When to advance Swan?

[vector2]

Below is a link to the guidelines on repair of valvular heart disease under TEE. There is mention of CVP tracings and PA pressures in these guidelines, but they are certainly not emphasized. In most cases I have seen, these measurements do not play a major role in deciding intervention or not. Also in my experience, the severity (especially severe cases) of tricuspid pathologies is pretty obvious on TEE.

Your mention of symptomatology is also addressed in the guidelines specifically. If it's primary dysfunction, you're probably there to address the TV already, so discussion is gonna be mostly moot in the context of being under anesthesia as the vascular resistance and cardiac function variables have all changed. If secondary (most cases of TR), there are specific recommendations on intervention laid out in the guidelines.

It's worth noting that whatever we talk about is always in context of guidelines being studied and written by cardiologists who do TTE/TEE all day, every day, and see the effects of these valvular lesions on patient's long term outcomes in clinics and inpatient areas. Every TEE/CVP/PA pressure that's done intraoperatively is going to be confounded by the patient being under anesthesia, so in these cases of whether to intervene or not it's more appropriate imo to confirm findings with an available cardiologist. If what you're doing is complex enough where CVPs/PAs are the deciding factor, a cardiologist should be available for consultation either preoperatively or intraoperatively. You will never, ever go wrong getting a second set of eyes on a TEE that is equivocal.

2014 AHA/ACC Guideline for the Management of Patients With Valvular Heart Disease: Executive Summary: A Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines

www.sciencedirect.com

Here's the algorithm:

View attachment 364027

Thanks, I’m aware of the guidelines


And I fully agree with your points about the guidelines being written by cardiologists with long-term effects in mind, and the fact that GA affects loading conditions and hemodynamics in such a fashion that any grading of valvular lesion severity needs to be done with caution and in context of the preop findings.

To @T-burglar ’s point, his mention of hemodynamics in relation to severe TR was not about slam dunk cases where the TR was obviously massive or torrential and/or where the imaging or tricuspid annular dilatation was so obvious that repair was definitely indicated. And in regard to symptomatology, almost every adult surgical TVR/r performed is actually the second procedure being done during a pump run…since most TVR/r’s are occurring at the time of left sided heart surgery for the main symptomatic lesion. Indeed, intervention for primary symptomatic severe TR is vanishingly rare, which is why I don’t find the guidelines or the relative lack of class I indications to be the most helpful in the operating room.

Ultimately, we need to be asking ourselves, what are we actually worried about with a severe regurgitant valvular lesion? What actually kills the patient? In the case of MR, the hemodynamic and volume loading effects are deleterious upon 1. The LV, 2. The LA/pulmonary vasculature, and 3. The RV. And in the case of MR if you look at the echo guidelines, one of the most specific findings (other than the obvious 2d appearance of flail with a large flail gap/width) is holosystolic reversal of flow in the pulmonary veins, aka the echocardiographic representation of MR’s real hemodynamics. Analogously, in the case of AI, what’s most specific echo finding? Holodiastolic reversal of flow in the distal descending aorta.

And in the case of TR, as I alluded to in my earlier post, one of the most specific findings is holosystolic reversal of flow in the hepatic veins. This finding (in context of the preop findings, the effects of GA, the rest of the echo/ability to exclude other causes like RV cardiomyopathies, RV diastolic dysfunction, significant arrhythmias, constrictive processes) lets you know in an instant that the RV is moving so much blood forward and backward that it will have deleterious effects upon the RV, the pulmonary vasculature, the RA, and the rest of the body if left unchecked long enough. So it’s not just CVP in isolation that has value, but if you look at the CVP and it’s as high as the PAD, and there are obvious V waves, you are looking at the true hemodynamic representation of one of the most specific echocardiographic findings of severe TR, and I don’t think that can be ignored when advising a surgeon, especially if the echo isn’t of top tier quality.

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[T-burglar]

Below is a link to the guidelines on repair of valvular heart disease under TEE. There is mention of CVP tracings and PA pressures in these guidelines, but they are certainly not emphasized. In most cases I have seen, these measurements do not play a major role in deciding intervention or not. Also in my experience, the severity (especially severe cases) of tricuspid pathologies is pretty obvious on TEE.

