TEE

[deleted171991]

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In my mind decompensated heart failure and CS means no anesthesia unless for a lifesaving procedure.
If she has functional MR she needs optimization and likely MCS. I like Impella here, given the pulmonary edema (feel like it gives better offloading than an IABP).
If it's pap rupture she needs surgery. This seems pretty unlikely with 3 TTEs and no clear rupture. Did she get a trop?
Cardiac CT might give a quick answer to primary vs secondary MR.

Somebody in tachycardia and pulmonary edema for days will probably have up to MI-level trops.

 

[Ronin786]

Nice job @jeesapeesa

Also highlights the fact that we are once again not simple tube jockeys (despite the argument above). Bringing up these points to the cardiologists avoided an unnecessary procedure.

It also highlights how hard it is to kill a young patient.

 

[deleted171991]

very astute and partly correct. lots of frustrations with this place and one of the 3 facilities i work at with my group. i do think they are overwhelmed and they do the same things over and over since i just found out they repeated a TTE today with basically the same results. you are wrong with the intensivist part - they used to hold a contract that affiliated them with a large academic institution with which chiefs of anesthesia critical care department would moonlight here. that is gone and now there are still fellowship trained intensivists that give absolutely no pushback to the cardiologists.

In my understanding, this is a lady with un(successfully)treated coronary vasospasm. All she needs is a calcium-channel blocker +/- nitrate for the vasospasm, lasix/CPAP for the decompensated HF, and some form of BP/CO support while all of this is happening. And this was crystal clear after the first LHC, 10 days ago. What's so hard?

 

[dhb]

What's so hard?

You know that 😉

 

[itwasalladream]

Somebody in tachycardia and pulmonary edema for days will probably have up to MI-level trops.

Agree. But if by chance they're on the lower side it weighs against pap rupture.

I haven't treated much coronary vasospasm. Giving CCB/Nitrate/Lasix in someone with CS obviously is a bit concerning. Giving pressor is easy. But do you see any problems with pressor for BP when you're doing your best trying to dilate coronaries? That's why I'd lean toward MCS if it can be done safely.

 

[deleted171991]

Agree. But if by chance they're on the lower side it weighs against pap rupture.

I haven't treated much coronary vasospasm. Giving CCB/Nitrate/Lasix in someone with CS obviously is a bit concerning. Giving pressor is easy. But do you see any problems with pressor for BP when you're doing your best trying to dilate coronaries? That's why I'd lean toward MCS if it can be done safely.

I have always considered good intensive care to include a part of experimental medicine. In this case, one has to work to find the CCB/nitrate and low-dose pressor combo that works (e.g. low dose epi is a coronarodilator, even low-dose norepi may work, or maybe even a touch of a coronary constrictor alpha1-blocker).

Euvolemia/CPAP (i.e. decreasing preload) and coronarodilation (i.e. normalizing the EF) may just do the trick, too, and a pressor may not be needed, especially if the nitrate/CCB is administered as a titrated drip (not as a blind, long-acting medication, we'll check on the patient tomorrow). FREQUENT trial and error, until one finds what works in this particular patient, not set it and forget it.

Mechanical circulatory support would probably save a lot of headaches while playing this game. Also, outside of the cath lab, I imagine one would need frequent bedside focused echo, to look for (the disappearance of) WMAs, as a surrogate for coronary spasm, and, of course, at least an a-line.

This ain't my typical pathology either.

 

[Hoya11]

Feels like you're not reading my posts before you reply to me.

Thx I read it I just didnt think that fact would significantly change my management or any decision making processes here

These decisions are always hard without actually seeing the patient, but I think we were in the same camp of wanting to get it done without a freak out

 

[Hamhock]

"staged PCI revealed normal coronaries"

We were told She had coronary vasospam and now has MR with clean coronaries. How do know she has coronary artery disease and why would you treat her for that when she doesn't have it?

There is a great discussion here. It was a pleasure to read.

I am also convinced, based on the OP presentation, that this case has been managed by the non-proceduralists poorly.

I am also not convinced that the original diagnosis (vasospasm) is correct.

I am hearing more and more about SCAD (spontaneous coronary artery dissection) being confused with vasospasm and demand type 2 NSTEMI. It seems gender, age, and the otherwise "clean" coronaries of this patient strongly hint at this diagnosis also.

Thoughts? Is the OP able to provide any more updates? Maybe another interventional cardiologist could review the images again...

Of course, regardless of this, the patient needs some management of pulmonary edema.

HH

 

[dchz]

I am also not convinced that the original diagnosis (vasospasm) is correct.

I am hearing more and more about SCAD (spontaneous coronary artery dissection) being confused with vasospasm and demand type 2 NSTEMI. It seems gender, age, and the otherwise "clean" coronaries of this patient strongly hint at this diagnosis also.

I am not an interventional cards so i might be talking out of my ass.

I believe the incidence of SCAD is much lower than vasospasms. Nothing from the history completely rules out the vasospasms either. I've seen vasospasms get stented - where a young person has angiographic proven STEMI but then normal angiographic coronaries a week later (which i think what the OP is trying to say). From my rudimentary understanding of the cardiology world, i believe that diagnosis is not rare in the stated patient population.

However, I do believe that this is less like likely to have pap muscle rupture from vasospasms in a 37 year old (LAD isn't the sole supply to either pap muscles), with vasospams or otherwise.

I do believe the pulm edema is contributed more by the MR than the "CHF" (MR is causing the CHF here is another way to phrase it). Which is why I am very much for doing the TEE now.

 

[dchz]

Another point worth bringing up that needs a good understand of both anesthesiology and cardiology here:

When you provide the anes, your anesthetic really matters (more so than just that you make sure they don't die).

Your anesthetic technique could affect the MR depending on the SVR decrease. i.e. when you give sedatives that decrease the SVR and the MAP goes from 85 to 65, the MR artificially look better on TEE, which why this study will take longer than the usual no-thrombus-in-the-LAA study. If a thorough echocardiographer is performing the TEE, they should ask you for a phenylephrine challenge.

