Thoughts about this case?

[ucsfgaspain]

Here's one for you all to monday morning quarterback. Go ahead and roast me but give me your best thoughts about how you would have done this case and what actually happened.

I finished my scheduled cases and get an add on case.

64 y.o. female with mixed tissue connective disease (unclear how this manifests), s/p CVA in 04 with no residual, OSA, pulm hypertension supposedly severe i.e. PA pressure estimated on TEE as 60ish, initially admitted for SOB. TTE shows a pericardial effusion that was drained by cardiology. 600 cc's of fluild was aspirated 5 days ago. On CT was seen to have mediastinal and axillary lymphadenopathy. Scheduled today for lymph node biopsy. Surgeon like GA or a big MAC i.e. a GA but without a tube.

I preop the patient and she states that she feels a lot better after the tap 5 days ago. EKG shows no electrical alternans, I don't determine any pulsus paradoxis (?sp) on PE. Lungs sound clear, airway looks somewhat sketchy but I thought that I could get a tube in with a bougie (we don't have a video laryngoscope). She's going at 112 with a pressure of 130/70's.

I take her back. Preox her. As I preox her, I just get that bad feeling and mix some epi up in a 250 bag to 4 ug/cc. I debated whether to do an a line before she goes to sleep but thought it's only a lymph node sampling no more than 30 minutes so screw it. Set my BP to go off every minute. INduce with 12 of etomidate and test my airway and she's easily maskable. Give roc (50) and take a DL. Immediately know that it ain't a great airway can't see squat and angles are all wrong. Go with millers and can't get anything but get no view whatsover. No problem cuz she's an easy mask and call for the fiber.

This is when it got exciting. I've got a half a MAC of sevo on now and BP's are great 140 systolic and HR in the 110's just basically like when she is awake. I'm trying to hyperventilate her to keep her from going hypercarbic. The pulse ox then craps out. Uh Oh. Great CO2 and great pressures. Fiber comes along with another one of my colleagues. He takes a look at her skin color and knows that I'm in the crapper. Although the interesting thing was that she had the cyanotic look only in the upper body.

I go to town with the fiber and easily pass the fiber into the trachea. But we can't get the damn tube to not get hung up. We try f***ing everything rotation...praying..cursing.the damn tube just won't come off. I still have no f+++ing sat. I'm droping a load into m pants now but she's maintaing great ET CO2 and her pressure are rock solid in the 140's she's a little bit faster at 120 or so.

I drop a fast trach in and get a tube in. We then get an a line in and drop a TEE in. A line first sample doesn't look good. You know that not bright red color so I'm bumming. I'm waiting for the istat to get back and we do a quick TEE. RV dilated, pericardial effusion, and a hyperdynamic heart. I call in our CV anesthesiologist. He does a quick perusal and agrees though he thinks that he may see something in the PA. He calls for his 3 d echo. (they get all the cool toys) and as he puts his TEE in her. Her pressures just go to pot. I ended up pushing 4, 10, 20 ,100 and 200 ug of epi to get a decent pressure on her.

In the end TEE ends up not helping diagnosis the cause of her crump on me. I had the CV aneshtesiologist, cardiologist, and cardiac surgeon in the room as I'm titrating in an epi drip to keep this woman alive. Needless to say we cancel the case, I roll her intubated into the CV ICU.

Interestingly, the ABG come back and guess what it was...7.14/44/115/-14. This was of course on 100% O2. So my questions are, what the hell happened. Why the metabolic acidosis?

The two scenarios that I could conjecture is 1) she despite my best efforts got hypercarbic and hypoxic and crumped with her pulm hypertension 2) was the upper body rash, anaphylaxis to roc?

Good thing that came out of this...She is totally awake extubated and totally neurologicallly intact. I told her that she took 10 years off my life. Extremely nice lady and one that I hope I never see again.

Okay, have at it.

Peace.

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[jetproppilot]

WOW.

What a case!!

Thanks for sharing. And congrats on your stellar reactions.

My best guess is that despite your very appropriate dose of etomidate, even though its much less of a negative inotrope than propofol, it was enough to restrict forward flow, especially right sided, in light of the pericardial effusion, dilated RV and pulmonary hypertension.

Those three things together aint a good mix....pericardial effusion, dilated RV and pulm HTN.

A dilated RV with pulm pressures in the sixties can't tolerate any pharmacologic insult.

Oxygenation goes down the tube since the just-barely-hanging-on RV is now totally in the crapper after induction.