Your mention of symptomatology is also addressed in the guidelines specifically. If it's primary dysfunction, you're probably there to address the TV already, so discussion is gonna be mostly moot in the context of being under anesthesia as the vascular resistance and cardiac function variables have all changed. If secondary (most cases of TR), there are specific recommendations on intervention laid out in the guidelines.

It's worth noting that whatever we talk about is always in context of guidelines being studied and written by cardiologists who do TTE/TEE all day, every day, and see the effects of these valvular lesions on patient's long term outcomes in clinics and inpatient areas. Every TEE/CVP/PA pressure that's done intraoperatively is going to be confounded by the patient being under anesthesia, so in these cases of whether to intervene or not it's more appropriate imo to confirm findings with an available cardiologist. If what you're doing is complex enough where CVPs/PAs are the deciding factor, a cardiologist should be available for consultation either preoperatively or intraoperatively. You will never, ever go wrong getting a second set of eyes on a TEE that is equivocal.

2014 AHA/ACC Guideline for the Management of Patients With Valvular Heart Disease: Executive Summary: A Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines

www.sciencedirect.com

Here's the algorithm:

We’ve read the guidelines front to back dude. I realize it’s not emphasized there. If I have to explain to you why imaging doesn’t fully replace invasive data, or why it’s a good idea to always correlate imaging clinically . Well I just won’t because I don’t have the energy.

In the end you have to use your head to make a diagnosis. you don’t need a different set of eyes on a tee study to make a diagnosis. If it’s that questionable Then you need different, additional information entirely.

 

[vector2]

This is fair, but the intersection of patients where you have to combo of the above factors (complete inability to evaluate both the right atrium AND tricuspid valve on TEE AND TTE on both live AND doppler, with absence of non valvular imaging indicators of severe disease (hepatic vein reversal)) seems to be vanishingly small. At that point, I would think you have to question whether the diagnosis was made appropriately if the windows are that terrible, because my guess would be the mitral valve that's likely causing the problem would be impossible to image as well.

I'm not saying that CVP or PA tracings are worthless for evaluating this pathology, just that in my time of working with the people who literally write the guidelines, they haven't brought it up as being all that significant of a marker, and I've never seen it make or break the pathology in a single case.

In any case, the gestalt of findings is going to be what usually drives management in TEEs. It's excellent to be able to back up findings with hard numbers, but if you're really that on the edge of an intervention, the risks and benefits of that additional operation I would think would tend to be nearly equal to non-operative management. If it could go either way, then it could go either way, and no one would fault a person for making the recommendation as a consultant and/or subsequently taking or not taking the advice as a surgeon.

When I get around to it I’ll upload some clips from the case in the picture above where the CVP was unexpectedly 24 with V waves. Pt with history of PPM coming for CABG, poorish TTE windows preop stating normal TV and trivial TR. On TEE he also made bad images. RV mildly enlarged with normal function, RA qualitatively enlarged, TV annulus probably not at 4cm although measurement by TEE has not been validated. Able to pick up large’ish area TR color jet, certainly much more than what the preop echo stated. But unable to visualize tricuspid leaflets well in any view. Unable to visualize how PPM and swan were interacting with the leaflets as they crossed the valve. Unable to visualize the vena contracta.

He did have holosystolic reversal of flow in the hepatic veins, though. So if I put the picture together and I’m talking to another echocardiographer, I can probably make a decent case that the TR is quite significant. However (and I don’t know if your experience is similar to mine), a whole bunch of CT surgeons 1. Have very strong opinions about changing cannulation and fixing TR when that wasn’t the preop plan 2. Are just as likely to nod and stare blankly at being told a pt has holosystolic reversal as they are to acknowledge something is wrong. But you know one thing I find they do understand? An insanely high, systolically pulsating venous pressure apparent on hemodynamics that’s confirmed when they look at the RA and then subsequently see a huge column of blood upon venous cannulation. In my case, unfortunately they didn’t want to do bicaval and look at the valve (pt is still doing OK but has signs of venous congestion and mildly elevated LFTs/bili/ammonia postop; two TTEs ordered have been unable to get any windows), but I do feel better about making that recommendation when invasive hemodynamics supported the gestalt of the TR being severe.