Furthermore, what about the reflexive bradycardia 2/2 phenylephrine push?? Theoretically, the MR could also be under diagnosed 2/2 lower cardiac output. Which is why I would use EPI here rather than dobutamine or milirinone as my inotrope of choice. The combination of both increased inotropy and SVR increases the sensitivity of the test. But one also has to take into account the chance of possible false positives as well - the increase of both inotropy and SVR could show severe MR when it is only moderate under normal loading conditions. One of the things I would do is ensure the BP reaches a map of 85 before I say there is no severe MR. The patient really needs a good experienced echocardiograher here.

Lastly, if there is IABP in, do you turn off the IABP during the test? I would argue that one SHOULD turn off the IABP, as it significantly lowers afterload and can decrease the sensitivity of the test.

Thoughts? @bigdan , @vector2 , @Newtwo ?

 

[deleted162650]

Another point worth bringing up that needs a good understand of both anesthesiology and cardiology here:

When you provide the anes, your anesthetic really matters (more so than just that you make sure they don't die).

Your anesthetic technique could affect the MR depending on the SVR decrease. i.e. when you give sedatives that decrease the SVR and the MAP goes from 85 to 65, the MR artificially look better on TEE, which why this study will take longer than the usual no-thrombus-in-the-LAA study. If a thorough echocardiographer is performing the TEE, they should ask you for a phenylephrine challenge.

Furthermore, what about the reflexive bradycardia 2/2 phenylephrine push?? Theoretically, the MR could also be under diagnosed 2/2 lower cardiac output. Which is why I would use EPI here rather than dobutamine or milirinone as my inotrope of choice. The combination of both increased inotropy and SVR increases the sensitivity of the test. But one also has to take into account the chance of possible false positives as well - the increase of both inotropy and SVR could show severe MR when it is only moderate under normal loading conditions. One of the things I would do is ensure the BP reaches a map of 85 before I say there is no severe MR. The patient really needs a good experienced echocardiograher here.

Lastly, if there is IABP in, do you turn off the IABP during the test? I would argue that one SHOULD turn off the IABP, as it significantly lowers afterload and can decrease the sensitivity of the test.

Thoughts? @bigdan , @vector2 , @Newtwo ?

Dude, just put in the tube and turn the dial mmkay.

 

[vector2]

Another point worth bringing up that needs a good understand of both anesthesiology and cardiology here:

When you provide the anes, your anesthetic really matters (more so than just that you make sure they don't die).

Your anesthetic technique could affect the MR depending on the SVR decrease. i.e. when you give sedatives that decrease the SVR and the MAP goes from 85 to 65, the MR artificially look better on TEE, which why this study will take longer than the usual no-thrombus-in-the-LAA study. If a thorough echocardiographer is performing the TEE, they should ask you for a phenylephrine challenge.

Furthermore, what about the reflexive bradycardia 2/2 phenylephrine push?? Theoretically, the MR could also be under diagnosed 2/2 lower cardiac output. Which is why I would use EPI here rather than dobutamine or milirinone as my inotrope of choice. The combination of both increased inotropy and SVR increases the sensitivity of the test. But one also has to take into account the chance of possible false positives as well - the increase of both inotropy and SVR could show severe MR when it is only moderate under normal loading conditions. One of the things I would do is ensure the BP reaches a map of 85 before I say there is no severe MR. The patient really needs a good experienced echocardiograher here.

Lastly, if there is IABP in, do you turn off the IABP during the test? I would argue that one SHOULD turn off the IABP, as it significantly lowers afterload and can decrease the sensitivity of the test.

Thoughts? @bigdan , @vector2 , @Newtwo ?

There is a reason that the ACC/AHA guidelines continue to de-emphasize certain measurements, particularly on the last MR guideline update. Qualitative measures or load dependent measures are good to get a general gestalt, but we shouldn't be making decisions about whether to repair or replace a valve based on those.

The 2017 guideline emphasizes vena contracta, Rvol/R%, and EROA. VC is theoretically load independent, same for Rvol based on continuity, and same for PISA EROA. 2d PISA poses a problem though because obviously a real PISA isn't really hemispherical, and it's reaaaallllyyyy not hemispherical in the case of functional MR where it's more crescentic shaped.

What I consider "gold standard" for echo is a VC in ME-AVLAX perfectly cutting A2-P2 that is >0.7 cm, a 3D vena contracta area, and/or RVol by continuity using 3d trace of mitral annulus and LVOT for the areas or Rvol by MR VTI x 3d vena contracta area. If you use those measurements plus have supporting data like PV S wave reversal and E velocity inflow 1.2-1.5 m/s, then I think you can be confident in severe MR even without using inotropes or pressors for provocation.

 

[kidthor]

There is a reason that the ACC/AHA guidelines continue to de-emphasize certain measurements, particularly on the last MR guideline update. Qualitative measures or load dependent measures are good to get a general gestalt, but we shouldn't be making decisions about whether to repair or replace a valve based on those.

The 2017 guideline emphasizes vena contracta, Rvol/R%, and EROA. VC is theoretically load independent, same for Rvol based on continuity, and same for PISA EROA. 2d PISA poses a problem though because obviously a real PISA isn't really hemispherical, and it's reaaaallllyyyy not hemispherical in the case of functional MR where it's more crescentic shaped.

What I consider "gold standard" for echo is a VC in ME-AVLAX perfectly cutting A2-P2 that is >0.7 cm, a 3D vena contracta area, and/or RVol by continuity using 3d trace of mitral annulus and LVOT for the areas or Rvol by MR VTI x 3d vena contracta area. If you use those measurements plus have supporting data like PV S wave reversal and E velocity inflow 1.2-1.5 m/s, then I think you can be confident in severe MR even without using inotropes or pressors for provocation.

That’s cool and all but the cardiology fellow will probably do the exam with a cardiology attending who doesn’t do this often. Soooo...