Sounds like your numbers were pretty good for a while which gave you a false sense of security acutely....then you said pressures went to crap... it seems perfusion had been decreased from the right heart chain of events....induction, a slight-but-catastrophic decreased inotropicity of (the already dilated) RV which has to still push against very high pulmonary artery pressures, flow to the pulmonary vascular tree diminishes which adversely affects oxygenation, flow to the LV diminishes, yeah the LV is still working but aint gettin' much flow from the right side, systemic pressure falls, acidosis ensues.....

Wouldda been interesting to see an SVR and an MVO2 during this period. And a CO.

I'm a non-invasive-alist when it comes to hemodynamic monitoring in the OR, and I hate to say this because I generally think they're pretty useless in the OR (actually anywhere), but a CCO-SWAN may have helped you identify this ladies hemodynamic picture pre-induction, and helped you in your pharmacologic intervention after the intraoperative event.

But then again, maybe not, since you wouldda pulled out the epi anyway.

You said the heart was hyperdynamic......one can see a hyperdynamic myocardium sans bloodflow (kinda like an EMD picture).

With all that said,

I probably wouldntve floated a SWAN.

I probably would've put in an A line, but your lack of one didnt affect your stellar actions.

As far as the airway and induction is concerned, I wouldda replicated it if I decided GA was needed.

Could it have been done with a cuppla milligrams of midaz? Could you have done it under a real MAC?

Face it, Dude, this lady was sick to begin with.

If you're puttin' people with dilated RV/pulm HTN/pericardial effusions to sleep, bad s hit may happen.

So often when something goes awry we point the finger.

I ain't gonna do that.

Sounds to me like you stepped up to the mike with micatin.

 

[militarymd]

Cool case.....sounds like one of the VERY FEW cases of acute myocardial failure secondary to anesthesia agents.

I 've seen the upper body cyanosis before in folks who get very hypercarbic and hypoxic

 

[Planktonmd]

Here is how I see it:
Pulm hypertension + Failing RV pre-op add to that positive pressure ventialtion and hypoxia because of multiple attempts to intubate: the result ----> Acute increase in Pulm. pressure and acute RV failure which would explain the SVC blood pooling and the upper body cyanosis that you mentioned.
I am curious, why did you think that you absolutely need to intubate this woman?
Would it have been less eventful if you just induced with Etomidate, inserted LMA and let her breath spontaneouly?

 

[ucsfgaspain]

PlanktonMD,

I agree with you that leaving an LMA in and just trying to hyperventilate by increasing respiratory rate may have been the way to go. I don';t thinlk I would have let her breathe sponatneously since her CO2 would rise and exacerbate her pulm hypertension. I htink I just kind of got got tracked in to thinking of controlling her airway definitively as things went south./ It's always good to throw cases out there so that I can get feedback. The only thing that argues against the hypoxia/ hypercarbia etilogy for her crumping is the ABG I got was done right after and I mean within 15 seconds after I got the ETT tube in through the fast trach. I don't think that I would have gotten a 7.15/44/115 that quickly i.e. she should have had a way higher CO2 and I don't think she would have rebounds in her PaO2 that quickly. This gas was done when she had the awful cyanotic look in the upper body but hemodynamically was stable. What do you think? Her gas after two amps of bicarb (I know controversial) and a bunch of epi, i.e. when she actually had the CV collapse on me. was 7.5/35/132. I'm still confused by this lady since I don't think I can make everything fit nicely. But then again...pt. don't read med school books so the rules don't always apply.

BTW I do love my practice, cuz without the help of my colleague. I know for sure that this nice lady would have had a one way ticket to the big playground in the Sky.

The best part of the case? The surgeon coming up to me and saying, "Why are you guys doing all that stuff? this case is only 30 minutes." My reply,, "Dude, your case is like zero seconds .... cuz she's trying really hard to die."

 

[Planktonmd]

PlanktonMD,

I agree with you that leaving an LMA in and just trying to hyperventilate by increasing respiratory rate may have been the way to go. I don';t thinlk I would have let her breathe sponatneously since her CO2 would rise and exacerbate her pulm hypertension. I htink I just kind of got got tracked in to thinking of controlling her airway definitively as things went south./ It's always good to throw cases out there so that I can get feedback. The only thing that argues against the hypoxia/ hypercarbia etilogy for her crumping is the ABG I got was done right after and I mean within 15 seconds after I got the ETT tube in through the fast trach. I don't think that I would have gotten a 7.15/44/115 that quickly i.e. she should have had a way higher CO2 and I don't think she would have rebounds in her PaO2 that quickly. This gas was done when she had the awful cyanotic look in the upper body but hemodynamically was stable. What do you think? Her gas after two amps of bicarb (I know controversial) and a bunch of epi, i.e. when she actually had the CV collapse on me. was 7.5/35/132. I'm still confused by this lady since I don't think I can make everything fit nicely. But then again...pt. don't read med school books so the rules don't always apply.