 

[vector2]

That’s a really cool case man, good to hear about this happening. But it sounds like my last paragraph ended up reasonably true. You had some good evidence to suggest severe regurgitation, but the surgeon was hesitant to change the plan based on the rec. Hard to fault as you never know whether your surgeon is comfortable with what they see or the length of the case. Idk what goes into those guys calculus for deviating from the original plan tbh

Sometimes they just won’t listen to us. In that case I find it helpful to have their favorite imaging cardiologist come in the room and back up what we say, and some surgeons don’t even have us do the tee and only go w their favorite cards person.

Sounds like you made the case well but at the end of the day the surgeons have to deal w the complications and follow up so it’ll be their call ultimately. We just do the best we can I think, and I won’t push them unless something blatant is there (like new or worsening AS on a cabg that wasn’t seen)

Ignoring surgeon idiosyncrasies for a sec, from an echo standpoint how good a case for severe was made, though? I think one of the biggest emphases in newer echo and valve guidelines has been the emphasis on primary vs secondary + mechanism, mechanism, mechanism. I couldn’t tell them the mechanism. I couldn’t see the leaflets. There was no vena contracta to share. There was no EROA to share. RV function was normal. TV annulus wasn’t clearly dilated. MPAP mildly elevated. Jet area is suggestive but not diagnostic. And flow reversal, while pretty specific, is still a supporting measure that shouldn’t really be used in isolation.

With the flow reversal, we know the CVP will have a V wave, but one thing we can’t derive from echo in the setting of severe TR is an accurate CVP. I think it does change the calculus, at least in my case, cause we do lines before induction/GA/PPV. And his awake was still ~18-20. Echo in valvular disease gives us amazing structural information, but we’re merely estimating the hemodynamic data that comes the cath lab. We don’t get that data as often as to avoid the invasive aspect, but that doesn’t mean that data doesn’t matter.

Indeed, I think there’s been a renaissance in the usage of catheter hemodynamics. There’s not an advanced heart failure cardiologist worth their salt who doesn’t use swans and data like CVPCWP, PAPi, CPO, and CO/CI/MVO2 in the treatment of high SCAI class CS. And in the case of TR, the move away from only using echo is already underway. This JACC paper from 2019 will likely be quite influential in the next guidelines:

https://www.jacc.org/doi/10.1016/j.jcmg.2018.11.034?_ga=2.84787801.1942180246.1672436334-2078311854.1672436334

 

[vector2]

I like your thoughts on cvp as a proxy for right sided filling pressures. I’d never say it’s useless except for fluid resuscitation purposes. In fact it’s such an easy thing to do it’s certainly worth checking assuming your tee won’t give you the info you want

Perhaps you’re right about heart failure cards people and their use of PACs. I’ve seen their cvicus and ccus and they do indeed like them, though I think if you have only a hammer, many things start to look like nails.

Assuming what they do is actually helpful, it Shouldn’t be long until we have evidence against this statement.

“Similar to general medical ICU patients, data supporting the value of PAC in patients with severe heart failure are equally lacking. As an example, one randomized study of 433 patients with heart failure (ESCAPE) reported no difference in mortality (10 versus 9 percent), or the length of hospital stay (8.7 versus 8.3 days) between those who had or did not have a PAC in place [26].”

Taken from UpToDate on severe cardiogenic shock. They don’t mention any trials that refute this result, which should be fairly easy to do if there’s really signal there. Just my thoughts on your last paragraph.

Or maybe it’s just too complicated for all us dumb folks who “don’t know how to interpret the data,” as is the classic response from the PAC crew. I tend to reserve my heaviest skepticism for people who disagree with expert consensus and guidelines without offering their own evidence. There isn’t much, if any, secret sauce left in medicine that the average specialist or generalist can’t replicate.

As always, the onus is on the expert to prove their stuff works, not the traditionalists to prove it doesn’t 😉

I appreciate all the thoughtful back and forth!

Agreed that CVP is pretty useless for fluid resuscitation.

