0:02

Hello and welcome to Noon Conference hosted by Modality.

0:05

Noon Conference connects the global radiology community through free live

0:09

educational webinars that are accessible for all and is an opportunity to

0:13

learn alongside top radiologists from around the world.

0:17

Today, we are honored to welcome Dr.

0:18

Mark Goslin for a lecture entitled Contrast Dynamics on Chest

0:22

CTA. Dr. Goslin earned his medical degree from McGill

0:25

University and completed his radiology residency at the University of

0:29

Vermont, followed by a fellowship in cardiopulmonary imaging at

0:32

Stanford University. He later joined Oregon Health

0:36

& Science University, where he led the cardiopulmonary imaging division and oversaw

0:40

the radiology program for medical students from 2001 to

0:44

2016. He's currently a faculty member at Vision

0:47

Radiology, where he continues to contribute to the field of medical

0:50

imaging. At the end of his lecture, please join him in a

0:54

Q&A session where he will address questions you may have on today's topic.

0:57

Please remember to use that Q&A feature to submit your questions, so we can get to

1:00

as many as we can before our time is up.

1:03

With that, we're ready to begin today's lecture. Dr.

1:06

Goslin, please take it from here.

1:08

Okay. Thank you very much. Well,

1:12

hi, everyone. Um, I'm Mark, and I'm gonna talk to you a

1:16

little bit of today on a different topic.

1:19

It's gonna be, uh, pulmonary CTAs, and

1:22

oh, we read a lot of them. You know? They're very

1:25

common. But what I'd like to do is kind of take you through

1:29

it from a slightly different perspective, and it's looking at the

1:32

contrast in cardiac dynamics to come up with some

1:36

ancillary kind of physiologic information, as well as kind of look

1:40

at some of the pitfalls that can occur.

1:43

So the objectives today is to go through some of the normal contrast

1:47

dynamics, such as transient interruption of contrast; looking at some

1:51

of the cardiac chamber changes that can occur when things are

1:55

altered, say, with, like, increased pulmonary pressures, myocardial

1:58

failure, tricuspid regurgitation.

2:01

Then we're gonna kind of look at the relationship of poor

2:04

opacification with contrast in the left heart

2:08

chambers and the IVC contrast reflux, and how that

2:12

relates to blood flow velocity and other physiologic

2:15

information. And then we'll finish with the pitfalls of this,

2:19

where there are flow-related artifacts

2:23

that, unfortunately, not uncommonly, are called pulmonary

2:26

emboli, which when there is not.

2:31

So up front, the goals are

2:34

this: taking a look at your CTAs from a

2:38

slightly different perspective, kind of trying to get you out of the

2:42

rut of saying, "Well, there's no opacification in the pulmonary

2:45

arteries, PE." And it's like, well, let's, let's slow down

2:49

here. Let's look at this differently.

2:52

Let's introduce and kind of incorporate looking at the contrast

2:56

dynamics in your reads, following that flow

3:00

to deduce the patient's underlying cardiopulmonary status

3:05

and trying also to reduce the risk of false

3:09

positive PEs. Now, when I go through these

3:12

examples, they're-- all of these concepts are sort of interrelated, 'cause

3:16

when one part goes, the others tend to

3:20

also be present. Okay? Now, looking at contrast

3:24

is not unique. I mean, we teach it with liver imaging,

3:28

right, with the dynamics and enhancement patterns, the kidneys, the

3:32

brain, all of these different things.

3:34

But I don't believe this has really been emphasized as

3:37

much in the typical curricula for CTA.

3:41

Now, let's go through some

3:45

initial patient exams. All right?

3:47

And then we're gonna come back to them as we go through the talk.

3:50

So this is the first one. You can see a CTA

3:54

here. The report was

3:57

indeterminate because of a poor bolus, and you can see there's not

4:01

opacification of some of the pulmonary vessels.

4:05

Another patient, dyspnea with bilateral lower extremity, evaluated for embolus.

4:09

Well, there's poor opacification of the left lower lobe pulmonary

4:13

arteries. There's pleural effusion. There's ascites.

4:17

There's a kind of a dilated heart.

4:20

Contrast, not a lot in the thoracic aorta.

4:23

Hmm. We'll come back to

4:25

it. What about this? You start

4:29

looking at your CTA, and you see the aorta look like this.

4:31

Contrast is coming in. Two questions.

4:35

What can you predict about the blood flow velocity in this patient?

4:40

And two, what do you need to be very, very careful of

4:44

when you start looking for pulmonary embolus in a patient with

4:48

this sort of contrast dynamics?

4:53

Another one, radiology report. There's an acute pulmonary embolus in

4:57

the distal left lobar artery extending into the left

5:00

upper lobe. Hmm.

5:06

Last one, COVID patient, substernal chest pain.

5:09

Radiology read, left lower lobe, multiple

5:13

pulmonary emboli.

5:17

All right.

5:21

So in a normal CTA, what we'd like is, obviously, you

5:25

have your-- the, the technologist puts the cursor on the pulmonary artery,

5:28

right? And then it triggers the, the response once it gets to a certain

5:32

level.

5:34

We'd like to see the contrast seen throughout the pulmonary arteries, the pulmonary

5:37

veins, the left heart, and the thoracic aorta.

5:42

Now, there's a, a phenomenon called transient interruption of contrast,

5:46

and that's actually a normal feature.

5:48

It, it usually is associated with normal pressures and good forward

5:52

flow. The other thing is you don't tend to see a

5:55

continuous contrast reflux into the inferior vena

5:59

cava. All right? I said continuous.Anatomically

6:03

the heart really should have a nice curved

6:06

interventricular septum the right um ventricular

6:10

wall should be curved and thin, less than four millimeters and the

6:14

pulmonary artery, you know, three centimeters, three point one

6:18

I usually don't measure it as much.

6:20

I actually compare it to the ascending aorta at the same level

6:24

because they really should be the same diameter.

6:27

Because remember, people are like snowflakes, right?

6:29

So absolute measurements are just kind of a rule of thumb, but

6:35

this is a normal CTA, and you can see there's normal opacification,

6:38

thoracic aorta, the superior vena cava's got contrast coming

6:42

in, nice rounded, curved right ventricle,

6:45

thin-walled, curved interventricular

6:48

septum, uh opacification, left

6:51

ventricle, and opacification of the pulmonary

6:55

arteries and veins. Fairly, fairly

6:57

reasonable. Little bit of cardiac motion

7:01

artifact is very common, right?

7:05

So let's go a little bit into transient interruption of contrast.

7:08

Again, I, I actually consider this a normal flow

7:11

contrast phenomenon, and it is a brief interruption of

7:15

unopacified blood coming up from the inferior vena cava.

7:18

It occurs when you take a deep breath in.

7:21

Deep breath in pulls in the inferior vena cava and superior vena

7:25

cava, uh blood. But the superior vena cava has contrast coming

7:29

in, but the inferior vena cava is unopacified.

7:32

So when you see it, it usually indicates a normal

7:36

cardiac output and good forward flow, right?

7:39

Because it's able to take all of that contrast coming into the superior

7:42

vena cava, and it can take in all of the

7:46

unopacified blood from the inferior vena cava, mixing it in the right

7:50

atrium, ventri-- right ventricle, and then into the pulmonary

7:54

arteries. Now, there's a variable change in density, and there's a

7:58

lot of confounding variables here. What's the patient's size?

8:01

What was the contrast volume? What's the patient's pulmonary pressures

8:05

and right heart filling pressures?

8:07

And in patients who get severe transient interruption of contrast,

8:11

this can actually interfere with

8:14

interpretation. Okay? So this is a

8:18

person who, on the scanner, this is an expiration.

8:22

Contrast is in. It's already gone through the circuit, and this is right

8:25

after they take a deep breath in. And you can see the unopacified blood from the

8:29

inferior vena cava fills the right heart and then

8:33

eventually the pulmonary arteries.

8:37

So, uh, this is my liver, by the way.

8:40

I was just experimenting as a resident, and this is

8:44

the inferior vena cava during my expiration.

8:47

And then I took a deep breath in, and it, it was amazing.

8:50

It just, pfft, just closed. All the blood just went right into

8:54

my right atrium, and the IVC collapsed.

8:58

So it-- this is a normal sort of

9:01

physiologic process. They did do a

9:04

study,

9:06

um, to follow up on the transient interruption paper, and they did find,

9:10

yeah, this is exactly what's happening.

