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waterbottle10

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Another case discussion for the experts here on this forum. 75 year old with atrial fibrillation on Eliquis, brought in with fractured hip. Orthopedic surgery books the procedure 3 days later (unclear why delayed) for hemiarthroplasty. Labs are fairly OK, nothing absurd. Hct 28, On TTE 1 day ago, there is large pericardial effusion (unknown etiology) with evidence of right atrial collapse, right ventricle inversion, respiratory variations. Diffuse hypokinesis, with LVEF 35%. However, patient's vitals are currently stable without support and is not complaining of dyspnea while lying in bed. Cardiology was consulted, and wrote a 'clearance note', stating nothing to do prior to procedure as patient is currently stable. While I believe the patient will most likely survive thru the procedure under general anesthesia, I do also believe there is significant increased risk of intra/post op morbidity/mortality due to the large effusion compressing on the heart. Proceed? Thoughts?

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Another case discussion for the experts here on this forum. 75 year old with atrial fibrillation on Eliquis, brought in with fractured hip. Orthopedic surgery books the procedure 3 days later (unclear why delayed) for hemiarthroplasty. Labs are fairly OK, nothing absurd. Hct 28, On TTE 1 day ago, there is large pericardial effusion (unknown etiology) with evidence of right atrial collapse, right ventricle inversion, respiratory variations. However, patient's vitals are currently stable without support and is not complaining of dyspnea while lying in bed. Cardiology was consulted, and wrote a 'clearance note', stating nothing to do prior to procedure as patient is currently stable. While I believe the patient will most likely survive thru the procedure under general anesthesia, I do also believe there is significant increased risk of intra/post op morbidity/mortality due to the large effusion compressing on the heart. Proceed? Thoughts?
Call the cardiologist and ask him or her why he doesnt think it needs to be drained prior to procedure? Does cards not know general anesthesia drops preload and you cannot quantify the drop so he needs to drain it! . Probably best to monitor introp with TEE if he doesnt want to drain it and a preinduction aline. I would make a couple of phone calls to your seniors to make sure you are comfortable proceeding with the case.
 
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Call the cardiologist and ask him or her why he doesnt think it needs to be drained prior to procedure? Does cards not know general anesthesia drops preload and you cannot quantify the drop so he needs to drain it! . Probably best to monitor introp with TEE if he doesnt want to drain it and a preinduction aline. I would make a couple of phone calls to your seniors to make sure you care comfortable proceeding with the case.

Per the cardiologist, who claims it was also discussed with the chair of their department, patient is currently hemodynamically stable, therefore there is no indication for them to drain it.

I'm at a good hospital in an under-served area, so unfortunately, we do not have the fancy equipment such as TEE.
 
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Stable pericardial effusion shouldn't be a big problem, she sounds like she's compensating.

Besides drainage, which the experts feel is unwarranted, and has its own risks, there's not much else you need to address.
 
Stable pericardial effusion shouldn't be a big problem, she sounds like she's compensating.

Besides drainage, which the experts feel is unwarranted, and has its own risks, there's not much else you need to address.

at my hospital, these experts would clear anybody for surgery unless they are actively having massive MI .
 
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Vitals are stone cold normal? Very, very unlikely someone has a clinically significant pericardial effusion or tamponade without tachycardia. +-hypotension or borderline hypotension depending on how well they're compensating. Even though I'm a bit worried by the echo findings (esp if PPV given during general anesthesia), remember that tamponade is a clinical diagnosis.

Also, did this lady have an echo ordered for any particular reason? Or did someone just see 75yo with afib and shotgunned a bunch of labs and tests?
 
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Vitals are stone cold normal? Very, very unlikely someone has a clinically significant pericardial effusion or tamponade without tachycardia. +-hypotension or borderline hypotension depending on how well they're compensating. Even though I'm a bit worried by the echo findings (esp if PPV given during general anesthesia), remember that tamponade is a clinical diagnosis.

Also, did this lady have an echo ordered for any particular reason? Or did someone just see 75yo with afib and shotgunned a bunch of labs and tests?

would you only drain this patient if she were in TAMPONADE? isn't the whole point of optimizing, to prevent bad stuff from happening? if shes in tamponade, the OP would prob be doing a different case
 
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would you only drain this patient if she were in TAMPONADE? isn't the whole point of optimizing, to prevent bad stuff from happening? if shes in tamponade, the OP would prob be doing a different case

I didn't really say in my previous post whether you should drain it or not- I'm more just commenting that the echo findings aren't an indication alone to hammer page cards and go to the cathlab for a drainage, esp in light of normal HR, normal BP, and ability to lay flat without any dyspnea. That being said, a drainage of the effusion might very well be indicated- but not necessarily because of hemodynamic reasons- more because we might need a diagnosis of whether the effusion is slow hemorrhagic from eliquis or malignant or something else. Now, if you tell me that you put your finger on her carotid pulse, had her valsalva (or slapped on CPAP mask at 15cmH20), and then you couldn't feel anything...maybe I'm thinking twice about doing a bit of drainage before inducing GA.


