0:00

All right, everyone. Well, that was the block

0:03

of pulmonary hypertension, but

0:06

There's a lot of good stuff in there, but through a lot of other things

0:09

that you will see how well some of this stuck.

0:13

Form an assessment time is fun time, right? No grades.

0:16

This is just for fun to see

0:19

if you know.

0:20

We were pretty effective at getting this information to you.

0:23

So we're going to kind of go through a few questions a few

0:26

cases.

0:27

Of the information that we covered and feel free

0:30

to pause this during the

0:33

questions. Okay. Most of all have fun.

0:37

All right. So let's go with the first one clinical manifestations associated

0:40

with pulmonary artery hypertension the pre-capillary

0:43

etiology include all the

0:46

following except you can take a look at those.

0:49

discian exertion bilateral or extremity

0:52

pinning edema

0:54

pulmonary edema or distended elevated jvp

0:59

This is the pulmonary arterial hypertension. And remember

1:02

what the definition of the arterial part was. It was the pre-capillary.

1:06

So pause if you want, so I'm going to move on.

1:09

The answer was pulmonary edema. So the pre-capillary

1:12

cause is Right heart failure

1:15

symptoms that's elevated jvp. That's pitting edema

1:18

dismionic exertion right ventricular

1:21

heave a BMP could be elevated, but there

1:24

is no pulmonary edema.

1:27

No pulmonary demon Paul if there's pulmonary edema or

1:30

evidence of congestive heart failure. Then you start also considering

1:33

the post capillary cause and you need

1:36

to consider the post capillary cause because if you treat these

1:39

patients with pulmonary,

1:42

Hypertension from post capillary cause with pulmonary

1:45

vasodilators a lot of them can go into

1:48

acute congestive heart failure or even

1:51

right ventricular failure.

1:53

Because you've increased the flow and the pulmonary

1:56

artery, but it's the opposite side of the capillary

1:59

bed. That's blocking it and hasn't been addressed. So that

2:02

just acutely causes the pulmonary.

2:05

Um right ventricle to fail.

2:10

Okay, all of the following.

2:14

Imaging findings are associated with moderate to severe pulmonary hypertension.

2:19

except I know these exceptions are never

2:22

fun, but

2:23

Here we are right normal, right

2:26

atrial chamber size pulmonary artery size greater than

2:29

3 centimeters or larger than the a sending aorta or more specifically

2:32

greater than 3.4 centimeters right ventricular

2:35

anterior wall greater than 4 millimeters reflux

2:38

of hypertens contrast into the

2:41

dilated IVC and hepatic veins.

2:44

So all of these Imaging findings are associated

2:47

with monitors severe pulmonary hypertension, except one of them.

2:50

Okay positive if you want because I'm moving on

2:53

well, the answer was the normal right atrial size

2:56

with pulmonary hypertension. The pressures

2:59

are going to elevate in the right side of the heart the right

3:02

ventricle and right atrium will dilate when it dilates there's tricuspic

3:05

regurgitation which causes further dilation and

3:08

more tricuspid which causes further dilation

3:11

and then reflux of hyper dense contrast into

3:14

the inferior vena cava and hepatic veins and over

3:17

time. You'll get right ventricular hypertrophy.

3:22

question 3

3:23

the most relevant site of obstruction to

3:26

identify an Imaging in a patient with pulmonary hypertension is

3:31

you all better get this one, right?

3:33

Pre-capillary capillary post capillary it's not

3:36

important. All of these are treated the same.

3:40

Positive if you want but better not okay. It's

3:43

post capillary right post capillary. And

3:46

that's the one that I mentioned that we treat them

3:49

with pulmonary artery vasodilators. But the obstruction is

3:52

the left ventricular chamber failure mitral

3:55

stenosis pulmonary inclusive disease, whatever

3:58

the cause you can go into a cute pulmonary

4:01

edema and/or right heart failure.

4:05

Okay.

4:07

So this is an example of patient pulmonary hypertension big

4:10

main pulmonary artery low bar pulmonary arteries

4:13

are big right atriums big one Lefty trims

4:16

big too.

4:17

And patient has some evidence of cephalization. Remember

4:20

cephalization is a sign of chronic pulmonary venous

4:23

hypertension.

