sethco

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I always enjoy the case presentations around here and it's been a while since I contributed, so here was a fun case

54 y/o male underwent Sternotomy for CABG/MVR/MAZE/LLAA 2 months ago after presenting with an NSTEMI. BMI 42, recent hx of Meth and Marijuana use, current everyday smoker with questionable COPD (PFTs were fine), OSA on BiPAP while at hospital (non-compliant at home), and AFib on Elliquis. Surgery went uneventfully, had a Mitral Valve Repair (simple ring), good flow in coronaries, NSR during postop course, extubated postop day 1, and discharged 4 days later. Only thing worth noting was that it took 85k units of Heparin to get his ACT therapeutic for CPB. After initiating CPB, 2 units FFP were given for severe Heparin Resistance (Of note, he was not on a Heparin gtt preop, but was on a therapeutic Lovenox bridge for his Atrial Fib). Hospital system completely out of Anti-Thrombin III and says it is on a national shortage

6 weeks later....

Presented to the ED with AFib with RVR, Acute Kidney Injury and new onset Pulmonary Edema/CHF. EP consulted and decided to do a TEE/CV. CV was successful with conversion back to Sinus. However, TEE showed Ring dehiscience with Severe MR, Severe TR, EF 35-40 (previously normal), Mild AI, and moderate RV dysfunction. No evidence of vegetation. Pt medically optimized with plans for Redo MVR, possible TVR. During workup, pt gets a CT of Chest/Neck which finds an 80% Stenosis of the airway at the level of the glottis and thyroid cartilidge without external compression. According to previous records, pt was an easy Intubation with MAC 3 and 8.0 ETT. Pt was exubated within 12 hours postop. Pt admits to "throat problems" over past couple of years that has not worsened since his first surgery. Pt notes occasional difficulty clearing mucus, occasional wheezing, and occasional bloody secretions. Denied any orthopnea. During medically optimization, ICU staff also treats him for "COPD exacerbation" with a steroid course and antibiotics. Pt placed on Milrinone and was diuresed which reversed his Acute Kidney injury to the point that Creatnine is now at baseline.

Surgeon wants to do a minimally invasive MVR (Repair, possible Replace) through a Right Thoracotomy. Let's stop here and hear others plans

Have a couple videos of the Ring Dehis but can't figure out how to add it from my iPhone.
 
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dchz

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congratulate pt on not having AV disruption, then prop roc tube.



In all seriousness:

Problem list:
Possible AT3 deficiency
Severe MR/TR (TR prob 2ndary)
Possible difficult airway with subglottic stenosis
A fib/AKI
Surgeon expectation of minimally invasive technique


M: a line TEE
A: ensure maskable, DLT -> bronchial blocker -> mainstem L side -> abandon minimally invasive technique
I: Big
D: prop roc
S:
-lay the foundation for full sternotomy in surgeons mind.
-pray to your diety of choice that you don't cause AV disruption with your coronary sinus cathether
-FFP in room
 
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fakin' the funk

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ENT and/or pulm needs to take a look at that larynx/subglottis
 
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How did the patient look from a pulmonary standpoint after diuresis and the steroid/abx course? Assuming his pulm complaints are what they appear to be, I agree with what’s been said above: biggest issues are this subglottic stenosis and managing surgical expectations re approach. Is the surgeon concerned about a sternotomy bc of something specific on a scan, or is he/she just avoiding a redo stenotomy empirically?
 

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What’s the question here, exactly? Am I missing something that makes this more complicated?

Sounds like urgent surgery. Can’t really wait for full oncologist work up. Go to the OR, induce as you would any other heart failure patient (I’m an Amidate guy) and have ENT do a flexible bronch through the tube to evaluate prior to your case. If you need lung isolation, use a blocker. Keep extubated at the end.
 
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sethco

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ENT and/or pulm needs to take a look at that larynx/subglottis

Pulm says medically optimized. ENT and CT surgeon discuss and ENT thinks not causing enough symptoms that it would take priority over the Mitral and RV dysfxn. In my opinion, I didn't know what to really make of this "new" finding. I had no problems with the first Intubation and he was no worse when I saw him before his second surgery, so I leaned towards agreeing with the order
 

sethco

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How did the patient look from a pulmonary standpoint after diuresis and the steroid/abx course? Assuming his pulm complaints are what they appear to be, I agree with what’s been said above: biggest issues are this subglottic stenosis and managing surgical expectations re approach. Is the surgeon concerned about a sternotomy bc of something specific on a scan, or is he/she just avoiding a redo stenotomy empirically?