BTW I do love my practice, cuz without the help of my colleague. I know for sure that this nice lady would have had a one way ticket to the big playground in the Sky.

The best part of the case? The surgeon coming up to me and saying, "Why are you guys doing all that stuff? this case is only 30 minutes." My reply,, "Dude, your case is like zero seconds .... cuz she's trying really hard to die."

Spontaneous ventilation doesn't always mean hypercarbia and I bet you that mild hypercarbia is better hemodynamically for this lady than switching to controlled pos. pressure ventialtion.
Think about it like you would handle a patient with tamponade, they usually crash the moment you start Pos. pressure ventilation.
If you are really concerned about CO2 then you could use some pressure support with the LMA if your machine alows you.
What I am trying to say is that it's always better to taylor the anesthetic to the situation because everything you do that is not absolutely needed can have bad consequences.
My approach to this case would have been: Sorry, we are giving this lady some versed and you are going to do good local anesthesia and get that biopsy done.

 

[Noyac]

Why was she so acidotic? She has a huge base deficit -14 which was present pre-op. Are you saying that her pericardial effusion had not recurred?

I would have either not done the case if she looked really bad pre-op and would have asked cardiology to assure me that the effusion wasn't back. But I assume that she didn't look too bad since you did the case.

I also would have pushed the surgeon to do it under local with minimal sedation in someone like this. If I needed real sedation I would have used Ketamine most likely. With small amounts of versed of coarse.

Its so easy to Monday Morning QB.

 

[drccw]

UCSFGASPAIN: you've gotten some helluva cases it sounds... fun practice....

That surgeon dropped a really winner add-on... gotta love when they don't appreciate how sick a patient is.. sounds like this gal's Rv was at the tipping point of the Starlign curve... and a little of anything just knocked her down and off into the toilet... that's what sucks about pulmonary hypertension.. it's a mean mean beast that scares the bejebus out of me-> and when you have a failing/failed RV then that is the worse... through in a pericardial effusion and the waters are quite muddled... how do you offload the RV, how do u decrease the PVR... HA.... everyone can conjecture, gesticulate about what to do; ie avoid hypoxia hypercarbia, and whatever but the truth of the matter is that really pulm HTN kills quickly and there ain't too many option-> inhaled NO? maybe if your hospital can get it... milrinone? I'ld be hard pressed to get that started quickly without any invasive monitoring... sounds like you did the best to let this women not celestially discharge on you....

what could you have done differently? Refuse to do this case? maybe.. it's always easy to second guess yourself, especially in the aftermath... Not put her to sleep? that's a thought... I personally wouldnt put a LMA in her as my primary plan... if I would do a GA, then my instinct would be to tube her.... MAC... probably not a bad place to go... have the come to Jesus talk with her and the surgeon... show the surgeon a big honking syringe of lidocaine and have him go to town.. I assume he was going after the axillary nodes.... Would I throw dexmedotomidine in? I like it; have used it in pulmonary hypertensives... so maybe....

but in the end it sounds like you did what was right... you recognized that something was amiss, you called for help and she did of...

 

[Planktonmd]

Why was she so acidotic?

My guess she was acidotic because she had acute RV failure secondary to Positive pressure ventilation and hypoxia.
Her cardiac output was probably very low for a while until they started her on epinephrine.

 

[Jeff05]

lymph node bx can be done with 2 of midaz and plenty of local.
that would have been my recommendation to the surgeon.

if a surgeon came up to me, i would have professionally stated that without appropriate preparations this patient has a real chance of dying even with MAC (which i think is more challenging and dangerous than GA)



otherwise
1. preinduction a line - in my opinion the length of the procedure does not determine the anesthetic. you MUST be able to control BP closely.

2. a very controlled smooth induction. 12 of etomidate without narcotic and then prolonged airway manipulation - her SVR and PVR must have gone through the roof. losing the airway and making her hypoxic and hypercarbic further increased her PVR.

