Cardiac case. Practice for echo boards.

This forum made possible through the generous support of SDN members, donors, and sponsors. Thank you.

sevoflurane

Ride
20+ Year Member
Joined
Jul 16, 2003
Messages
6,019
Reaction score
3,774
Boards are coming up next week. Hope this thread helps (sorry 'bout the crappy pics).

38 y/o brittle and difficult to control type I diabetic presents for CABG. She received an outpatient cath which revealed severe 4 vessel disease. HBAic is 13.5. Now blind in both eyes due to DM. + for Diabetic neprhopathy (cr 1.9) + neuropathy and + HTN.

Induction and lines go in fine. Tee probe is placed.

Comment on the following images:

:boom:

Members don't see this ad.
 
Last edited:
  • Like
Reactions: 1 user
Before I comment further, I will note the E' velocity of 13.5 cm/s and E/E' of 5.27.
 
  • Like
Reactions: 1 user
Members don't see this ad :)
Before I comment further, I will note the E' velocity of 13.5 cm/s and E/E' of 5.27.


Ah. Ok. So can't be PN. Been a while since I've done some serious diastology.

Of note, I studied more diastology for the advanced exam than any other topic and maybe had 3 Qs. Very disappointed.
 
The E/A transmittal Doppler combined with the S<D pulmonary venous doppler would suggest pseudonormal physiology. However, the E' is greater than 8 cm/s, which would suggest normal diastology. This would have to take in account how much you trust the E' as a predictor of diastolic dysfxn under general anesthesia. I heard some people say that you can't trust that algorithm under GA and speckle tracking is more accurate. Did you happen to measure the LAP by Doppler and were all of the measurements taken while holding ventilation?

In addition, the inferolateral wall measures 1.84 cm, which would classify this patient as severe concentric LVH. The LA appendage also has a velocity >40 cm/s, which would make this patient lowering risk for thrombus if that's what your looking at in the last slide. Maybe that last slide is the RUPV?
 
With severe LVH why would you care about pseudonormal or not? isn't diastolic dysfunction a given?
 
With severe LVH why would you care about pseudonormal or not? isn't diastolic dysfunction a given?


I'm not sure this is true. This patient is 38 y/o and has not gone through the diastolic changes that occur with increasing age and LVH doesn't necessarily mean diastolic dysfunction. I will agree that with this degree of hypertrophy one would expect some decrease in complience .

Prognostically, pseudonormal pattern is very different than a fixed restrictive relaxation pattern (IIIB)-which is not reversible with a valsalva, RTburg, Nitro, etc. Quantifying the degree of diastolic dysfunction is important for prognosis and as a way to monitor medical management as some patients can and will regress to varying degrees.
 
The E/A transmittal Doppler combined with the S<D pulmonary venous doppler would suggest pseudonormal physiology. However, the E' is greater than 8 cm/s, which would suggest normal diastology. This would have to take in account how much you trust the E' as a predictor of diastolic dysfxn under general anesthesia. I heard some people say that you can't trust that algorithm under GA and speckle tracking is more accurate. Did you happen to measure the LAP by Doppler and were all of the measurements taken while holding ventilation?

In addition, the inferolateral wall measures 1.84 cm, which would classify this patient as severe concentric LVH. The LA appendage also has a velocity >40 cm/s, which would make this patient lowering risk for thrombus if that's what your looking at in the last slide. Maybe that last slide is the RUPV?

Great response sethco. :thumbup:

Yep. > 40 cm/s and no SEC = low probability of thrombus.

Speckle tracking is supposed to be preload and afterload independent, but so is tissue doppler imaging and strain rate.

Yep. All taken during apnea. I did not have time to measure LAP.

So I reviewed the images with cardiology out of my own curiosity. They do encounter this pattern on rare occasion in the setting of LVH.
These images were taken while we we're priming the pump. So if she did have a pseudonormal pattern decreasing preload (like a valsalva) would have revealed a TMF E:A ratio less than 1, yet E:A was 1.28. I didn't show it here, but DT was nml and Pulm A reversal wave velocity was 18-20 cm/s... arguing a normal relaxation pattern. Weird.

Definitely not what I expected. Maybe HB can add some input here.
 
Great responses. We can keep on talking about diastology, but we can simultaneously keep the case going for fun. So you continue your exam and you see this. Anything abnormal?
 
Last edited:
To be honest, I first thought the short axis views were somehow foreshortened (i.e. cut obliquely through the heart, not straight across it), since the inferior wall looks so much thicker than the anterior. The 4C view you just posted doesn't look to me like like outrageous LVH.

But if the LVH is real, then yeah, it's a bit of a diagnostic conundrum. One of those "indeterminate diastolic function" calls where some data looks normal (like the tissue Doppler) and some doesn't. I think most of it looks normal.