9:12

When you take a deep breath, there is a caval augmentation

9:16

of blood flow into the right atrium, and the inferior vena cava was

9:20

much greater than the superior vena cava.

9:23

You know, it drains more organs, it has more blood.

9:26

And they actually suggested doing these CTAs without doing these

9:30

deep breaths to kind of reduce the severity

9:34

of the transient interruption of contrast.

9:37

So this is kind of what you're seeing on an, on a CT, um, this

9:41

is right after inspiration. They start scanning, and then you see the

9:45

unopacified blood coming into the right atrium and ventricle.

9:48

It fills it, and then really there's quite a bit of decreased

9:53

density. This is much more of a severe form.

9:56

But look what happens to the pulmonary artery.

9:58

So if you're only looking at the pulmonary arteries, you could

10:01

be, you know, tricked into thinking, "Hey, they're, they're not opacified.

10:05

They were up here. These are bilateral pulmonary

10:08

emboli." When in fact, they, they are

10:10

not. And it can be quite severe.

10:14

So again, when you look at these things, you want to look at it from a different

10:17

perspective. You want to kind of incorporate looking at the contrast

10:21

dynamics as you're interpreting this.

10:24

If you simply are looking at the pulmonary arteries,

10:28

things like this could get called emboli.

10:33

The key here is that it often occurs at the same level, and there's no

10:37

vessel expansion, right? A lot of acute emboli, there's a bit of a vessel

10:41

expansion, but not with transient interruption.

10:45

It's simply the contrast column got interrupted and

10:48

mixed, okay? If you, if you're not sure, look at the

10:52

right heart on the preceding images, and you'll see the unopacified

10:56

blood coming up. And it's not a poor bolus

11:00

because you'll still see that hyperdense contrast coming down the

11:03

superior vena cava. So it's still coming

11:07

down, and there's contrast in the left side heart, but

11:11

there's less opacification of the pulmonary artery in the middle.

11:15

That would be transient interruption of contrast.

11:18

And again, it, it's a variable decrease, but when it's pretty severe,

11:22

it can lead to interpretations such as indeterminate, poor

11:26

bolus, or worse, false positive diagnosis of

11:30

pulmonary embolus. This one is a nice

11:33

example. Bloo-- uh, contrast still coming in the superior vena

11:37

cava. There's contrast, nice opacification

11:41

of the thoracic aorta, but the pulmonary artery density has

11:44

decreased quite a bit. And you look at the preceding, and you can see the right

11:48

ventricle and atrium. This is transient interruption of

11:51

contrast. This unopacified blood simply made its way through the

11:54

circuit, and it got called bilateral pulmonary emboli.

12:00

That's a false positive. So case

12:03

one.What do you think?

12:06

Well, poor bolus is actually incorrect.

12:09

It's not a poor bolus. There's still contrast coming down the superior

12:13

vena cava. So this is classic

12:17

severe transient interruption of contrast.

12:21

Um, it can also be mistakenly called pulmonary emboli.

12:24

That would be unfortunate. So in this

12:28

case, even if you just kind of said, "Well, it's indeterminate because of transient

12:32

interruption of contrast," suggest this, um,

12:36

and I'll give the suggestions. But

12:39

now, let's start shifting. What about the contrast

12:43

that's going in the superior vena cava and then ends up in the inferior vena cava

12:47

and hepatic veins?

12:49

Well, that's not very common in the normal patient, but you can still sort of see

12:53

it a

12:55

bit. The-- and especially in the smaller, more petite patients

12:59

or with lower cardiopat capacities, the contrast

13:03

comes in, and especially at a high rate, it might kind of

13:06

overfill and then reflux down

13:09

briefly. The key will be that the, the inferior vena cava

13:13

and the hepatic veins are not dilated.

13:16

It simply just kind of goes in and then comes back

13:19

out. Okay? So in

13:23

discontinuous, you might see a little blip of contrast here and

13:26

there. That's okay, too.

13:29

When a patient, um, when the heart, the right atrium, and right

13:33

ventricle contract, there's often, even in normal patients, a

13:37

little bit of blood which will scoot back into the inferior vena cava because

13:41

there is no valve there, and hepatic veins.

13:44

So you might see a little discontinuous reflux.

13:47

That's also normal.

13:51

This is a nice example. This is a, a normal patient.

13:53

There's a little bit of contrast in the hepatic veins, inferior vena

13:57

cava, but it's only temporary, okay?

14:01

This discontinuous is fine. This one at, at

14:05

first, you know, you look at it, and you're like, "Well, this is not discontinuous.

14:08

This is a-- this is quite a bit of reflux." But the veins are

14:12

not distended. And then when you look at the patient, you see that, you know,

14:16

it's kind of a smaller heart. It's more of a petite

14:19

person. And what I equate this to is like a kettle of

14:23

water, and that everybody, you know, people

14:27

are snowflakes, and everyone has a different kind of cardio-

14:31

cardiac capacity, cardiovascular capacity, like a

14:34

kettle. And when you're under

14:37

eighteen, in pediatrics, we give contrast based on

14:41

kilograms, right? One to two cc's per kilogram.

14:44

So we, in pediatrics, we recognize that the amount of contrast

14:48

you give should be tailored to the patient's

14:51

weight/body habitus. But once you turn eighteen,

14:55

you know, for practical reasons, we simply just give the same amount.

14:59

Well, we're all a bit different. So if you have a small kettle

15:03

and you give the same amount of contrast, it will overflow, and this

15:07

would be what we're seeing here, this continuous hepatic

15:10

reflex or reflux without

15:12

dis-distension. Larger patients or pregnant patients,

15:16

you give the same amount of contrast, you can't completely fill that kettle.

15:21

And so now you are open to more severe

15:25

transient interruption of contrast

15:28

and not see this.

15:30

So

15:31

trying to reduce the severity of t- of transient interruption of

15:35

contrast,

15:36

you know, you could scan during mild inspiration or mild expiration,

15:40

right? Trying to reduce that inspiratory huge amount

15:44

of, of augmented flow. Or you could kind of

15:48

adjust

15:50

in your protocols the amount of volume,

15:53

right, of contrast based on the kilograms, kinda like the

15:57

pregnancy, a sliding scale. Um, the other thing you can do,

16:01

obviously, is repeat it if it's really that important.

16:03

But like I say, usually in the setting of severe

16:07

transient interruption of contrast, usually

16:10

that's physiologically normal. That tells you the pressures are normal.

16:14

So even if there was maybe a small embolus, it's not causing right heart

16:18

strain. You know, it's, you know, it's most

16:22

likely, though, it's gonna be negative.

16:25

So now let's shift. All right. So you're reading.

16:29

You see non-opacification or, you know, it looks like a filling

16:33

defect in the right lower lobe. That's a PE.

16:36

Well, are you sure? Was it sharply marginated?

16:40

Is there expansion? You know? Or was there

16:44

contrast dynamics here that suggest there might be altered

16:47

flow, uh, mixing artifact, you know, something a little bit

16:51

more relevant? I love this sign from Canada because it's

16:55

not that this is wrong, but this is probably a little bit more

16:59

clinically useful.

17:02

So altered dynamics. We'll start off with contrast

17:05

reflux. And when you see this continuous IVC

17:10

reflux and into the hepatic veins with

17:13

distension, that usually correlates with poor

17:17

forward flow. What are some causes of poor forward flow?

17:20

Again, all of this is interrelated.

17:22

Elevated right heart pressures, poor, um, so you can't really

17:26

feel the right atrium and right ventricle, uh, reduced cardiac

17:30

output, myocardial failure, pulmonary stenosis, tricuspid

17:34

regurgitation, that's a big one, just goes right on

17:36

down. Um, one of the, uh,

17:40

things about, uh, IVC contrast reflux is that you tend not

17:44

to see transient interruption of contrast.

17:46

So if the heart function or forward flow

17:50

is maintained relatively, you know, well

17:53

enough, then you should see a very well

17:57

opacified pulmonary arteries, assuming they made it all the way through to the

18:01

pulmonary veins and left heart.

18:04

So transient interruption of contrast, often not seen in

18:08

the setting of a continuous IVC contrast

18:11

reflux.So when you see it, you

18:14

start looking for the potential causes.

18:17

Again, it's the, it's the contrast dynamics that are kind of alerting you on where

18:21

to go next. So you see these are patients where you

18:25

have continuous reflux, there's distension of the

18:29

veins

18:31

that you need to find out why. So let's go through a few.

