Compensation and decompensation in heart failure | NCLEX-RN | Khan Academy

Compensation and decompensation in heart failure | NCLEX-RN | Khan Academy

– [Voiceover] So what do we mean when we say compensation? Well, let’s remember that heart failure, you have this decreased ability to meet your body’s demands, right? Well, your heart and body have this way of trying to make up for
this decreased ability and increase the blood you supply, and that’s called compensation. Because you’re compensating
for this decreased supply. But in heart failure this can lead to something called decompensation. So eventually you can’t compensate anymore and your symptoms start to get worse and heart failure gets worse. So there are a couple main
ways we try to compensate. And each of these ways either
increase your stroke volume or increase your heart rate. And remember that cardiac output equals stroke volume times heart rate. So if you increase either one of those you’re gonna increase your cardiac output. The first thing we’re gonna look at is activating your
sympathetic nervous system. And this is like your
fight or flight response. So, for example, what
if you’re hiking along in the woods and you see this bear? Your sympathetic nervous
system is gonna kick in. And your heart rate’s
definitely gonna go up and your stroke volume is
definitely gonna go up. And so your body is preparing you to either fight or flight, or run away. So when your cardiac output goes down your sympathetic nervous system kicks in. And it uses these receptors on the heart that tell the heart to one, beat or contract
harder with more force which increases your stroke volume. And two, to beat faster, which increases your heart rate. But if you use these too much they start to down-regulate. Or decrease in amount. So you know, there’s less of them. And less receptors means your heart won’t respond as it did before. So think of it like this. What if you’re moving? And you call a bunch of your friends over to try to help you move your stuff. And you know, they’re glad
to come over and help you. And so you move your stuff and then you decide next week, oh, I want to move again. So you call them up again and say “hey, I need some more help”. And they’re like okay, I
guess it’s kinda weird, but I’m gonna come help you. And then they come. But then the next week you’re like, oh, I’m gonna move again. And then you keep doing
this week after week and those friends are gonna start to well one, question why
you’re moving so much. And two, they’re gonna stop maybe answering your phone calls. It’s sorta the same thing with your sympathetic nervous system. When you activate it too much it’s gonna start helping less and less. So the next big way we
can compensate is by increasing this thing called preload. Now preload is defined as this
pressure in the ventricles. So in this lower chamber, after it’s filled but before it contracts. So during diastole. When it’s filled, the walls
and the heart muscle cells are all stretched out because it’s like filling
up a water balloon. So you put the water in
it and then the water causes that balloon to expand, right? So the more you fill in, the higher this pressure or preload. So as you keep filling, the
walls stretch more and more and we get higher pressures or preload. To do this, to fill more, to get more blood in those ventricles your body releases these specific hormones like antidiuretic hormone,
or we call it ADH sometimes, or aldosterone, to increase
this filling volume. So if the ventricles used to
have about 100 milliliters at the end of diastole, now maybe they have a little more, like 115 milliliters. This extra little bit
might not seem like a lot, it’s like one tablespoon, but it’s enough to
stretch the heart chamber and muscles just a little more. So that’s great, but why
does increasing the preload, or filling pressure, increase
the force of contraction, and so your stroke volume? Well, think of it like
stretching a rubber band. The more you stretch the rubber band the more force it’ll
snap back with, right? Okay, so there’s a lot
going on here, right? So let’s go one step at a time. So as you fill the
ventricles with more blood it stretches those muscles out, right? And just like the rubber band did, when you stretch it out it contracts, or it snaps back with more force. And when it contracts with more force, you get more stroke volume, you get more blood ejected. And so this guy named
Frank-Starling saw this and kind of decided to cut corners and create this law that says, as you increase your
pressure or your preload, you also increase your stroke volume. And that’s the Frank-Starling law. Sweet, so increasing preload
increases stroke volume and therefore, your cardiac output, and is one way we can compensate. But again, like over activation of the sympathetic nervous system, this is a real delicate balance. So these muscles now contract
with more force, right? But that means that they use
up more energy to do that. And therefore, they need more blood. And if there’s no additional blood flow coming to the heart muscle cells, they can begin to die off. So let’s get back to that first analogy where that guy’s moving all the time. But this time maybe he decides, oh, I’m gonna pay my friends to help. And so all the sudden
they all come running back and then they help him move in and they kinda support his weekly moves. But then all of a sudden he starts moving every other day, and he’s not increasing their pay. Well, they start to get overworked, and without more money,
they’re gonna leave, right? It’s kinda the same thing
with our muscles cells. They’re contracting harder
and they’re working harder. So they need more oxygen and more blood, but they’re not getting that
so they start to die off. So we just saw that
when you contract harder you eject more blood. Well, besides increasing preload, there’s one more way we can do that. And that’s gaining
muscle, that’s bulking up. This is also called
myocardial hypertrophy, where your heart gains muscle mass. And when it gains muscle
it contracts harder because it’s stronger. So to try to make up for this
decrease in stroke volume or this death of cardiomyocytes,
or heart muscle cells, these surviving cardiomyocytes become elongated and they grow. And this causes the heart
muscle as a whole to get larger. So you get this enlarged heart muscle. So it’s like the ones that don’t die are like whoa, I gotta start bulking up so I can take over for these guys that aren’t contracting anymore. And these bulked up muscle
cells contract harder, they eject more blood and
they increase cardiac output. Perfect. But as we know, this usually
comes at a cost, right? Well, more work means more oxygen and more blood supply. But with heart failure we know
that that’s not an option. And so without an increased supply these bulked up cells get overworked and then they start to die off. Not only that, if the
heart muscle gets too big the chambers start to get smaller and so there’s less blood
that can fill in the chambers. So those were the three
modes of compensation. You can activate your
sympathetic nervous system. You can increase your preload. Or you can gain muscle, which is called myocardial hypertrophy. And so for each of these, our goal is to increase cardiac output. By either heart rate or stroke volume. But like we saw, when you use any of these too much it leads to unintended consequences. And eventually heart failure gets worse. And this is what we call decompensation. So when you overuse the
sympathetic nervous system your receptors start to go away. And you end up with a lowered response. When you increase preload, you muscle cells stretch
and then contract harder, but this costs more oxygen and then eventually leads to cell death. Similarly with hypertrophy, these bigger muscles also use more oxygen. And without that the cells die. So not only that, these three can often
feed back on each other. Like the death of muscle cells
from an increased preload might result in hypertrophy, because those remaining
cells start to bulk up. And this increases cell death even more. And then as the heart weakens from this it might stimulate the
sympathetic nervous system to try and beat harder and faster, which further progresses heart failure. Most of the time it’s
really difficult to pinpoint which one was the initial culprit. But the major takeaway
should be that compensation, regardless of its intentions, is often a major contributor
to worsening heart failure and eventually decompensation.

40 Replies to “Compensation and decompensation in heart failure | NCLEX-RN | Khan Academy”

  1. Khan academy never fails to amaze me. Thank you for presenting this topic in a way that is simple and easy to understand, and with awesome graphics that really help drive the point home! I don't think I could make it through nursing school without these amazing videos!

  2. It's really not elasticity so much as optimization actin-myosin cross-bridge alignment that increases force of contraction in stretched heart muscle, producing the Frank-Starling effect.

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