 4 out
of 20 that are working. And I could actually just
rewrite that as 4 out of 20 works out to– what? 20%. So 20% of my myosin
heads are working. So that’s not great, but
it’s not awful, either. So to sum this up, at 9:00 AM
I was walking along the river. And at that time, at
the end of systole, if you actually wanted to
see how much of my myosin was actually working,
you’d say 20%. Now that night, 9:00 PM, an
interesting thing happened. I also headed out, went outside. And wanted to do one
last little look around. And I encountered a scary
animal, a scary beast, I would even say. And this animal had
four legs– and let’s see if you can
recognize it– had a striped tail and
a striped body. And this horrible,
horrible little creature is none other than a raccoon. So this is my little raccoon
with a ugly little face. And this raccoon, like many
raccoons do, scared me. And you should
know, I do actually in fact have a fear of raccoons. And so this was a very
scary event for me. I shrieked, and I
was not too happy. So what was going on in
my heart at that time? Let’s actually do a
little cut-paste job. All right, so now I’m
basically just going to try to cut and
paste some of this, and I’ll erase the parts
that are not relevant. So I’ve got something like that. And let me just
quickly erase the parts that I know I’m
not going to want. So let’s start there. I’ve got my
sympathetic nerves that are now going to be going crazy. I’m going to just draw a giant
arrow because they are going to be driving a message
down there saying, hey, this raccoon is awful and scary. Let’s just get lots and lots
of neurotransmitter released. So they’re going to
just release tons and tons of neurotransmitter. And that is an important issue. This is how signals get passed. And so, of course, now
all of my receptors are jamming that signal. And of course, that
signal means that calcium is going to flood my cell. All of a sudden, I have
much more calcium in my cell than I used to, tons
and tons of calcium. And in fact we know
that this is the key way that our nerves are able
to communicate a message. They basically help by
sending ions into cells. So now our cell is
jam-packed full of calcium. And so now I can just kind of
scatter calcium everywhere, just kind of sprinkle
it all over the place. And let’s see what happens now. So I’ve got calcium everywhere. And same question as before–
how many myosin heads, rather, are going to be working for us. So let’s just circle the
ones that are working for us. We still have a few
that are not going to be working because
they’re blocked by the wrong-polarity actin. But these are actually
now all recruited. All of these are. And on the other side, I’ve
got some recruitment over here. So I’ve got lots and lots
of myosin heads recruited. I’ve got– let’s see if I can
count it up– 5, 10, 11, 12. So I’ve got 12 out of 20. Or that works out to
60%, so 60% up from 20%. I’m going to make a little bit
of space on our canvas now. But just kind of think
about that, the fact that at 9:00 AM in
the morning my heart, at the end of systole,
was cranking out at 20%. And now it’s working at 60%. So what does that mean exactly? How can we put that
together in an image that we can kind of remember and
think about and make sense of? So for this part,
I think it would be helpful to go back to
our pressure-volume curves. So we’ve got this idea
that at the end of systole, we have a relationship
called the end-systolic pressure-volume relationship. I’m actually going
to draw it out here. Something like that. This is a sketch of our
end-systolic pressure-volume relationship. And we know– and yellow
will be our 9:00 AM. Let’s just kind of
keep that in mind. This is what was happening in
the morning as I was relaxed. And at the end of systole,
I said we had about 20% of our myosin heads working. So if I was– let’s
just take a spot here, and I could take any spot. I’m just choosing it randomly. And let’s say this is
the volume at that spot. And if I fill it in with
blood, it would look like that. And at this point,
we’ve got our workers. Remember, our workers represent
how much force of contraction there is. So our workers are yanking
this way and that on this rope. And our worker– I’m just
going to quickly sketch out– maybe looks like that. And we’ve got another worker
down here– long arms, apparently. And if I was to look
at my workers’ faces– because I’ve drawn the
faces very, very small, it’s hard to see
them– they’re yanking. It’s not like they’re–
they’re not lazy. They’re not just standing there. But they’re yanking, and
this is the face of someone that’s working,
let’s say at 20%. Now, at that same moment, let’s
say instead of yanking at 20%, let’s say I yanked at–
I don’t know– 60%. Just to make it kind of
the same as the other one. If I was yanking
at 60%, well, now I would actually
create more pressure. So same volume. And I’m actually going to just
kind of sketch higher– maybe something like this. So at that same volume, it
would basically look like this. And I’ve going to try to draw
the exact same volume so you believe me. This is, let’s say, the same
volume– about the same, anyway. And here, let’s fill
it up with blood. We’ve got our two workers
doing kind of the same thing. We’ve got workers yanking
on this left ventricle. And these workers are
working much harder. So they’re working much more
diligently than previously. And they’re yanking, of
course, same directions, opposite from each other. And these workers, if you
were to stare at their face, you’d notice they’re
really into it. They’re really, really
trying to– grr. They’re really, really
trying to pull apart on that left ventricle, And as they are working so
much harder– and actually, maybe I should even write
the percentage in here. Let’s write 60% here. They’re working so much harder. What that does is for any
given volume, the same volume, they’re going to have
a much higher pressure. So these are going to be able
to drive a higher pressure. And that’s what you see, right? This volume is the same. I’ve tried to sketch
it to be the same, but now you can see it’s
the same exact point. And yet the pressure
is much higher. Now, going back– and this
is, of course, our 9:00 PM. This is when I was scared. This is my 9:00 PM sketch. Now, going back to the 9:00
AM, the morning sketch, let’s say I was to pull a little
bit of volume off of my heart. Well, the pressure would fall,
and it would keep falling. And so remember,
this is how we even created this line
in the first place. And it kind of ends down here. And at 9:00 PM in the evening,
I could do the exact same thing. I could say, well, if I drop
the volume a little bit, I’ll get a lower pressure. And if I drop the volume again,
I’ll get at a lower pressure. And it eventually also
heads down to the same spot. Because remember, you
do need a minimum amount of volume, some
minimum amount, to be able to even generate pressure. And that’s going to be the
same minimum amount for both of the situations. So you need that
same minimum amount. But as you go higher
from that point, you actually go along
a different slope. And so really what
you’re creating is two lines of a
different slope. And the difference is really
reflected in our percent work. So our 60% line is
different from our 20% line. And I could even test you. I could say, well, what
if I was to draw a line? I’m going to just make a
little bit of space now. What if I was to draw a line
somewhere in the middle? What if I drew a green
line that looked like this? What would be your guess as
to what percent work that is? And you would say,
well, you know, it looks like something
between 20 and 60. I don’t know– maybe 40%. So this would be your guess
just by looking at the line. So what you’re saying,
or what I’m saying, really, is that you can
change the slope of the line up or down. And what that
reflects is how hard your muscle is contracting. And that goes back
to the myosin heads that you’re using to contract. And so what this
really means, the slope of the line in these three
lines that I’ve drawn here, really reflect an idea
called contractility. And you’ll see contractility
mentioned all the time. And all it really means
is the slope of that line. And you can change
the slope of the line. The main way is through calcium. So calcium– more or
less calcium– changes the slope of the line. And remember, that’s how
our sympathetic nerves work. So this is kind of the main
way that our sympathetics change or affect that line. Sympathetic nerves. And finally, I want
to make sure that you don’t get the idea that
that’s the only way to change contractility. You can also change
the pH, or you can change the temperature–
all of these things will affect how well
myosin can work. Because of course,
myosin is a protein, and proteins need an
ideal pH or temperature. But I mentioned that
just so you know that. But truthfully, the one that
we always seem to talk about or always think
about is this one. And the main reason is
because that’s something that our sympathetics have
gotten so good at controlling.