18:34

One, pericardium. Right? Pericardium that's

18:38

constrictive or with tamponade will constrict

18:42

the right atrium and right ventricle filling, so it limits

18:45

it. So it really can't get in there, so when that superior vena cava

18:49

contrast is coming down, it goes to go in the right atrium, the right atrium

18:53

just kinda says, "Uh, no. Stop. Go into the waiting room down

18:57

in the inferior vena cava. We'll get to you when we get to you." All

19:01

right? Now, with pericardial effusions, the

19:04

ones that are concerning are the exudative.

19:07

So you can have very large transudative effusions, but it's

19:11

h- difficult for the, the fluid to generate that much

19:14

pressure to constrict the right heart.

19:18

Exudative, uh, pericardial effusions, now they can generate

19:22

that pressure to straighten out and c- um,

19:26

compress the right ventricular free wall

19:30

anteriorly and the right atrium, limiting the

19:33

filling. It can be diffuse, right, it can be

19:37

focal, and the-- you'll notice it because the right atrium will be

19:41

compressed and the right ventricle, it will start, instead of having that rounded

19:45

appearance, it's gonna start looking triangular.

19:47

It's gonna look triangular. And then when things get really

19:51

severe, you'll start getting straightening of the

19:54

intraventricular septum. That's one of the last things to go, so once you see that,

19:58

it's like, "Oh, my God." Make phone calls.

20:03

So this is a patient,

20:05

hyperdense, IVC, hepatic vein,

20:08

contrast reflux, some di-distension of the inferior vena cava and hepatic

20:12

veins. You come up, and you see the right atrium is distended,

20:17

and the right ventricle is constricted into more of a triangular

20:20

shape. So it's almost like there's a, a vice grip on it.

20:24

So this is actually constrictive pericardium, um,

20:28

chronic constrictive pericardial disease.

20:31

Okay?

20:33

Another patient. Reflux. Hyperdense contrast into the inferior vena

20:37

cava. All right. There's a large pericardial

20:41

effusion. If you look very carefully, there is enhancement,

20:45

enhancement to the pericardium that indicates

20:48

what? This is probably exudative, so this is

20:52

automatically going to be a little bit more concerning.

20:55

Then you look at the right ventricle, and it's the right atri-- the

20:59

right ventricle wall is now flattened, right?

21:02

So this is exerting the pressure and narrowing the right ventricular

21:06

chamber, and the reflux of contrast because it

21:10

cannot move forward. The other thing is there were multiple

21:14

MIs, old MIs. So the left ventricle is not very robust either.

21:18

So this is, this is very concerning, because this is a cardiac

21:21

tamponade in evolution.

21:25

So again, what you wanna see is nice, rounded right ventricle,

21:29

thin-walled, okay?

21:32

This triangular appearance, not good.

21:36

This usually indicates a constrictive pericardial or cardiac

21:39

tamponade, especially if there's enhancement along

21:43

the pericardium. Okay. Myocardial

21:47

failure. Well, you can get

21:51

reflux, but in this case, the filling

21:55

is inhibited because the heart can't pump out the

21:59

blood fast enough, and the, and the contrast is gonna-- again, the

22:03

contrast is just following the blood where it's going.

22:06

It's going to go into the inferior vena cava.

22:08

It's not gonna make its way well into the pulmonary arteries or

22:12

the left heart. So when you see poor opacification

22:17

of these structures, this reflects a much slower blood

22:21

flow, okay? Usually, with myocardial

22:25

failure, the left ventricle may be dilated and thin-walled.

22:29

You still have that normal rightward convexity of

22:33

the intraventricular septum. Now, one of the other things I've noticed

22:37

is that when you're looking at this, and again, you start to interrogate that

22:41

heart, you'll notice you see the heart structures really

22:45

clear, almost as if it was cardiac gated.

22:48

That's another pretty good sign, because this reflects

22:52

either severe bradycardia,

22:55

but more likely, when you have a dilated heart,

22:58

this is markedly reduced contractility.

23:02

The heart isn't moving very much, so when the scan is obtained,

23:06

you're seeing the heart structures very

23:09

clearly.

23:11

So

23:13

this is, again, beautifully reflected

23:17

on the contrast flow. So it's coming in the superior vena cava

23:20

immediately. Right when you start, you say, "Oh, man, thoracic aorta

23:24

has no contrast in it.

23:27

Okay, this, this is a problem." We already know that there's probably gonna

23:30

be some very significantly reduced flow.

23:34

And then you look, yeah, uh, a

23:38

lot of IVC and, um, hepatic vein contrast

23:42

reflux, distension, okay? That's the waiting

23:45

room. Pulmonary arteries are opacified, but

23:49

not the pulmonary veins, right? Not the pulmonary

23:52

veins. So this is a markedly reduced

23:56

cardiac ejection fraction, 'cause the left ventricle is disten-

23:59

dilated. Um, you know, estimate about less than twenty

24:04

usually. When I see that there's no contrast in the thoracic

24:07

aorta, I usually find that it's maybe around a twenty percent or less

24:11

ejection fraction. You don't have to say that in your reports, of

24:15

course, justIt's just an observation.

24:18

So the other thing you notice is that the margins are, like,

24:22

really sharp. Really sharp. You can see the, the

24:26

myocardium, the chambers, the trabeculation,

24:30

the moderator band in the right ventricle apex.

24:32

You see these structures very well when the...

24:36

in dilated cardiomyopathy, as opposed to normal where

24:40

the heart kind of beats with a more robust contractility, you're

24:44

gonna have a little bit more blurriness and motion artifact.

24:47

The motion artifact is normal. The clarity, not so

24:51

much. Okay? So

24:55

another patient, you can see immediately, uh, the pulmonary artery

24:59

is enlarged. There's reflux of hyperdense contrast into the dilated

25:02

inferior vena cava. There's a paucity of contrast in

25:06

the pulmonary veins, left atrium, left

25:09

ventricle. Uh, this is a person with

25:13

reduced flow and you, you know, I mean,

25:17

you can come up with that and just say, "Hey, this is, this is a cardiac

25:21

issue, uh, poor ejection fraction most likely,

25:24

um, based on the altered contrast dynamics."

25:30

So let's go to case two, the patient two.

25:33

This was the dyspnea patient. When you look at it, you can see there's

25:37

contrast reflux into a dilated inferior vena

25:40

cava, that the heart structures are relatively

25:44

clear. There's the moderator band, just like I mentioned.

25:47

And the wall of the myocardium, left ventricle, is

25:50

thin. There's dilation of the right atrium.

25:53

This is a patient who's got bilateral lower extremity swelling

25:58

because they have a dilated cardiomyopathy and poor forward

26:01

flow.

26:04

Okay. Uh, reflux from tricuspid regurgitation.

26:08

This pretty much you can tell whenever you see the right

26:11

atrium, right atrium, is moderately to severely dilated.

26:15

Pretty much when you see that, there's gonna be tricuspid

26:19

regurgitation, because remember, the, the heart chambers dilate

26:23

in the setting of increased volume.

26:25

They hypertrophy in the setting of increased

26:29

pressure. So when you have marked

26:32

dilation, say of the right atrium, that's increased

26:36

volume, and that will be because the tricuspid

26:39

regurgitation, where the blood flows back and forth between the right

26:43

ventricle and atrium, and it also refluxes down into the

26:46

inferior vena cava. Usually, with tricuspid

26:50

regurgitation, the interventricular septum remains

26:54

normally convex,

26:56

okay? So this is a patient with markedly dilated right

27:00

atrium, a little bit of maybe dilation right

27:03

ventricle, reflux of hyperdense contrast, dilated

27:07

IVC, tricuspid regurgitation.

27:12

So another patient with pulmonary hypertension.

27:14

You can see automatically that, oh, there's reduced forward flow because

27:18

there's a paucity of contrast in the left ventricle, thoracic

27:22

aorta. There is a distended and dilated right

27:25

atrium. There is hyperdense reflux into the inferior vena

27:29

cava, which is dilated. This is all pulmonary

27:32

hypertension, and you can see also hypertrophy of the right ventricle,

27:36

greater than four millimeters. This is hypertrophy, so it's

27:40

long-standing. So this is a patient with pulmonary hypertension, tricuspid

27:43

regurgitation, poor forward flow.

27:46

Again, contrast dynamics, cardiac chamber, you can k- get a lot

27:50

of information about a patient's cardiopulmonary status.

