Action potentials in cardiac myocytes | Circulatory system physiology | NCLEX-RN | Khan Academy
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Action potentials in cardiac myocytes | Circulatory system physiology | NCLEX-RN | Khan Academy

Let’s figure out how a
heart squeezes, exactly. And to do that, we have
to actually get down to the cellular level. We have to think about
the heart muscle cells. So we call them
cardiac myocytes. These are the cells
within the heart muscle. And these are the cells that
actually do that squeezing. So if you actually were
to go with a microscope and look down at
one of these cells, it might look a
little bit like this, with proteins inside of it. And when it’s relaxed, these
proteins are all kind of spread apart. And when it’s squeezing
down, because each cell has to squeeze for the
overall heart to squeeze, these proteins look
completely different. They’re totally overlapped. And that overlapping is
really what we call squeezing. So this is a squeezed
version of the cell. And the first one was
a relaxed version. And the trigger that kind
of gets it from squeezing– and of course actually, I
should probably draw that too. The fact that, of course, at
some point it has to go back to relaxed to do it
again, to beat again. But the trigger for
squeezing is calcium. So it’s easy to get confused
when you’re thinking about all this kind of squeezing relaxing
all this kind of stuff. But if you just keep
your eye on calcium and think about the fact
that calcium is the trigger, then you’ll never get confused. You’ll always be
able to kind of find your way in terms of where
the heart is in its cycle. So I’m going to draw for you the
heart cycle, and specifically the cycle of an individual cell. This is what one cell is
going to kind of go through over time. And the heart cycle, or the
cycle for a cell, a heart cell, is going to be
measured in millivolts. We’re going to use millivolts
to think about this. And you could use, I guess,
a lot of different things. But this is probably one
of the simplest things to kind of summarize
what’s happening with all of the
different ions that are moving back and
forth across that cell. Now the major
ions, the ones that are going to mostly
influence our heart cell, are going to be calcium,
sodium, and potassium. So I’ll put those three on here. And I’m putting them
really just as benchmarks just so you can
kind of keep track of where things
would like to be. So calcium would like
to be at 123 millivolts. Sodium at 67. And what that means is that if
these were the only ions moving through, then sodium would
like to keep things positive. And potassium, on
the other hand, would like to make the
membrane potential negative. So this scale is
actually the scale for the membrane potential. And if we move up
the scale, if we go from negative to
something positive, this process would be
called depolarization. That just means going
from some negative number up towards something positive. And if you were
to do the reverse, if you were going to from
something positive to something negative, you’d call
that repolarization. So these are just a couple of
terms I wanted to make sure that we’re familiar
with, because we’re going to be able
to then get at some of the interesting
things that happen. I’m going to make some space
here inside of this cell. So let’s start with a
little picture of the cell. So let’s say that
this is our cell here. And I’m going to draw in
little gap junctions, which are little connections
between cells. So maybe a couple there. Maybe one there and
maybe one over here. And let me label that. So these are the gap junctions. And also let’s draw
in some channels. So we have, let’s say, a
potassium channel right here. We know the potassium
likes to leave cells. So this is going to be the way
that potassium’s going to flow. And it’s going to leave behind
a negative membrane potential, right? And let’s say potassium
is the main ion for this cell, which it is. Then our membrane
potential is going to be really, really negative. In fact, if it was the only
ion, it would be negative 92. But it’s not. It’s actually just
the dominant ion. So it’s over here and
our membrane potential is around negative 90. And it continues
around negative 90. So let’s say nothing
changes over a bit of time. So we stay at negative 90. So this is what things look
like with the dominant ion that our cell is permeable
to being potassium. Now a neighboring
cell, let’s say now, has a little bit of
a depolarization. So it goes positive
and through the gap junctions leak a little bit
of sodium and some calcium. So this stuff starts leaking
through the gap junctions, right? Now what will happened to
our membrane potential? Well it was negative
90, but now that we’ve got some positive ions
sitting inside of our cell, our cell becomes a little
bit more positive, right? So it goes up to,
let’s say, here. And it happens pretty quickly. So now it’s at negative
70 up from negative 90. So at this point,
you actually get– I’m going to erase
gap functions– but now that you’re
at negative 70, you actually get new
channels opening up. And I haven’t drawn
them yet, and I’m going to erase sodium
and calcium just to make some space. But you get new
channels opening up. And these are going to
be the sodium channels. So let me draw those in. Sodium channels. And there’s so many of them. Lots and lots of these fast
sodium channels open up. And I say fast
because the sodium can flow through very quickly. So the sodium starts gushing in. And you know that’s going
to happen because there’s a lot more sodium on
the outside of a cell than the inside of a cell. And so sodium