 

[jeesapeesa]

just a quick update. i was on call sunday and had a chance to drop by and see how she was doing. looked and felt better ... nasal cannula off and noticed she didn't have any shortness of breath and no drop in oxygen saturation while talking to me - also had a chance to walk around the room/increased activity. HR has been steady at the 90s range with slight improvements in BP from the last time i saw her. nothing was done over the long weekend - no IABP/impella placement. additionally she was kicked out of the ICU and downgraded. Kounis syndrome being thrown around and she was tested for it but really unclear what the allergy, if any, were/was. anyways, i'm sure this week will provide some more insight on her ongoing care. thanks for all your great responses!

 

[Hork Bajir]

Great discussion in this thread... But also, with all of the extremely interesting and lively intellectual debate here, lol at the patient getting better with pretty much no intervention. Goes to show how once again, the practice of good medicine is to do as little as possible

 

[MoMoGesiologist]

just a quick update. i was on call sunday and had a chance to drop by and see how she was doing. looked and felt better ... nasal cannula off and noticed she didn't have any shortness of breath and no drop in oxygen saturation while talking to me - also had a chance to walk around the room/increased activity. HR has been steady at the 90s range with slight improvements in BP from the last time i saw her. nothing was done over the long weekend - no IABP/impella placement. additionally she was kicked out of the ICU and downgraded. Kounis syndrome being thrown around and she was tested for it but really unclear what the allergy, if any, were/was. anyways, i'm sure this week will provide some more insight on her ongoing care. thanks for all your great responses!

You mean all these anesthesiologists advocating IABP, impella, central line and pressors, etc ended up not knowing better than the cardiologists? Shocker!

In all seriousness, was surprised at how quickly and strongly people advocated for mechanical circulatory support. Is there any strong indications for MCS? What happened to medical optimization first?

 

[deleted697535]

Great discussion in this thread... But also, with all of the extremely interesting and lively intellectual debate here, lol at the patient getting better with pretty much no intervention. Goes to show how once again, the practice of good medicine is to do as little as possible

Well yes and no.
Getting better on an IV lasix drip isnt exactly nothing, nor is it sustainable. She needs that Mitral repaired unfortunately.

@dhcz
Re MR under GA. I very rarely downgrade the severity of a regurgitant lesion under GA when the primary op is for MV repair/replace. As outlined already the loading conditions are so drastically different under GA plus they're likely diuresed to a wafer pre-op etc etc etc.
I tend to trust our cardiologists TTE a lot. It doesnt sound like the op's institution is that overall trustworthy

If the pre-op diagnosis is severe MR and the plan is MV repair/replace then i consider my job to be to tell the surgeon the feasibility of repair vs replace as its accepted repair has far better outcomes.

Then my assessment is which leaflet/scallop is the culprit and tell them which repair to do or which valve to insert, plus show them the surgical view on 3d. Make sure the circ is out of the way, look for incr risk of SAM etc

I cant remember the last time ive used IABP/pressors to try not repair a mitral. Ive certainly seen many times where i would have to ask the surgeon to repair at least moderate MR. Sometimes they listen, sometimes not

 

[vector2]

You mean all these anesthesiologists advocating IABP, impella, central line and pressors, etc ended up not knowing better than the cardiologists? Shocker!

In all seriousness, was surprised at how quickly and strongly people advocated for mechanical circulatory support. Is there any strong indications for MCS? What happened to medical optimization first?

Most everyone here wrote bipap/CPAP, diuresis, inotropes first. And if you look at the end of the previous page, ppl including myself were advocating MCS after OP posted the day after his original post saying the pts hemodynamics were still bad, oxygenation was bad, and LV function was worse than previously thought on repeat echo.

Additionally, OP has never provided a bunch of supportive information like renal fnx, liver fnx, lactate, SVO2, CI, i.e. things that would sway the decision for MCS one way or another...

 

[deleted697535]

Its another discussion but there is a growing body of evidence that impella's dont improve outcome. Weve certainly not had much luck with our program.

balloon pumps have been around for so long but their body of evidence isnt fantastic either. And thats for definitive post infarct patients. This lady didnt even have a stent did she and had clean coronaries a couple days later so i dont even know where she would fit in the scheme of things?

 

[jeesapeesa]

should have added that except for hyponatremia her kidney, liver function tests, thyroid tests were normal. early on leukocytosis had resolved.

 

[MoMoGesiologist]

Most everyone here wrote bipap/CPAP, diuresis, inotropes first. And if you look at the end of the previous page, ppl including myself were advocating MCS after OP posted the day after his original post saying the pts hemodynamics were still bad, oxygenation was bad, and LV function was worse than previously thought on repeat echo.

Additionally, OP has never provided a bunch of supportive information like renal fnx, liver fnx, lactate, SVO2, CI, i.e. things that would sway the decision for MCS one way or another...

I get what you are saying and agree. However there are some posts here saying IABP would be high up on their list of interventions and they can’t believe cardiologists would manage their patients this way.

Now having the end result, we can say retrospectively all this patient needed was diuresis (plus likely eventual mitral valve repair). But this discussion makes me think of all the patients who were “super sick” who got a bunch of interventions, that maybe what they needed was less and likely were “sick” from iatrogenic harm. I’m sure we have all had that attending who does waaayyy too much for what should have been a simple anesthetic.

 

[vector2]

we can say retrospectively all this patient needed

Retrospectively if we MMQB it we can say a lot of things, so retrospectively is neither here nor there and we should try to avoid hindsight bias just because this lady with a bizarre clinical course happened to do well. Based on what OP told us, I'm more of the opinion that OP's cardiology department didn't make a decision to withhold MCS based on clinical judgement but more because of expediency. With the initial presentation of borderline cardiogenic shock, coronary malperfusion of some sort, frank pulmonary edema, high FiO2 requirement, severe MR, and ?ruptured pap or torn chord as described in the original post, MCS (impella, IABP) is well within the standard of care and some might even argue one of the first interventions that should be considered early assuming a large dose of lasix, CPAP, inotrope infusion doesn't immediately begin to stabilize the patient.