27:54

And so this leads us into another cause, right?

27:57

Right heart pressures are elevated.

28:00

Uh, the right ventricle is gonna oftenly be a bit dilated or there might

28:04

be some hypertrophy. Hypertrophy automatically means

28:08

it's chronic, okay? And in these patients with

28:12

elevated pulmonary pressures, pulmonary hypertension,

28:15

the interventricular septum will start straightening at about sixty to

28:19

sixty-five millimeters of mercury systolic.

28:22

That's pretty high, right? So that's one of the last things to change.

28:27

So right ventricle, elevated pulmonary pressures, there's

28:30

acute and there's chronic. Chronic, there'll often be hypertrophy

28:35

and some tricuspid regurgitation.

28:39

So this is a patient with chronic, this is chronic thromboemboli.

28:42

The pulmonary arteries are enlarged, hyperdense contrast

28:46

reflux, the right atrium's dilated, there's some tricuspid

28:49

regurgitation, there's hypertrophy of the right ventricle.

28:52

This is chronic cor pulmonale. There is straightening of the interventricular

28:56

septum. That indicates that the pulmonary pressures are probably over

29:00

sixty, sixty-seven, right? In this case, they were seventy.

29:03

So all of that information is here.

29:06

And notice how there's also poor forward flow, as there's no real

29:10

blood or contrast in the left heart and thoracic

29:13

aorta. Okay? Another patient.

29:17

This is, again, reflux. You can see that right atrium is really

29:20

dilated. There's actually, in this patient also, there is an

29:24

atrial septal defect. The pulmonary pressures in this person, unfortunately, are

29:28

very high.

29:31

Now, this is more of the acute, and I'm gonna just spend a little time on

29:34

this. Sometimes you do a pulmonary

29:37

CTA, and there's a pulmonary embolus. That's right.

29:40

So in that setting, when should you be concerned?

29:44

Well, I get at least a little

29:48

bit more concerned when I see right heart strain.

29:51

To me, that's the most important. In fact, that's the first thing I look

29:55

at. Is there

29:57

cardiac changes and contrast dynamics here that would suggest to me that

30:01

the patient has right heart strain?

30:03

And in this patient who's got bilateral distal

30:06

lobar, distal main and lobar emboli, you can see they're

30:10

emboli, they're sharply marginated, there is actually pretty

30:13

severe right heart strain here. And there's straightening of the interventricular

30:17

septum, there's dilation of the right

30:19

atrium.Reflux of hyperdense contrast

30:23

this would be

30:25

a bit more concerning. This is the kind of patient who's gonna

30:28

have problems.

30:31

So in the setting of pulmonary embolus, acute right ventricular strain, and

30:35

it is not associated with clot burden, I cannot overestimate this enough.

30:39

It is not associated with clot burden, and it's

30:43

actually not associated with the so-called saddle embolus.

30:46

People get all worked up, "Hey, there's a saddle embolus." It's like,

30:49

yeah, yeah, there, there might

30:52

be. Is there right heart strain?

30:56

The most important thing you've gotta look for for pulmonary emboli

30:59

is, is it in the distal main or lobar

31:02

arteries? When you see it there, that has a

31:06

very high propensity to develop right heart strain.

31:10

So it's not so much the saddle or the clot burden, as are

31:14

the distal main and are the dist-- or proximal

31:18

lobar arteries, are they involved?

31:21

And if they are, you're probably gonna have right ventricular

31:25

strain. Okay? Patient has distal lobar

31:29

arteries. Notice they're sharply marginated.

31:32

In this patient, again, when you're looking for right ventricular strain,

31:35

you, you know, the estimate to get the RV/LV

31:39

ratio, usually I like to see about one

31:42

point-- over one point zero. Uh, one point two

31:46

has a much higher specificity. And you measure at

31:50

the widest point about a centimeter from the valve plane,

31:54

tricuspid valve, mitral valve, about a centimeter, and

31:58

then you get your measurement. It doesn't have to be at the same level, because

32:01

remember, when the heart kind of starts to dilate, it might

32:05

kind of curve and shift. So you might have to kind of go up and

32:09

down a little bit. But try to measure it about a centimeter from the valve

32:13

plane. Okay? There's a

32:16

saddle embolus.

32:20

Is there any right heart strain? There is

32:22

not. There is not.

32:26

Distal lobar, is there right heart strain?

32:28

Yes, there is. Okay.

32:33

It's not that the saddle can't, right?

32:35

It's just

32:37

it's not as strongly associated. So the RV/LV

32:41

ratio, which we looked at, you know, I use about one point one, one point

32:45

two. Straightening the interventricular septum when you're looking for it is a

32:48

little harder because the septum, uh, doesn't straighten

32:52

just all the way through at first. Uh, I find that the

32:56

base tends to straighten first, but it remains

33:00

curved at the, um, apex, and then

33:04

with increasing, uh, strain or pressures,

33:08

that finally starts to flatten last. Okay?

33:12

And you'll see they're, uh, hyperdense.

33:14

Now, the other thing I use is the interatrial septum,

33:18

um, because that one is a lot more compliant

33:22

than the interventricular. So when the interatrial septum is bowed

33:25

into the left atrium, that's a pretty good sign there's elevated filling

33:29

pressures in the right heart. Okay?

33:32

So RV/LV ratio, one point three. There's your measurement, one

33:36

centimeter. There's no right ventricular hypertrophy.

33:40

You'll notice that the, the distal, or sorry, the apical

33:43

interventricular septum is still a little curved, right?

33:46

This is the last thing to kind of flatten.

33:49

This is usually where you look first.

33:51

Um, you can see again distal lobar, um,

33:55

or sorry, distal main, kind of proximal lobar emboli, reflux

33:59

of hyperdense contrast. And in this patient who had chest

34:03

pain,

34:05

also subtly, they had

34:07

poor enhancement here in the myocardium, consistent that they were

34:11

actually having ischemia and an MI, because

34:15

right ventricular strain in the setting of a lot of coronary artery disease is

34:18

kinda like a stress test, right? And so they may have elevated troponins and

34:22

chest-- substernal chest pain, but that usually indicates that they might be

34:26

having some ischemia. Um, patient

34:30

with right heart strain, emboli, you--

34:34

One of the things that if-- I find is when they're hypoxic, they usually have

34:38

a PFO, and you can see the contrast dynamics here

34:42

with the hyperdense contrast in the right atrium going

34:45

into an open PFO. Now, PFO

34:49

is usually a flap and it stays closed, but in the setting of increased pressure,

34:53

that may open, and

34:55

there comes the contrast.

35:00

In fact, this patient has got, uh, bilateral distal main

35:04

emboli, right heart strain, oof, r- a lot of

35:07

severe flattening, even at the apex, bowing of the

35:11

interatrial septum. But when you start looking at the interatrial septum, you see

35:15

this, and you're like, "What the heck?" Well,

35:19

that turns out to be an embolus

35:21

that's passing, bypassing the heart, and

35:25

coursing up into the PFO to go,

35:29

unfortunately, to the other side of the lung, where it can

35:32

do a great deal of damage. Again, the function of a lung

35:38

is it's a filter. It stops the emboli, and then it chops it

35:41

up. You don't want it going to the other side,

35:45

where, you know, a lot more severe complications can

35:49

happen.

35:52

And remember, these changes are dynamic.

35:54

They, uh, they reflect the patient's cardiopulmonary status

35:58

at that time. So, you know, this patient

36:02

had an embolus. All right. There's your reflux straightening.

36:05

They've been treated. Um, this is a month

36:09

later. Everything returned back to normal. Okay?

36:13

So it's a dynamic process that reflects the patient's cardiopulmonary

36:17

status.

36:19

So let's start shifting now. Okay, so we've kinda gotten through

36:23

some of this, so nowIn the setting of

36:27

patients with altered and reduced flow

36:31

velocity, what are some of the pitfalls we can run

36:34

into? So when you start

36:38

seeing the reduction in flow, it can be globally within the

36:41

pulmonary vessels and in the systemic

36:45

and or regional. And I'm gonna emphasize this because this is

36:49

where I see a lot of the mistakes. When

36:53

the flow-- blood flows in the pulmonary artery, it's not all just

36:57

uniform all the time, especially if there's some

37:00

abnormality in the lung, there can be some

37:03

vasoconstriction that could be acute or chronic, there'll be

37:06

differences in flow velocity even within the

37:10

lung.