gushes in, and it’s going to drive the membrane
potential very quickly up to a very positive range. Now it would go all
the way, let’s say close to 67, maybe
not exactly 67, because you still have those
potassium ions leaving. But close to it,
if not for the fact that these voltage-gated
channels actually close down. So these sodium channels
are voltage-gated. And they will actually
close down just as quickly as they opened up. To show that, I’m actually
going to do a little cut paste. I’m going to just
draw this cell here. And I’m going to
move it down here. So we’ve got our
cell just as before. And now these voltage-gated
channels, they close down. So let me get rid of
all these arrow heads. But we’re already now
in positive range. So at this point, you
could say our channels have caused a depolarization. And let me just quickly
show these shut downs so that you don’t get confused. There’s no more sodium
flowing through. You still have some
potassium leaking out, but that’s kind of
as it’s always been. And in addition to those
potassium channels, that little channel
I’ve drawn here, you have new potassium channels
that open up down here. And these are actually
voltage-gated potassium channels. So you had them before. They existed. But they were actually not open. So let me just draw little x’s. And the only reason
they flipped open is because the
depolarization happened. You had a negative
go to a positive. So now that our cell is
in positive territory, actually let me write
in positive 20 or so, our potassium voltage-gated
channels open up. So these voltage-gated
channels open up. And you can guess
what’s going to happen. Like which direction
do you think that the membrane
potential will go? Well, if the sodium channels
aren’t gushing the sodium inwards and potassium
is leaking outwards, now you’re going to have a
downwards repolarization. So now potassium is causing
the membrane potential to go back down. And let’s say it gets
to about positive 5. And if it continued, again, it
would go all the way back down to negative 90. But an interesting new
development occurs. At this point, I’m going to
actually cut paste again. And I’ll show you what happens
next, which is that calcium– this is the thing I said keep
your eye on the whole time, right?– calcium finally
kind of starts leaking in. So let me get rid of this. And this is the key idea, right? I don’t want to forget
that this is potassium. So you still have potassium
in the same over here. But now calcium leaks in. And let’s draw that over here. So you have these calcium
voltage-gated channel that allow calcium to come it. So you’ve got calcium coming
in, potassium leaving. Now think about what will
happen in this situation. So calcium is going
to want to rise the membrane potential this way. Potassium leaving
is going to want it to continue
going down this way. And because both are
happening simultaneously, you basically get
something like this. You get kind of a flatline. So because both
events are happening, both potassium leaving the cell
and calcium entering the cell, you get this kind of flatline. And the membrane potential
stays kind of around the same. And so it can just
write something similar, something like positive 5. Just so we’re clear,
these are also voltage-gated calcium channels. So to round this out, then
what happens after that? So you have so far, so good. We have all these channels
coming in to our cells and allowing different
ions passage. And now we get to
something like this. And I’m going to try to
clean this up a little bit. And what happens is that the
calcium channels actually close just as suddenly
as they opened. So now you don’t have any
more calcium coming in. And if calcium was
the only thing that was keeping this
membrane potential going flat– you know, I said
that the potassium makes it want to go down,
but the calcium was making it flat– well,
what will happen now? Well, if again you have just
those potassium channels open, well then you’re going to
have the membrane potential go back down. It’s going to go back
down to negative 90 or so. So this is kind of the last
stage, where those potassium channels are going back down. And those voltage-gated
potassium channels also close at this point. So finally, they
close down as well. And so now that
they’re closed, you’re going to finally get back to
just your initial state, which was having a little bit of
potassium kind of leaking out of this cell. And those voltage-gated
channel have shut down now. So now that you’re at negative
90, you stay down there. And this process is
ready to begin again. The last thing I want to say is
the stages, how they’re named. So this is state four, this
kind of baseline negative state that the relaxed muscle cell is. And then this action potential,
when it finally fires and it hits that
negative 70, this is actually considered
a threshold. This is our threshold. When it gets to that point,
we call that stage 0. And then on the
other side of stage 0 you have stage 1, 2, and 3. So stage 1 is that point
when just the potassium channels first open up,
the voltage-gated ones. And then stage 2 is when they’re
balanced with the calcium channels. And stage 3 is again when you
have just potassium channels, voltage-gated ones
that are open. And then you get back
to stage 4 again. So this would be stage 4. And because stage 0 is happening
so rapidly, because this is so fast, we actually call
this a fast action potential. So compare that to how
the action potential goes in the pacemaker cells,
where it’s much slower. This fast action potential
is a result of those really, really amazingly quick
voltage-gated sodium channels.