Another thing to keep in mind, you should be very careful about draining large, chronic effusions. I had a case where too much volume was drained off too quickly on one and the lady went into what I'm pretty sure was a syndrome like this.
 
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I forgot to mention that her TTE also showed diffuse hypokinesis with EF 35%; added onto my 1st post, in case anyone cares for this discussion
 
I've done a couple "large" pericardial effusions of unknown etiology, one for pericardial window and other was some other unrelated procedure.

Both did perfectly fine.

I've also done a "small" pericardial effusion pericardial window, and developed significant instability after induction.
 
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at my hospital, these experts would clear anybody for surgery unless they are actively having massive MI .

Are people dying all over there?

In residency, I had neurotic attendings who would cancel or have a public meltdown over anything other than "healthy" rolling in. Thankfully we had cardiologists who would give their blessing so things can get done. Maybe the pendulum has swung and now they're too liberal with their clearances?
 
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Are people dying all over there?

In residency, I had neurotic attendings who would cancel or have a public meltdown over anything other than "healthy" rolling in. Thankfully we had cardiologists who would give their blessing so things can get done. Maybe the pendulum has swung and now they're too liberal with their clearances?

the problem is its extremely uncommon to have intraoperative mortality... its kind of like the hyponatremia thread. hyponatremia is associated with significant post op m/m. im sure 99++ % of the time we can get a patient thru a case even if the Na is 125. doesn't mean the patient is optimized for the procedure. the goal should be to reduce overall M/M, not just get the patient thru a case and dump the patient back to the primary team and it's a job well done
 
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Vitals are stone cold normal? Very, very unlikely someone has a clinically significant pericardial effusion or tamponade without tachycardia. +-hypotension or borderline hypotension depending on how well they're compensating. Even though I'm a bit worried by the echo findings (esp if PPV given during general anesthesia), remember that tamponade is a clinical diagnosis.

Also, did this lady have an echo ordered for any particular reason? Or did someone just see 75yo with afib and shotgunned a bunch of labs and tests?

I definitely remember learning in medical school that tamponade is a clinical diagnosis but now that I think about it, what exactly does that mean in 2019? I did some reading and I see no strict diagnostic criteria for tamponade. Classic signs include the triad low blood pressure, JVD, muffled heart sounds but it sounds awfully outdated in 2019. (I imagine most large pericardial effusions will have 'muffled' heart sounds, and JVD is not very specific). Obvious tamponade cases are obvious, but it's those borderline cases that I question. What if blood pressure is normal, but JVD and muffled heart sound is present, +/- tachycardia? How many symptoms and signs do you need to call it tamponade? What mix/match of these do you need to call it tamponade?
 
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I definitely remember learning in medical school that tamponade is a clinical diagnosis but now that I think about it, what exactly does that mean in 2019? I did some reading and I see no strict diagnostic criteria for tamponade. Classic signs include the triad low blood pressure, JVD, muffled heart sounds but it sounds awfully outdated in 2019. (I imagine most large pericardial effusions will have 'muffled' heart sounds, and JVD is not very specific). Obvious tamponade cases are obvious, but it's those borderline cases that I question. What if blood pressure is normal, but JVD and muffled heart sound is present, +/- tachycardia? How many symptoms and signs do you need to call it tamponade? What mix/match of these do you need to call it tamponade?

When I say clinical diagnosis in 2019, I don’t mean Beck’s triad. I use a mixture of clinical and echocardiographic signs to gauge the overall gestalt.

Not having tachycardia is a huge indicator against a diagnosis of tamponade. Not having tachycardia (in the absence of conflating factors or medications) means that pt is has enough beat to beat diastolic filling to generate an adequate cardiac output.

While not as sensitive as tachycardia, I do pay attention to the bp. Hypotension is obviously indicative. Normal or borderline normal can go either way. If the pt is HR 120, sweating their a$$ off, looks anxious, dyspneic, then I don’t look at an sbp 102 and think, oh yea pt’s doing great. OTOH, lying in bed, hr 85, sbp 110, huge pericardial effusion- I’m not that concerned. BP is still a tricky one because you don’t want to misinterpret a high SVR/low CO/normalish MAP scenario incorrectly. So in addition to bp, is the pt mentating ok, warm extremities, good cap refill, making urine, normal lactate etc.