3. you saw a potentially difficult airway in a patient who absolutely could not be hypoventilated and chose to put her to sleep...

4. i know, i know, in private practice you do whatever and it's skillful gold and everything learned in academics is WRONG. but, this patient SHOULD have had a swan.

5. you should have avoided volitile anesthetics - her RV was preload dependent, which you decreased with venodilation. also, volitiles are myocardial depressants.


here's what happened physiologically. her RV was on the edge of failure. by inadequately blunting response to intubation and hypoventilating the patient you spiked the PVR and she went into FLORID RV failure.

that's why she was blue - there was almost no blood going into the lungs. she had a metabolic acidosis chronically 2/2 high lactate from hypoperfusion, this was likely exacerbated when her forward flow was impeded further.

 

[Planktonmd]

4. i know, i know, in private practice you do whatever and it's skillful gold and everything learned in academics is WRONG. but, this patient SHOULD have had a swan.

A Swan for a lymph node biopsy?
Are you serious?
I am assuming you are saying that a Swan is needed if we need to do GA on this patient, do you really believe that you can't give this patient safe GA without a Swan?

 

[Jeff05]

like i said, the procedure is not always the indication for the type of monitoring. in this case it's the patient.

technically, yes, if this patient has GETA she should have a swan. (can it be done without, of course.) and a preinduction a line. because what happened was not a surprise.
i would have been surprised if nothing bad happened. i really appreciate the original poster writing up the case - it makes for great learning.

jet - i disagree with you, these actions were not "stellar". this patient should have never been managed in this way. a huge part of anesthesiology is anticipating. this is a classic case - all these events were anticipated, but NOTHING was done to prepare for them. a bag of epi was mixed (anticipating something bad), but appropriate monitors or induction or airway management was NOT applied.

the most important idea is not to dwell on what we WOULD have done, it is to learn and DO the right thing in the future.
if i have a patient like this in the future - refer to a center with a good CV anesthesiologist. if not possible, preinduction a line and swan. smooth
induction. nitric oxide and milrinone ready to go.



HEMODYNAMIC MONITORING FOR PAH
Invasive hemodynamic monitoring must be applied because
of the possibility of severe circulatory instability.
Continuous knowledge of the mean and transpulmonary
pressure, PVR, preload and afterload indexes, and RV and
LV function is mandatory to better manage the sudden
changes of cardiorespiratory status.6 Radial
artery cannulation, a pulmonary artery catheter (PAC)
equipped with a fast response thermistor capable of assess-
ing RV ejection fraction (RVEF%) and ventricular filling
through RV end diastolic volume calculation (RVEDV),
PiCCO System (Pulsion Medical System, Munich, Ger-
many), and transesophageal echocardiography (TEE) are
always adopted in this institution. Pharmacologic interven-
tions, volume therapy, vasoactive drug administration, and
ventilatory adjustment are better guided on real-time data
integration derived from different monitoring methods.

A Swan for a lymph node biopsy?
Are you serious?
I am assuming you are saying that a Swan is needed if we need to do GA on this patient, do you really believe that you can't give this patient safe GA without a Swan?

 

[Planktonmd]

like i said, the procedure is not always the indication for the type of monitoring. in this case it's the patient.

technically, yes, if this patient has GETA she should have a swan. (can it be done without, of course.) and a preinduction a line. because what happened was not a surprise.
i would have been surprised if nothing bad happened. i really appreciate the original poster writing up the case - it makes for great learning.

jet - i disagree with you, these actions were not "stellar". this patient should have never been managed in this way. a huge part of anesthesiology is anticipating. this is a classic case - all these events were anticipated, but NOTHING was done to prepare for them. a bag of epi was mixed (anticipating something bad), but appropriate monitors or induction or airway management was NOT applied.

the most important idea is not to dwell on what we WOULD have done, it is to learn and DO the right thing in the future.
if i have a patient like this in the future - refer to a center with a good CV anesthesiologist. if not possible, preinduction a line and swan. smooth
induction. nitric oxide and milrinone ready to go.



HEMODYNAMIC MONITORING FOR PAH
Invasive hemodynamic monitoring must be applied because
of the possibility of severe circulatory instability.
Continuous knowledge of the mean and transpulmonary
pressure, PVR, preload and afterload indexes, and RV and
LV function is mandatory to better manage the sudden
changes of cardiorespiratory status.6 Radial
artery cannulation, a pulmonary artery catheter (PAC)
equipped with a fast response thermistor capable of assess-
ing RV ejection fraction (RVEF%) and ventricular filling
through RV end diastolic volume calculation (RVEDV),
PiCCO System (Pulsion Medical System, Munich, Ger-
many), and transesophageal echocardiography (TEE) are
always adopted in this institution. Pharmacologic interven-
tions, volume therapy, vasoactive drug administration, and
ventilatory adjustment are better guided on real-time data
integration derived from different monitoring methods.

