Welcome back. In this talk, we're going to cover valvular
And there are a lot of different ways that we can have the
heart valves affected,
causing either stenosis or regurgitation.
And when the valves don't work to limit flow in one
direction or another,
then we have potential secondary complications that can be
This is just showing you the heart pumping.
It's a very vigorously pumping heart, just going from the
left to the right on your screen.
We have blood that comes in the right atrium,
goes across the tricuspid valve into the right ventricle,
the right ventricle squeezes it out through the pulmonic
valve, going to the lungs.
Blood returns oxygenated from the lungs to the left atrium.
And then, from the left atrium across the mitral valve, into
the left ventricle
which squeezes it out through the aortic valve.
We're going to talk about each of these valves and the
pathologies that can occur with them.
And there are certain valves that are more predisposed to
disease, such as the mitral valve.
Valves that are relatively uncommonly affected, the pulmonic
And we'll talk about, again, insufficiency and stenosis.
So, stenosis, what is that? Well, it's basically the valve
doesn't open completely.
It becomes stiff usually due to excess connective tissue or
And when that happens, as is shown here with aortic valve,
you have a valve that doesn't open completely, and that
impedes forward flow,
giving you a jet stream going out, you see across the aortic
valve into the aorta,
but it also means that the left ventricle behind it has to
work that much harder.
In insufficiency, the valve is incompetent.
Again, we're looking at the aortic valve, it's not closing
So, when you have a filling during diastole, that valve
Instead, the blood is regurgitating back from the aorta into
the left ventricle.
This is not going to necessarily require the heart to
but there is going to be a volume overload.
We are basically dumping contents of the left ventricle
recurrently back into the left ventricle.
And over time, that can also be a cause of heart failure.
Also, keep in mind that if you have insufficiency that's
we're not pumping all that blood out to the rest of the
So, you may have relative hypotension and malperfusion of
all of the organs throughout the body.
Functional regurgitation can occur for a variety of reasons,
and it can stem from, in this particular case, we're going
to look at the mitral valve,
so the atrial ventricular valve, the mitral valve,
and the regurgitation can occur as a result of incompetence
or defect in a number of support structures.
So, the annulus, the ring of fibrous connective tissue that
holds the valve leaflets,
needs to be competent. It can't be dilated. It can't be too
It needs to maintain its normal circumference in order to
keep the valve leaflets
so that they can appropriately coapt, close against one
The valve leaflets need to be intact. If there's a hole in
them, if the valve is destroyed,
if the valve is too fibrotic, the valve won't close
and may become stenotic or regurgitant.
The chordae tendineae of the atrioventricular valves are
also very important.
They connect the valve leaflets to the underlying papillary
and they need to be of the appropriate length and tensile
The papillary muscles connected to the left ventricular wall
are also important.
They need to contract appropriately and relax appropriately
to allow the valve to open and close respectively.
And the ventricular wall, the configuration, the geometry of
that ventricular wall,
has also got to be about right. Otherwise, as we'll see if
the valve - if the ventricular wall dilates,
then we pull those papillary muscles apart which pull on the
and the valve leaflet won't close. So, the ventricular wall
also makes a difference.
So, all of these structures are important for the function
of the atrioventricular valves.
Now, we've been talking about the mitral valve in
but if you just shift over to the right, the tricuspid valve
has all the same requirements
in order for it to maintain its normal valvular structure
Here's just an example of now where the chamber dilates. The
Everything else is fine. The annulus is fine, the leaflets
are fine, the chordae is fine,
the papillary muscles are actually okay, but the chamber now
has a different geometry,
and that dilation pulls the papillary muscles down and
And now, the leaflets can't coapt. And so, that will lead to
It's a structurally normal valve but can't properly close.
So, things like ischemic heart disease can very easily cause
And as we'll talk about when there's mitral insufficiency,
blood is now going to be squeezed primarily through the
through the open valve, into the left atrium, and that
pressure then translates back up into the lungs.
We have functional regurgitation with a completely normal
valve in this case.
So, the clinical consequences clearly depend on which valve
And we can see that we're jumping around to the different
but tricuspid valve insufficiency has a different kind of
consequence versus mitral insufficiency.
Tricuspid is going to affect the venous circulation
Mitral incompetency is going to affect the pulmonary venous
circulation rather than the systemic.
Aortic stenosis versus pulmonic stenosis will have effects
that you can, in your own mind, think through.
So, the nature of the valve or which valve is involved is
The degree of impairment, clearly, has an impact as well.
So, if you have severe stenosis such as that, then that's
going to be much more of an effect
than if it's a relatively minor calcification and stenosis
And then, the tempo of the disease onset.
So, if it's very rapid, say, an infective endocarditis
where you have a sudden destruction of the aortic valve,
that's going to lead to acute massive rapidly fatal
However, if things go relatively slowly, such as mitral -
rheumatic mitral disease,
it's a slow degeneration, takes months to years, even
and for long periods of time, there will be adaptation of
the underlying myocardium,
and the other structures that will allow it to be well
tolerated for extended periods until we reach,
at some point, a tipping point where its symptomatology
And then, it also depends on how well the heart can respond.
So, if you have a very good circulation and no
you can tolerate valvular stenosis for longer.
You can have hypertrophy of the myocytes
because you're providing adequate nutrition, adequate
So, with pressure overload in a valvular stenosis case, you
get concentric hypertrophy.
And if that goes slowly enough in a heart that has really
good coronary arteries,
you can compensate for a long, long period of time.
And conversely, if you have ischemic heart disease,
you may not tolerate a valvular stenosis that well.
Valvular insufficiency, in another hand, gives you a volume
which tends to give you what's called eccentric hypertrophy.
And the difference between concentric hypertrophy versus
has to do with the alignment of the sarcomeres within the
Concentric hypertrophy means that, in fact, you have
increase in wall thickness.
Eccentric hypertrophy means you have increase
in the diameter of the ventricle
Both, over time, will lead to heart failure.
But it's important to note stenosis leading to pressure
and valvular insufficiently leaving - leading to volume
can have different kind of adaptation consequences for the