About James Carlton

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100 thoughts on “Action potentials in cardiac myocytes | Circulatory system physiology | NCLEX-RN | Khan Academy

  1. Rishi Desai, is my best teacher.

    Learned a lot about Heart and how it functions.

    Thank you so much sir.

    I see a dedication and sincerity behind the video. Hope someday i too become somebody who could pass on the knowledge i earned from you.

    Your proud student

  2. Excellent! I wish I watched this video, instead of trying to figure this out from the text for an hr 🙂 Thank you!!!!

  3. PERFECTLY EXPLAINED! But is an action potential the reason you get an influx of Ca2+ ions, just like a in a neurone?

  4. I don't get how after the stage three ( where lots of K out and Na in ) we back to the stage four ? shouldn't be an activity for the Na-K pump to return the normal membrane status ? 

  5. so calcium flows in after the sodium channels close right? In skeletal muscles the calcium flows in after the action potential has been reached to cause contraction, so is that the reason why calcium flows into cardiac myocytes as well? And does it also happen due to the action potential being reached? I'm a little confused about how this differs to skeletal muscle & the role of calcium exactly. In skeletal muscles does the calcium also enter after the sodium channels close & potassium channels open?

  6. Great vid, really helped me understand how a positively charged potassium ion leaving the cell can result in making the overall cell negative. Everything else just fell into place. Thanks. One question: by 'voltage gated channel' does that mean like it's based on a concentration gradient of which state the ions would ideally be? e.g. K+ at -92, Na+ at +67…

  7. So when or how the pottasium gets back into the cell? In every single phase pottasium is leaving the cell, wouldn't the cell eventually lose all potassium ions? In no step it ever says how it goes back in… I'm thinking sodium potassium pump but I'm not sure how that wouldn't alter the membrane potential… PLEASE HELP

  8. Does anyone know why a cardiac muscle can't produce a tetanic contraction unlike a skeletal striated muscle?

  9. I want to mention the role of Na-K ATPase pompe in the keeping of negative potentiel of cardiac myocytes …so helpful explain..thank's

  10. How's that +20mV peak value calculated? Shouldn't it be close to equilibrium potential of sodium (which is around +60mV)?

  11. Does the voltage gated potassium channels are not supposed to remain open during the resting stage of AP of Myocardial cells?

  12. This was great. A million times better than the teacher i med school

    I only have an small constructive critic. I had explained how the ionic balance returns to place in stage 4, If I was completely new to this I would not be able to understand how with all the Na+ in and the K+ out the cell would be able to start a new potential:

  13. does the intracell voltage come from neg90 to neg70 because of k slow out follw ???is not k ion and its outfollow will lead to more intra cell neg voltage

  14. What triggers the close of the calcium channels at +5mV? I understand that they're voltage gated but if no voltage change occurs due to potassium leaving simultaneously, ie the 'flat line', what causes the calcium channels to close off?

  15. Slow (L-type) Calcium channels actually begin to open in phase 0 once the membrane potential reaches 30mV -40mV. However, the effects aren't manifested until phase 2, as shown in the video, when the three types of K+ channels (I-to, I-k, and I-k1) slows down outward conduction speed to maintain the plateau.

  16. When does the potassium come back into the cell? It can't lose it forever. Also, when do sodium and calcium leave the cell? The cell can't accumulate them forever. (By forever of course I mean for the life of the person.)

  17. So does that flat line act as a delay to keep the cardiac myocyte contracted long enough for the blood to be forced out of the atria and ventricles?

  18. Thanks for the video. I have a question. What about Cl− ions? Do they participate in the generation of the action potential in cardiac myocytes?

