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Arterial elastance (Ea) and afterload | Circulatory system physiology | NCLEX-RN | Khan Academy

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    Let's go ahead and use
    our pressure volume loop.
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    I'm going to sketch
    out how afterload
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    would make things
    change on this.
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    So let's just quickly
    sketch this out.
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    I'm going to put
    pressure over here.
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    And I'm going to start
    out with just two lines.
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    First, and this is
    probably the one
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    I want you to keep
    an eye on, this
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    is the end systolic pressure
    volume relationship.
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    And then I'm going
    to also put on there
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    the end diastolic
    pressure volume
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    relationship,
    something like that.
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    And so these are kind
    of the first two lines
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    that we know are going to
    be helpful in sketching out
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    our pressure volume loop.
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    Then we have this
    other line, right?
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    We have this EA line.
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    This is Arterial Elastance.
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    And there's a good formula here
    that is very, very helpful.
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    It's the pressure at the end
    of systole over stroke volume.
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    Remember, any elastance
    is kind of thinking along
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    the lines of a
    pressure over a volume.
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    And this red dot represents the
    pressure at the end of systole.
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    And this other red dot here
    is going to kind of show you
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    where it crosses the
    x-axis, the volume.
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    And that's helpful because
    then we can kind of quickly
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    figure out what the
    stroke volume would be.
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    This would be our
    stroke volume here.
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    So we have it sketched out.
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    And I can actually
    take this and now
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    draw in the PV loop,
    which would be something
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    like this kind of
    chugging along.
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    And you might be tempted
    to make it cross right
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    there at the point where the
    purple line is, but remember,
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    we have to go a little bit
    further because that's not
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    where the volume is going to be.
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    The volume is actually going to
    be a little bit further along.
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    So to be true to
    that, I'm just going
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    to draw it a little bit further.
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    But I wanted to draw
    the first line just
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    to show you how you might
    have thought it looked.
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    But that is not
    where it crosses.
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    And then, of course,
    you have contraction,
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    and you have ejection
    of blood into the aorta.
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    So this is our pressure
    volume loop, right?
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    This is what it looks like.
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    And at the top of this
    loop, we have ejection.
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    This is where blood,
    I said, is coming out
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    of the left ventricle
    and going into the aorta.
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    And if I actually just kind of
    trace around this part of it--
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    this is ejection--
    you would probably
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    remember that this is where
    something important is taking
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    place.
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    And specifically, I'm
    talking about afterload.
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    Remember, we actually
    defined afterload.
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    According to this part of
    the pressure volume loop,
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    we said-- and this is
    going back to Laplace.
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    We said that
    afterload is basically
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    wall stress happening
    during ejection.
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    So during the entire
    ejection phase,
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    the wall stress is
    what our afterload is.
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    And we actually simplified
    this to-- or not simplified,
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    but kind of wrote
    this out, I should
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    say, to Laplace's
    law, which is pressure
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    times radius of
    the left ventricle
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    during ejection divided
    by 2 times the wall
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    thickness during ejection.
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    So this is the
    formula for afterload.
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    And we have to
    remember that it's
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    occurring during
    the entire ejection,
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    during the entire
    part I traced out.
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    But for simplicity,
    because a lot
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    of times we don't actually
    sit there and calculate
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    all the different
    points, we oftentimes
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    look to this value, this
    pressure at the end of systole.
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    Because, of course,
    this is definitely
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    one of the points
    during ejection.
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    You could say the final moment
    of ejection would be that point
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    right there , where the
    pressure is end systolic.
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    And so we often use
    that value to kind of be
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    a marker for what
    afterload is doing.
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    And remember, we know that
    pressure and afterload
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    are very closely related.
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    You can see it in the
    formula right there.
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    So we do use the end systolic
    pressure as a marker.
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    And I guess now the
    question I want to pose
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    is what would happen if we
    actually increased that number?
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    What if we increased the
    pressure at the end of systole?
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    What would happen?
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    So on the graph it would
    basically look maybe something
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    like this, where now
    your value is higher.
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    This is our new pressure.
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    This is the new pressure
    at the end of systole.
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    I'll put p prime.
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    And if that's the new pressure
    at the end of systole,
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    then we have to think through
    what else would change?
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    I guess that's the question.
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    And you know, of course, the
    first thing to think about
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    is the fact that this is
    going to drop down, this line.
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    And if our pressure
    has gone up, then you
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    know our stroke
    volume has gone down.
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    So our stroke volume is going to
    be a little bit more contracted
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    or smaller.
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    And you remember now
    we have a formula.
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    I may actually just jot
    down the formula for us,
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    just make a little bit of space.