4:24

So this would be a patient. You want to be very careful about giving

4:27

pulmonary artery vasodilators to IE.

4:30

Don't do it. You got to treat the

4:33

heart.

4:34

side the post capillary side

4:36

another patient with mitral stenosis cephalization

4:39

vessels are dilated up high

4:42

constricted low. That's how you differentiate it from

4:45

shunt vascularity. It's one way.

4:47

Main pulmonary arteries big the left atrium is definitely enlarged

4:50

here. So is the right ventricle so

4:53

Pulmonary artery vasodilators. Probably not

4:56

a good idea here.

4:58

replace the mitral valve

5:01

All right question 4 35 year old female with a

5:04

new diagnosis of pulmonary artery hypertension well around the radiologist

5:07

would hopefully pick this up on the radiograph mean pulmonarities big.

5:11

Well, right ventricle is very large. What do you see with

5:14

the pulmonary vessels? Well, these are large.

5:17

You know left atrium looks okay left ventricle looks

5:20

okay, but this is large and then as you go down

5:23

to the lower, these are the same size.

5:26

So as opposed to cephalization these vessels are the

5:29

same size.

5:31

So what would likely be the

5:34

etiology for this patient's pulmonary hypertension just

5:37

based on the radiograph.

5:39

It's a chronic hypoxia from diffuse lung disease

5:42

left to right into cardiac shunt mitral stenosis.

5:46

No, identifiable etiology scene get a

5:49

pulmonary CTA.

5:51

So positive if you want.

5:53

But in this case, it's a wonderful example of an

5:56

intercardiac shunt in this case an atrial septal

5:59

defect.

6:00

Long-standing shunt vascularity increase

6:03

flow. It actually causes

6:06

the pulmonary arteries to dilate and then eventually the pressures

6:09

increase

6:12

All right.

6:15

Is patient has severe pulmonary artery hypertension. They

6:18

have right ventricular hypertrophy here pretty severe.

6:22

now

6:24

notice this

6:25

the descending thoracic aorta looks narrow.

6:29

Are small small diameter? Why well?

6:33

Right ventricular Percy, right atrial dilation small

6:36

caliber thresh. Aorta. What's the etiology here? Well, it's

6:39

right there. There's a large membranous defect

6:42

in the interventricular septum right

6:45

here large left to right shunt causes

6:48

the pulmonary artery hypertension also reduces

6:51

the flow to the aorta, so it doesn't tend to

6:54

dilate to a normal size.

6:58

Severe pulmonary hypertension. This is a patient with

7:01

voice severe pulmonary hypertens is very Advanced looking see

7:04

the low bar arteries, but there's also pulmonary artery calcification remember

7:09

Are to intimal calcification to the pulmonary arteries is usually

7:12

seen with systemic pressures and usually is

7:15

that's present with a left to right shunt.

7:19

This patient had a VQ scan. What do you think showed

7:22

because at this point, you know, you're in isomingus physiology.

7:26

That's right. The particles some went to the

7:29

lung in the pulmonary arteries and a lot of them ended up in the brain or

7:32

the kidneys because they went over into the systemic circulation

7:35

through the shunt.

7:39

question five Imaging findings characteristic for

7:42

transient Interruption a contrast

7:45

Which one?

7:46

Decreased the pacification of the pulmonary arteries at different

7:49

levels no contrast in the superior

7:52

vena cava with decreased pulmonary artery opacification.

7:56

reflux of hyperdense contrast into the inferior vena

7:59

cava

8:00

decreased opacification of the pulmonary arteries with

8:03

contrast in the aorta and superior

8:06

vena cava

8:08

So pause this if we want.

8:12

It's actually decreased opacification of the pulmonary arteries

8:15

at the same level. It's got to be the same level not different

8:18

levels.

8:19

With hyperdense contrast still coming into the

8:22

superior vena cava.

8:24

And of course contrast seen in the aorta that indicates the

8:27

contrast colon was interrupted.

8:30

Usually seeing the setting of good forward flow or normal

8:33

cardiac output or relatively normal pulmonary

8:36

pressures or pressures at least or not

8:39

severely elevated.

8:41

Okay.