  19. I love you guys, but I have to say that I think there is something wrong in this video.
    The voltage-gated Ca+2 channels don't "actually close just as suddenly as they opened", if they did there wouldn't be a flatline.
    Actually their name is L-type Ca+2 channel, L for long lasting.
    Unlike the Na+ channels of stage 0 which they actually close just as suddenly as they opened.
    Unless I have misunderstood you, if that is I apologize.

  20. tbh, at the plateau stage membrane potential is slightly decreasing, due to the bigger number of k-channel( a little difference)

  21. There is something I don't understand, where does the Na+/k+ ATP fit in all of this, I mean, I never see Na+ coming out of cells in this explanations. 🙁

  22. I don't understand one part though. How does potassium ions enter the myocardial cells if they keep leaving the cells. The myocardial cells does not have an infinite supply of K ions right?

  23. I have two questions: What happened with all the calcium and Sodium that got inside the cell; 2) how does the cell recover K+ ? it seems to be loosing it all the time?

  24. How is K+ always leaving and Na+ and Ca++ always entering? The cell would run out of Potassium at some point right?

  25. At what stage does contraction happen? And how does Acetylcholine play a role in cardiac muscle action potentials?

  26. HELP! I took potassium when I wss badly dehydrated got bad heart pain n pressure took calcium to counteract n it felt better next morning another calcium which put my heart into contraction it seems to go all into heart making worse I then took magnesium to try counteract it n a few days later after alot of cardiac symptoms my heart released the lock it was such a relief. I thought it was better or all the tightness or contraction released when I resumed supplements I took a dose of potassium the whole lot seeped into heart n it constricted up tightened n felt very uncomfortable. thats 2 weeks ago n it hasnt released yet. im figuring with all the trauma from k supplements n calcium while badly dehydrated during vomiting bug my gates of channels were malfunctioning n that k dose seeped all into heart n is now stuck there unable to move putting my heart into constant state of hyperkalemia even in total loss in body stores back achy n legs cramping. im in nightmare situation I dont know how to undue the potassium in myocites too much n my heart cant excrete excess..iv had to take potassium msny times n this never.happens I dont get any symptoms just twitching when its building back into muscles..all my ecgs are coming out with peaked t waves.n abnormal t waves on iii section..this is proving my theory.of hyperkalemua coz its.stuck in hesrt even though blood levels normalized ages ago…help heart needs expertese help…should I take a potassium channel opener? would that help my hesrt release excess k out or is it in cells of hesrt now could some protein your talking about.push out? this is most unusual circumstances I know but its happened…my heart is very uncomfortable breathlessness like air not fully flowing around or from tightness like something stuck in there preventing it from going into normal relaxed.state.
    any advice please im desperate?
    khan acadamy or anyone plz

  27. Question: originally we see Ka leaving and Na and Ca going in and bringing the cell to more positive charge, now what confuses me is that at final phase where more Kan leaves the cell and ca enter the cell brings the cell to negative? The very end ca continues to go in and more Ka goes out then how comes it switches to negative when we initially understood that the more Ka leave the cell the more positive the cell becomes. Wish someone brings this clear to me thanks

  28. The moment that you realize several thousand dollars worth of lectures in university is nothing compared to free YouTube videos…

  29. Sorry to sort of necro the comments here but one thing I'd like to clarify: how does a positive ion (potassium) produce a negative membrane potential? Do you just mean that it is negative relative to sodium? I'm guessing that isn't the reason given your graph so if anyone can explain that would be great! Thanks 🙂 great videos!

  30. This is just superb, I have been researching "thyroid solution diet reviews" for a while now, and I think this has helped. Have you ever come across – Yannabarn Vanish Thyroid – (Have a quick look on google cant remember the place now ) ? Ive heard some amazing things about it and my neighbour got cool results with it.

  31. What about the sarcoplasmic reticulum and it’s release of calcium when calcium begins to influx into the cell?

  32. How does Calcium exit the cell? You explained how it enters in the beginning but how does it exit after the action potential to maintain balance?

  33. just read a physiology book they say permeability of K+ goes down when Na+ goes up, i don't understand , in the video it's said that K+ gated opens so permeabilty should go up.

  34. Please, I have Q how their
    are two action potentials one in myocyte and other in SA node?
    I didn't understand the main ideai 😢

  35. So if potassium is always slowly or fastly leaving the cell, at what point does the potassium re-enter? It can't leave forever, otherwise at some point there won't be any potassium left to leave… I think this video is missing some steps.

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