37:11

Okay? You have a pneumonia or fibrosis in the lower

37:15

lobes, that blood flow is gonna be slower than, say, the

37:19

mid and upper lobes. This will be

37:22

reflected in how the contrast

37:24

flows. Okay? So slow

37:28

flow i- the biggest clue is that there'll be poor or absent

37:32

enhancement to the pulmonary veins, the left

37:35

heart, and the thoracic aorta. Clued in already.

37:39

So this is your first clue. Okay, wait a minute, there's...

37:42

Flow's altered, let's see if we can see the reasons, and then we went through some

37:46

of the reasons for it.

37:49

Incorporate this information into your

37:52

dictation, alter your search a little bit more, kind of looking a

37:56

little bit closer at the heart, the pulmonary arteries, chambers,

38:01

and then get yourself ready

38:04

for the artifacts, 'cause if the flow is so

38:08

slow, there's probably gonna be a couple of

38:12

artifacts there. So this

38:16

is case three. When you see this on your

38:20

CTA, what can you predict about the blood flow

38:23

velocity? It's reduced. It's

38:27

reduced. And we'll start making a search for

38:29

why. Two, what should you be

38:33

careful when you look at? You have to be careful of flow

38:37

artifacts.

38:40

Flow artifacts are very common with patients

38:43

with reduced flow. So this would be an example.

38:46

Patient with... And you can see it. All right.

38:49

Immediately, there's reduced flow.

38:51

There is a contrast reaching the pulmonary arteries, no

38:55

transient interruption of contrast because there's no way the

38:59

inferior vena cava unopacified blood can actually get up there.

39:03

In fact, it's probably got hyperdense contrast reflux

39:06

back. Then you look, and it's like, okay, there's a

39:10

dilated right atrium, probably some tricuspid regurge, there's reflux

39:14

into the coronary veins. You know, there's no

39:18

opacification of the left ventricle, and then you start looking in the pulmonary

39:21

arteries, and there's enhancement here.

39:24

But as you go down, that enhancement is

39:27

lost. So the contrast flow

39:31

hasn't really made its way down into the right

39:35

and left lower lobe pulmonary vessels.

39:37

You can see how they are unopacified.

39:42

These are your artifacts. Mixing artifact, which is

39:45

basically the leading edge of the contrast,

39:49

kind of moving through slowly and mixing with the

39:53

unopacified. It's gonna give you a spiral, ill-defined

39:56

kind of appearance that changes from image to image.

40:01

The other is that there's just no opacification.

40:05

All right? No opacification. And these are the dangerous ones.

40:09

These are the ones I see called emboli,

40:13

not uncommonly.

40:16

So there was a study that was published,

40:20

and they found that of all pulmonary

40:22

CTAs, one-quarter of them were false

40:26

positives. One quarter. Now, that's high.

40:30

Um, I haven't seen that high, but

40:33

it, it's common. It's very common.

40:37

And it-- I'm not gonna really get into the whole thing

40:41

of, you know, false positive versus overdiagnosis.

40:45

They are completely different. And what we're gonna talk

40:49

about here and focus on is more of

40:51

accuracy, but I'm gonna let you know that accuracy does not

40:55

necessarily mean better patient outcomes.

40:58

That's a whole 'nother topic, too.

41:01

But accuracy in trying to reduce false

41:04

positives, that would improve patient

41:08

outcomes. So we're gonna focus on reducing false

41:12

positives. That's, that's just what I'm gonna talk about.

41:15

I won't get into the whole patient outcomes, um, of

41:19

small emboli because, you know, frankly, the literature suggests it's

41:23

better just to not call those, but...

41:26

Now, in their study, one out of, uh, ten or so,

41:30

just somewhere around there, had

41:33

false positives based on mixing artifacts.

41:37

Now, I, I gotta believe that might be a little underreported or, or maybe it

41:40

was in their patient population. But from what I've

41:44

seen, reading for across the country, um,

41:48

the big causes of false positives are non-opacification

41:52

regionally, mixing artifact, and then, then the last

41:56

one is motion artifact. These are the big

41:58

three.

42:01

And the reason I'm gonna focus on reducing the false positives, 'cause once you

42:05

push that ball down the hill and call it an embolus,

42:10

you don't know what's gonna happen, 'cause that ball gets into motion, and it's

42:13

difficult to stop, and then too many people start to get involved, too many

42:17

clinicians, downstream complications, and most of the time,

42:21

without the radiologist even knowing this has

42:24

happened. So you wanna pause a little bit in the setting

42:28

of altered kind of slow flow before you start calling

42:32

emboli.It's not to say it's not there, just

42:36

slow down

42:38

and the treatment ramifications you are sending a patient on a different

42:42

trajectory once you diagnose it, right?

42:44

They're now going on anticoagulation, their medical epic chart or

42:48

whatever they're using has changed.

42:50

So now they come back into the ER with chest pain, and there's the history of PE.

42:54

Well, you know they're gonna get a CTA, um, follow-up

42:57

visits. Complications of the wallet are a big one,

43:00

right? And then there's others, but

43:04

let's see if we can't reduce the false positives.

43:06

So let's look at this a little bit closer.

43:09

These are patients with clearly altered and reduced

43:13

flow for the reasons that we've talked about, and some tricuspid

43:16

regurg. Now, take a look at the pulmonary arteries.

43:19

As you go down, you start to notice that this one on the left,

43:23

lower lobe, you see all of them at the same level, start to fade

43:27

away. They start to fade away till they're

43:29

non-opacified. They're still opacified on the left

43:34

but not... Or on the right, I'm-- I apologize.

43:36

Not on the right, but not the left.

43:41

If you are only looking at opacification without

43:45

taking in the whole concept of what's going on cardiopulmonary-wise

43:49

with this patient, this gets called

43:53

pulmonary emboli. There's no expansion of the vessels.

43:56

There is a gradual decreasing opacification

44:00

with some mixing artifact in there too, but

44:04

this is not an emboli.

44:09

You can see another patient going down, and then there's just this

44:12

non-opacification, non-opacification in the left

44:16

lower lobe. Okay? There's no vessel

44:19

expansion, and this gradual transition is important,

44:23

so you do not call these emboli. If you want, you

44:27

just say indeterminate in the left lower lobe. That's fine.

44:30

That, there's nothing wrong with that.

44:32

If you see expansion of the vessels,

44:35

maybe it is, but still, you might wanna

44:40

be a little careful in calling it. R-recommend a repeat, look for lower

44:43

extremity DVT or something else.

44:47

And remember, the flow is not just globally reduced, but it can be regionally

44:51

reduced. So this is a patient who's got

44:54

reduced cardiac, um, flow outpo-- uh, sorry,

44:57

reduced cardiac ejection fraction, slow flow, poor

45:01

opacification of the left heart and the thoracic

45:04

aorta. The blood is in the pu-- or the contrast is in the pulmonary

45:08

arteries, but as we go into the right lower lobe, you start to notice it

45:12

fades out as compared to the left. You can see the

45:15

difference. Okay? And as you go

45:19

lower, you start to see this is not

45:22

opacified. These are still opacified until the very

45:26

end, and then they're not opacified.

45:29

So there's overall slow flow. The right side is

45:33

much slower than the left, kinda giving you a little asymmetry,

45:38

and this can be very misleading unless you look at the whole

45:41

thing. So this patient actually had bilateral lower lobe

45:45

fibrosis with chronic vasoconstriction destruction.

45:48

There's de-reduced flow. Right was greater than left, and they had an

45:52

elevated right hemidiaphragm eventration, which of course, is a

45:55

weakness, so there's reduced flow on the right, greater

45:59

than left, and overall it was reduced.

46:02

The interpretation, bilateral right lower lobe emboli.

46:06

Y-you know, no, no hedge in there, just bilateral lower lobe

46:10

emboli. That's a false

46:12

positive. Okay? Another patient,

46:17

if this is all you had and you see that this isolated

46:20

vessel artery right here

46:23

is actually non-opacified. You go up higher, it was

46:26

opacified, and then it faded off on the right in some areas.

46:30

The left still is opacified. This could be a difficult one.

46:34

Is this an embolus? Is this non-opacification?

46:36

Is it an in situ thrombus, for heck?

46:39

And

46:40

in this person, they actually had an abdomen CT, so you've

46:44

got this delayed venous, and then you find, oh,

46:47

nope, it's opacified. So this was just a non-opacified

46:52

pulmonary artery, but you could see if you didn't have the

46:55

delayed venous, that could be called

46:58

embolus. Another patient who's got

47:02

severe consolidation, vasoconstriction.