 

[MoMoGesiologist]

Retrospectively if we MMQB it we can say a lot of things, so retrospectively is neither here nor there and we should try to avoid hindsight bias just because this lady with a bizarre clinical course happened to do well. Based on what OP told us, I'm more of the opinion that OP's cardiology department didn't make a decision to withhold MCS based on clinical judgement but more because of expediency. With the initial presentation of borderline cardiogenic shock, coronary malperfusion of some sort, frank pulmonary edema, high FiO2 requirement, severe MR, and ?ruptured pap or torn chord as described in the original post, MCS (impella, IABP) is well within the standard of care and some might even argue one of the first interventions that should be considered early assuming a large dose of lasix, CPAP, inotrope infusion doesn't immediately begin to stabilize the patient.

Maybe the heart docs were being expedient and lazy. Or maybe they know what they’re doing. Guess we will never know.

Also if you have a paper or guideline on when MCS should be one of the first interventions considered, would be happy to learn

 

[vector2]

Maybe the heart docs were being expedient and lazy. Or maybe they know what they’re doing. Guess we will never know.

Also if you have a paper or guideline on when MCS should be one of the first interventions considered, would be happy to learn

Just to clarify, I said "first interventions that should be considered early assuming a large dose of lasix, CPAP, inotrope infusion doesn't immediately begin to stabilize the patient." So, if she is failing medical therapy, this lady potentially meets three possible indications for MCS that I can think of if she has ischemic (ruptured pap) severe MR, 90% prox LAD vasospasm or thrombus requiring PCI in setting of severely reduced LV function, or is going to undergo a mitraclip or surgical mitral repair.

2015 SCAI/ACC/HFSA/STS Clinical Expert Consensus Statement on the Use of Percutaneous Mechanical Circulatory Support Devices in Cardiovascular Care: Endorsed by the American Heart Assocation, the Cardiological Society of India, and Sociedad Latino Am

Although historically the intra-aortic balloon pump has been the only mechanical circulatory support device available to clinicians, a number of new d…

www.sciencedirect.com

Additionaly, I highly recommend Kapur's lecture on MCS because it really highlights the importance of mechanical LV decompression (unloads LV, LA, pulmonary bed, RV) and the weaknesses of traditional decompensated HF therapy (inotropes, IABP, etc).

 

[dchz]

Kounis syndrome being thrown around and she was tested for it but really unclear what the allergy, if any, were/was. anyways, i'm sure this week will provide some more insight on her ongoing care. thanks for all your great responses!

 

[deleted171991]

just a quick update. i was on call sunday and had a chance to drop by and see how she was doing. looked and felt better ... nasal cannula off and noticed she didn't have any shortness of breath and no drop in oxygen saturation while talking to me - also had a chance to walk around the room/increased activity. HR has been steady at the 90s range with slight improvements in BP from the last time i saw her. nothing was done over the long weekend - no IABP/impella placement. additionally she was kicked out of the ICU and downgraded. Kounis syndrome being thrown around and she was tested for it but really unclear what the allergy, if any, were/was. anyways, i'm sure this week will provide some more insight on her ongoing care. thanks for all your great responses!

You mean she won't get mitral valve surgery? What a shock! 😛

 

[deleted171991]

Great discussion in this thread... But also, with all of the extremely interesting and lively intellectual debate here, lol at the patient getting better with pretty much no intervention. Goes to show how once again, the practice of good medicine is to do as little as possible

Now you know why I am a minimalist, as you can see from my first post in this thread.

First Do No Harm, AKA medicine 101 for the last two thousand years.

The art of intensive care is not knowing what to do, but what and when not to.

Absent a iatrogenic intervention, many patients will get better with the proper supportive care. Intensivists are not gods; we are stewards. In the hands of a good intensivist, Mother Nature can be the best doctor.

 

[dchz]

@vector2 I think we disagree here in some places but agree in others:

There is a reason that the ACC/AHA guidelines continue to de-emphasize certain measurements, particularly on the last MR guideline update. Qualitative measures or load dependent measures are good to get a general gestalt, but we shouldn't be making decisions about whether to repair or replace a valve based on those.

The 2017 guideline emphasizes vena contracta, Rvol/R%, and EROA. VC is theoretically load independent, same for Rvol based on continuity, and same for PISA EROA. 2d PISA poses a problem though because obviously a real PISA isn't really hemispherical, and it's reaaaallllyyyy not hemispherical in the case of functional MR where it's more crescentic shaped.

All mitral regurg measurements (qualitative and quantitative) are load-dependent: RVol/R% Regurgitant volume%, Vena Contracta (VC), EROA (Effective regurgitant orifice area), are all load-dependent. MR it self is load-dependent so it should follow that all measurements are load-dependent. EROA and VC are less theoretically less load-dependent because a small area change can mean a big change in flow, so it's harder to detect the change in a smaller dimension due to the margin of error.

According to the 2014 AHA/ACC guidelines, VC is only 1 of the quantitative measures that should be taken into account in the context of the big picture. I don't believe the 2017 guideline change any of the diagnostic criteria but i'd be happy to be corrected. I do agree with you that PISA isn't a hemisphere and prone to a lot of errors. Personally, I feel that VC is just as prone too error. It's about as user-dependent as Vp.

What I consider "gold standard" for echo is a VC in ME-AVLAX perfectly cutting A2-P2 that is >0.7 cm, a 3D vena contracta area, and/or RVol by continuity using 3d trace of mitral annulus and LVOT for the areas or Rvol by MR VTI x 3d vena contracta area. If you use those measurements plus have supporting data like PV S wave reversal and E velocity inflow 1.2-1.5 m/s, then I think you can be confident in severe MR even without using inotropes or pressors for provocation.

I disagree with the 2D VC measurement. The valve cordes do not read the text book, sometimes you have to sweep to the edge of A1 to get the MR. Also how do you know your VC is in line with the the actual direction of flow?? How do you know your LAX view is actually lined up perpendicular to A2-P2 commissure? How do you know the VC you get at 120 degree isn't foreshortened when you should be at 135 degrees? I don't like the VC measurement at all to be honest, but it's only my personal opinion.