In regard to CCUs and their tools, I don't think the characterization of "only having a hammer" is quite fair. After all, unlike a lot of intensivists managing shock, CT/CCM anesthesiologists and CCU cardiologists are typically more than capable of doing TTE and TEE when need be. In the echo thread, I posted some clips of a low EF MVR who had post cardiotomy shock and had to go back to the cathlab for impella placement a few hours after arriving in the ICU. In my opinion, assessing his biventricular function with the pulmonary artery pulsatility index, continuous CO, MVO2, and integrating that data with his lactate, acid base status, UOP, echo, and other clinical features was just much more practically useful and helpful than the alternatives.

No doubt, there is a dearth of high quality evidence for PAC, but pointing to an almost 20 yr old trial done in the age before GDMT for heart failure or widespread mechanical circulatory support like impellas doesn't negate the reality on the ground today. And to be clear, I support the use of PACs in cardiogenic shock, not just any decompensated heart failure. There is low quality retrospective evidence in existence such as this paper looking at 2.7 million pts which showed improved survival to discharge with PAC in CS, but unfortunately we're stuck with expert consensus until the PACCS trial is done.

And as far as that goes, SCAI says:

For all patients with suspected cardiogenic shock, an invasive hemodynamic assessment is recommended for the diagnosis and to expedite therapy. Specific hemodynamic criteria for cardiogenic shock are systolic blood pressure <90 mm Hg for >30 min or a fall in mean arterial blood pressure >30 mm Hg below baseline; PCWP >15 mm Hg; and a cardiac index (CI) of <1.8 L/min/m2 without hemodynamic support or <2.2 L/min/m2 with support 46-48. Patients with chronic heart failure and younger adults with acute heart failure can present with hemodynamic criteria for shock without suggestive bedside findings.

https://onlinelibrary.wiley.com/doi/full/10.1002/ccd.26888

And some more context and history about how we ended up here where PAC has had a resurgence even with a bunch of negative older trials can found in this interesting article here:

https://www.ahajournals.org/doi/full/10.1161/CIRCULATIONAHA.119.043080

 

[T-burglar]

Vector 2 has a lot more energy for these kinds of debates than I do.

It's been a theme throughout my medical career that we have to keep reminding ourselves, as evidenced by the literature, to step back and consider the whole picture and not fall victim to tunnel vision regarding one diagnostic modality.

Some day you if you're bored you should really take a step back and look at the depth and breadth of literature to consume about aortic stenosis alone. There's so much to read you could probably spend an entire career on JUST echocardiographic evaluation of aortic stenosis if you wanted to be a true expert. Why is it that we can't nail down this diagnosis completely with just ultrasound? Why do we still need CT scans, and catheter pullback studies.. Why do we sometimes still just throw up our hands and just assume the aortic valve is the cause of a patients symptoms even though all their diagnostics produce discrepancies. Here's a few selected articles from my "latest in aortic stenosis" folder:

Transvalvular Flow Rate Determines prognosis in severe aortic stenosis.pdf
Resting aortic valve area at normal transaortic flow rate reflects true valve area in suspected low-gradient severe aortic stenosis.pdf
Normal flow low gradient severe AS (WHAT?).pdf
Low-Flow Aortic Stenosis - flow rate does not completely replace SVi.pdf
Low gradient aortic stenosis and projected AVA.pdf
Indexing AVA for BSA signficantly increases the number of patients classified as severe AS, but these reclassified patients have fewer adverse valve related events.pdf

The idea that echocardiography alone is all you ever need to consider is simply wrong. In fact, many times the imaging plays more of a supporting role to other diagnostic information. A regurgitant lesion can look impressive on color and even meet some of the semiquantitative or quantitative criteria for severity, but if there's no evidence of any real hemodynamic effect in the invasive pressure traces, then arguing to intervene requires CAREFUL consideration.

 

[vector2]

I think a lot of management is driven too by the individual’s tendency towards doing more or less invasive things, and the desire to use more or less data points in creating an assessment.

For my part, I’m a minimalist. That’s my nature, and my laziness that comes through. When it comes to GDMT I let the simpler, more obvious criteria guide my goals. Lactate level, urine output, blood pressure can all be reasonably integrated to assess whether someone is in shock or not, particularly in the surgical population.