With echo, three things I need to see to support my clinical diagnosis:
IVC plethora- if you have a 1.2 cm ivc that’s collapsing wildly with sniffing, it ain’t tamponade
RV diastolic impingement/collapse - a sensitive and specific sign of impending badness
Mitral inflow velocity or vti variation- not as sensitive but I’ll certainly pay attention to 25% peak to trough variations

Without getting more details on your pt I can’t really tell you what I think, but what I wrote above is the general way I think about whether I need to escalate things.
 
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When I say clinical diagnosis in 2019, I don’t mean Beck’s triad. I use a mixture of clinical and echocardiographic signs to gauge the overall gestalt.

Not having tachycardia is a huge indicator against a diagnosis of tamponade. Not having tachycardia (in the absence of conflating factors or medications) means that pt is has enough beat to beat diastolic filling to generate an adequate cardiac output.

While not as sensitive as tachycardia, I do pay attention to the bp. Hypotension is obviously indicative. Normal or borderline normal can go either way. If the pt is HR 120, sweating their a$$ off, looks anxious, dyspneic, then I don’t look at an sbp 102 and think, oh yea pt’s doing great. OTOH, lying in bed, hr 85, sbp 110, huge pericardial effusion- I’m not that concerned. BP is still a tricky one because you don’t want to misinterpret a high SVR/low CO/normalish MAP scenario incorrectly. So in addition to bp, is the pt mentating ok, warm extremities, good cap refill, making urine, normal lactate etc.

With echo, three things I need to see to support my clinical diagnosis:
IVC plethora- if you have a 1.2 cm ivc that’s collapsing wildly with sniffing, it ain’t tamponade
RV diastolic impingement/collapse - a sensitive and specific sign of impending badness
Mitral inflow velocity or vti variation- not as sensitive but I’ll certainly pay attention to 25% peak to trough variations

Without getting more details on your pt I can’t really tell you what I think, but what I wrote above is the general way I think about whether I need to escalate things.

So assuming the patient does not currently have tamponade on the floor, what criteria do you use to decide to proceed? We know the patient's cardiac status will most likely be worse after induction of anesthesia and PPV, even worse if surgeon gets unanticipated bleeding (no TEE). I get of course if the patient is already in tamponade pre-op, it has to be fixed but what if not actively in tamponade? If this patient was instead getting a colon resection for cancer, with this TTE, and a cardiology note saying "not in tamponade, proceed with surgery", would you proceed?

I don't remember the exact TTE details off the top of my head right now but like I mentioned in first post, there is at least "large pericardial effusion (unknown etiology) with evidence of right atrial collapse, right ventricle inversion, respiratory variations. Diffuse hypokinesis, with LVEF 35%. " I believe there is 25% mitral variations, but I have to double check.
 
So assuming the patient does not currently have tamponade on the floor, what criteria do you use to decide to proceed? We know the patient's cardiac status will most likely be worse after induction of anesthesia and PPV, even worse if surgeon gets unanticipated bleeding (no TEE). I get of course if the patient is already in tamponade pre-op, it has to be fixed but what if not actively in tamponade? If this patient was instead getting a colon resection for cancer, with this TTE, and a cardiology note saying "not in tamponade, proceed with surgery", would you proceed?

I don't remember the exact TTE details off the top of my head right now but like I mentioned in first post, there is at least "large pericardial effusion (unknown etiology) with evidence of right atrial collapse, right ventricle inversion, respiratory variations. Diffuse hypokinesis, with LVEF 35%. " I believe there is 25% mitral variations, but I have to double check.


What’s their vitals and general clinical condition? The afib is def going to compound some things too. Do we know if the decreased EF is new?
 
I sure would like to have this pericardial effusion drained unless some cardiologist can tell why we shouldn’t.
 
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Another case discussion for the experts here on this forum. 75 year old with atrial fibrillation on Eliquis, brought in with fractured hip. Orthopedic surgery books the procedure 3 days later (unclear why delayed) for hemiarthroplasty. Labs are fairly OK, nothing absurd. Hct 28, On TTE 1 day ago, there is large pericardial effusion (unknown etiology) with evidence of right atrial collapse, right ventricle inversion, respiratory variations. Diffuse hypokinesis, with LVEF 35%. However, patient's vitals are currently stable without support and is not complaining of dyspnea while lying in bed. Cardiology was consulted, and wrote a 'clearance note', stating nothing to do prior to procedure as patient is currently stable. While I believe the patient will most likely survive thru the procedure under general anesthesia, I do also believe there is significant increased risk of intra/post op morbidity/mortality due to the large effusion compressing on the heart. Proceed? Thoughts?
If Cardiology does not want to evacuate that effusion (I have seen idiots who refused to do so even when the patient needed pressors, because "the echo did not meet criteria" -> the patient died), I would treat is as tamponade. Hence "fast, full and forward", pre-induction A-line, maintain spontaneous ventilation, LMA.

This is urgent surgery, stop futzing around, discuss risk vs benefits with patient and surgeon and go from there.
 