I like the 3D color EROA measurement but it also runs into problems of foreshortening and frame rate. (most X8-2t probes with Epic7C machines only gets like 8Hz frame rate if you do 3d with color). I am a HUGE fan of the 3D ejection volume to calculate the ERV, but a lot of electrocardiographers don't do this and it's never been "validated" by any study as far as I know. Still, i think this is the most reliable measure, but it still should be taken into the context of the big picture.

I used to be a big fan of the S wave reversal but then it was explained to me by an experienced cardiologist that it's merely a proxy measure of a previously not very sensitive finding during fluoroscopy - If they did an LV gram while doing a LHC, it would clue them in if they see the pulm vein tracing during the fluro shot. The S wave reversal was just an echography proxy measure for that but it's very non-sensitive.

To sum this up I am not sure if there is any set way to do it. It takes an experience person years to understand all the nuances and i still got a ways to go. The measurement of MR is not an exactly science either, because you have to then take into account if this is primary or secondary. The data and evidence on primary is overwhelming while secondary MR is still somewhat in a gray area.

However, I do believe that we should account of the load conditions when doing the TEE. The most experienced cardiologists do this, e.g. we always do a phenylephrine challenge after the mitraclip if the BP is low - make sure the clip actually did something and not just the general anesthesia making it better.

 

[deleted171991]

@vector2However, I do believe that we should account of the load conditions when doing the TEE. The most experienced cardiologists do this, e.g. we always do a phenylephrine challenge after the mitraclip if the BP is low - make sure the clip actually did something and not just the general anesthesia making it better.

Is that why you didn't care that much about diuresing the patient to euvolemia, and insisted on getting her TEE done while in pulmonary edema? 😛

 

[dchz]

Is that why you didn't care that much about diuresing the patient to euvolemia, and insisted on getting her TEE done while in pulmonary edema? 😛

No, the reason is that the pulm edema would never get better if it was primary MR and the pt would just sit there "medically optimizing" for days while getting worse 😛

 

[deleted171991]

No, the reason is that the pulm edema would never get better if it was primary MR and the pt would just sit there "medically optimizing" for days while getting worse 😛

Not true.

Even a primary MR can be optimized in multiple ways, especially if the patient has been iatrogenicized already. In this case, it would have been diuresis (she was already tachycardic and borderline hypotensive).

Doing a TEE in a medically unoptimized patient condemns a patient to possibly unnecessary surgery.

 

[dchz]

Goes to show how once again, the practice of good medicine is to do as little as possible

Someone is a big fan of the fat man! rule #13

You mean all these anesthesiologists advocating IABP, impella, central line and pressors, etc ended up not knowing better than the cardiologists? Shocker!



In all seriousness, was surprised at how quickly and strongly people advocated for mechanical circulatory support. Is there any strong indications for MCS? What happened to medical optimization first?

I think you might be joking, but this is a perfect example of result-oriented thinking. From the way the patient was described to us, TEE would be the next step in diagnosis. There was a significant chance this patient could have been getting worse.

Retrospectively if we MMQB it we can say a lot of things, so retrospectively is neither here nor there and we should try to avoid hindsight bias just because this lady with a bizarre clinical course happened to do well. Based on what OP told us, I'm more of the opinion that OP's cardiology department didn't make a decision to withhold MCS based on clinical judgement but more because of expediency. With the initial presentation of borderline cardiogenic shock, coronary malperfusion of some sort, frank pulmonary edema, high FiO2 requirement, severe MR, and ?ruptured pap or torn chord as described in the original post, MCS (impella, IABP) is well within the standard of care and some might even argue one of the first interventions that should be considered early assuming a large dose of lasix, CPAP, inotrope infusion doesn't immediately begin to stabilize the patient.

Exactly this!

Maybe the heart docs were being expedient and lazy. Or maybe they know what they’re doing. Guess we will never know.

We will know when we get the TEE, but at this point it's most likely 2ndary MR.
What if this turned out to be primary MR and the patient should have been repaired when we wait a week "optimizing"? now the patient is in kidney failure while in the ICU and operative risk just sky-rocketed? IMO everything @vector2 and @bigdan said are spot on.

The patient just GOT LUCKY. I'd rather be lucky than good any day. But the problem is we can't rely on luck to practice medicine.

Not true.

Even a primary MR can be optimized in multiple ways.

Yes, optimized by mitraclip, resection repair, or neocord. not optimized by iatrogenicized refusal to help facilitate a TEE.

 

[deleted171991]

Yes, optimized by mitraclip, resection repair, or neocord. 🤓

If one fluid overloads a patient, or does anything else that increases regurg (e.g. hypertension) or ischemia (thus adding a secondary MR component), one can transform a mild-moderate MR into a severe-looking one. This case was a classic example.

Surgeries should be reserved for patients who cannot be fixed medically. Ergo, any patient should be optimized medically to the maximum possible extent, before working her up for a possible surgery. The best surgeons cancel surgeries that their patients don't need anymore, even on the day of surgery.

You've been among surgeons/cardiac anesthesiologists for too long. Knee-jerk. Remember when "primary" appendicitis was cured only by surgery? 😉

 

[dchz]

Well yes and no.
Getting better on an IV lasix drip isnt exactly nothing, nor is it sustainable. She needs that Mitral repaired unfortunately.

@dhcz
Re MR under GA. I very rarely downgrade the severity of a regurgitant lesion under GA when the primary op is for MV repair/replace. As outlined already the loading conditions are so drastically different under GA plus they're likely diuresed to a wafer pre-op etc etc etc.
I tend to trust our cardiologists TTE a lot. It doesnt sound like the op's institution is that overall trustworthy

I cant remember the last time ive used IABP/pressors to try not repair a mitral. Ive certainly seen many times where i would have to ask the surgeon to repair at least moderate MR. Sometimes they listen, sometimes not

I don't think anyone is advocating IABP instead of a MV repair, I think most are advocating that it's a temporizing measure, or at least I'm advocating it as a temporizing measure in order to diagnose the MR, then manage accordingly.