With that in mind, it will come as little surprise to you that I don’t favor MCS like impella or balloon pump as a standard therapy in almost any situation, simply because American medicine in general is overly expensive primarily because of our interventionist/over testing nature, and I haven’t read or heard of much compelling evidence that nearly any MCS device is useful compared to GDMT except as a bridge to transplant or durable solution when transplant isn’t an option.

Having said all that, I’m not ICU trained, and the endless debates they have about whether to give a 250cc fluid bolus on rounds made me want to jump out a window. For what it’s worth I think pulm crit trained internal medicine folks are the most discerning and evidence driven docs I’ve seen, so I defer to a lot of what they say, even over cardiologists.

Except sodium bicarbonate in lactic acidosis. Useless until proven otherwise haha

I'm an intensivist. I generally subscribe to the zentensivism school. In the vast majority of SICU patients I have, I try to do as little as possible to them, but rather just try to gently facilitate the things that are going to help their bodies heal themselves.

That being said, I also remain skeptical when a tool has fallen so far out of favor for so long that people treat its avoidance like a religious tenet. I don't think cardiac anesthesia or cardiac critical care is the same as it was when the prior "swan has no benefit" studies were being done. There were almost no tools to treat cardiogenic shock if it didn't respond to revascularization (in the case of AMI shock), inotropes, and a balloon pump. Echocardiography was also more primitive then. The evaluation of venous congestion using VexUS didn't exist. CHF GDMT didn't exist (entresto, SGLT2i's). I'm not surprised swans didn't change the outcomes of heart failure in the year 2005 when the treatment for heart failure, itself, hadn't changed since the year the swan came out.

I also agree that MCS has the potential to be way overused (and in many cathlabs impellas are thrown in without a moment's hesitation even in pts who shouldn't have one), but like everything else, it is a tool that has its time and place, and I think that includes more than just as a bridge. In the post-cardiotomy shock MVR I described in the other thread, in the pre-MCS/pre-impella era that 50 year old man is dead. On max inotropes/vasopressors and an IABP his MVO2 was 38, his pH was 7.09, and his lactate was 22. With three days of unloading with an impella (which really does have unique characteristics and benefits as far as ventricular rest and unloading) and a bit of an prolonged ICU stay, the guy managed to get stepped down to the floor two days ago on no inotropes, no oxygen, no dialysis.

 

[vector2]

All I’m really saying is that if these things are such slam dunks, someone just needs to actually do the studies and I’ll shut up about it.

I agree with the sentiment that we need high quality RCTs. Unfortunately we prolly gotta wait until 2025-2026 before what should be a definitive study on PACS in CS comes out.

However, it should be noted that when talking about critically ill patients (and presumably those in CCU as well), trials demonstrating an unambiguous mortality benefit are a pretty big ask, and furthermore, it may not even be the right question to ask depending on what intervention we're studying.

Josh Farkas of the PulmCrit blog (who is probably one of the most minimalist intensivists in practice) laid it out very well in this two part tour de force.

PulmCrit- Chasing mortality endpoints is a fool's errand

"There is no mortality benefit for that." How many times have you heard that? The implication is usually the same: that intervention is a waste of time. A smart, evidence-based clinician wouldn't bother with it. But, what does it actually mean if there is no proven mortality benefit?

emcrit.org

PulmCrit - It’s insane to keep using mortality as a primary endpoint in critical care trials

There, I’ve said it. That’s a bit of a bold statement, but it seems to be supported by the evidence. failure to prove mortality benefit A post in

emcrit.org

 

[Beeftenderloin]

He's saying hemodynamics would be a major deciding factor on whether to tell a surgeon if significant TR on echo needs intervention (much in the same way PASP > 50 mmHg supports the diagnosis of severe MR).

In the assessment of valvular disease, we have all sorts of quantitative and semiquantitative measures informing us of severity, but ultimately the doppler derived regurgitant volume or the vena contracta of the regurgitant jet or X other echo parameter is not nearly as important as pt symptomatology, adverse cardiac remodeling, or other end-organ dysfunction caused by the lesion. CVP of 20 with large V waves (i.e. holosystolic reversal of flow in the hepatic veins) is telling us that the TR will have deleterious effects upon the liver, kidneys, bowels, and heart if left untreated long enough.