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Vitals are stone cold normal? Very, very unlikely someone has a clinically significant pericardial effusion or tamponade without tachycardia. +-hypotension or borderline hypotension depending on how well they're compensating. Even though I'm a bit worried by the echo findings (esp if PPV given during general anesthesia), remember that tamponade is a clinical diagnosis.

Also, did this lady have an echo ordered for any particular reason? Or did someone just see 75yo with afib and shotgunned a bunch of labs and tests?
Some would be surprised how many idiots physicians continue beta-blockers, or give inappropriate doses of them.

And just because cardiac tamponade is not detectable at rest, it doesn't mean it can't show up the moment one pushes the patient above his/her low functional reserve.
 
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If Cardiology does not want to evacuate that effusion (I have seen idiots who refused to do so even when the patient needed pressors, because "the echo did not meet criteria" -> the patient died), I would treat is as tamponade. Hence "fast, full and forward", pre-induction A-line, maintain spontaneous ventilation, LMA.

This is urgent surgery, stop futzing around, discuss risk vs benefits with patient and surgeon and go from there.
i would strongly recommend draining first and i wouldn’t start without a clear plan for how this effusion is getting urgently drained if (when?) this patient decompensates .

i very nearly learnt this the hard way
 
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Another case discussion for the experts here on this forum. 75 year old with atrial fibrillation on Eliquis, brought in with fractured hip. Orthopedic surgery books the procedure 3 days later (unclear why delayed) for hemiarthroplasty. Labs are fairly OK, nothing absurd. Hct 28, On TTE 1 day ago, there is large pericardial effusion (unknown etiology) with evidence of right atrial collapse, right ventricle inversion, respiratory variations. Diffuse hypokinesis, with LVEF 35%. However, patient's vitals are currently stable without support and is not complaining of dyspnea while lying in bed. Cardiology was consulted, and wrote a 'clearance note', stating nothing to do prior to procedure as patient is currently stable. While I believe the patient will most likely survive thru the procedure under general anesthesia, I do also believe there is significant increased risk of intra/post op morbidity/mortality due to the large effusion compressing on the heart. Proceed? Thoughts?
Is Cardiac output monitoring (via) A-line available to you?
 
there is large pericardial effusion (unknown etiology) with evidence of right atrial collapse, right ventricle inversion, respiratory variations. Diffuse hypokinesis, with LVEF 35%.

was that official TTE read by cardiologist?

Stable pericardial effusion shouldn't be a big problem

does normal vitals = stable effusion? if there are signs of right atrial collapse, and right vent inversion, this isn't an stable effusion to me based on those echo reads.


With echo, three things I need to see to support my clinical diagnosis:
IVC plethora- if you have a 1.2 cm ivc that’s collapsing wildly with sniffing, it ain’t tamponade
RV diastolic impingement/collapse - a sensitive and specific sign of impending badness
Mitral inflow velocity or vti variation- not as sensitive but I’ll certainly pay attention to 25% peak to trough variations

Bingo. But right vent inversion felt like another way to state #2?

I don't remember the exact TTE details off the top of my head right now but like I mentioned in first post, there is at least "large pericardial effusion (unknown etiology) with evidence of right atrial collapse, right ventricle inversion, respiratory variations. Diffuse hypokinesis, with LVEF 35%. " I believe there is 25% mitral variations, but I have to double check.

I like to think i'm as much of a cowboy as the next guy. But why risk it with given documented RV inversion?? you said it. it's gonna get worse with the vent and PPV. You don't even have a TEE available to diagnose other stuff. just because she has a pericardial effusion doesn't mean other cardiac stuff can't happen intra op for this 75 year old. If you stated twice like that then i believe it's probably an official cardiologist read. Sizes of effusion is not sensitive or specific, but the bolded stuff is where the medical legal stuff can really hang you. even though they "cleared" it, the echo finding is supposed to point you towards the bad effusion.

My willingness to do this case would also change if I had a long needle and a curvilinear probe handy.
 
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Is Cardiac output monitoring (via) A-line available to you?

Man it would be great if there is a magical monitor that tells you what the cardiac output is without an invasive PA cath.

But just because the flowtrac spits out a number doesn't mean you should trust it. All the assumptions of a flowtrac extrapolation are not met here. The number that it spits out means nothing IMO.
 
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If Cardiology does not want to evacuate that effusion (I have seen idiots who refused to do so even when the patient needed pressors, because "the echo did not meet criteria" -> the patient died), I would treat is as tamponade. Hence "fast, full and forward", pre-induction A-line, maintain spontaneous ventilation, LMA.

This is urgent surgery, stop futzing around, discuss risk vs benefits with patient and surgeon and go from there.
That would be my approach.
 
Bingo. But right vent inversion felt like another way to state #2?