Have you looked at the TTE images that they are using to make these "reads"? It's like watching a flip camera phone video from 2008 while the TEE images are like HD TV. I only recently come to realize that we put a lot of faith in some very suboptimal images.

Do you check your mitral valve repair with a phenylephrine challenge? I don't, most don't, but i'm wondering if we should.

 

[dchz]

If one fluid overloads a patient, or does anything else that increases regurg (e.g. hypertension), one can transform a mild-moderate MR into a severe-looking one. Why is this so hard to comprehend?

Surgeries should be reserved for patients who cannot be fixed medically. Ergo, any patient should be optimized medically to the maximum possible extent, before working her up for a possible surgery.

I can't tell if you're purposely making up arguments to mess with me. Surgical management of primary MR has a mortality benefit over medical management. One can also medically optimize the patient from a hemo concentrator on the CPB machine, I assure you it works better than furosemide.

When OP presented the case, the decision point should be made early to differentiate from primary MR. If the patient has secondary MR, we should medical manage the patient, as I stated on my first reply.

If your proposed course of action is to wait and see and hope it's secondary MR, I disagree with that management. Hence i'm in the camp to facilitate the TEE.

 

[deleted171991]

I can't tell if you're purposely making up arguments to mess with me. Surgical management of primary MR has a mortality benefit over medical management. One can also medically optimize the patient from a hemo concentrator on the CPB machine, I assure you it works better than furosemide.

When OP presented the case, the decision point should be made early to differentiate from primary MR. If the patient has secondary MR, we should medical manage the patient, as I stated on my first reply.

If your proposed course of action is to wait and see and hope it's secondary MR, I disagree with that management.

There is primary MR and primary MR.

Because you didn't bother to optimize the patient, even with a primary MR you would not have been able to eliminate a possible secondary component, hence overestimating the severity of the primary disease (plus almost nothing is truly load-independent in cardiac echo, because of the Frank-Starling mechanism).

I may not be a cardiac person, but this is just logical.

I'll let @bigdan shut me up. He's usually pretty good at proving me wrong.

 

[dchz]

There is primary MR and primary MR.

 

[deleted171991]

I understand that one cannot sit around and wait forever with a primary lesion, even if medically optimized, because the LV may get affected. But not all primary MR is surgical.

In this case, there was a good chance that the patient had a secondary ischemic (+/- iatrogenic) component. Hence that primary lesion was not that clearcut to me, even from the beginning.

There was a possibility that the primary lesion was basically asymptomatic even during physical effort, absent coronary spasm +/- fluid overload.

Anyway... let's agree to differ. I am not pulling your leg.

 

[dchz]

I'll let @bigdan shut me up. He's usually pretty good at proving me wrong.

I'm no big dan, but he might be busy doing a liver. Here is my source:

2014 AHA/ACC Guideline for the Management of Patients With Valvular Heart Disease

Exert from section 7.1.1 Diagnosis and Follow-Up:

"It may be difficult to diagnose severe acute MR with TTE due to narrow eccentric jets of MR, tachycardia, and early equalization of LV and LA pressures. In cases where TTE is nondiagnostic but the suspicion of severe acute MR persists, enhanced mitral valve imaging with TEE usually clarifies the diagnosis. TEE can be especially helpful in detecting valvular vegetations and annular abscesses that may further accentuate the need for a more urgent surgical approach. In the presence of sudden acute and hemodynamic instability after MI with hyperdynamic LV function by TTE and no other cause for the deterioration, TEE should be performed as soon as possible, looking for severe MR due either to a papillary muscle or chordal rupture. "

Here is the study that the recommendation is based on:

Horstkotte D., Schulte H.D., Niehues R., et al. (1993) Diagnostic and therapeutic considerations in acute, severe mitral regurgitation: experience in 42 consecutive patients entering the intensive care unit with pulmonary edema. J Heart Valve Dis 2:512–522.

 

[deleted171991]

I'm no big dan, but he might be busy doing a liver. Here is my source:

2014 AHA/ACC Guideline for the Management of Patients With Valvular Heart Disease

Exert from section 7.1.1 Diagnosis and Follow-Up:

"It may be difficult to diagnose severe acute MR with TTE due to narrow eccentric jets of MR, tachycardia, and early equalization of LV and LA pressures. In cases where TTE is nondiagnostic but the suspicion of severe acute MR persists, enhanced mitral valve imaging with TEE usually clarifies the diagnosis. TEE can be especially helpful in detecting valvular vegetations and annular abscesses that may further accentuate the need for a more urgent surgical approach. In the presence of sudden acute and hemodynamic instability after MI with hyperdynamic LV function by TTE and no other cause for the deterioration, TEE should be performed as soon as possible, looking for severe MR due either to a papillary muscle or chordal rupture. "

Here is the source that this is based on:

Horstkotte D., Schulte H.D., Niehues R., et al. (1993) Diagnostic and therapeutic considerations in acute, severe mitral regurgitation: experience in 42 consecutive patients entering the intensive care unit with pulmonary edema. J Heart Valve Dis 2:512–522.

I emphasized my point (click to expand the quote, please). They were so nice to even include it in the guidelines. 🙂

Let me make a parallel: one can't have ARDS until one doesn't rule out fluid overload or CHF. The same way, one can't judge a primary MR until one doesn't optimize the patient to eliminate all the possible sources of secondary MR.

 

[MoMoGesiologist]

Someone is a big fan of the fat man! rule #13





I think you might be joking, but this is a perfect example of result-oriented thinking. From the way the patient was described to us, TEE would be the next step in diagnosis. There was a significant chance this patient could have been getting worse.




Exactly this!



We will know when we get the TEE, but at this point it's most likely 2ndary MR.
What if this turned out to be primary MR and the patient should have been repaired when we wait a week "optimizing"? now the patient is in kidney failure while in the ICU and operative risk just sky-rocketed? IMO everything @vector2 and @bigdan said are spot on.

The patient just GOT LUCKY. I'd rather be lucky than good any day. But the problem is we can't rely on luck to practice medicine.