Patient looked about the same as he did before the first surgery.

Surgeon A did the first surgery. He does not do any minimally invasive Valves. He goes out of town for a week right as this patient gets readmitted. His partner, Surgeon B, highly prefers minimally invasive Valves. For Mitrals/Tricuspids, I'll put in a 15 FR SVC Return Cannula +/- PA Endovent, +/- Retrograde Coronary Sinus Catheter. But yes, he would also like to avoid a Redo Sternotomy

The other issue in this case is he will have trouble getting to the aorta for cross Clamp. Solutions?
 
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AdmiralChz

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Patient looked about the same as he did before the first surgery.

Surgeon A did the first surgery. He does not do any minimally invasive Valves. He goes out of town for a week right as this patient gets readmitted. His partner, Surgeon B, highly prefers minimally invasive Valves. For Mitrals/Tricuspids, I'll put in a 15 FR SVC Return Cannula +/- PA Endovent, +/- Retrograde Coronary Sinus Catheter. But yes, he would also like to avoid a Redo Sternotomy

The other issue in this case is he will have trouble getting to the aorta for cross Clamp. Solutions?

I don’t get involved in surgical decision-making like this. Surgeon B needs to Do surgeon A the courtesy of calling and seeing what he or she would prefer to do as it is A’s original patient (and complication). A may come back into town and do the case.

I still don’t see what’s sticky about this case in particular. The surgical considerations are largely academic and theoretical for us.
 
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sethco

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I don’t get involved in surgical decision-making like this. Surgeon B needs to Do surgeon A the courtesy of calling and seeing what he or she would prefer to do as it is A’s original patient (and complication). A may come back into town and do the case.

I still don’t see what’s sticky about this case in particular. The surgical considerations are largely academic and theoretical for us.

Surgeon B offered to optimize the patient until A got back to town. Surgeon A declined and told B to just do the surgery himself (with another surgeon), as the repair became more complicated.

As an aside, I never said we shouldn't do this case minimally invasive. If the surgeon is good at it, I'm all for it. Would anybody decline to do a minimally invasive approach on this patient? If so, why? It's one thing to not be comfortable with it and it's another thing to think it's bad for the patient
 
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anaesthetic

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Surgeon B offered to optimize the patient until A got back to town. Surgeon A declined and told B to just do the surgery himself (with another surgeon), as the repair became more complicated.

As an aside, I never said we shouldn't do this case minimally invasive. If the surgeon is good at it, I'm all for it. Would anybody decline to do a minimally invasive approach on this patient? If so, why? It's one thing to not be comfortable with it and it's another thing to think it's bad for the patient

Seems like surgeon B is way more comfortable doing minimally invasive. If he thinks he can do it, I'm all for it, keeping in mind conversion to full sternotomy if he can't get to what he needs to and the consequences of that. Speaking hyperbolically, I'd rather have someone who's done 1000 surgeries the same way than someone who's done 1000 different surgeries once.
 
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dchz

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It's one thing to not be comfortable with it and it's another thing to think it's bad for the patient
I'm interested in hearing how many people out there are actually doing this minimally invasively.
 
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vector2

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If the pt had right heart failure and severe TR when presenting for the initial surgery, a TV band would've been done as well. Now, if the TR is still severe and/or the TV annulus is over ~4cm when you get him in the OR for the redo after he's been diuresed and medically optimized, should TV repair be done, or do we hope that re-fixing the mitral will solve the issue since it's acute/ sub-acute?
 
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anaesthetic

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If the pt had right heart failure and severe TR when presenting for the initial surgery, a TV band would've been done as well. Now, if the TR is still severe and/or the TV annulus is over ~4cm when you get him in the OR for the redo after he's been diuresed and medically optimized, should TV repair be done, or do we hope that re-fixing the mitral will solve the issue since it's acute/ sub-acute?

He’s a potential re-do chest with severe TR and new moderate RH dysfunction. I think that’s a class I indication to repair the TV, although I’m sure it’s debatable. Shouldn’t take much time to throw stitches or a ring around it, although doing it minimally invasive would probably present some different challenges if not just the operative time issue. The chances of TR progression over time are pretty high and reoperation for isolated TR would be disastrous for this patient.

