0:00

All right, everyone. We're gonna shift gears a

0:03

little bit on the pulmonary hypertension. I'm gonna

0:06

try talking about something that is not commonly taught. We're

0:09

going to actually look at the contrast Dynamics on a

0:12

CT, especially a CT pulmonary angiogram and

0:15

how can that help you deduce what's

0:18

going on with the patient's cardiopulmonary physiologic status?

0:22

The Dynamics of the contrast floor. I'll give you a

0:25

lot of information. So we're going to look at two really

0:28

common ones one is called transient Interruption a

0:31

contrast and the other is when you see

0:34

IVC contrast hyperdense contrast reflux into

0:37

the inferior, vena cava and hepatic veins

0:40

will also look at some of the exceptions to these rules

0:43

to

0:44

okay. So again normal pulmonary

0:47

CTA. This is what we would like to see Transit Interruption

0:51

of contrast is very common.

0:54

There should be no.

0:56

Significant or no flow of hyperdense contrast

0:59

into the infrarian cave of this reflex.

1:02

Anatomically you want to see the interventricular septum convexing

1:05

towards the right ventricle. You want

1:08

the right ventricular wall into your wall,

1:11

which is very thin paper thin no more than four millimeters

1:14

and the pulmonary artery diameter.

1:17

If you're taking a test.

1:20

It's three centimeters.

1:22

I think it's probably better to kind of use a higher

1:25

number, but definitely 3.5 or

1:28

over. It's probably not going to be normal.

1:31

Nice way to do it though. If you don't feel like measuring that's

1:34

fine with me the ascending aorta and the

1:37

pulmonary artery really should be of the same diameter so

1:40

you can kind of eyeball.

1:43

All right brief Interruption a contrast. That's

1:46

what transient Interruption of contrast is.

1:49

This Uno pastified blood comes up from the inferior vena

1:52

cava when you take a deep breath in

1:55

this huge negative pressure in the thoracic cavity

1:58

just sucks the blood right on up

2:01

from the inferior vena cava now, there's no contrast coming

2:04

in there. So it's going to cause an interruption and cause

2:07

the contrast density to descend. The hounds

2:10

field unit numbers will be sent.

2:12

It's often seen in the setting of

2:15

normal cardiac output and normal right

2:18

heart and arterial pressures because we

2:21

have all this high flow IB

2:24

contrast coming in the security of an achieve.

2:27

Filling up the right agent.

2:29

Now you take a breath in and you can also take in all of

2:32

this unopathified IVC blood mixing it

2:35

in that is a very high functioning

2:38

system. So

2:41

it's indicative of good Ford flow and it's a variable

2:44

amount of change in density because there's a lot of variables that

2:47

affect it.

2:49

So how do you diagnose transient Interruption of contrast on

2:52

a CTA? What you're going to be seeing is there's going to be this Interruption

2:55

of the contrast bolus column. You'll

2:58

see the unapasified blood coming into the

3:01

right atrium and the right ventricle. The pulmonary arteries would

3:04

be well opacified.

3:06

Then on the later images as you go up the

3:09

pulmonary arteries will now have a decreased density

3:12

which could possibly look like an embolus. What's the

3:15

key they're unapacified bilaterally at

3:18

the same level and there is no vascular

3:21

expansion.

3:23

That's key. No vascular expansion same level and

3:26

then you look in the proceeding earlier images. There's the

3:29

end of pacified blood.

3:31

Why isn't this a late contrast bolus because there will

3:34

still be hyperdense contrast coming into

3:37

the superior vena cava.

3:39

So you'll see that and know it's not a late bolus.

3:42

It is simply an interruption of the contrast column.

3:47

This is what it looks like on a pacified blood

3:50

coming into the right atrium. Then in The ventricle notice

3:53

the pulmonary arteries are well opacified.

3:56

This unapacified Blood fills the right ventricle and

3:59

then starts to fill the pulmonary arteries.

4:02

So you look there and if all you're looking at

4:05

is the pulmonary arteries. Whoa, that could be embolite. Wait

4:08

a minute all the same level. No expansion.

4:12

You look in the earlier images and you see the unaplacified blood

4:15

coming up.