47:05

There's no sharp edges here. This is a gradual

47:09

transition, mixing artifact into non-opacification.

47:12

No expansion of the vessel.

47:15

Do not call this an embolus. You can see that the patient has a very

47:19

poor cardiac output to start with.

47:21

There's severe hyperdense contrast reflux into the

47:25

hepatic veins, um, and it's just

47:28

very, very slow flow into the

47:32

right, and that's what the contrast is showing.

47:35

In embolus, we usually have sharper edges

47:38

again.

47:40

All right? So let's go back to our case.

47:43

Oh, sorry, not quite. This is another case of mixing artifact.

47:47

Now, mixing artifacts are a little more difficult, I think,

47:51

because they have a very, a variable appearance, and

47:55

they can be seen in the aorta, right, and in

47:59

the pulmonary arteries. They're usually very wispy, right?

48:03

Wispy, they change shape, a little turbulent

48:06

flow, and a lot of times I think you can tell

48:10

because they change shape and appearance on each image

48:14

rather than kind of solid, and they don't tend to have quite the

48:18

sharp margins. You can see how the margins are a little

48:21

indistinct. Turbulent flow, though, I gotta

48:24

admit, I've seen some that are, ooh, they are tough to,

48:28

to figure out. I mean, you get-- sometimes it does give you a little

48:32

bit of a sharper edge. The key is, does it touch the

48:35

wall? Um, does it change appearance

48:39

with each image?And again, you see the

48:43

mixing artifacts in the setting of low cardiac output or slow

48:48

flow.

48:50

This is from Radiopedia, and this one is like an example I just

48:54

mentioned, that you don't want to have to read this.

48:57

So it's reduced output. You can see there's less

49:01

opacification in the thoracic aorta, and then you start to see what looks like a

49:04

mixing artifact. Then it starts to kind of become

49:07

sharper. This is-- There's no expansion of the vessel,

49:11

but, you know, these are-- these can be very

49:14

tricky. Um, this patient actually had venous

49:18

imaging after, and you saw that, no, there is

49:22

nothing there. That was all mixing artifact.

49:25

So it's-- I understand when these are called

49:29

emboli. It's just I-- what I'm trying to do

49:33

is, is to have you incorporate a little uncertainty

49:36

in your diagnosis when you see these kind of

49:40

contrast dynamics.

49:42

You have a patient here who's got what looked like a little

49:45

maybe thromboembolus,

49:49

maybe, but it's not touching the wall, there's no

49:51

expansion, kind of a little turn

49:55

here. This was a tough one. But again,

49:59

thankfully, you see on the

50:02

delayed imaging, because they had an abdomen, it was gone.

50:06

So it was really more of a flow artifact and maybe related to the sharper

50:10

algorithm.

50:12

So let's go back to our last case here.

50:16

So this was the person who has no contrast in the

50:20

thoracic aorta and has what looks to me to be a

50:23

mixing artifact. It's, it's heterogeneous, it

50:27

changes shape,

50:30

and there's just kind of a reduced opacification.

50:34

Unfortunately, this was not hedged.

50:36

This was called definitely a left upper lobe pulmonary

50:39

embolus. Now, the reason

50:43

I'm showing you this is because you might recognize

50:46

this. This was the same patient that I showed you

50:50

as an example of cardiac tamponade.

50:55

And

50:57

that wasn't diagnosed either. That was just a large

51:01

effusion and no constrictive appearance.

51:05

And it's like, okay, this is a huge

51:09

setup for a disaster at this point, right?

51:12

The patient got the scan because of hypotension, thinking it was a pulmonary

51:16

embolus. It's not a pulmonary embolus, it's mixing artifact.

51:21

No expansion. You then put them on

51:24

anticoagulation with an exudative effusion and cardiac

51:27

tamponade, and things are not gonna go

51:30

well. Okay? So

51:35

let's put all of these pieces together. Again, they're all interrelated.

51:39

Contrast, dynamics, cardiac chamber,

51:43

and flow artifacts. Put them all together.

51:47

This is your last one, and everything is here.

51:51

So this is a patient who's had substernal chest pain.

51:54

The radiology read, and I read the report,

51:58

no hedging, "Multiple left lower lobe pulmonary emboli, trace

52:02

pericardial effusion." Okay. Let's look at

52:06

this again. Let's incorporate these features.

52:09

First and foremost, there's no opacification within the left atrium and

52:13

the left ventricle. The thoracic aorta has no

52:17

contrast. The pulmonary veins don't have contrast, so we

52:21

know

52:22

that the flow is altered, that it's slow, and that

52:26

in this person, it is probably related to the cardiac

52:31

output. There's the moderator band.

52:32

Notice how sharply demarcated this is.

52:36

The left ventricle's a bit, a little bit dilated, but there

52:39

may be a little bit of myocarditis here, a little bit of cardiomyopathy.

52:43

I'm not sure, but the ejection fraction is not robust.

52:47

There is reflux of contrast into the inferior vena cava and coronary

52:51

sinus. Forward flow is altered, right?

52:53

It's going into the waiting room.

52:56

Okay. Let's move on to the next, the

52:59

pericardium. Yeah, there's a little fluid, but this is

53:02

indistinct. It's actually more thickening and a little bit of

53:06

indistinctness. There's a subtle bit of possible

53:09

enhancement, maybe, but at least you wanna kind of go, "What was

53:13

that history again? Substernal chest pain.

53:16

Could this be pericarditis?" Okay?

53:19

Lastly, you look at the pulmonary vessels, and they're

53:23

both opacified, but the left is a little bit less opacified.

53:26

It's starting to transition. You go up a little higher, and you can

53:30

see the contrast is moving very slowly.

53:33

You get into some mixing artifacts, and then there's just

53:36

non-opacification of the left lower lobe vessels.

53:40

The right was used as a reference. You can't do that, right?

53:44

Because you can have regionally different flow.

53:47

So this is simply non-opacification of the left lower lobe

53:50

pulmonary vessels, secondary to global and more

53:54

left lower lobe regionally slow flow

53:57

with mixing artifact, too. Okay? Is there an emboli

54:01

there? I don't know. You can always say it's indeterminate in the left lower lobe

54:05

if you want, but it's unlikely. So the patient comes

54:09

back in a week with the same symptoms after being put on

54:12

anticoagulation. Well, they were looking for another

54:15

embolus. Well, there wasn't one in the first place.

54:18

You can see in this one, where it was scanned a little later, there was absolutely

54:22

nothing down there. It was the chronic atelectasis and

54:24

vasoconstriction. The new problem is they've developed

54:28

a large pericardial effusion, which we know is probably going to

54:32

be blood. There is constriction of the right

54:36

ventricle free wall and atrium. The triangular shape

54:40

is starting to form.

54:43

This is gonna be cardiac tamponade from an acute hemopericardium

54:47

based on the anticoagulation from the false

54:49

positive.The

54:54

summary here, contrast flow. It's used

54:58

in a lot of other areas to try to get you out of the rut

55:01

of the CTAs, because they were-- there's just so many.

55:05

After a while, you just, you know, it's just kind of mind-numbing.

55:09

Try incorporating the flow dynamics into your

55:13

report. See if you can maybe make this a little more

55:16

interesting, and understand

55:19

how that even good for, like, transient interruption of

55:22

contrast, which is normal, when it's severe, it can

55:25

interrupt, uh, the contrast

55:29

column, and it makes your report and

55:33

evaluation a little bit more difficult.

55:36

Continuous reflux of contrast, unless the patient's very

55:39

petite, is not normal, and you wanna look for

55:43

causes of the elevated heart pressures, tricuspid

55:46

regurge, or reduced ejection fraction.

55:49

And when you see it, be very careful when you're interpreting the pulmonary

55:53

arteries. Watch out for mixing artifacts and flow relate-- and

55:57

non-opacification. Okay? For the

56:00

chambers, when the right atrium's enlarged, there's probably

56:04

tric-tricuspid regurgitation. It's actually fair to say that in your report

56:08

if you wish. I do, 'cause it, it's likely there.

56:11

And thin myocardium, clarity of the

56:14

structures, you know, probably reduced cardiac output,

56:18

contractility. For P-- For pulmonary emboli, when you

56:22

actually see them, it's right heart strain that is important to be

56:26

able to deduce whether it's present or not.

