00:01
Let's look at the
etiology of heart failure.
00:03
Something bad had to
happen to the heart.
00:06
It all starts with
a cardiac insult, right?
And you have this cardiac insult,
which leads to decreased
cardiac output. Tada.
00:16
But wait a minute, we've talked
about a lot of other things, right.
00:19
But what I want you to keep in mind
that cardiac insult is all
those things we've talked about,
what could it be?
An MI of alveolar disease,
ischemic disease, core, all those
things that can cause the heart
to be insulted or harmed, which
lead to a decreased cardiac output.
00:41
That means not enough blood
or volume is going to be
pumped around to my tissues
to meet my metabolic needs,
and to keep fluid where it's
supposed to be kept, right,
and it's appropriate space.
00:52
So there's some
insult to the heart.
00:55
We've talked about all the
things that can insult the heart,
that leads to a
decreased cardiac output.
01:00
Here's how the body responds.
01:02
That's what a
compensatory measure is.
01:05
So, heart is damaged,
decreasing cardiac output.
01:09
Here's how the body
tries to compensate.
01:12
You've got the RAAS,
which you remember
from blood pressure,
SNS stimulation. Remember?
That's my fight or flight system
where you're going to really come,
everything goes faster.
01:22
heartbeats faster,
things move faster,
and myocardial adaptations.
01:27
Well, it means that tissue
is actually going to get bigger.
01:31
Sometimes you'll hear it
called myocardial remodeling.
01:34
So, you take a hit cardiac insult.
01:37
Cardiac output to the point
where cardiac output is lowered
three main ways the body is going
to compensate or try to respond.
01:46
So, let's break these down
a little bit more.
01:48
Now, I know, you remember the RAAS,
the Renin-angiotensin
-aldosterone System, right?
This is the one that helps raise
your blood pressure because
when the body senses,
"Whoa, whoa, whoa, whoa,
that's not an adequate
blood pressure for us,"
that the kidneys,
they squirt out renin.
02:07
Well, they're going to connect up
with the livers angiotensinogen
and that's going to give you
angiotensin I.
02:14
Now, angiotensin I
connects with ACE,
Angiotensin Converting Enzyme,
then you come up with
a bad [unintelligible],
you got angiotensin II.
02:27
This causes really intense
vasoconstriction and
ends up hanging on to sodium
and you hang on to water,
so you end up with more volume,
because aldosterone tells your body
to hang on to sodium.
02:43
Wherever sodium goes,
water follows.
02:46
When I have more water on board,
I have more volume on board.
02:50
So there are two ways this system
that starts with a body recognising
blood pressure's not adequate
to perfuse all my tissues.
02:58
Renin + angiotensinogen =
angiotensin I + ACE = angiotensin II.
03:05
When angiotensin II
is available in the body,
it causes potent vasoconstriction
and fluid reabsorption.
03:14
So, that's the way it raises
blood pressure.
03:19
Now, remember, the RAAS what
is meant to keep us safe,
but if your heart
isn't functioning well,
this could be a real problem.
03:28
Now the second compensatory
measure is SNS stimulation.
03:33
Keep in mind, the heart has
taken a hit cardiac insult
the decreased cardiac output
is the result.
03:40
One way you respond is the RAAS,
we just talked about it.
03:43
The second way is SNS, sympathetic
nervous system stimulation.
03:48
Now, when this happens,
all these neurotransmitters
that are released cause
increased heart rate
in contractility.
03:56
Okay, so what would that feel
like to you?
If your heart rate was
pumping faster and harder?
Would that increase
your workload or decrease it?
Well, clearly, this would increase
the workload of the heart.
04:10
Faster heart rate, pumping harder,
that's what contractility
is how hard it pumps.
04:16
This is going to be really
challenging for a struggling heart.
04:19
In fact, it can be
a recipe for disaster.
04:22
Because all of this is happening
in an already exhausted heart.
04:27
We've got more fluid on board,
and we've got the vessels
constricted, because of the RAAS.
04:34
We've got the heart beating faster
and harder because of the SNS.
04:39
And the third one is
myocardial adaptations.
04:43
So, here's a healthy heart.
04:45
We've got a real close up picture
of the wall there.
04:48
I love that where they show
you the cardiac cells there.
04:51
You've got blood moving through
that star arrow that shows us,
"Wow, that looks pretty good."
Pretty good systemic output
there, right, stroke volume.
04:59
Now, let's look at what
happens when the heart muscle
seems to be impacted
by the workload.
05:05
Look at that left ventricular wall,
what's changed?
See how thick it's become?
It can't compress
and relax as much.
05:14
Look how much smaller
the left ventricle is now
than it used to be
in the previous picture.
05:20
And look what the artist
has left for you in that arrow.
05:23
See how it is much
smaller in this picture?
Yeah, that's to let you know
when the body starts making
these adaptations in the heart
because it's been working
so hard initially,
it got bigger to try to help,
but now it's just way too
big and thick and floppy.
05:39
It's not effective in pushing out
the amount of blood volume
your body needs.
05:44
So, let's look at all
three of these together.
05:47
I know we've walked through them,
but think about
what are the things that could
be considered a cardiac insult?
Can you write a quick list
of them on your slides?
Now, when all of those
things happen to the point
that you have a
decreased cardiac output,
that's when these
compensatory measures kick in.
06:06
A decreased cardiac output
the equals a lower blood pressure.
06:11
When it's too low,
the RAAS kicks in.
06:16
And that's when you have
vasoconstriction
and extra volume on board.
06:19
In addition, the sympathetic
nervous system is stimulated
and your heart rate will
be faster and harder.
06:27
The last one does not help.
06:30
Myocardial adaptation means the
myocardium becomes hypertrophied.
06:35
Big and not effective.
06:37
Remember, each one of these
three compensatory measures
can be happening in a heart
that's already struggling
and that's when it becomes
especially problematic.
The lecture Heart Failure: Etiology and Compensatory Measures (Nursing) by Rhonda Lawes, PhD, RN is from the course Heart Failure (Nursing).
What compensatory measures in heart failure are caused by stimulation of the sympathetic nervous system? Select all that apply.
What compensatory measures in heart failure are caused by the Renin-angiotensin-aldosterone system? Select all that apply.
What causes all incidences of heart failure?
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