often with thickened heart muscle.
Now, there are a number of compensatory mechanisms
that the body sets off when it sees heart
failure. Remember, I mentioned them just a
few moments ago. What are the compensatory
mechanisms? Well, let’s think, why would
the body compensate for decreased cardiac
output, for decreased pumping of the blood?
The reason the body compensates is because
it interprets heart failure as if there had
been a hemorrhage - a blood loss, or dehydration.
In other words, the reduced pumping ability,
the body interprets as, “Oh, there’s a
lack of blood from a hemorrhage or there’s
a lack of fluid in the circulation because
of dehydration”. And it sets off a whole
bunch of compensatory mechanisms aimed at
holding on to fluid, water and salt.
Unfortunately, this is exactly the opposite
of what we would want because in holding on
to fluid, you actually create the setting
where patients put some of that fluid into
the tissues, both in the legs as edema or in
the lung as pulmonary edema. So, the activation
of these… of the neurohumoral system that
is central nervous system initiated activity
to correct the heart failure situation actually
makes the situation worse.
These systems work great if there’s dehydration -
you’re caught in the desert without water.
They work great if there’s a hemorrhage,
you’ve been cut somewhere or you’re bleeding
from an ulcer in your stomach, but they work
unfortunately, in a negative manner in a patient
with heart failure.
Let’s just talk for a moment about why these
compensatory mechanisms work. They work because
of something I mentioned before, Starling’s
Law. The so called "Rubber Band Law of the
Heart" - the more you fill it, the more it
contracts. So, what the compensatory mechanisms
are trying to do is to increase the filling
of the heart so it will squeeze more. As I’ve
said, unfortunately, that leads to elevated
pressures that back up in the system and result
in edema. But, the rubber band law of the
heart says that the force of contraction is
related to how much you stretch the heart
muscle cells and this increases contractility.
So, you see why the body is trying to increase
the pumping ability of the heart and this
works fine if it’s a hemorrhage or dehydration,
but it doesn’t work well when the patient
has heart failure. So remember, stroke volume
is the number of cubic centimeters that the
heart puts out with each time it squeezes
times heart rate, that’s cardiac output.
So, when we have a reduction in stroke volume
because the heart has been injured, sometimes
you’ll even see the heart rate go up because
the central nervous system says, “Oh, cardiac
output is falling, we have to increase the
heart rate, we have to increase our ability
to hold on to salt and water and increase
the blood volume and use the Starling law
to increase the contractility of the heart.”
Again, unfortunately, it’s not the right
setting for that and this leads to overfilling
of the circulation, increased pressures in
the circulation and increased fluid getting
out into the lungs and into the tissues.
So, the central factor in heart failure, of
course, is depression of the heart muscle
at least for systolic heart failure. But also,
in diastolic heart failure, the heart is supposed
to actively relax and there’s also depression
of that, but the commonest form of heart failure,
as you’ve seen in the previous slide, was
systolic and it is usually because there’s
been some injury to the heart muscle, most
commonly from ischemic or coronary artery
disease with heart attacks. And again, we’ve
talked about the compensatory mechanisms,
here are the compensatory mechanisms listed.
First of all, they're initiated by the central
nervous system. One of them is a signal that’s
sent to the kidneys and that the kidney actually
does on its own. The kidney is the regulator
of the blood pressure in the body, it sees
a drop in blood pressure, a drop in cardiac
output and it releases compounds in something
called the renin-angiotensin system which
holds on to salt and water. It's hormones
that actively tell the kidney, “Hey, don’t
pee out… sodium and water, hold on to
it because the circulatory system needs some
There are also hormones that are released
from the pituitary, so called anti-diuretic
hormone, which tells the kidney, “Hey, hold
on to water, don’t let the water go out
in the urine.” In addition, you also will
have activation of the sympathetic nervous
system which is part of the flight or fight
system. This sends adrenaline to the heart
muscle to try and get it to contract more
vigorously and it also clamps down a little
bit on the periphery in an attempt to shrink
the volume that the heart has to pump into.
All of these compensatory mechanisms you can
see, they work great if we’re talking about
dehydration or hemorrhage, but they work in
the wrong direction when the patient already
has a depressed left ventricle.
The other thing that happens is that the heart
muscle remodels, it reconstructs itself, if
you will. You can see in this diagram on the
left, there’s one form of remodeling - left
ventricular hypertrophy where the ventricle
markedly thickens. For example, with aortic
stenosis, as we talked about with the patient
in the last lecture. On the other side is
the sort of thing you see in a cardiomyopathy.
The heart dilates, thickens a little bit,
but predominantly what it does is it dilates.
And you’ve all heard someone say, “Oh,
so and so is in trouble, they have a ‘big
heart’.” That’s because the heart’s
dilated. That’s often the final stage of
heart failure when the heart has exhausted
all of its other compensatory mechanisms to
get the cardiac output up, then you start to
see this dilatation of the left ventricle.
Now, again, we talked about the different