I think the heart is young enough that it still actively relaxes, and that diastolic function is therefore near- normal, though there are probably elevated filling pressures afoot ( at least while awake) that will throw off some indices.

Also S isn't always less than D on that trace, which is interesting.

But enough speculation, let's talk about the right heart...
 
  • Like
Reactions: 1 user
Agree. Right side overload. Pulm HTN? What does color look like across V septum? ME AV SAX with color please?
 
Here is some color. What view is this and what's going on here?
 
Last edited:
Your 4-chamber view looks like the RV makes up the majority of the apex in relation the the LV. The RV is definitely enlarged. The last picture you posted is a modified bicaval view showing lack of coaptation of the tricuspid valve (likely due to the RV enlargement) and tricuspid regurgitation. I agree with the above about the severe LVH and normal appearing diastology.
 
Members don't see this ad :)
Your 4-chamber view looks like the RV makes up the majority of the apex in relation the the LV. The RV is definitely enlarged. The last picture you posted is a modified bicaval view showing lack of coaptation of the tricuspid valve (likely due to the RV enlargement) and tricuspid regurgitation. I agree with the above about the severe LVH and normal appearing diastology.
 
Yep. TR. What do you tell the surgeon?


Suggest a ring annuloplasty.

I recently did a 4 v Cabg in a bad diabetic. Put probe down and found mod type 1 MR. Surgeon "That's fine, she's not getting a ring." Ok. Still had mod MR after bypass. Frustrating.
 
Suggest a ring annuloplasty.

I recently did a 4 v Cabg in a bad diabetic. Put probe down and found mod type 1 MR. Surgeon "That's fine, she's not getting a ring." Ok. Still had mod MR after bypass. Frustrating.

Yep. This part of the case is analogous to a type I MR jet. :thumbup:

I'm really skeptical about calling stuff out in the OR. So based on the VC by itself (even though the true VC was 8.8mm), I didn't feel comfortable telling our surgeon to go ahead and do a ring annuloplasty. So I went hunting a little further.

Here is another image.


Hmmm... what's going on here? o_O
 
Last edited:
Is there anything else we can do in order to secure the diagnosis and treatment plan? How do we interpret the above CWD profile and the below PWD profile?



What if I told you the IVC measured 25mm? What can be inferred with this measurement?
 
Last edited:
Severe TR based on hepatic S wave blunting.

Not hepatic (although would show same) but still S wave blunt in IVC.
 
Last edited:
  • Like
Reactions: 1 user
According to the guidelines the TR is severe by VC (>7mm). The CWD profile also goes along with severe TR based on the sharp early peaking appearance of the TR jet. There is systolic blunting. If I had to make this call, I would say mod-severe TR. The IVC is also dilated (>2.1cm). Are they just doing the cabg or is there another valve issue. I'm reviewing the new 2014 ACC AHA valve guidelines now. Class I indication to repair or replace if doing a left sided valve. Haven't found data when doing just a CABG. This is a tough call. The pulmonary htn isn't that bad at all if you assume RAP of 15. You had a CVC in, what was your CVP?
 
They don't mention what to do with TR during a CABG anywhere in the 2011 guidelines. What did you tell them?
 
They don't mention what to do with TR during a CABG anywhere in the 2011 guidelines. What did you tell them?

Another great answer Dr. Beaker.

Anything else we can do before we pop over the drapes and share our findings?
 
According to the guidelines the TR is severe by VC (>7mm). The CWD profile also goes along with severe TR based on the sharp early peaking appearance of the TR jet. There is systolic blunting. If I had to make this call, I would say mod-severe TR. The IVC is also dilated (>2.1cm). Are they just doing the cabg or is there another valve issue. I'm reviewing the new 2014 ACC AHA valve guidelines now. Class I indication to repair or replace if doing a left sided valve. Haven't found data when doing just a CABG. This is a tough call. The pulmonary htn isn't that bad at all if you assume RAP of 15. You had a CVC in, what was your CVP?

Naaaice. :thumbup: Early peaking vs late peaking in HOCM. :claps:

... and our inflow velocity is >1 m/s.
 
After doing a basic exam, look at each valve carefully. See if there is any other valvular pathology to address as well which would make the call to fix the TR easier. If I were in your shoes, I would tell them the TR should be addressed. We are in the chest for a CABG, and the risk goes way up for a re-do sternotomy to fix it later.
 
So I did a couple more measurements because if we were going to do this I wanted to be 100% positive it was the right thing to do.

Pisa Radius was 1.1cm with a nyquist of 30 cm/s.
Jet Area = 10.5 cm^2
I also measured the TV annulus both in the 4 chamber and RV inflow-outflow. Both measurements were >2.6 cm.