It is, but again it's the overall picture. IVC plethora is like 97% sensitive whereas RAI or RVDC might be ~60-70% sensitive, and its sensitivity goes down significantly as the duration of collapse during the cardiac cycle decreases. Not to mention, this lady is in afib so who knows how that's gonna cloud some of the echo picture.

I think you make a good point tho that this lady could run into all sorts of trouble intraop, and having those words in the echo report is going to be devastating from a medicolegal standpoint even if tamponade isn't the cause of the intraop trouble.
 
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Per the cardiologist, who claims it was also discussed with the chair of their department, patient is currently hemodynamically stable, therefore there is no indication for them to drain it.

I'm at a good hospital in an under-served area, so unfortunately, we do not have the fancy equipment such as TEE.

Frequently in medicine we do things not because of what the patient looks like in front of us but because of “anticipated clinical course”. The patient with the bad TBI with GCS of 9-10 doesn’t technically meet criteria for intubation, but you tube em now because your not gonna send them down to CT so they can decompensate and die down there.

Yes they are hemodynamically stable now with normal pre-load, peripheral vascular resistance and spontaneous negative pressure ventilation. But the second you push induction meds, drop pre-load, Initiate PPV and give a cardiotoxic/vasodilatory general anesthetic this patient is going to decompensate and it’s going to be on your shoulders.

Cardiologists SHOULD be aware of this, but it never ceases to amaze me what a black box anesthesia is to virtually all other specialties.

This needs drainage.
 
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If Cardiology does not want to evacuate that effusion (I have seen idiots who refused to do so even when the patient needed pressors, because "the echo did not meet criteria" -> the patient died), I would treat is as tamponade. Hence "fast, full and forward", pre-induction A-line, maintain spontaneous ventilation, LMA.

This is urgent surgery, stop futzing around, discuss risk vs benefits with patient and surgeon and go from there.

Is it an urgent surgery? The surgeon has been sitting on this broken hip for three days. Granted he was probably waiting for the Eliquis, per the same cardiologist’s recommendation who “cleared” the patient...

In any event, I think from all the discussion we can all agree that no one knows for sure exactly how PPV is going to affect the patient’s physiology and hemodynamics. It’s just a matter of whether you want to assume the (potentially small) risk of the patient circling the drain. I sure as hell wouldn’t and would tell the bone doctor to sit on the fracture for another couple hours until I can find a cardiologist to put a needle in this thing.
 
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It is, but again it's the overall picture. IVC plethora is like 97% sensitive whereas RAI or RVDC might be ~60-70% sensitive, and its sensitivity goes down significantly as the duration of collapse during the cardiac cycle decreases. Not to mention, this lady is in afib so who knows how that's gonna cloud some of the echo picture.

I think you make a good point tho that this lady could run into all sorts of trouble intraop, and having those words in the echo report is going to be devastating from a medicolegal standpoint even if tamponade isn't the cause of the intraop trouble.


I think you mean specificity??? my understanding is that the sensitivity is high and specificity is low.
 
Drain this $hit. If necessary take a large BP cuff in holding, get a borderline low BP and send them back to cardiology because “now they got worse”. Sometimes you gotta play the game......
 
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Thanks for all the comments. Glad my decision was inline with most of your thoughts as well! I also thought that the cardiologist was not taking the anesthesia into account. They did take a look at the echo and even with that said the patient is cleared because vitals are stable. The patient was also getting her home dose beta blockers on the medicine floor (metoprolol 12.5). Drainage was finally done, and patient did fine!
 
Did you guys do the evacuation before the hip surgery??
Thanks for all the comments. Glad my decision was inline with most of your thoughts as well! I also thought that the cardiologist was not taking the anesthesia into account. They did take a look at the echo and even with that said the patient is cleared because vitals are stable. The patient was also getting her home dose beta blockers on the medicine floor (metoprolol 12.5). Drainage was finally done, and patient did fine!
 
Thanks for all the comments. Glad my decision was inline with most of your thoughts as well! I also thought that the cardiologist was not taking the anesthesia into account. They did take a look at the echo and even with that said the patient is cleared because vitals are stable. The patient was also getting her home dose beta blockers on the medicine floor (metoprolol 12.5). Drainage was finally done, and patient did fine!
We need more details! How’d you do induction and airway?
 