So let me ask you this:
You want to put a PA catheter i every patient with pulmonary hypertension getting GA?
You do realize that most of your COPD patients have pulm. hypertension and many of them have severe Pulm. hypertension but no one had measured it.
What criteria are you going to use for PA insertion in these patients?
And one more point:
Who said a CV anesthesiologist in a big center is better for this kind of patient than a slick private practice warrior who knows how to give anesthesia without killing people?
You can put any one to sleep safely if you know how, trust me on this one.

 

[Jeff05]

MOST COPD patients do NOT have clinically sig PAH (1). this particular patient has SYMPTOMATIC RV failure, ie symptomatic severe PAH, that bought her a swan.

1. Pulmonary hypertension is a common complication of chronic obstructive pulmonary disease (COPD). The increase in pulmonary artery pressures is often mild to moderate. However, 5–10% of patients with advanced COPD may suffer from severe pulmonary hypertension and present with a progressively downhill clinical course because of right heart failure added to ventilatory handicap. The prevalence of clinically significant severe pulmonary hypertension in COPD is roughly estimated to be of 1–2/1,000.
Pulmonary Hypertension and Right Heart Failure in Chronic Obstructive Pulmonary Disease. The Proceedings of the American Thoracic Society 2:20-22 (2005)

 

[Brian Fantana]

Here's one for you all to monday morning quarterback. Go ahead and roast me but give me your best thoughts about how you would have done this case and what actually happened.

I finished my scheduled cases and get an add on case.

64 y.o. female with mixed tissue connective disease (unclear how this manifests), s/p CVA in 04 with no residual, OSA, pulm hypertension supposedly severe i.e. PA pressure estimated on TEE as 60ish, initially admitted for SOB. TTE shows a pericardial effusion that was drained by cardiology. 600 cc's of fluild was aspirated 5 days ago. On CT was seen to have mediastinal and axillary lymphadenopathy. Scheduled today for lymph node biopsy. Surgeon like GA or a big MAC i.e. a GA but without a tube.

I preop the patient and she states that she feels a lot better after the tap 5 days ago. EKG shows no electrical alternans, I don't determine any pulsus paradoxis (?sp) on PE. Lungs sound clear, airway looks somewhat sketchy but I thought that I could get a tube in with a bougie (we don't have a video laryngoscope). She's going at 112 with a pressure of 130/70's.

I take her back. Preox her. As I preox her, I just get that bad feeling and mix some epi up in a 250 bag to 4 ug/cc. I debated whether to do an a line before she goes to sleep but thought it's only a lymph node sampling no more than 30 minutes so screw it. Set my BP to go off every minute. INduce with 12 of etomidate and test my airway and she's easily maskable. Give roc (50) and take a DL. Immediately know that it ain't a great airway can't see squat and angles are all wrong. Go with millers and can't get anything but get no view whatsover. No problem cuz she's an easy mask and call for the fiber.

This is when it got exciting. I've got a half a MAC of sevo on now and BP's are great 140 systolic and HR in the 110's just basically like when she is awake. I'm trying to hyperventilate her to keep her from going hypercarbic. The pulse ox then craps out. Uh Oh. Great CO2 and great pressures. Fiber comes along with another one of my colleagues. He takes a look at her skin color and knows that I'm in the crapper. Although the interesting thing was that she had the cyanotic look only in the upper body.

I go to town with the fiber and easily pass the fiber into the trachea. But we can't get the damn tube to not get hung up. We try f***ing everything rotation...praying..cursing.the damn tube just won't come off. I still have no f+++ing sat. I'm droping a load into m pants now but she's maintaing great ET CO2 and her pressure are rock solid in the 140's she's a little bit faster at 120 or so.

I drop a fast trach in and get a tube in. We then get an a line in and drop a TEE in. A line first sample doesn't look good. You know that not bright red color so I'm bumming. I'm waiting for the istat to get back and we do a quick TEE. RV dilated, pericardial effusion, and a hyperdynamic heart. I call in our CV anesthesiologist. He does a quick perusal and agrees though he thinks that he may see something in the PA. He calls for his 3 d echo. (they get all the cool toys) and as he puts his TEE in her. Her pressures just go to pot. I ended up pushing 4, 10, 20 ,100 and 200 ug of epi to get a decent pressure on her.