This came up the other day for me. Was read as mild on TTE. Took first look, everything’s a little off axis but the portions of the tricuspid I can see look okay. CVP is 18 with big ass V waves though, prompting me to look harder. Then and sure enough, found the severe TR up high between the septal and anterior leaflets.

 

[T-burglar]

This came up the other day for me. Was read as mild on TTE. Took first look, everything’s a little off axis but the portions of the tricuspid I can see look okay. CVP is 18 with big ass V waves though, prompting me to look harder. Then and sure enough, found the severe TR up high between the septal and anterior leaflets.

Nice. This is why I shake my head when I hear places have stopped placing PA catheters for heart surgery. If you do this you’ll miss important pathology, misdiagnose things, or both .

It’s a little more complicated for MR because it’s accepted that severe MR can exist without a high PCWP or V waves on the PA trace. But the information is still useful to help interpret the imaging. And I’ve been alerted to the development of new MR post bypass by the appearance of new V waves when I wasn’t looking for it. And I’ve made interventions based on this information .

It’s more than just regurgitation. There’s a wealth of important diagnostic information from PA catheters.

 

[anes121508]

Post-op ICU care where 90% of the ICU RNs are 1-2 years out of nursing school. Also serves as another set of numbers to help guide management intra-op and assuage surgeons/nurses/NPs. Not completely useless, IMO, despite having minimal/no impact on M/M.

You ever try to do POCUS on a fresh heart with dressings/tubes in place on a hefty patient? I have. It’s not easy. We do ICU TEEs as well, but that’s a headache for everyone involved and delays care by a couple of hours compared to a set of numbers from a PAC/CCO monitor.

Surgeons like them, ICU likes them, cardiology likes them, and I don’t mind placing them. As soon as I try to change the culture based on “data,” the sooner they throw me under the bus for not placing one.

literally same boat as you

i only do it for them, all cases (hearts) get one

i'm an employee so i don't get paid for it

feel like eventually ill have a complication from one and not sure how ill defend "so this patient was a two vessel cabg with normal lvef and you don't use the swan yet you put one in?"

ill be hung to dry for sure

anyone refuse to do it for the icu folks?

 

[anes121508]

Nice. This is why I shake my head when I hear places have stopped placing PA catheters for heart surgery. If you do this you’ll miss important pathology, misdiagnose things, or both .

It’s a little more complicated for MR because it’s accepted that severe MR can exist without a high PCWP or V waves on the PA trace. But the information is still useful to help interpret the imaging. And I’ve been alerted to the development of new MR post bypass by the appearance of new V waves when I wasn’t looking for it. And I’ve made interventions based on this information .

It’s more than just regurgitation. There’s a wealth of important diagnostic information from PA catheters.

so you believe you would possibly miss severe tr or mr in some cases without a swan? I dunno...agree good info, but i have a hard time using that example to justify putting them in

 

[anes121508]

Just to cherry-pick your nonsense statement about the CVP. A high fidelity CVP trace is my gold standard for advising the surgeon on whether to intervene on a tricuspid valve en passant in cardiac surgery. There are some imaging elements to consider but by and large if there are no significant V waves or elevated CVP then there is no benefit to be expected from intervening on a tricuspid. There are many reasons that it is tough to be sure about the severity of TR by imaging alone. I’d also place way more emphasis on the CVP trace than the TEE in evaluating RV systolic and diastolic function, presence of significant pericardial disease, whether I’m overloading the RV with my rate of volume administration.

The list goes on. Do you do cardiac surgery? Or just read articles about how the CVP is useless .

in part of your post you said that there is no benefit to fixing the tr if there aren't V waves or elevated cvp ....can you please direct me to where you get that from?

also interesting that you will advise them on wether to intervene on a valve...i have shifted to more of an approach that centers around I tell them the grading and the cause of the regurgitation and leave the decision to them...ever have blowback after arguing to intervene on a valve?

