Diastolic heart failure pathophysiology | Circulatory System and Disease | NCLEX-RN | Khan Academy

Diastolic heart failure pathophysiology | Circulatory System and Disease | NCLEX-RN | Khan Academy


– [Voiceover] Diastolic
heart failure is similar to systolic heart failure in that the heart doesn’t pump enough blood
to meet the body’s demands. Okay, but how it is different? Well, if you look at diastolic,
that kind of clues us into how it’s different. And if we remember that
diastole is that phase in the cardiac cycle where the heart’s just filling with blood, so the heart’s all relaxed and blood’s filling into the ventricles and that’s called diastole. So diastolic failure means that the heart’s not
filling with enough blood. And so, if you just compare the two, if you just eyeball them, you’ll notice how much less room there is with diastolic failure. And if we bring back our
most favorite analogy ever, the water bottles, if you
squeeze the healthy one, water ejects out, that’s great. But with diastolic
failure, what if the bottle is not filled with as much
water and you squeeze it? Obviously, less water is gonna be ejected ’cause there’s less in
there in the first place. It’s the same thing with the heart. So, if there’s less blood in
the heart in the first place, it’s gonna have a lot harder
time meeting the body’s demands in ejecting as much blood. So less filled means less ejected. Also, remember how a systolic failure had a lower ejection fraction which is that fraction of blood
ejected with each beat. That’s because there’s
about the same amount or possibly even more
filled into the ventricles with systolic failure,
but there’s less ejected. So naturally, you’d have
a lower ejection fraction. It makes sense. But since diastolic heart failure has both filled and ejected
lower, so both are lower, sometimes your ejection
fraction can be the same as with a healthy heart, and we would call that a
preserved ejection fraction. Okay, that seems a
little confusing, right? Well, let’s do an example and
show how that might happen. Recall that ejection fraction is equal to your volume ejected, which you can also call
your stroke volume, divided by the total blood filled which we can also call
end diastolic volume because it’s the volume
at the end of diastole. Let’s say your stroke volume is 70 ml, say your end diastolic volume is 120 ml. This would be considered “healthy”; 70 divided 120 equals 58%. Okay, that’s within our normal range. What if stroke volume is equal to 46 ml
because of heart failure? It’s a lot lower, it’s pumping less blood. But your end diastolic volume
is also lower, it’s 80 ml. Forty-six divided by 80 is still 58%, technically in a normal range. So clearly, the stroke volume
and the blood being pumped out is lower, but that’s kind of covered up by your end diastolic
volume being lower, too. But just because that
ejection fraction’s preserved, that doesn’t mean we’re out of the woods. It’s still heart failure. But how does this diastolic heart failure get to look so much different
than systolic failure? Well, there’s pretty much two ways. The first way is hypertrophy
which essentially means like growth of muscle. When we’re gonna talk about that, we mean ventricular muscle growth. When these grow, they take up more space, and since there’s more space
being taken up the by muscles, that means there’s less
space to fill, right? Secondly, is that these muscles, these growing muscles get stiffer. They don’t stretch as
much when they relax. Even though they’re growing, there are these dead
muscle cells in here, too, because it’s heart failure
and that’s a main component is death of muscles cells. So these dead muscle cells
leave this fibrotic scar tissue and this fibrotic tissue is like a bunch of connective tissue and that connective tissue
has a lot lower compliance. Basically, compliance is the
ability for the ventricle or for any tissue to passively stretch and expand during filling. This is super important for the heart because more stretch, more compliance means that it can fill more,
it could get more blood. Think of like filling a water balloon. When you put water into it, what happens? Well, it gets bigger, it expands. But this is like passive, the water is forcing it to get bigger. Now think about filling up
one of those glass flasks from Chemistry class. I mean, I’m gonna be really extreme here just to make a point, but, what’s gonna happen when
you fill it up is just, it’s not gonna get bigger,
it’s not gonna change shape, it’s just gonna fill up
all the way and then start to overflow and spill all over. That’s because it’s a lot less compliant. It’s probably one of the