Indications for Surgery for Tricuspid Regurgitation Many other articles discussing this, but this is a decent review.

We had a surgeon who threw in TV annuloplasty rings not uncommonly for MVRs with RH issues/TR, especially if the annulus was dilated > 40 mm. He was quick so it was a non-issue, and patients did well.
 
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vector2

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He’s a potential re-do chest with severe TR and new moderate RH dysfunction. I think that’s a class I indication to repair the TV, although I’m sure it’s debatable. Shouldn’t take much time to throw stitches or a ring around it, although doing it minimally invasive would probably present some different challenges if not just the operative time issue. The chances of TR progression over time are pretty high and reoperation for isolated TR would be disastrous for this patient.

Indications for Surgery for Tricuspid Regurgitation Many other articles discussing this, but this is a decent review.

We had a surgeon who threw in TV annuloplasty rings not uncommonly for MVRs with RH issues/TR, especially if the annulus was dilated > 40 mm. He was quick so it was a non-issue, and patients did well.

I don't dispute the high level of evidence for TV repair in patients who have concomitant mitral disease or other LH disease who are now going for operative repair. However, in the vast majority of those patients neither the mitral nor tricuspid became diseased overnight and it took years if not decades to develop primary mitral disease and the functional TR that followed. It makes me wonder what this pt's tricuspid looked like before his first mitral surgery.
 
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Hork Bajir

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Probably an analogous situation to the patient who infarcts the PM pap and pops a chordae, goes urgently for MVr, and has concomitant RH dilation w/ significant TR. I’m assuming most surgeons would band the TV in that scenario- or would they not?
 

sethco

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I don't dispute the high level of evidence for TV repair in patients who have concomitant mitral disease or other LH disease who are now going for operative repair. However, in the vast majority of those patients neither the mitral nor tricuspid became diseased overnight and it took years if not decades to develop primary mitral disease and the functional TR that followed. It makes me wonder what this pt's tricuspid looked like before his first mitral surgery.

Completely agree.

With the first surgery, the TV was trace and annulus measured 36 mm. So, we didn't fix it at the time.

Now, there is Severe TR with a dilated annulus measuring 41 mm.

We debated a lot about this because we certainly didn't want to have to come back a third time
 
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vector2

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Completely agree.

With the first surgery, the TV was trace and annulus measured 36 mm. So, we didn't fix it at the time.

Now, there is Severe TR with a dilated annulus measuring 41 mm.

We debated a lot about this because we certainly didn't want to have to come back a third time

The TV annulus was already dilated the first go around (>35 mm or 21 mm/m2), but just not dilated enough to hit that classic 40-42 mm number to pull to the trigger. I would be inclined to re-steronotomy and fix TV and MV. Surgeon B may be good at minimally invasive but even the best MICs take longer than fully opening the chest. Why add unnecessarily to this already sick pt's pump and X-clamp time?


e: just FYI for everyone, that "40 mm" number is validated for a specific apical 4ch obtained with TTE. We may think the 2d TEE ME4ch right-focused view of the annulus is a good approximation, but afaik this hasn't been validated.
 
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J Peterman

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We do robotic mitrals at our shop so I’m an open book to discuss MIS if people are interested.

It’s only 6 weeks since the initial sternotomy so likelihood of significant intrathoracic adhesions is probably unlikely. Sternotomy as backup sounds reasonable. Also highly unlikely the tracheal narrowing is brand new since the case 6 weeks ago, especially given the short period of intubation postop. Plan A, DLT, Plan B blocker. ENT nasopharyngoscopy preop would be nice to have noted but not entirely necessary.

The TR is purely secondary to L sided failure and we probably wouldn’t touch that. Recommendation to fix TR with annular dilation >40mm is 1C evidence. Our surgeon maintains he sees significant improvement and remodeling after fixing L sided disease and we rarely intervene on the TV during mitral surgery unless the TR is severe by our intraop TEE.
Re: cross clamping, I thought the endoballoon was being discontinued if it isn’t already off the market. Our surgeon prefers a Chitwood clamp anyways so we rarely use the endoballoon.

Major concern here is how diseased the mitral annulus is here and how difficult re-repair vs replacement might become especially via a MIS incision. Fortunately it doesn’t sound like there are signs of infection or perivalvular abscess. If you do enough longer pump runs (>3h) via R anterior thoracotomy incisions and you’ll start to see “Robot lung”...
 
