0:00

Okay moving on to case number five.

0:04

This is a 57 year old man.

0:08

Who has shortness of breath?

0:10

And to stack distended neck fans.

0:15

I'm showing you.

0:17

the four chamber

0:19

and mid ventricular short axis in a

0:23

series

0:24

that is steady state free procession.

0:27

synonym

0:29

from a cardiac MRI

0:32

and see if you can identify the

0:36

abnormalities

0:38

on these two series

0:49

Okay. Well we can start.

0:51

With the easy findings the patient has small bilateral

0:54

prolifusions right greater than

0:57

left.

0:58

We don't see anything in terms of opacities and

1:01

the lungs except for maybe a little bit of atelectasis in

1:04

the right one base.

1:06

and the primary abnormalities that

1:09

were

1:11

Looking to describe in this case involve the heart

1:14

and the contraction.

1:17

of the ventricles

1:21

we can look at the the chambers of the heart and I'll tell

1:24

you the right atrium looks a little bit prominent left atrium.

1:27

Although not a easy to appreciate Years also

1:30

a little bit big.

1:33

The ventricular chamber of volumes don't look abnormally increased.

1:39

the Striking finding

1:42

is not a systolic finding but a diastole.

1:47

and it's the

1:49

To and fro motion we refer

1:52

to it as the acceptable bounce.

1:56

Of the interventricular septum. So it's a diastolic.

2:01

septal bounce

2:03

and you can see it on both the

2:06

four chamber and short axis fuse

2:09

during diastole

2:11

There's this high frequency to and for emotion.

2:14

And what does this tell us?

2:17

This tell us tells us that during diastole. There

2:20

is a ventricular filling dependence.

2:23

So there's an interdependence between

2:26

the ventricles so that as one ventricle say

2:29

the left ventricle starts to fill.

2:32

Pressure in it builds up and it pushes the

2:35

septum very quickly towards the right ventricle. Well

2:38

the right ventricle.

2:40

Also is filling and as the pressure builds there.

2:43

It pushes the septum back towards the left and this

2:46

is all happening very quickly.

2:48

This ventricular interdependence tells you.

2:53

That it's very likely that the pericardium.

2:57

Is somehow constraining?

2:59

The ventricle

3:01

And this is these two Sinai movies

3:04

are virtually diagnostic of the pathology

3:07

here, which is constrictive pericarditis.

3:12

Now these patients present with

3:15

symptoms of poor.

3:20

Cardiac output and impaired cardiac

3:24

films and that's because of this ventricular Independence

3:27

where the pericardium basically acts like

3:30

Saran wrap around the ventricles and it forces them

3:33

to behave in a manner in which the filling is

3:36

dependent between them.

3:38

the

3:40

the pathology in pericard constricted pericarditis

3:43

is that you have an acute usually an

3:46

acute insult causing pericarditis the

3:49

two membranes of visceral and parietal pericardium

3:52

become kind of sticky they fuse together.

3:56

And form this Saran Wrap like envelope around

4:00

the the ventricles.

4:04

The pathophysiology as I

4:07

just described gives a presentation that's very

4:10

similar to restrictive cardiomyopathy which

4:13

is when the ventricles just don't fill very well due to

4:17

a number of other causes such as infiltrative

4:20

cardiomyopathies sarcoid hypertrophic cardiomyopathy

4:25

amyloid the ventricles. Just don't feel well.

4:29

but for

4:30

the same reasons we see

4:34

impaired filling in a clinical scenario distended

4:37

neck themes peripheral edema that

4:40

sort of thing. It's very important to distinguish constrictive pericarditis

4:43

from restrictive cardiomyopathy because

4:47

this is treated surgically and restrictive

4:50

cardiomyopathy is treated medically and

4:53

you don't want to take a person

4:56

with restrictive party myopathy to

4:58

the operating room

5:02

so the pathophysiology is as I described the pericardium

5:05

becomes rigid because of a prior inflammatory

5:08

insult.

5:09

It becomes fibrotic and causes this

5:12

ventricular interdependence and decreases the stroke volume.

5:16

The etiologies are multiple and

5:20

many of them are shown here with various.

5:24

likelihoods

5:28

at cardiac MRI we look for a

5:31

number of different features to help

5:34

us make this diagnosis in general.

5:37

We like to see a pericardium that looks at normally thinking greater

5:40

than three millimeters.

5:43

Because of the poor filling of the

5:46

ventricles you get dilated.

5:49

vena cava dilated Atria

5:53

and dilated hepatic names and

5:59

as I said the left atrium not as well see here.

6:03

You also have often a tubular shape to

6:06

the right ventricle. We didn't see that in our

6:09

index case.

6:11

in addition to the sigmoid bounce

6:17

you see a sigmoid.

6:19

I'm sorry, in addition to the septal bounce. You see

6:22

a sigmoid configuration of the interventricular septum,

6:25

but you can appreciate there's this s shape configuration

6:28

of the septum. That's a

6:31

common finding as well. And this tends to be an accurate

6:34

way for making the diagnosis. Now. I'm

6:37

going to show you a companion case that's going to

6:41

show an alternate.

6:44

presentation at cardiac MRI

6:47

This is a 64 year old female who had severe rheumatoid

6:50

arthritis and a three-week history of this meal

6:53

on exertion.

6:54

She had leg swelling and a five

6:57

pound weight gain.

6:58

Echo should a large pericardial effusion with diastolic

7:01

white atrial collapse and that's a a somewhat

7:05

dire finding when you

7:08

see the right atrium collapse during diastole. That's

7:11

an indicator of pericardial tamponade. So

7:14

this patient went on to get a pericardiocentesis 300

7:17

cc's of a straw color fluid was

7:20

aspirated.

7:21

Normal fluid as I mentioned earlier is about

7:24

10 to 50 cc's in the pericardium.

7:28

The pericardiocentesis found inflammatory cells and

7:31

a negative culture.

7:33

Now her are a pressure right

7:36

atrial pressure remained elevated even after the

7:39

pericardiocentesis and she had this cardiac

7:42

MRI.

7:44

And if you look at this cardiac Mr. In the

7:47

same.

7:49

Cardiac axes that we just saw four chamber and

7:52

mid ventricular short axis. We can see the pericardial

7:55

effusion.

7:58

But we also see a sigmoid configuration of the interventricular

8:01

septum and a diastolic septal

8:04

bounce. So

8:07

what is this what's going on here? We have a pericardial effusion. So

8:10

we know the visceral and parietal pericardium are

8:13

not fused.

8:14

But the the pathophysiology I shouldn't

8:17

say that they say the the cardiac physiology

8:20

the contractile physiology is

8:23

identical to that which we would just saw in constrictive

8:26

pericarditis. And this is a uncommon variant

8:30

of constrictive pericarditis. This is called

8:33

effusive constrictive pericarditis. It's

8:36

an atypical form of constricted paraparaditis where

8:39

the visceral pericardium is fibrotic and

8:42

an effusion is present and so the visceral pericardium

8:45

itself scars down and becomes

8:48

the Saran wrap. It doesn't have

8:51

to fuse to the parietal pericardium. You get the

8:54

same outcome from hemodynamics standpoint.

8:58

The CMR findings are otherwise the same.