Now. Let's take a step back and look at our data.

1) LA enlargement
2) RV enlargement (some degree of apex forming geometry)
3) VC of 8.8 cm (probably tips the scale the most)
4) Jet area 10.5
5) Pisa radius of 1.1 cm w/ a nyquist limit of 30 cm/s
6) IVC > 20mm ( = elevated R atrial pressure) with D>S wave
7) Early peaking triangular appearing regurgitant jet
8) Severely dilated TV annulus leading to a central jet.
9) PA pressures in the 50's

All data harvested under General anesthesia = underestimates the severity of everything above.

In addition, this patient is 38 y/o and if her TV isn't fixed during her CABG, it most certainly will be in the future as her R heart geometry has already been altered. Failure to address the TV would likely lead to increase morbidity and a second sternotomy/open heart procedure in the future.

After a short discussion, we elected to add a TV annuloplasty as we felt she would benefit from it in the long term. The ring repair was easy.

With the ring in place, TV rergurgitation was nearly nonexistent before we left CVOR. In the end, it was a relatively easy call.
 
  • Like
Reactions: 1 user
Thanks for the case Sevo. I enjoyed it. Good luck to everyone taking the exams this year. It was a fun test.
 
Thanks for the case Sevo. I enjoyed it. Good luck to everyone taking the exams this year. It was a fun test.

No problem. :thumbup:
Good luck to everyone taking it next week.
I hope some lurkers out there can get something from the case presented.
Maybe some of you studs can post a case.

I'll cash out with some random pics. Thank you all for playing over the last couple of days. :artist:

1. You come off bypass and get this picture. What is being measured here and what does it show?


2. Diagnosis?

F4.large.jpg


3. Diagnosis?

Video-3.gif


4. Diagnosis?

255v64n01-13190111fig6.jpg
 
Last edited:
1. dP/dT- measure of LV function. His is 1000mmHg/s. >1200 is normal
2. Is that a before and after? A. looks like LV noncompaction. maybe cardiac lipoma
3. atrial myxoma
4. 3D artifact?
 
Agree with above, except number 4. It looks like ring dehiscence. Had a case like this couple months ago. Initially the CFD fooled me because none of the regurgitant flow through the that big hole was turbulent and the patient also had moderate MR through the ring that was turbulent.

BTW, how did you put in the video of the myxoma? Is that an avi file?
 
Agree with above, except number 4. It looks like ring dehiscence. Had a case like this couple months ago. Initially the CFD fooled me because none of the regurgitant flow through the that big hole was turbulent and the patient also had moderate MR through the ring that was turbulent.

BTW, how did you put in the video of the myxoma? Is that an avi file?


Correct on the dehiscense.
The myxoma is a file borrowed from Duke University.
 
So I did a couple more measurements because if we were going to do this I wanted to be 100% positive it was the right thing to do.

Pisa Radius was 1.1cm with a nyquist of 30 cm/s.
Jet Area = 10.5 cm^2
I also measured the TV annulus both in the 4 chamber and RV inflow-outflow. Both measurements were >2.6 cm.

Now. Let's take a step back and look at our data.

1) LA enlargement
2) RV enlargement (some degree of apex forming geometry)
3) VC of 8.8 cm (probably tips the scale the most)
4) Jet area 10.5
5) Pisa radius of 1.1 cm w/ a nyquist limit of 30 cm/s
6) IVC > 20mm ( = elevated R atrial pressure) with D>S wave
7) Early peaking triangular appearing regurgitant jet
8) Severely dilated TV annulus leading to a central jet.
9) PA pressures in the 50's

All data harvested under General anesthesia = underestimates the severity of everything above.

In addition, this patient is 38 y/o and if her TV isn't fixed during her CABG, it most certainly will be in the future as her R heart geometry has already been altered. Failure to address the TV would likely lead to increase morbidity and a second sternotomy/open heart procedure in the future.

After a short discussion, we elected to add a TV annuloplasty as we felt she would benefit from it in the long term. The ring repair was easy.

With the ring in place, TV rergurgitation was nearly nonexistent before we left CVOR. In the end, it was a relatively easy call.
What did the preop echo show?
 
1. dP/dT- measure of LV function. His is 1000mmHg/s. >1200 is normal
2. Is that a before and after? A. looks like LV noncompaction. maybe cardiac lipoma
3. atrial myxoma
4. 3D artifact?

Cardiac lipoma... they can occur anywhere, but often arise in the intramyocardial tissue or pericaurdium.

255v62n03-13135149fig02.jpg


Lipotamous Hypertrophy of the intraatrial septum:

F3.large.jpg


This is a cool TTE: Apical obliteration seen in endomyocardial fibrosis/hypreisinophilic syndrome.

F1.large.jpg
 
Top