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vector2

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Major concern here is how diseased the mitral annulus is here and how difficult re-repair vs replacement might become especially via a MIS incision.

Precisely. Even for shops that have high volume MICS, how often is the reop being done minimally invasively, especially for something like this where the guy has BiV failure, resolving pulm edema and AKI, heparin resistance, tracheal stenosis, and such poor protoplasm that the ring had a 3/4 dehiscence....
 
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dchz

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just FYI for everyone, that "40 mm" number is validated for a specific apical 4ch obtained with TTE. We may think the 2d TEE ME4ch right-focused view of the annulus is a good approximation, but afaik this hasn't been validated.

This can't be stressed enough. HUGE % of our evidence for measurements are just adopted from the TTE measurements: e.g. normal parameters for size. I would keep this in mind when helping to make decisions...

exceptions to this rule: c-sep distance was a TEE study, except Maslow did it in the 4 chamber view when he should have done the long axis view. (he claims at the time of the study he only had 4 chamber data available. I think he should re do it with long axis).
 
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J Peterman

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IMO all these measurements should be done with a 3D TEE dataset using MPR for any sort of reproducibility (knowing exactly where you are cutting your 2D slice) and correlation with surgical measurements in the field.
 
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dchz

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IMO all these measurements should be done with a 3D TEE dataset using MPR for any sort of reproducibility (knowing exactly where you are cutting your 2D slice) and correlation with surgical measurements in the field.

how many surgeons actually ask you to do this? (how many of them actually understand what MPR is?)
 

AdmiralChz

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how many surgeons actually ask you to do this? (how many of them actually understand what MPR is?)

+1. I have yet to see a surgeon actual use real time MPR data (I have seen some from TEEs done pre-op). This includes big academic centers and community practice (wouldn’t have time to do it in the latter anyway).
 

dchz

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+1. I have yet to see a surgeon actual use real time MPR data (I have seen some from TEEs done pre-op). This includes big academic centers and community practice (wouldn’t have time to do it in the latter anyway).

I have had surgeon ask me to measure things. But they don't know the difference if i'm foreshortened or done in 3d w/o MPR. they just need a number in ballpark to start.
 
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sethco

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Great responses. Thread went in a direction that I didn't think it was going to go on.

I saw this guy the morning of surgery. He came to me still on a Milrinone gtt. Had been diuresed for about a week. CXR looked better and Renal function had improved to baseline. No wheezing or stridor present on exam. Questioned him again and he says no further progression of sx since first surgery.

Asked a colleague who was free in the morning to provide an extra set of hands just in case. Perc Cric set in the room and Surgeon in the room, but highly doubted I would need either. Plan A was induce with Prop/Sux and DL as I did for the first surgery with ETT of various sizes. Plan B was LMA to Trach if nothing would pass the Glottis (very unlikely). Induced with Propofol and test ventilated (Haven't done test ventilation before paralytics since Residency) and was fine, then gave Sux. Grade 2 view with maybe 50% narrowed glottic opening. Put a 7.5 ETT without resistance. Might have been pretty difficult trying to pass a double lumen past the Glottis and didn't want to tube exchange at the end anyway. Put a bronchial blocker in the right mainstream and got good separation

Since I was able to get good lung separation, we were able to proceed with the Right Thoracotomy approach. I put in a 15 FR SVC, and 9 FR Introducer with Retrograde CS in the IJ and 8 FR CVC in the SC. I was, in particular, worried about his previous Heparin resistance. FFP was immediately available, but AT3 still on national backorder. I instructed my perfusionist to draw an ACT immediately when we got in the room along with a Heparin assay. Then, right before I put in my lines, gave 10k Heparin and rechecked the ACT for response. In both cases, no Heparin resistance was evident, so I proceeded with the lines and then flushed with additional Heparin after lines were in place.

Intraop TEE showed the above images, along with Mod-Severe TR with a dilated annulus and Mild AI. After getting exposure through the Right lateral chest, IVC cannula was placed in the Femoral. In addition, an endoaortic balloon "Clamp" was advanced into the Aortic Root. Exposure was good while on CPB. Because there were multiple jets, Replacement was the course of action. In addition, because the Tricuspid was originally trivial, we wanted to leave it alone, come off bypass and then reassess. Upon separation from CPB, TR was now mild.