Another case discussion for the experts here on this forum. 75 year old with atrial fibrillation on Eliquis, brought in with fractured hip. Orthopedic surgery books the procedure 3 days later (unclear why delayed) for hemiarthroplasty. Labs are fairly OK, nothing absurd. Hct 28, On TTE 1 day ago, there is large pericardial effusion (unknown etiology) with evidence of right atrial collapse, right ventricle inversion, respiratory variations. Diffuse hypokinesis, with LVEF 35%. However, patient's vitals are currently stable without support and is not complaining of dyspnea while lying in bed. Cardiology was consulted, and wrote a 'clearance note', stating nothing to do prior to procedure as patient is currently stable. While I believe the patient will most likely survive thru the procedure under general anesthesia, I do also believe there is significant increased risk of intra/post op morbidity/mortality due to the large effusion compressing on the heart. Proceed? Thoughts?
Who are these cardiology jokers?
Did they report tissue doppler across the mitral/tricuspid in inspiration/expiration

Either way, this thing should definitely be drained pre-op because of "evidence of right atrial collapse, right ventricle inversion"
The rest is irrelevant.

If i had to do it, it'd be fast full tight and light with aline ketamine boluses, until glidescope is tolerated then spray the cords and maintain with low dose volatile. stick of epi 10mcg/ml in one hand and the name of the cardiologist that cleared written everywhere over the chart. I wouldnt do pac, i would do tee
 
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Man it would be great if there is a magical monitor that tells you what the cardiac output is without an invasive PA cath.

But just because the flowtrac spits out a number doesn't mean you should trust it. All the assumptions of a flowtrac extrapolation are not met here. The number that it spits out means nothing IMO.

Perhaps.

When I have had the opportunity to use CO from an A-line and the CardioQ, I have found they track very nicely together. (I highly trust CardioQ). I think they are great trend monitors. But full disclosure, I like monitors and data. I’m a big fan of anesthesia depth monitors and have used peripheral venous pressure trends often.

But maybe in certain conditions the CO monitors don’t trend well. But what condition would a patient have that when the CO fell by bunch that the flotrac would not decrease, or maybe even increase?
 
Who are these cardiology jokers?
Did they report tissue doppler across the mitral/tricuspid in inspiration/expiration

Either way, this thing should definitely be drained pre-op because of "evidence of right atrial collapse, right ventricle inversion"
The rest is irrelevant.

If i had to do it, it'd be fast full tight and light with aline ketamine boluses, until glidescope is tolerated then spray the cords and maintain with low dose volatile. stick of epi 10mcg/ml in one hand and the name of the cardiologist that cleared written everywhere over the chart. I wouldnt do pac, i would do tee

i recently tried to intubate someone without paralytic (unrelated to this topic), bolused some midaz and ketamine... and then could not open his mouth at ALL. Fully clenched. super fail
 
.
Perhaps.

When I have had the opportunity to use CO from an A-line and the CardioQ, I have found they track very nicely together. (I highly trust CardioQ). I think they are great trend monitors. But full disclosure, I like monitors and data. I’m a big fan of anesthesia depth monitors and have used peripheral venous pressure trends often.

But maybe in certain conditions the CO monitors don’t trend well. But what condition would a patient have that when the CO fell by bunch that the flotrac would not decrease, or maybe even increase?
You must love random number generators. :)
 
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i recently tried to intubate someone without paralytic (unrelated to this topic), bolused some midaz and ketamine... and then could not open his mouth at ALL. Fully clenched. super fail
What did you use to topicalise/sedate? What was the ddx of why you couldn't open his mouth and how did you treat it?

.overall it's just a glorified afoi so do all the same things you would do for afoi
 
But full disclosure, I like monitors and data.

I’m a big fan of anesthesia depth monitors and have used peripheral venous pressure trends often.
For what? What's the evidence?

There's been 3 big anesthesia depth monitor trials. All have not shown benefit ultimately

There has been no big generally accepted periphal venous pressure trials. Central venous pressure has long since been accepted as inaccurate almost always so I can't imagine how a peripheral vein can give any form of useful info. There's just so many potential confounders
 
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Is your cardiologist Donald trump ?

That effusion is almost surely Blood and best case scenario is spontaneous on eliquis, but it could be something much worse with a fib and (new?) dysfunction.

Lots of things need to be investigated but aren’t for some unclear reason. The heart condition needs to be sorted out before trying any other bloodletting. How can a cardiologist essentially write “signs of early tanponade” then in the same paragraph write “nothing else to do”
 
How can a cardiologist essentially write “signs of early tanponade” then in the same paragraph write “nothing else to do”
But did he approuve the use of zofran via meticulous examination of the QTc?
 
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Advise anesthesia avoid hypotension, avoid excess iv fluids, Provide Adequate oxygenation. rcri=1 => 6% 30 day mortality.

Thanks cardiology
 
Perhaps.

When I have had the opportunity to use CO from an A-line and the CardioQ, I have found they track very nicely together. (I highly trust CardioQ). I think they are great trend monitors. But full disclosure, I like monitors and data. I’m a big fan of anesthesia depth monitors and have used peripheral venous pressure trends often.