56:28

And hypertrophy of the right ventricle or left ventricle, that's

56:32

usually a chronic process in the setting of increased

56:36

pressure. Again, increased volume within the heart will

56:40

cause dilation. Increased pressure will cause

56:44

hypertrophy, and that's usually a more chronic process.

56:49

So with that, I will stop. I hope you found it

56:53

helpful. I will hang out as long as you want if you have any

56:56

questions, and you'd like to go over.

57:00

Thank you so much for that fantastic lecture.

57:03

Really appreciate it. We do have a couple questions in that Q&A

57:07

box, if you're able to pop that open.

57:10

Uh, Q&A box.

57:10

It might be-

57:11

Q&A box.

57:12

I-

57:13

I will find it. Um...

57:15

Might be at the top of your Zoom right now.

57:19

Hmm.

57:21

If not, I can read it off to you.

57:23

Oh, Q&A. Okay.

57:25

Perfect.

57:25

All right. Here you go. Do you have a cutoff value, um,

57:30

that you measure the pulmonary trunk to assess whether it's going to be suboptimal?

57:33

No, I don't. I know the,

57:37

the teaching is two fifty. Some teach two

57:40

hundred. I would like it more than two fifty,

57:44

if possible. Um,

57:47

when I start to see that it's, you know, a little

57:51

low, just visually, uh, I sometimes put the Hounsfield

57:55

unit on it. What I do in the setting

57:59

when I see, like, it's two hundred or maybe a hundred and fifty to two

58:03

hundred, is rather than just say it's indeterminate, because I've seen a lot of

58:07

radiologists just say that, and maybe because they have so many exams to read,

58:11

let's just move through. I don't know.

58:13

I actually narrow the windows a bit and just kind of go through

58:17

it. And I, I do say that, you

58:20

know, once you get a little more peripheral, and I start seeing maybe a lot more

58:24

mixing or poorer pacification, then I would

58:28

say, "I can only kind of say that there's no central,"

58:32

but I also would say, "I don't see any expansion or right heart

58:35

strain or other things." But I don't really have a

58:39

value, um,

58:43

for me. And the other thing is,

58:45

two hundred Hounsfield units in a thin patient,

58:49

I, I'll still be able to read that. I can see

58:52

that. Two hundred in a very

58:56

large person, yeah, probably not gonna

59:00

be able to see much. So it's not strictly just the

59:03

Hounsfield. It's the Hounsfield in the setting of

59:07

also the quantum model and patient size.

59:11

Okay? All right. Let's, let's keep going.

59:15

Is it possible to have a poor opacification of the aorta and left

59:18

ventricle in normal flow in your early phase? Yes.

59:21

If the technologist put the cursor in the wrong area, right?

59:25

They put it on the superior vena cava, yeah,

59:28

it could be normal, and you didn't give it enough time.

59:32

Um, other than

59:33

that,

59:37

mm,

59:39

no. I would favor if...

59:43

I would favor if the aorta and left ventricle don't have good

59:46

opacification. I have seen this very

59:50

rarely in pregnant patients who have a very

59:53

increased blood volume and hyperdynamic

59:56

circulation, that it-- they get

60:00

severe tricusp-- or severe transient interruption of

60:03

contrast that flows through very quickly, and there's

60:07

decreased opacification of the left ventricle and

60:10

aorta. That was just a really rapid,

60:14

severe transient interruption. That's about the only time I've seen

60:17

it, other than a very new tech putting the

60:21

cursor in the wrong area.

60:24

So pretty much, if you, if you don't see opacification of the thoracic aorta and

60:28

left ventricle, just make an assumption first that this is

60:32

actually slow flow and work it that way.

60:35

Okay. Next one. How do you approach suggesting

60:39

chamber enlargement given the cardiac phase?

60:43

Do you rely more on subjective, gestalt, or measurements?

60:46

Ugh. Thanks, Joel. Um,

60:49

yeah. I actually don't have a

60:52

measurement. Um,

60:55

I actually look a little bit more at

60:59

the, um-The

61:02

size, if it kind of touches and looks like it's more

61:06

than the fifty percent rule that we use in the radiograph, that's kind of a good

61:10

sign. The other for me I found useful is

61:14

when the atria are dilated, and I don't really have a measurement,

61:18

but you start to see this distension, like the left atrial

61:21

appendage normally should be kind of triangular,

61:25

kind of elongated. And when I start seeing it convex

61:28

out, that's a pretty good sign that the

61:32

heart, when I say, "God, the heart looks a little big," maybe it's

61:36

just a bigger person. And then I go look at the left atrial

61:39

appendage, and I see that it's a bit more rounded, and I

61:42

go, "Yeah, I'm gonna call that. I'm gonna call that some

61:46

enlarged heart." If I see that it's kind of still thin,

61:50

the left atrial chamber looks okay, the right atrial chamber looks fine, there's

61:54

no reflux, then I probably won't call it.

61:58

Uh, but I don't have an absolute measurement because, you

62:02

know, the heart, just like

62:05

a lot of the different organs of the body, are really different.

62:09

So

62:10

hopefully that's helpful. Okay, is there a way to reduce

62:14

cardiac motion during CTA PE?

62:18

Um, I mean, you can cardiac gate it.

62:22

Um, otherwise, uh, I don't think so.

62:26

I, I don't mind the cardiac motion too much.

62:30

I actually use it, so I didn't mention that.

62:32

But when I'm looking at a CTA, and

62:37

I see that there might be some emboli, and I look at the heart,

62:41

and I see a lot of motion artifact, I

62:45

then think, "This patient is tachycardic, so these would

62:49

be

62:50

more symptomatic." Um, if I-- So cardiac

62:54

motion to me, when I see it excessively, I s- I kind

62:58

of make an assumption that they may be

63:01

tachycardic, right? Because it's moving very fast.

63:05

Just the opposite

63:07

of this so-called, you know, the clear heart of

63:11

decreased contri- contractility and dilated

63:14

cardiomyopathy. Patients with

63:17

tachycardia, it'll be very blurry.

63:21

So I actually kind of use that information.

63:24

Is there a Hounsfield unit that c- can distinguish mixing in the pulmonary

63:28

arteries versus embolus?

63:33

I haven't used it. Um,

63:37

I, I don't use the Hounsfield units much, you can probably

63:41

tell. Uh, so

63:44

it should be... If it's an acute embolus,

63:48

it would might be helpful because it'll be a higher Hounsfield

63:52

unit than the actual blood because it's clotted blood, right?

63:56

If it's more of an subacute to chronic embolus,

64:00

it's actually gonna be a little lower.

64:02

So

64:03

I don't usually use the Hounsfield unit.

64:06

I, I look to see, are the margins sharp?

64:08

Is it against the wall? Does it seem to change shape?

64:12

If I'm not sure, at least I'll mention that I think this might be

64:16

indeterminate

64:18

and give a suggestion, usually kind of lower extremity ultrasounds or

64:21

something, um, rather than, than just calling it

64:25

PE. Um, I promise you, you're gonna see

64:29

these patients where

64:32

these artifacts are gonna be very difficult to

64:34

distinguish. The take-home

64:38

point I'm hoping to impress upon you is,

64:42

don't just call it an embolus and, and move on to the

64:45

next. Just look at it a little bit

64:49

deeper. Do you see clues that can help you?

64:52

And if you're not sure, use the word indeterminate

64:56

and give a suggestion. Okay?

65:00

Okay. So is it better to be descriptive rather than say

65:03

indeterminate? Well, yeah, I... You gotta say

65:07

something. So you gotta, you gotta come up with a

65:10

conclusion. Uh, but I agree. I... The

65:13

description, I think, helps us with our thinking

65:17

as we go through it.

65:21

There's a greater move in radiology to be descriptive and not

65:27

give a diagnosis.

65:30

I, on a personal opinion, do not agree with that at all.

65:34

We are not descriptive radiologists, we are diagnostic

65:36

radiologists. Can this examination

65:40

diagnose

65:42

what we need to know? If it

65:45

can't, then it, it is

65:48

indeterminate, and what do we need to

65:51

do?

65:54

I hope that answers your question.

65:56

Um,

65:57

I find that when I describe things,

66:01

it helps my thought process, and then in my report

66:04

impression, I'll come up with a conclusion

66:08

rather than a repeat of the description.

66:12

All right. In c- in the case which you had

66:16

shown where artifacts mimicked an embolus, had a

66:19

follow-up venous,

66:22

but since most PE protocols do not have this

66:26

abdomen, how do you deal with the real-life scenario? Just like I mentioned.