I work at a center that does a lot of Minimally invasive Valves, including Redos. So, our surgeons are very comfortable with this approach. If the first surgeon had admitted the patient and done the Redo it would have been a Replacement via Sternotomy. Also, if I couldn't achieve lung isolation, that would have affected the surgical approach.

The Tricuspid issue was certainly debated. We generally reserve repair for TR that is at least moderate with an annulus size greater than 40mm when also doing a Mitral. Obviously, there are issues with this as Vector pointed out. It also has to be realized that TR will get better under General Anesthesia.
 
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dchz

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It also has to be realized that TR will get better under General Anesthesia.

Is it better if you're lung isolating? i'd imagine the down lung causes a significant PVR increase and actually makes it worse?
 

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The point about valve pathology “looking better” under GA is moot if you do a hemodynamic challenge to restore parameters to “awake” BP if hypotensive or SVR decreased. In the case of MR, that involves a pressor infusion, usually Neo. Same way you might use Dobutamine to characterize LFLG AS.

I can’t say I see TR getting worse under OLV with any regularity except when patients have significant pHTN (talking near-systemic PAP here, and it’s usually secondary in the setting of MR).

Nice case and prudent approach to the airway with excellent planning with B&C in the room and available with a 2nd our of experienced hands. My only suggestion: why not use Roc for the induction paralytic considering you actually have a reversal agent for that drug in case it hits the fan (assuming you have access to Sugammadex)?
 
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sethco

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Nice case and prudent approach to the airway with excellent planning with B&C in the room and available with a 2nd our of experienced hands. My only suggestion: why not use Roc for the induction paralytic considering you actually have a reversal agent for that drug in case it hits the fan (assuming you have access to Sugammadex)?

At this particular hospital, Sugammedex is very hard to come by. Have to fill out forms everytime I want to use it. Real pain doing this and then waiting for pharmacy to deliver it. Can't imagine trying to reverse an induction dose in this patient with the limited supply
 
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vector2

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Is it better if you're lung isolating? i'd imagine the down lung causes a significant PVR increase and actually makes it worse?

Can you find any studies that actually measure global PVR in OLV? I was of the impression that vascular compliance in the dependent lung is able to mostly compensate for the hypoxic pulm vasoconstruction in the nondependent lung and thus total PVR only increases slightly.
 

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how many surgeons actually ask you to do this? (how many of them actually understand what MPR is?)

For mitral repairs/replacements I show our surgeon 3D views of the valve in the surgeon's view (and rotated to view along the coaptation plane) with and without color to show him where the jet(s) are coming from and areas of leading edge prolapse/flail/tethering etc. As for values, for every case I give him the following: C-sept, AMVL & PMVL heights, intertrigonal distance, lateral annulus to circumflex minimum distance, end diastolic AP & lateral to medial mitral annular diameters. 3D vena contracta area if we are making an assessment of severity. If C-sept is close and parameters suggest higher SAM risk he'll usually want to look at the ME LAX view to assess the area of upper septal hypertrophy. He is VERY echo savvy, and these parameters help him formulate a surgical plan. I get all those values using MPR.

Post-repair, he wants to know gradients, coaptation depth & height (get those with MPR as well), and obviously presence of SAM and any potential leaks around the band/ring. If you use or practice with MPR a lot you can get these values quickly.
 
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dchz

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Can you find any studies that actually measure global PVR in OLV? I was of the impression that vascular compliance in the dependent lung is able to mostly compensate for the hypoxic pulm vasoconstruction in the nondependent lung and thus total PVR only increases slightly.

I could not. I do not have any high level data on this, unfortunately.
 

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M: a line TEE
A: ensure maskable, DLT -> bronchial blocker -> mainstem L side -> abandon minimally invasive technique
I: Big
D: prop roc
S:
-lay the foundation for full sternotomy in surgeons mind.
-pray to your diety of choice that you don't cause AV disruption with your coronary sinus cathether
-FFP in room
I didn't know @FFP takes consults
 
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anes121508

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This can't be stressed enough. HUGE % of our evidence for measurements are just adopted from the TTE measurements: e.g. normal parameters for size. I would keep this in mind when helping to make decisions...

exceptions to this rule: c-sep distance was a TEE study, except Maslow did it in the 4 chamber view when he should have done the long axis view. (he claims at the time of the study he only had 4 chamber data available. I think he should re do it with long axis).