Yes, optimized by mitraclip, resection repair, or neocord. not optimized by iatrogenicized refusal to help facilitate a TEE.

You really want this TEE...

If the pt is getting worse despite medical mgmt, then yes I agree with you. This pt wasn’t even on CPAP. Also, in the original post, pt was satting 100% on 11L. Who knows if PaO2 was 100 or 500.

I like TEE as much as the next person. My post is made to highlight we need to get basic medical management done first before we move into fancy stuff. I don’t think pt “just GOT LUCKY” because she responded to diuresis. Would be nice to get a cardiologist or CT surgeons opinion.

 

[dchz]

I emphasized my point (click to expand the quote, please). They were so nice to even include it in the guidelines. 🙂

Let me make a parallel: one can't have ARDS until one doesn't rule out fluid overload or CHF. The same way, one can't judge a primary MR until one doesn't optimize the patient to eliminate all the possible sources of secondary MR.

I'm no big dan, but he might be busy doing a liver. Here is my source:

2014 AHA/ACC Guideline for the Management of Patients With Valvular Heart Disease

Exert from section 7.1.1 Diagnosis and Follow-Up:

"It may be difficult to diagnose severe acute MR with TTE due to narrow eccentric jets of MR, tachycardia, and early equalization of LV and LA pressures. In cases where TTE is nondiagnostic but the suspicion of severe acute MR persists, enhanced mitral valve imaging with TEE usually clarifies the diagnosis. TEE can be especially helpful in detecting valvular vegetations and annular abscesses that may further accentuate the need for a more urgent surgical approach. In the presence of sudden acute and hemodynamic instability after MI with hyperdynamic LV function by TTE and no other cause for the deterioration, TEE should be performed as soon as possible, looking for severe MR due either to a papillary muscle or chordal rupture. "

Here is the study that the recommendation is based on:

Horstkotte D., Schulte H.D., Niehues R., et al. (1993) Diagnostic and therapeutic considerations in acute, severe mitral regurgitation: experience in 42 consecutive patients entering the intensive care unit with pulmonary edema. J Heart Valve Dis 2:512–522.

LOL am i doing this right?

 

[deleted171991]

LOL wtf are we doing?

I can be stubborn, too. 😀

 

[deleted171991]

LOL am i doing this right?

"As soon as possible" only if "no other cause for the deterioration". 😛

The latter has priority.

 

[vector2]

@vector2 I think we disagree here in some places but agree in others:

All mitral regurg measurements (qualitative and quantitative) are load-dependent: RVol/R% Regurgitant volume%, Vena Contracta (VC), EROA (Effective regurgitant orifice area), are all load-dependent. MR it self is load-dependent so it should follow that all measurements are load-dependent. EROA and VC are less theoretically less load-dependent because a small area change can mean a big change in flow, so it's harder to detect the change in a smaller dimension due to the margin of error.

Yea man, I agree, that's why I also said *theoretically* load independent (assuming we're not talking about rheumatic MS with concomitant MR where the regurgitant orifice is relatively fixed throughout the cardiac cycle).

According to the 2014 AHA/ACC guidelines, VC is only 1 of the quantitative measures that should be taken into account in the context of the big picture. I don't believe the 2017 guideline change any of the diagnostic criteria but i'd be happy to be corrected. I do agree with you that PISA isn't a hemisphere and prone to a lot of errors. Personally, I feel that VC is just as prone too error. It's about as user-dependent as Vp.

I disagree with the 2D VC measurement. The valve cordes do not read the text book, sometimes you have to sweep to the edge of A1 to get the MR. Also how do you know your VC is in line with the the actual direction of flow?? How do you know your LAX view is actually lined up perpendicular to A2-P2 commissure? How do you know the VC you get at 120 degree isn't foreshortened when you should be at 135 degrees? I don't like the VC measurement at all to be honest, but it's only my personal opinion.

Sorry, my fault, I was mixing up my guidelines. I was referring to the updated 2017 JASE Recommendations for Noninvasive Evaluation of Native Valvular Regurgitation in which RVol and RF assumed more prominence, E Wave inflow changed to 1.2 from 1.5 m/s, cautioned that 2d EROA for secondary MR may be underestimating severity, emphasized CMR. You are correct that the algorithm from 2014 to 2017 ACC/AHA did not change significantly.

Let me clarify what was talking about when I said making sure your beam is ME-AVLAX and you are cutting through A2-P2 to use 2d VC. I specifically mean that your MR is also coming through A2-P2 (which you have confirmed looking at the leaflets with a 3d surgeons view) because hopefully you are evaluating someone who has the most common primary lesion which is P2 prolapse. Obviously it's nonsensical to use 2d VC if your jet is eccentrically directed in a medial to lateral or lateral to medial or another oblique to the AVLAX orientation. Very specifically, to use 2d VC I think your 2d image with CFD needs to capture 1. flow acceleration 2. the VC 3. the main jet body in the same plane. If you don't have all those things in your picture then you are correct that 2d VC is probably garbage. And even if you have all those things, obviously you should never use just one measurement in one plane to make a diagnosis.

Now, you might ask why I am using VC if I have have the ability to use 3d to check my orientation and leaflet pathology. It's because frequently I don't have access to an epic 7 or GE vivid and I have to use a POS portable cx-50 that only has 3d zoom and goes to 2hz if I activate CFD with 3d on.

I like the 3D color EROA measurement but it also runs into problems of foreshortening and frame rate. (most X8-2t probes with Epic7C machines only gets like 8Hz frame rate if you do 3d with color). I am a HUGE fan of the 3D ejection volume to calculate the ERV, but a lot of electrocardiographers don't do this and it's never been "validated" by any study as far as I know. Still, i think this is the most reliable measure, but it still should be taken into the context of the big picture.

Even with poor frame rate, 3d EROA or VCA, 3d RVol (along with 3d volumetric [assuming good endocardial border definition], which I should've mentioned, which is just waiting for validation) are the likely gold standards for mitral regurg echocardiography if you look at their R coefficients compared to the true gold standard which is CMR.