But maybe in certain conditions the CO monitors don’t trend well. But what condition would a patient have that when the CO fell by bunch that the flotrac would not decrease, or maybe even increase?
There’s enough numbers on the monitor. no need to take a simple straightforward case and make it way too complex...
 
For what? What's the evidence?

There's been 3 big anesthesia depth monitor trials. All have not shown benefit ultimately

There has been no big generally accepted periphal venous pressure trials. Central venous pressure has long since been accepted as inaccurate almost always so I can't imagine how a peripheral vein can give any form of useful info. There's just so many potential confounders

PVP is actually a much better trend monitor than CVP - but whatever. Also, have we really decided CVP trends aren't correct? We can see consistent cases where CVP numbers drop over time but actual venous pressures rise over time - or the converse? I don't care about an absolute number - I would agree that is not very helpful. If you never use it - it's fine. It's not like you can't get the info in other ways.

Regarding your comment about anesthesia depth monitor. Show me a single study that shows the BIS doesn't trend well to anesthesia depth (careful now...I'm not talking about recall...I'm talking about anesthesia depth trends).

This topic has been discussed lots of times on here so we don't need to rehash -

But I will just say this.

If I am using BIS - and I give a propofol bolus, the number seems to ALWAYS decrease. But I'd like you to prove me wrong. Show me a good example over 20 patients where you give a propofol bolus and the BIS increases. Also, it seems to ALWAYS INCREASE when I decrease my anesthetic depth. Prove me wrong though. Show me a case where in 20 patients, you significantly decrease anesthetic depth (and without doing anything else), the BIS drops. It is in no way - a random number generator. You know why? Because it's science. That number changes based on EEG - and EEG absolutely changes with anesthetic depth (so the BIS number will absolutely change).

Now before you say anything, I know you could come up with examples in your own experience where the BIS didn't work correctly and the numbers were funny. But let me ask you this...has that ever happened to your A-Line? Has your pulse ox ever given funny numbers? did you then immediately dismiss the value of A-Lines in ALL CASES or the value of the pulse-ox because in this patient the monitor was not being reliable? Not at all..and the reason is - because you are astute enough to know when your monitor was not acting like it should.

So all I ask is that you NOT be hypocritical. Fine if you don't like the BIS because this one time you found it gave funny numbers. Okay. But you then HAVE to apply that to all the monitors you use. And basically you will then hate ETCO2 monitoring, pulse ox, BP cuffs, A-lines, and Tidal Volume reports, and many other things. Good luck with that.

(oh and by the way - the study with awake patients giving each other Sux doesn't count. That doesn't change what I am saying. Do other things affect the number? Yep...but again...remember, you are astute and paying attention to stuff and the info that the monitor is giving you).
 
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Ok well, we dont need to derail the thread but...
1 - You made the semi-profound 'i like data statement' as if the rest of us are too primitive to understand, Therefore i think the burden of proof should be on you! So far you have produced anecdotes and asked me for evidence!
2 - What is BIS? Does anyone outside of the company know? How does it handle etomidate, ketamine, dexmed? The isolated forearm technqiue you dismiss is a major flaw in bis. It may or may not be fixed. We dont know what bis is so how can we know? Ketamine and etomidate would be very close at hand for this lady. Propofol bolus is basically instant death for this lady pre drainage, i know you're not suggesting giving this to her but i prefer to keep things on topic
3 - I dont think i am hypocritical. I am critical however especially of people using CVP and even more so peripheral venous pressure. This lady has a very large pericardial effusion. How do you reconcile all the variables to interpret either? Where do you place your peripheral cannula? Upper limb lower limb? What if you're in lateral position? What trend are you looking for? Number goes up therefore effusion is now becoming a tamponade?

Im trying to understand better how you use these things and how i can justify them to give a better outcome. So far i dont see anything.
Recall is the absolute least of my worries.
 
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Very late to this party, but...

No way I am touching that patient until the pericardial effusion is drained. Not only should it be drained in its own right (unknown etiology, right?), you know, anesthesia stuff. I generally find perioperative recommendations from cardiologists to be useless - all theory, usually on an outpatient-type timescale, with no clinical context especially for our work where seconds to minutes matter.

I have also been told by cardiologists that "epinephrine is not an inotrope," not to use phenylephrine in AS, and that the patient with a lactate of 8, hr 130, large pericardial effusion wasn't in tamponade because of some transmitral flow bs. Use your common sense.
 
Literally had the same patient yesterday.

A few things that stood out to me:

Tamponade is a clinical diagnosis. My pt had none of the 3 signs mentioned by vector above (even though A Fib makes mitral inflow worthless). The patient had a syncopal episode. So even without RV diastolic collapse and the IVC collapsed with sniff, the cardiologist still elected to drain the fluid. Even though no one called it tamponade.