I’ll send this his way and see what he thinks . I sort of remember it as 5ch
 
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anes121508

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IMO all these measurements should be done with a 3D TEE dataset using MPR for any sort of reproducibility (knowing exactly where you are cutting your 2D slice) and correlation with surgical measurements in the field.

Agreed. Wish more people understood this.
 

anes121508

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how many surgeons actually ask you to do this? (how many of them actually understand what MPR is?)

I tell them it’s just like ct slice planes.

Our mitral guy loves mpr and he has a decent understanding of echo.

I make all my measurements with mpr and save them like that for the calcs. Echo techs and cards folks noticed when they are seeing people post op. I think it’s slowly catching on
 
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anes121508

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The point about valve pathology “looking better” under GA is moot if you do a hemodynamic challenge to restore parameters to “awake” BP if hypotensive or SVR decreased. In the case of MR, that involves a pressor infusion, usually Neo. Same way you might use Dobutamine to characterize LFLG AS.

I can’t say I see TR getting worse under OLV with any regularity except when patients have significant pHTN (talking near-systemic PAP here, and it’s usually secondary in the setting of MR).

Nice case and prudent approach to the airway with excellent planning with B&C in the room and available with a 2nd our of experienced hands. My only suggestion: why not use Roc for the induction paralytic considering you actually have a reversal agent for that drug in case it hits the fan (assuming you have access to Sugammadex)?

I remember reading something that actually said making the hemos normal still doesn’t make it apples to apples with mr. opinions?
 

anes121508

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For mitral repairs/replacements I show our surgeon 3D views of the valve in the surgeon's view (and rotated to view along the coaptation plane) with and without color to show him where the jet(s) are coming from and areas of leading edge prolapse/flail/tethering etc. As for values, for every case I give him the following: C-sept, AMVL & PMVL heights, intertrigonal distance, lateral annulus to circumflex minimum distance, end diastolic AP & lateral to medial mitral annular diameters. 3D vena contracta area if we are making an assessment of severity. If C-sept is close and parameters suggest higher SAM risk he'll usually want to look at the ME LAX view to assess the area of upper septal hypertrophy. He is VERY echo savvy, and these parameters help him formulate a surgical plan. I get all those values using MPR.

Post-repair, he wants to know gradients, coaptation depth & height (get those with MPR as well), and obviously presence of SAM and any potential leaks around the band/ring. If you use or practice with MPR a lot you can get these values quickly.

I should join your place. Really nice your surgeon on board too. Makes for a good working relationship.
 

anes121508

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Great responses. Thread went in a direction that I didn't think it was going to go on.

I saw this guy the morning of surgery. He came to me still on a Milrinone gtt. Had been diuresed for about a week. CXR looked better and Renal function had improved to baseline. No wheezing or stridor present on exam. Questioned him again and he says no further progression of sx since first surgery.

Asked a colleague who was free in the morning to provide an extra set of hands just in case. Perc Cric set in the room and Surgeon in the room, but highly doubted I would need either. Plan A was induce with Prop/Sux and DL as I did for the first surgery with ETT of various sizes. Plan B was LMA to Trach if nothing would pass the Glottis (very unlikely). Induced with Propofol and test ventilated (Haven't done test ventilation before paralytics since Residency) and was fine, then gave Sux. Grade 2 view with maybe 50% narrowed glottic opening. Put a 7.5 ETT without resistance. Might have been pretty difficult trying to pass a double lumen past the Glottis and didn't want to tube exchange at the end anyway. Put a bronchial blocker in the right mainstream and got good separation

Since I was able to get good lung separation, we were able to proceed with the Right Thoracotomy approach. I put in a 15 FR SVC, and 9 FR Introducer with Retrograde CS in the IJ and 8 FR CVC in the SC. I was, in particular, worried about his previous Heparin resistance. FFP was immediately available, but AT3 still on national backorder. I instructed my perfusionist to draw an ACT immediately when we got in the room along with a Heparin assay. Then, right before I put in my lines, gave 10k Heparin and rechecked the ACT for response. In both cases, no Heparin resistance was evident, so I proceeded with the lines and then flushed with additional Heparin after lines were in place.