least compliant things we can think of. It’s the same with the heart
with a bunch of fibrous connective tissue. It can’t relax and it
can’t passively expand, and it can’t fill completely. So that’s what’s going on
with diastolic heart failure, but how does it get like that and how do we get these
enlarged and stiffened muscles? Well, just like systolic
failure, it’s a secondary disease which means that this growth
and stiffening is caused by some kind of underlying disease
that’s been there before. The big one that we tend
to understand the most is chronic hypertension
or high blood pressure. So when the pressure in
your blood vessels goes up, they become harder to pump against. Harder to pump into. This is kinda like blowing into a straw versus like a big tube. Which one do you think it’s
gonna be harder to blow air to? It’s probably the smaller one, right? Well, it’s sort of like
that for the heart. Except the heart has to pump blood through these narrowed vessels, and this is way more difficult to do. So what does your heart do? Well, it bulks up. It gains muscle and it gets bigger, so it can pump against
these high pressures. Now, both diet and diabetes
can both contribute to higher blood pressure and hypertension. Those are definitely big risk
factors for hypertension. And therefore, diastolic heart failure. The second underlying
disease is aortic stenosis, and stenosis from the
systolic heart video we know is a narrowed valve. Specifically, we’re gonna talk
about this valve right here, this aortic valve. Then that valve goes out
from the left ventricle and pumps into an artery called aorta. It’s similar to hypertension. It’s a lot harder to pump blood through this narrowed
opening, as opposed to a valve that’s opening all the way. What happens? Well, the heart muscle again
bulks up and gains muscle so it can try to pump harder
through this smaller valve. Now, this is a little
tricky though, right? Because we remember that this can also lead to systolic failure. So, what gives? Well, unfortunately, a lot
of the mechanisms behind why in one case it might lead
to this growth of muscles like in diastolic heart failure or it might lead to this
series weakening of the muscles like in systolic heart
failure are pretty complex and honestly, a lot of
these mechanisms are unknown in still big areas of research. Next up, we have cardiomyopathies which means heart muscles diseases and sometimes this can
be a little general, but for diastolic heart
failure in particular, there’s two that we’re gonna focus on. The first one is
hypertrophic cardiomyopathy which we can kinda figure out by the name. Hypertrophic or hypertrophy
means muscle growth. This cardiomyopathy causes muscle growth and this is often
without an obvious cause. The second is restrictive cardiomyopathy which cases stiffer
and more rigid muscles. This restricts the
ventricles from expanding. These two cardiomyopathies kinda hit the nail in the head, right? Because with diastolic heart failure, you have either stiffer
muscles or enlarged muscles. Finally, there are some
other causes and risk factors like old age and coronary
artery disease, even, but like I said before, some of these cross path with systolic failure. Again, a lot of the
mechanisms behind that are largely unknown. Especially as to why one
might lead to systolic failure and one might lead to diastolic failure. These are still big areas of research. With diastolic heart failure, the heart muscles either get bigger, they get stiffened or both. When this happens, less blood
fills in to the ventricles and the heart can’t
passively expand as much and therefore, it can’t relax completely. Ultimately, you end up with this cycle that leads to worsening heart failure. So you start with some underlying disease like hypertension or stenosis that makes it a lot harder
to pump blood to the body. To try and make it
easier, the heart muscles increase in size and they
get bigger, and then bulk up. These bigger muscles do more
work, so they need more oxygen. But with heart failure, you
can’t supply more oxygen so this leads to cell death, and that cell death causes
this fibrosis and this stiffening of the heart muscle tissue. Then that feeds back
into a lower blood supply making it even harder to pump blood. You could also have other diseases like hypertrophic cardiomyopathy that directly affects muscle size or restrictive cardiomyopathy that directly affects stiffening. This cycle progresses and
heart failure gets worse.

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