11 thoughts on “What is contractility? | Circulatory system physiology | NCLEX-RN | Khan Academy

  1. I'm glad you liked it. I am going to put contractility, preload, and afterload all together so we can see how they all affect stroke volume and cardiac output in one easy diagram.

  2. Contractility is a fuzzy concept – How "hard" is the heart muscle squeezing? One way to get a sense for contractility is to measure how "hard" it's working at a specific point in time (but this doesn't tell you what it's doing the rest of the time, does it?). The time point that we usually choose is at end-systole. At this time point, the left ventricle's elastance is maximized. So we often simplify all of this to say that LV contractility = LV peak elastance.

  3. I've got a test about the heart (the mechanics and electrics), bloodvessels, lungs and kidneys in two weeks, so if you need any ideas for new videos, there you go. These are really helping me out! 🙂

  4. I really love your videos! Have my physiology exam in a couple of weeks and you are just a teaching genius!
    I just have a couple of questions:
    1. what do you mean by "they are the wrong polarity"? I'm having trouble understanding it from your diagram, the white Ca2+ dots seem to be in similar positions, but some of the actin is the right polarity and some isn't, and the ones that are are recruited.
    2. Will the end diastolic volume be the same for each of the slopes or will it decrease with and increase in the contractility?
    Thank you so much! Please come teach at my university!!!

  5. I am trying to finish my AEMT/ Paramedic and it is been so, so hard to pass my program this it is my second try. The main problem is Bc my teacher is not good explain things. I am a very strong visual person. Is the main pathway to learn for me. And he doesn't have time for teach that way. I really appreciate your video so, so, much. God Bless your knowledge of teaching. Specially for me that I am a ADD student.

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