4:16

Eventually, it goes through the whole circuit and

4:19

then it is in the aorta. Why isn't this

4:22

a late contrast bolus? Because there's still

4:25

hyperdense contrast coming in the superior vena cava.

4:29

This is a ultrasound showing the inferior vena

4:32

cava transverse Dimension. This is an expiration. You

4:35

can do this on yourself. What happens

4:38

when you take a deep breath in well, the inferior vena cava

4:41

just collapse is just like that. It just

4:44

gets sucked right up in to the right atrium.

4:48

As long as the pressures are normal, and

4:51

there's good forward flow.

4:53

So this is a patient takes breath in on a

4:56

pacify blood comes up from the inferior vena cava and then

4:59

fills in the pulmonary arteries on a pacified at

5:02

the same levels. No expansion.

5:05

It's indicative of normal right heart pressures, and it's

5:08

very common, although variable in the

5:11

amount of density.

5:13

So I usually say, you

5:16

know in that setting where you see this on a

5:19

pacified transient eruption of contrast that there's unlikely to

5:22

be a cardio pulmonary

5:25

symptomatic what I mean by that is a cute heart

5:28

string kind of thing and shortness of breath present, although

5:31

sometimes, you know, you really can't tell

5:34

for sure but the physiology favors that

5:37

it's unlikely to be present.

5:39

This this patient actually was dictated as

5:42

having bilateral pulmonary employ.

5:44

What was it?

5:45

It was it was transient eruption of contrast. They

5:48

got started in heparin.

5:50

And then we did a redid it the next

5:53

day and there was nothing there.

5:56

so

5:57

how is that different from contrast reflux?

6:00

Contrast reflux is when you have this continuous column

6:03

of hyper dense, not discontinuous continuous calm

6:06

of hyperdense reflux, and it's often seen in

6:09

the setting of tricuspid regurgitation elevated right

6:12

heart pressures or a reduced cardiac

6:15

output.

6:16

Okay in this setting right when

6:19

they take a breath in.

6:21

That on our pacified blood is not coming up rather. The

6:24

contrast is asked to go wait in the inferior vena

6:27

cava and hepatic veins like a waiting room because

6:30

forward flow is impaired.

6:34

So this patient has hypertense contrast

6:37

in the dilated Superior Cava or inferior

6:40

vena. Cava, I'm sorry and you can see the right

6:43

atriums markedly enlarged the right ventricles

6:46

large. They're straightening the engine particular septum. There's hypertrophy of

6:50

the right ventricle. This is all pulmonary hypertension with tricuspid regurgitation.

6:53

You will not see transient Interruption

6:57

of contrast with this patient there forward

7:00

flow is reduced. The pressures are

7:03

high. They got tricuspid regurgitation and the contrast is

7:06

asked to wait in the inferior vena cava until

7:09

it can be a combinated.

7:12

What are some causes pericardium especially constrictive

7:15

pericardium or cardiac tamponade?

7:18

pulmonary artery either from embolite with

7:21

widespread vasoconstriction and right heart strain or

7:25

cardiac myocardial failure septal defects sensor thing

7:29

So this is a patient again pulmonary artery hypertension hypertense contrast

7:32

in the inferior vena cava and hepatic

7:35

veins ripentricular hypertrophy straightening an

7:38

interventricular septum pressures are elevated here.

7:41

This one is a little different. This is

7:44

actually due the contrast reflux to cardiomyopathy. They

7:48

have an injection fraction of approximately 10 to 15

7:51

percent.

7:52

Most of the time with cardiac failure you will not see

7:55

straightening of the interventricular septum or bowing of

7:58

the interatrial septum.

8:00

the other Clues and it's not in books, but

8:03

you won't see a pacification of the aorta

8:06

or much pacification left ventricle that

8:09

tells you the flow is very slow.

8:11

The second thing is look at this. I mean you can

8:14

see the popular muscles the moderator band you can

8:17

see the trabeculation. It's because you see it.

8:20

So well, there's not a lot of motion artifact because the heart

8:24

isn't really moving very much.

8:28

IBC reflux in the setting of constrictive pericardial disease

8:31

straightening of the right anterior ventricular wall

8:35

hyperdense contrast reflex

8:38

There is a rough correlation with the degree

8:41

of reflux. It's there a lot of confounding variables

8:44

though. But if you see the IBC reflux

8:47

extending well below the diaphragm that

8:50

usually goes along with pulmonary pressures of about 40 which

8:53

is moderate and if you

8:56

see straightening of the interventricular septum, this one's bit

8:59

better that usually correlates with severe

9:02

pressure elevation.