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    Maybe I'll just
    actually leave it.
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    That way, you can
    see everything.
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    But I'll put the
    formula over here.
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    We have our formula,
    which says that elastance,
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    or arterial elastance,
    equals pressure
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    at end systole divided
    by stroke volume.
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    And all that equals heart
    rate times resistance, right?
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    And in this case,
    I'm saying that I'm
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    going to increase
    this number, and I'm
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    going to decrease this number.
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    So what I've done is
    basically changed the slope.
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    So I know that the elastance
    is going to change.
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    And if I've done that, the only
    way to really accomplish that
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    would be to either
    increase the heart rate
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    or increase the resistance.
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    Already I'm getting some
    interesting information
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    about how this
    might have happened.
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    I can ask, hey, did that
    person's heart rate go up?
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    Or are their blood
    vessels more constricted?
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    Because one of those
    two things must
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    have happened to
    cause this increase in
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    afterload that I'm
    drawing for you.
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    And either way, to draw it out,
    it would be kind of the same.
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    You'd basically say, OK,
    well, if this is my new end
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    systolic pressure,
    I know that I need
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    to draw it so that the point
    where it crosses the volume
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    axis is the same.
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    And actually, I can
    make it kind of extend
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    on the other side, too.
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    I can say something like that.
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    And this is what would happen.
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    So one of the things
    I want to point out
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    is there is a difference
    between EA and afterload.
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    So let's talk about
    that difference.
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    When I talk about
    afterload, I really
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    want you to keep
    remembering or keep in mind
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    the fact that we're talking
    about the entire line, so
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    this entire area or this entire
    part of the curve, which I'll
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    redraw here, which would look
    something like this, right?
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    That entire thing
    is the afterload.
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    And we kind of simplified that.
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    I keep reminding us that we
    keep simplifying that down
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    to just pressure at end systole.
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    But really, afterload is more
    than just that one point.
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    But we use that as kind of
    a marker for how afterload
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    is doing at every other point.
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    And we can see pretty
    clearly that, of course,
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    the afterload has gone up at
    every point including the very
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    last point, which
    is end systolic.
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    And the new curve, of course,
    if I was just to draw it in,
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    would look like this.
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    Let me just keep a blue
    line so it stays steady.
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    The new line would
    look like this
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    and would actually come
    up like this and do this.
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    That would be my new line.
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    So the pressure volume
    loop does change.
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    And you can see that if
    afterload is pressure end
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    systole, if that's what
    we're using as our marker--
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    I guess maybe I should
    put it in quotes
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    just to make sure
    we don't actually
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    think that that's
    afterload because we know
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    that the definition of
    afterload is much more than just
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    that-- then EA is going
    to include part of that.
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    It's the end systolic pressure.
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    But it's also includes
    stroke volume.
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    So one of them is the
    pressure over volume
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    and the other is
    just the pressure.
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    And if we're
    thinking about that,
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    remember that many things
    are going to affect,
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    then, this end systolic
    pressure, many things,
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    including things like
    contractility will affect this.
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    And preload will affect this.
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    So many things are going
    to affect afterload.
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    But not too many things
    are going to affect our EA.
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    So remember, if you're having
    a change in EA, the things that
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    are going to change EA would be
    like heart rate and resistance.
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    So truly when you're
    breaking this down,
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    just try to keep this
    in mind that the formula
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    you want to always
    remember is this guy.
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    And this will always get
    you to the right answer,
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    that if you are
    thinking afterload,
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    you're really talking
    about everything
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    that could affect
    afterload including preload
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    and contractility, because
    all those things can affect
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    which direction this
    goes, because they
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    are going to change
    stroke volume.
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    Whereas if you're going to
    talk about the elastance,
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    then really the
    only things that are
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    going to change the overall
    elastance, this whole thing,
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    are going to be things like
    heart rate or resistance.
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    So it's actually pretty simple
    when you look at the formula.
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    But I know a lot of times people
    confuse the word "elastance,"
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    arterial elastance,
    with afterload,
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    and they think it could
    be the same thing.
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    And it's true that
    they're very related,
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    but they're not
    exactly the same thing.
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    So as a final
    point, in this case,
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    we increased the arterial
    elastance by either changing
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    the heart rate-- increasing it--
    or increasing the resistance .
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    But we could have also decreased
    the heart rate resistance,
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    and we would have seen a
    smaller arterial elastance.
Title:
Arterial elastance (Ea) and afterload | Circulatory system physiology | NCLEX-RN | Khan Academy
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Video Language:
English
Team:
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Duration:
09:33

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