Now, let us take a look at aortic dissection.
Now, we have completed peripheral vascular
disease, we have walked through venous insufficiency
and we also talked about peripheral arterial
disease. Let us take a look at aortic dissection.
What does that mean to you? It means that
literally the aortic, now what I'd like for you
to do is come out of the left ventricle, come
out of the aortic route, come through the
ascending aorta, the arch and then thoracic, stope
there, please. Why? Because clinically speaking
there are two major dissections, these are called Stanfords.
And it is important that you know the exact location
of that aortic dissection. I had you stop
at thoracic aorta. Are you picturing this?
And the two major components would be the ascending part of the
aorta or the thoracic aorta. Are you picturing
it? Good. These are the two places where, if
the aortic dissection was to take place, you
will then call it either Stanford type A,
A for ascending aorta or Stanford type B as
in thoracic aorta, distal aortic dissection. Is that clear?
Now, what are some of the predisposing factors
for developing an aortic dissection? Well let's take a look.
It is an emergency, stabbing back pain because there
is an actual dissection.
The pressure dissected right through the aorta
during the dissection, the lining of the aorta,
the intima tears and so now the intimate most
is the innermost, the middle portion is the
media, m and m. Those are the two layers that
I want you to pay attention to specifically.
Those are going to tear and when they do so
this is not a good situation. You might have
blood which then does what? Well they'll rob the blood from the
subclavian, it will lead the blood perhaps
back proximally into the pericardial cavity,
may result in cardiac tamponade. Sudden
rush of blood, isn’t this cardiac tamponade?
Of course, it is. Is this an emergency? Yes,
it is. What do you want to do? Remove. Surgery
is what you are thinking.
Risk factors include. This should make sense
to you. There is too much blood pressure,
excessive hypertension. Over a period of time,
it might cause complete rupture and dissection.
Marfan, you pay attention to "f" in Marfan.
Who is your patient with Marfan? Think about
Abraham Lincoln as an example of a typical
patient with Marfan. Tall, lanky, you have
your fingers that are quite elongated like
a spider, arachnodactyly. May be visual disturbance because
the f in Marfan is coding for the fibrillin gene
with chromosome F-15 which is then coding
for what part of your tissue? Elastin. So
this elastic tissue is not present, suspends
your ligament that places or holds the lens
in place, not there. Dislocation, subluxation of the lens.
So that is your patient with Marfan.
Go into aorta, what happens? Either the
is thoracic aorta or the ascending portion
in which the elastic tissue is not present
what happens? You are now prone to a dissection.
But before that, what then happens? A cystic
medionecrosis. It mean to say that the media
which is what portion of the blood vessel?
The middle portion of the aorta specifically,
will undergo necrosis in which you will form
a cyst like a cavity. If that is not properly
identified and corrected you are worried about
a dissection, which was which again? Stanford type A.
A is an ascending. Stanford type B would be the
thoracic aorta dissection.
Atherosclerosis risk factors. Ehlers-Danlos.
What do you know about this? Deficiency of
collagen depending as to which type and then
coarctation of the aorta. How much pressure
is there in coarctation of aorta? "Well Dr.
Raj, you didn’t tell me where." I understand that.
If it is distal you don’t have enough
pressure, but proximally what you have done?
You have introduced a resistor in a series.
What happens to the pressure proximal
to the resistor? Increased. That is where
the problem is, Too much pressure there, are you
prone to dissection? Yes, you are.