8:42

Bonus case I want you to apply this information. This is a real

8:45

case. All right, 40 year old female was referred to

8:48

your Institution for pulmonary artery hypertension workup from

8:51

a community hospital outside Echo demonstrated pulmonary artery

8:54

pressures.

8:55

Of 60 millimeters of mercury, which is

8:58

considered severe.

8:59

So when they arrive they got a CTA.

9:03

This is the CTA.

9:06

60 millimeters Mercury no interventricular septal

9:09

straightening. What's this?

9:13

Bolus of on a pass by contrast coming up from the inferior vena

9:16

cava transient Interruption of contrast. You

9:19

can see the unapasified vessels at the same level without expansion.

9:23

Transient Interruption and contrast is often seen the

9:26

setting of normal forward flow and pressures. There's no

9:29

rape ventricular perpetry to me. This is a normal study.

9:32

And they got the right heart cath, and it

9:35

was completely normal.

9:37

So that was using some contrast Dynamics here to suggest

9:40

that okay. I'm not sure what happened with that Echo. But

9:43

yeah, this patient does not have pulmonary hypertension.

9:47

All right, distinguishing higher lymph nodes

9:50

from chronic mural thrombine include all the following except again. This

9:53

is an accept one.

9:55

This should be straightforward differences in density between

9:58

the higher nodes and the mural thrombi is that helpful presence of

10:01

webs in other pulmonary arteries, that could be

10:04

helpful. I don't know. What do you think lobbyulated inner border

10:07

of the mural thrombi?

10:10

That's what expansion with chronic mural thrombi

10:13

or smooth inner border of the

10:16

higher lymph node.

10:18

Which of these would be helpful? Okay one is

10:21

not one is not.

10:24

Okay, which one?

10:25

Pause it because I'm going on.

10:28

It is the vessel expansion because vessels do not

10:31

expand in the setting of chronic thrombolic disease,

10:34

right? They do not expand the expansion of

10:37

the pulmonary artery in the setting of an embolus is actually

10:40

acute.

10:41

Okay, all the others were useful signs.

10:46

last one

10:47

28 year old female recent diagnosis pulmonary hypertension

10:50

on Reinhardt cast so they got the gold standard and

10:53

wasn't you know, they got the radar cap.

10:57

They had a normal left ventricular function.

10:59

And they had borderline elevated wedge pressures.

11:03

This was the CT that was done. And when you look at it, you

11:06

see these very subtle ground glass nodules very subtle

11:09

ground glass nodules.

11:12

Okay.

11:14

based on the information

11:16

and the Imaging

11:19

what do you think most likely?

11:21

hypersensitivity pneumonitis with chronic hypoxia

11:25

chronic thrombosymbolic disease

11:27

Pulmonary genocusive disease / capillary hemangiomatosis capillary

11:30

hemangiomatosis is very

11:33

much related to pulmonary phenocusive disease.

11:36

And so I put them together.

11:38

Scleroderma and autoimmune diseases. Hmm. Maybe

11:41

has lip maybe he has

11:44

scleroderma.

11:45

With some lip. What do you think?

11:49

added information

11:50

When the patient was started in a pulmonary vasodilators, she

11:53

developed acute congestive heart failure hydrostatic edema.

11:57

Now this that change your answer.

12:00

Is posit think about it? I'm going to

12:04

the answer was actually pulmonary vinoclusive disease

12:07

pulmonary capillary hemangiomatosis. Okay. These

12:10

are five to ten millimeters sort of hemorrhagic nodules in

12:13

the lung. It is a form of post-capillary pulmonary

12:17

hypertension cause this is

12:20

a very difficult one, but that was kind of the keys when

12:23

they gave pulmonary artery vasodilator. She actually got pulmonary

12:26

edema and that indicates. It's probably on

12:29

the post capillary level.

12:32

And remember the wedge pressures may not be elevated with

12:35

pulmonary occlus disease or Kepler hemangiomatosis

12:38

because the vessels that are involved the

12:41

venules are so small.

12:43

And the pulmonary artery catheter reflects the pressures

12:46

it's similar luminal diameters and greater,

12:49

but can miss the smaller.

12:53

So with that I hope you enjoyed the pulmonary artery

12:56

hypertension form an assessment and this block

12:59

of sessions.

13:01

Thank you very much.