 

[epidural man]

I have heard from almost all attendings that you should advance the Swan 1 cm at a time during systole. They say to listen to the pulse ox tone and advance with each beep.

However, one attending says that’s not real. He says the Swan is flow directed and the the tone is delayed due to computer processing. So he just advances at random timing.

Does anyone know if you should advance with each pulse ox beep, or is this dogma?

What is this mysterious “Swanz” you speak of?

 

[T-burglar]

Just had another case where I had to over read my partners echo because he glanced at the TR and said it was mild, but there were obvious V waves on the CVP and when I was putting the line in the neck there was pulsatility coming from the needle in the jugular. Sure enough with some careful examination we found an axial alignment that showed the TR hitting the posterior RA wall and systolic flow reversal in the proximal hepatic veins.

Here’s a great article

https://pubs.rsna.org/doi/10.1148/rg.297095715

 

[DesiredMemberName?]

Just had another case where I had to over read my partners echo because he glanced at the TR and said it was mild, but there were obvious V waves on the CVP and when I was putting the line in the neck there was pulsatility coming from the needle in the jugular. Sure enough with some careful examination we found an axial alignment that showed the TR hitting the posterior RA wall and systolic flow reversal in the proximal hepatic veins.

Here’s a great article

https://pubs.rsna.org/doi/10.1148/rg.297095715

I don’t understand what’s happening here. Your partner did a TEE, and then you placed the lines? Do you regularly have two anesthesiologists working on a heart case?

I agree cvp tracing can be helpful. We should use all the data we have available. However, a quick look at cvp could confuse cannon a waves (e.g. 2/2 AV dysynchrony) with large CV waves (e.g. 2/2 TR). Both could appear as higher than expected venous pulsatility with line placement.

Just as a quick glance at the cvp may confuse a valve issue with a rhythm issue, a quick glance at the TV on echo may underestimate the valvulopathy. If we are going to gather and interpret data, it should be done carefully.

 

[T-burglar]

Nobody should confuse cannon As with V waves

And yes we have two physicians

 

[dabears505]

I routinely confuse cannon As with V waves. Sorry.

 

[lunaire]

I find the PA cath to be one of the easiest diagnostic tool to be misread. You need to interpret the numeral values. You need to actually take in all the values with clinical context (instead of just cherry picking a single one). You need to be identify the waveforms properly. etc etc... I think PA cath is a useful diagnostic tool that can definitely lead to better outcome, but most clinicians are not necessarily trained properly in its use.

 

[nimbus]

I find the PA cath to be one of the easiest diagnostic tool to be misread. You need to interpret the numeral values. You need to actually take in all the values with clinical context (instead of just cherry picking a single one). You need to be identify the waveforms properly. etc etc... I think PA cath is a useful diagnostic tool that can definitely lead to better outcome, but most clinicians are not necessarily trained properly in its use.

Yep. I can often cure pulmonary htn with fentanyl 50mcg or propofol 50mg. Definitely need to interpret the data within context.

 

[PpfSuxTube]

in part of your post you said that there is no benefit to fixing the tr if there aren't V waves or elevated cvp ....can you please direct me to where you get that from?

also interesting that you will advise them on wether to intervene on a valve...i have shifted to more of an approach that centers around I tell them the grading and the cause of the regurgitation and leave the decision to them...ever have blowback after arguing to intervene on a valve?

100%
Im not a surgeon. I met the patient 1 hour ago. I dont tell surgeons to do anything. I tell them grading and if its there anatomical pathology but im not telling them to intervene or not

I will get a second opinion on the grading and if that person wants to go rogue thats fine, but not for me... not my job, never will be

 

[T-burglar]

in part of your post you said that there is no benefit to fixing the tr if there aren't V waves or elevated cvp ....can you please direct me to where you get that from?

also interesting that you will advise them on wether to intervene on a valve...i have shifted to more of an approach that centers around I tell them the grading and the cause of the regurgitation and leave the decision to them...ever have blowback after arguing to intervene on a valve?

If there is an incidental finding (not the primary valve disorder the patient is on the table for ) , I do discuss intervention in every case with the surgeon. They respect my insight about whether it makes sense to intervene or not.