Intraop TEE showed the above images, along with Mod-Severe TR with a dilated annulus and Mild AI. After getting exposure through the Right lateral chest, IVC cannula was placed in the Femoral. In addition, an endoaortic balloon "Clamp" was advanced into the Aortic Root. Exposure was good while on CPB. Because there were multiple jets, Replacement was the course of action. In addition, because the Tricuspid was originally trivial, we wanted to leave it alone, come off bypass and then reassess. Upon separation from CPB, TR was now mild.

I work at a center that does a lot of Minimally invasive Valves, including Redos. So, our surgeons are very comfortable with this approach. If the first surgeon had admitted the patient and done the Redo it would have been a Replacement via Sternotomy. Also, if I couldn't achieve lung isolation, that would have affected the surgical approach.

The Tricuspid issue was certainly debated. We generally reserve repair for TR that is at least moderate with an annulus size greater than 40mm when also doing a Mitral. Obviously, there are issues with this as Vector pointed out. It also has to be realized that TR will get better under General Anesthesia.

While on the topic...any tips to CS catheter placement with tee? 3D? I have zero experience with CS catheter.
 

sethco

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While on the topic...any tips to CS catheter placement with tee? 3D? I have zero experience with CS catheter.

I don't use real time 3d for placement. Only use a Modified Bicaval view where I can see the SVC, TV, and Coronary Sinus in the same view. Once I can see all three structures and the Catheter at the same time, small turns clockwise/counterclockwise will usually guide the Catheter to the CS ostium. Once engaged and Advanced 2-3 centimeters, I confirm by pressure tracing that I'm not in the RV before switching over to Fluoroscopy. The projection of the Catheter should be in a diagonal direction. I'll shoot a non-occlusive venogram with about 5-10 mL contrast to make sure I'm heading in the right direction and not off in a side branch. Then slowly inflate the balloon (usually 0.4-0.8 mL volume) until I see my pressure waveform become "ventricularized" and shoot an occlusive venogram to make sure the contrast is spreading to the Apex and lateral wall

With time, it starts to become much easier to engage the Os than navigating the coronary veins to get a good Venous occlusive shot (due to the catheter not advancing and bowing). I did a couple of them during fellowship and it took so much damn time, if we were even successful at all. Some of my older partners that have been doing this for a very long time can do this faster (while also talking on the phone!) than most can put in a PA catheter. They were great to learn from. I imagine with them it eventually becomes enough muscle memory no different than Intubations.

Here is a great primer on the CS catheter placement that Edwards Lifesciences put out a while ago

 
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J Peterman

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Ditto to the above post.

I’ll also use a floppy “Zip wire” we steal from our cath lab colleagues if necessary to negotiate more challenging CS anatomy or semi-occlusive Thebesian valves to Seldinger into the main CS lumen. Very very rarely will park it in the middle cardiac vein if it’s absolutely the best you can do. There is a very real risk of perforation if your catheter is bowing and you try to use force to advance past a side branch if you don’t know what you’re doing. This can result in tamponade. Keep the catheter in situ if you’re seeing a pericardial effusion. You could even theoretically use the catheter to drain the accumulation.
 
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J Peterman

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For mitrals, there is a lot more retraction/cardiac manipulation by the surgeon, so I’ll park the catheter in a bit more distal position (a few cm shy of the PLV branches) than for a port access AVR for example. Nothing worse than having the catheter in a good position and then having it pull out when the venous cannula comes up from the IVC, or fall out due to surgical retraction. Especially in an AVR and your surgeon hates using ostial perfusors.

I like to shoot a cine venogram once I think the catheter is optimally positioned to save in the system, showing ideal catheter position, no “blushing” (indication of potential perforation), and ideally contrast collateralizing around the apex and back via the middle cardiac vein proximal to where my ballon is inflated.
 

dchz

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I didn't know @FFP takes consults
He'll probably cancel the case. Saying, "first, do no harm".

I’ll send this his way and see what he thinks . I sort of remember it as 5ch

already asked him ;). he said many authors says it should be long axis and he agrees. but his data was based on 4 chamber.
 
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dchz

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How many of you leave the balloon up on the coronary sinus catheter?

I measure things in MPR just to keep my skills sharp, i often measure the annulus to see if they size the valve the same size. so far really good accuracy if you do it en face.
 

J Peterman

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After placement, balloon down. Balloon partially inflated when venous cannula coming up from the IVC via femoral vein to prevent dislodgement. Then balloon down, reinflated once we go on CPB and are about to start delivering plege.

Stays up for the pump run and deflated once Ao XC comes off.
 

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