Which again makes me wonder why this cardiologist elected recommended not to drain.... Even without good echo signs the threshold to drain was pretty low. Why not drain it with echo signs of impending collapse? Were they worried about the apixaban? was this the same guy that did neil armstrong and now he's gun shy?

Pulse pressure on non-invasive cuff can be misleading. Remember that the patient is afib and the cuff isn't measuring the same beat. so don't be mislead by a wide pulse pressure.
 
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PVP is actually a much better trend monitor than CVP - but whatever. Also, have we really decided CVP trends aren't correct? We can see consistent cases where CVP numbers drop over time but actual venous pressures rise over time - or the converse? I don't care about an absolute number - I would agree that is not very helpful. If you never use it - it's fine. It's not like you can't get the info in other ways.

Regarding your comment about anesthesia depth monitor. Show me a single study that shows the BIS doesn't trend well to anesthesia depth (careful now...I'm not talking about recall...I'm talking about anesthesia depth trends).

This topic has been discussed lots of times on here so we don't need to rehash -

But I will just say this.

If I am using BIS - and I give a propofol bolus, the number seems to ALWAYS decrease. But I'd like you to prove me wrong. Show me a good example over 20 patients where you give a propofol bolus and the BIS increases. Also, it seems to ALWAYS INCREASE when I decrease my anesthetic depth. Prove me wrong though. Show me a case where in 20 patients, you significantly decrease anesthetic depth (and without doing anything else), the BIS drops. It is in no way - a random number generator. You know why? Because it's science. That number changes based on EEG - and EEG absolutely changes with anesthetic depth (so the BIS number will absolutely change).

Now before you say anything, I know you could come up with examples in your own experience where the BIS didn't work correctly and the numbers were funny. But let me ask you this...has that ever happened to your A-Line? Has your pulse ox ever given funny numbers? did you then immediately dismiss the value of A-Lines in ALL CASES or the value of the pulse-ox because in this patient the monitor was not being reliable? Not at all..and the reason is - because you are astute enough to know when your monitor was not acting like it should.

So all I ask is that you NOT be hypocritical. Fine if you don't like the BIS because this one time you found it gave funny numbers. Okay. But you then HAVE to apply that to all the monitors you use. And basically you will then hate ETCO2 monitoring, pulse ox, BP cuffs, A-lines, and Tidal Volume reports, and many other things. Good luck with that.

(oh and by the way - the study with awake patients giving each other Sux doesn't count. That doesn't change what I am saying. Do other things affect the number? Yep...but again...remember, you are astute and paying attention to stuff and the info that the monitor is giving you).

I think we pretty much all agree with good evidence that the pericardial fluids should be drained. So I consider the main point of the thread to be over. So let's let the derailing begin.

Disclaimer: None of what i'm saying is meant to be an ad hominem attack on @epidural man . He is not the first one that's made these arguments and definitely won't be the last. So it's definitely worth while to discuss the topic. I do agree that no monitor is better than an astute clinician and the tool is only as good as the tool using it.

Claim: The monitor sucks and doesn't tell you what you need to know, but it is a better monitor as a trend.

E.g. CVP does not give you a good assessment of LV preload, but it will tell you which way the LV preload is going if you simply trend it. If the CVP went from 10 to 15, the LV preload must be higher at the CVP 15 compared to the CVP 10.

I find this idea not logically sound. If the initial data correlates poorly with the true quantity, then there should be no reason that the trend of the initial data would follow the changes in the true quantity except for random chance. Therefore, the reliability of the trend is then dependent on the % of the time that they move in the same direction.

In our example, the % of time they move in the same direction isn't overwhelming; there are 3 valves and lungs in the way between the RA and the LV. Imagine if the PVR increased and all else equal, the CVP would increase by the LV preload would actually decrease. There is a specific time in which they will trend the same direction: there are no valvular pathology and the PVR moves the same way as the CVP. How often can you claim that is the case?? How easily identifiable is that clinical situation ??? If you can't claim the case a huge % of the time and you can't clearly identify the situation which CVP and PVR decreases simultaneously, then CVP is worthless as a LV preload predictor.

The counter argument often goes. Of course you can't rely on a monitor 100% of the time, you have to use your clinical assessment along with the CVP. E.g. If CVP is high and there is decrease skin turgor then obviously the patient is dehydrated. I always wondered: If you can rely on skin turgor and the decrease of skin turgor completely invalidates CVP, why not just go pinch the skin rather than sticking an invasive line????!?!

end of rant, i'm tired and going to bed.
 
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the CV pressure alone is not nearly as useful as a study of both the pressure and the waveform morphology.

central venous pressures and waveforms are very useful but EVERYONE in our specialty forgets the information gained from analyzing the waveform.

Our systems generally have fidelity similar to those cardiologists use so there is no excuse to disregard it. And you should troubleshoot poor fidelity so you can have the information from a clear waveform.
 
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