66:30

Um, do the best you can. Do the best you can with

66:33

it. Uh, just do me a favor. If y- you don't see

66:37

expansion and there's altered contrast, please don't just say,

66:41

"It's an embolus." Okay? Just,

66:45

"This region is indeterminate. This may be an embolus,

66:50

but non-opacification or mixing artifact

66:54

is a distinct possibility." Would

66:57

suggest... You

67:01

can suggest a repeat with longer venous delays.

67:04

You can suggestBilateral lower extremity ultrasounds.

67:07

The reason I say that is because when people treat emboli, I mean, are you

67:11

treating this? No, these are gonna take care of.

67:14

The treatment is designed to what? Prevent the next one?

67:18

Well, that's in the legs. So if there's nothing coming up, and there's no clot

67:22

burden, what exactly are we treating?

67:26

So I, I... That's kind of where I'm, like,

67:30

if you're not sure, do a repeat of the chest

67:34

CTA with a longer delay or expiration if it's transient interruption of

67:38

contrast or one of these, or you could suggest bilateral lower

67:42

extremities. There's nothing there.

67:45

Well, that still could be a PE. Well, yeah, but if there's no right heart strain,

67:49

I... It's gonna be taken care of. Is there anything else coming up

67:53

from below? That would be good to know.

67:56

If there is, then treat. If there isn't,

68:00

eh, I, I would just let that go.

68:03

Okay. For RV/LV ratio, in your experience, is

68:07

insufficient to... Oh, the raw data.

68:09

Do you suggest measuring off manually redu...

68:12

If you wanna measure off the all

68:16

reformatted, yes, the reformatted's better.

68:19

I live in the real world, and the real world

68:21

is, no, I'm not gonna do that. I,

68:25

uh... The list is too long.

68:28

I'm gonna get an idea. And again, the, I find the contrast

68:32

dynamics very helpful here on whether there's

68:36

heart strain or not. I think that we, we focus a

68:40

little too much on all of these reformatted, and if you have

68:44

software that can do it immediately, great.

68:47

Um, if you don't, I don't think I would

68:50

bother reformatting it. Now, maybe there'll be software

68:54

where it automatically comes up in the near future.

68:57

But, uh, for now, um, I look at the

69:00

dynamics, I look at the chamber changes,

69:04

and then I'll kind of give that measurement as a rule of

69:07

thumb, knowing that the heart does shift

69:10

around when it dilates, 'cause that, it can happen.

69:14

And you can't, you may not be, you probably can't do it on the same

69:18

plane, and it might, and of course, I think it might be

69:21

accurate if you can do a three-dimensional or four-dimensional

69:25

view, but, you know, in the real

69:28

world, you probably have to move a little

69:32

faster. Okay. The CTA

69:35

findings in pulmonary hypertension in addition to enlarged pulmonary trunk

69:38

arteries, what are the CTA? Pulmonary hypertension, I have a whole talk on

69:41

that. Um, be

69:45

glad to give it at some point if you're interested.

69:48

The main thing is

69:50

the contrast dynamics, the size of the pulmonary arteries.

69:55

You might see mosaic lung perfusion or lung

69:58

attenuation. That's been attributed to chronic

70:01

thromboembolic, but you can see that with other causes

70:05

of advanced pulmonary hypertension.

70:07

It's just reflects the vaso, uh, throm, uh, thrombolytic

70:11

plexogenic destruction, which occurs whether

70:14

it's thrombogenic, uh, uh, thromboemboli

70:18

or non-thromboemboli. They look the same.

70:22

And, uh, the heart chamber changes.

70:24

The right ventricle's dilated. There's right free wall

70:28

thickening. There's reflux of contrast into the inferior

70:31

vena cava. The right atrium will be dilated with tricuspid

70:35

regurgitation. There'll be reduced forward flow and decreased

70:39

opacification of the left heart. Those would be the

70:42

main features of pulmonary hypertension.

70:46

Then you look for the etiology of the mural thrombi versus not mural

70:49

thrombi, or you look for, uh, left

70:53

or right shunts, um,

70:57

or you look for chronic pulmonary venous hypertension,

71:00

right? That's the most common cause.

71:04

Okay. Usually, how many weeks before a repeated case if it's

71:08

indeterminate? Um, that's a good question.

71:11

I, I think it depends on the acuity.

71:13

Um, if it's an ER patient, um, they may wanna know

71:17

before they leave, and, you know, I, I don't think that's

71:20

unreasonable, uh, to some degree.

71:22

So you could actually suggest the repeat there if you are reading

71:26

in, on that time. If this is a, a, a

71:31

patient exam that you're reading maybe the morning

71:34

from the night or a day later, uh, you know, you, you just

71:38

kind of call them and say, "Well," you know, "maybe they should have this

71:41

reevaluated." You can do it as an outpatient with the lower extremity ultrasounds

71:45

if you want, for the reasons I said, um, or you have them come back

71:49

in. If you see evidence of sort of right heart strain

71:54

kind of thing without the hypertrophy, maybe you

71:58

repeat the indeterminate findings a bit more sooner,

72:02

um, because those are the people who tend to have a

72:06

higher incidence of morbidity and mortality.

72:10

Okay? All right. Do you have any comment on radiologists use the

72:14

term strain in terms... I realize it's RP

72:17

literature, and I understand what they

72:20

mean. Signs of elevated right heart pressure instead of strain,

72:24

since strain is more specific for the echo world.

72:27

Wow, I love that. Uh, terminology, I get into that

72:31

stuff. Um,

72:33

you're right.

72:35

I like using, I would like to use signs of elevated right heart

72:39

pressures. I do actually say that on

72:41

occasion. The reason I say

72:45

strain is for

72:48

a more effective communication with the

72:50

clinicians. But I absolutely

72:54

agree with you. I, every time I say it,

72:58

I, I don't particularly relish that

73:01

term, because to me, this is

73:04

signs of acute elevated right heart pressures and

73:08

right atrial pressures, reduced filling.

73:11

You know, that's exactly what we're seeing.But,

73:16

um,

73:17

in that particular situation, I say

73:21

strain in my report because that's what

73:25

most physicians and clinicians seem to

73:28

understand in the context, especially a pulmonary embolus.

73:32

So it's just to improve that. Love,

73:36

love your thoughts on that, though.

73:39

How do you incorporate age in your reading? Ooh, with difference.

73:43

Ooh, very good. I don't

73:47

tend to incorporate the age.

73:49

Um,

73:52

the reason it... If-- But we can understand

73:56

that in patients who may be eighty, yeah,

73:59

they're more likely to have contrast, altered contrast dynamics in

74:03

heart chambers

74:05

based on, you know, many more years of developing a lot of

74:09

problems. Um,

74:12

but I don't incorporate the age because I have seen, and I showed a

74:16

couple actually, of younger people who had

74:19

cardiomyopathies. So

74:22

I tend to keep the age out. What I'd really

74:26

find would be more useful would be body habitus, but we can see that,

74:30

right? Usually, we can see the body habitus, and that one

74:34

is more relevant with regards to transient interruption

74:38

of contrast

74:39

severity and such because of contrast volume.

74:43

But other, I don't usually use

74:45

age.

74:48

Okay?

74:51

Okay. I guess-

74:51

I think you got them all.

74:53

I got them all. Okay.

74:54

Oh, wow. Thank you so much for staying on extra time to answer those

74:58

questions.

74:59

My pleasure. And this is my email. If you have, you know,

75:03

thoughts, uh, questions, or comments,

75:06

um, feel free to email me. Um, I'd be happy

75:10

to chat with you about any of this topic.

75:14

Again, I, I realize this is a different topic, but it

75:18

makes reading these CTAs a lot more enjoyable because

75:21

you're, you're really kinda diving into what's going on with these

75:24

patients. But I appreciate y'all listening

75:28

and hope it was worth it.

75:31

Appreciate you being here again, Mark. Such a pleasure.

75:34

Thank you for everyone else for participating in this noon conference.

75:37

We will email out a link to the replay later

75:40

today. Be sure to join us next week, Thursday, March twelfth at twelve

75:44

PM Eastern, where Dr. Grace Mitchell will deliver a lecture entitled

75:48

Pediatric MSK Trauma. You can register for that at

75:51

medality.com and follow us on social media for updates on future new

75:54

conferences. Thanks again for learning with us, and have a great

75:58

day.