Vena contracta area for severity grading in functional and degenerative mitral regurgitation: a transoesophageal 3D colour Doppler analysis in 500 patients

AbstractAims. Vena contracta area (VCA3D), derived by 3D colour Doppler echocardiography, has already been validated against cardiac magnetic resonance ima

academic.oup.com

Quantification of Functional Mitral Regurgitation by Real-Time 3D Echocardiography: Comparison With 3D Velocity-Encoded Cardiac Magnetic Resonance

The aim of this study was to evaluate feasibility and accuracy of real-time 3-dimensional (3D) echocardiography for quantification of mitral regurgita…

www.sciencedirect.com

I used to be a big fan of the S wave reversal but then it was explained to me by an experienced cardiologist that it's merely a proxy measure of a previously not very sensitive finding during fluoroscopy - If they did an LV gram while doing a LHC, it would clue them in if they see the pulm vein tracing during the fluro shot. The S wave reversal was just an echography proxy measure for that but it's very non-sensitive

I don't understand how the anecdote about fluoro negates its utility since (in my amateur opinion) it seems that it's gotta be a significant volume of blood refluxing retrograde during an LV gram to be able to pick up angiographic pulmonary vein blush. Regardless though, the hallmark of holosystolic pulmonary vein flow reversal isn't that it's sensitive- it's that it's a pretty specific marker of severe mitral regurgitation.

To sum this up I am not sure if there is any set way to do it. It takes an experience person years to understand all the nuances and i still got a ways to go. The measurement of MR is not an exactly science either, because you have to then take into account if this is primary or secondary. The data and evidence on primary is overwhelming while secondary MR is still somewhat in a gray area.

Agree.

However, I do believe that we should account of the load conditions when doing the TEE. The most experienced cardiologists do this, e.g. we always do a phenylephrine challenge after the mitraclip if the BP is low - make sure the clip actually did something and not just the general anesthesia making it better.

I think you have to account for the load conditions within reason, especially if your post-clip deployments are like mine where post-clip severity is usually the cardiologist "eyeballing" jet areas etc. Stuff like VC and EROA are going to have a bit of a dynamic change during the cardiac cycle as well, but ime I've never noticed a significant change unless the pt's volume status/contractility changed significantly or BP was 40+ points off the baseline.

 

[vector2]

TEE and "optimizing the pt" are not mutually exclusive. but let me quote the OP again:

"
37 yo F with coronary artery vasospasm: s/p LHC on 5/13 with 90% narrowing of the LAD. staged PCI revealed normal coronaries. acute systolic CHF: Patient in respiratory distress with bilateral crackles on exam. chest x-ray on 05/18 revealed new interstitial pulmonary edema. chest x-ray on 5/20 shows worsening infiltrates and/or edema. TTE on 5/14 revealed mildly increased LV wall thickness with normal systolic function and estimated LVEF 55-60%. TTE on 5/18 revealed LVEF 35-45% with akinesis of basal-mid inferior lateral myocardium with severe MR (possible ruptured chordae),
RVSP=31mmHg

she is currently tachycardic in the 120s and hypotensive with blood pressure ranging in 80s-90/50s-60s with s/s of acute respiratory failure on oximyzer 11 LPM most likely cardiogenic pulm edema from acute CHF. "


There is no way on earth one can look at the ACC/AHA guidelines and not think a TEE needs to be done in this scenario if the MR type and severity by TTE is indeterminate and there is high suspicion MR is contributing to her cardiopulmonary decompensation (inferior wall ischemia goes hand in hand with PM pap/chord rupture -> acute severe MR -> OR b/c it's a surgical emergency). @dchz is right.

 

[deleted697535]

I can't tell if you're purposely making up arguments to mess with me. Surgical management of primary MR has a mortality benefit over medical management. One can also medically optimize the patient from a hemo concentrator on the CPB machine, I assure you it works better than furosemide.

When OP presented the case, the decision point should be made early to differentiate from primary MR. If the patient has secondary MR, we should medical manage the patient, as I stated on my first reply.

If your proposed course of action is to wait and see and hope it's secondary MR, I disagree with that management. Hence i'm in the camp to facilitate the TEE.

What is the point of even replying to that guy. Claims to be a great ICU doc but doesnt do ICU and lets leave aside he said he hasnt looked after covid pt. Now he wants to tell everyone how to do cardiac anesthesia & surgery. Give me a break. Dude doesnt know 1 single thing about the mitral valve

What did he say, you cant diagnose primary MR until all causes of secondary are outruled? WTF? a P2 flapping in the wind can 100% be diagnosed and even coexist with secondary MR but still be repairable

 

[Southpaw]

What is the point of even replying to that guy. Claims to be a great ICU doc but doesnt do ICU and lets leave aside he said he hasnt looked after covid pt. Now he wants to tell everyone how to do cardiac anesthesia & surgery. Give me a break. Dude doesnt know 1 single thing about the mitral valve

What did he say, you cant diagnose primary MR until all causes of secondary are outruled? WTF? a P2 flapping in the wind can 100% be diagnosed and even coexist with secondary MR but still be repairable

He doesn’t claim to be a great ICU doc far as I can tell. He claims, and makes great points, that iatrogenesis is an absolute killer. He’s also a fellowship trained attending physician. You should stand down and learn to be a better trainee.

 

[deleted697535]

He doesn’t claim to be a great ICU doc far as I can tell. He claims, and makes great points, that iatrogenesis is an absolute killer. He’s also a fellowship trained attending physician. You should stand down and learn to be a better trainee.

Okay

He suggests and you agree with not repairing severe MR in or even investigating it with a TEE in a 37 yo F as it may be secondary. Is that correct?
Just give her lasix and send her home?

 

[Southpaw]

Okay

He suggests and you agree with not repairing severe MR in or even investigating it with a TEE in a 37 yo F as it may be secondary. Is that correct?
Just give her lasix and send her home?

No one said send her home. Some said diurese and non-invasive resp support prior to invasive investigation/consideration of surgical repair. Agree or not - it’s a fair point.