9:05

Average 67 in one study, but that's usually fairly elevated

9:08

pressures.

9:10

This patient has contrast reflux to the level

9:13

of the diaphragm. They had no interventricular septal

9:16

straightening the right ventricles normal their

9:19

pulmonary pressures were elevated to 35

9:22

as opposed to this patient chronic thrombolic disease

9:25

their pressures were 70 you can see there's a

9:28

great deal reflux of hyperdense contrast in

9:31

their straightening of intrudicular septum. You just say, this is

9:34

Advanced pulmonary hypertension.

9:37

now

9:38

When you see so much dilation and you can

9:41

see this IVC contrast. There's a little right ventricular

9:44

hypertrophy straightening an interventricular septum. Right atrium

9:47

is large whenever the right atrium dilates. It's

9:50

usually tricuspid regurgitation in this

9:53

case because the right ventricle was a little hypertrophy that suggests

9:56

something chronic. This is what the patient had and initially

9:59

say. Oh my God that looks like a large endless. Well, it's

10:02

it's not really there's a

10:05

vessel in it. There's a little bit of enhancement there

10:08

was vasoconstriction to the more peripheral

10:11

pulmonary arteries.

10:13

And it turned out to be a intimal sarcoma.

10:18

But why I show it is because these changes of

10:21

transient Interruption of contrast.

10:23

And inferior being a cable reflex our

10:26

Dynamic and can change when a

10:29

patient's cardiopulmonary physiology also changes.

10:33

So once they removed the intimal sarcoma, look what

10:36

the heart is doing now, there's no longer

10:39

interventricular straightening. There's transient Interruption

10:42

of contrast coming up.

10:44

From the inferior vena cava indicating the

10:47

forward flow has improved.

10:49

So, you know, it's a dynamic

10:52

process and you can use this ancillary information

10:55

to help kind of tighten up your reports if you

10:58

so desire.

11:00

Now what are the exceptions cardiovascular capacity

11:03

IVC flow rate and the flow rates too slow or

11:06

the cardiovascular capacities not matched with

11:09

the amount of contrast. Then you can see either

11:12

of these for instance. I want you to

11:15

consider very large person or maybe a pregnant patient

11:18

who's got a very large cardiovascular capacity

11:21

what you need to increase the flow rate and

11:24

contrast volume.

11:26

Otherwise, you'll get transient Interruption of contrast

11:29

pretty commonly, which we tend to see.

11:32

Small cardiovascular capacity, you know, maybe a petite

11:35

person. Well, if you give the same amount

11:38

you just gave to the last person you might see reflux of

11:41

contrast but no straightening of the internship

11:44

is septum or heart dilation. You just overflowed the

11:47

kettle

11:49

because remember one size doesn't fit all

11:51

for Pediatric patients. We give contrast

11:54

volume based on weight. Well at

11:57

the age of 18, we stop doing it and give

12:00

them all the same. Well that doesn't you know one size doesn't

12:03

fit all

12:04

So some people have a very large kettle which we don't completely fill

12:07

with contrast and you can see transient Interruption of

12:10

contrast and other people have small Kettle where

12:13

we overflow the contrast.

12:16

So this is a pregnant patient. You can see there's severe transient

12:19

Interruption of contrast here.

12:23

It's just because they got a large cardiovascular capacity. Their

12:26

heart is pumping it out very efficiently and

12:29

they suck up all that inferior vena cable

12:32

on a pacified blood.

12:34

As opposed to this person who you know,

12:37

it's actually a small heart. It's a small cardiovascular capacity

12:40

it overflows a kettle a bit

12:43

and you get reflux, but

12:46

So try anything Interruption contrast very common flow

12:49

phenomenon, very common and usually seen

12:52

in the setting of normal pressures and good forward flow reflux

12:55

of hyperdense contrast. You want to take a close look at

12:58

the heart pericardium and the pulmonary arteries.

13:02

The exceptions are with these the patient has a very large

13:05

cardiovascular capacity or a very small.

13:10

With that I thank you very much.