In the end TEE ends up not helping diagnosis the cause of her crump on me. I had the CV aneshtesiologist, cardiologist, and cardiac surgeon in the room as I'm titrating in an epi drip to keep this woman alive. Needless to say we cancel the case, I roll her intubated into the CV ICU.

Interestingly, the ABG come back and guess what it was...7.14/44/115/-14. This was of course on 100% O2. So my questions are, what the hell happened. Why the metabolic acidosis?

The two scenarios that I could conjecture is 1) she despite my best efforts got hypercarbic and hypoxic and crumped with her pulm hypertension 2) was the upper body rash, anaphylaxis to roc?

Good thing that came out of this...She is totally awake extubated and totally neurologicallly intact. I told her that she took 10 years off my life. Extremely nice lady and one that I hope I never see again.

Okay, have at it.

Peace.

You mentioned Mediastinal LAD, was there significant anterior LAD on CT? How fast do these airways take a turn down **** highway when NMBs are given which describes your situation (not being able to pass tube where the tracheobronchial tree may be collapsed). Combine this with the comorbidities of Severe PHTN, possible continued pericardial effusion s/p drainage, and you got yourself a great case! You see this mainly with pediatric anterior med masses, but adults as well Hodgkins LAD etc.

The Anesthetic Management of the Patient with an Anterior Mediastinal Mass.
Anesthesiology. 60(2):144-146, February 1984.
Neuman, George G. M.D. *; Weingarten, Alexander E. M.D. +; Abramowitz, Roy M. M.D. ++; Kushins, Lawrence G. M.D. ++; Abramson, Alan L. M.D. ; Ladner, William M.D. ++

 

[Planktonmd]

MOST COPD patients do NOT have clinically sig PAH (1). this particular patient has SYMPTOMATIC RV failure, ie symptomatic severe PAH, that bought her a swan.

1. Pulmonary hypertension is a common complication of chronic obstructive pulmonary disease (COPD). The increase in pulmonary artery pressures is often mild to moderate. However, 5–10% of patients with advanced COPD may suffer from severe pulmonary hypertension and present with a progressively downhill clinical course because of right heart failure added to ventilatory handicap. The prevalence of clinically significant severe pulmonary hypertension in COPD is roughly estimated to be of 1–2/1,000.
Pulmonary Hypertension and Right Heart Failure in Chronic Obstructive Pulmonary Disease. The Proceedings of the American Thoracic Society 2:20-22 (2005)

So what is "clinically significant" Pulm htn in your view?
and how do you know that a COPD patient has clinically significant pulm htn?
The main symptom of pulm htn is hypoxia and a COPD patient who is hypoxic is not very unusual as you know
So, who gets a PA catheter?
Only the ones with an Echo showing "clinically" significant pulm hypertension?
What if there is no echo? (the usual situation)
The point I am trying to make is: PA catheters don't transform a bad anesthetic into a good one, and that applies to all the other invasive monitors that you might think of.
Instead of wasting time on unnecessary monitors it's better to plan an anesthetic that suits the patient and the procedure.

 

[ucsfgaspain]

I love the discourse that everyone is having on this. So I went and visited her again today amazed at how she survived my anesthetic. I'm not sure what is going on with this lady. Now she's been in the unit day 3 since the incident. She is not intubated. She doesn't look as good as yesterday. Now someone explain to me what these gasses could possibly mean. On CPAP with an FIO2 of .4. 7.36/23/78/-11. When they took her off CPAP and ran her on FM I believe although they labeled the FIO2 as 1.0 so maybe a non rebreather the ABG showed 7.29/33/177/-10. Why is this woman still acidotic. I talked to the ICU team and they have no idea.

I just looked up her labs from home and I do see a couple things that may be helpful. Remembering from my internal medicine days I calculated her gap and she's got a NON-Gap Acidosis. Her creatinine has bumped up a lot int he last two days. She went from 0.86 prior to her "come to jesus moment" in the OR. To her last creatinine this a.m. of 1.68. That I know is not good. So is the acidosis due to RTA? She is going into renal failure right. That can't be good since her mortality risk has just increased dramatically right?

Her troponins bumped a little. Her troponin before my meeting her was 0.17. The one after my meeting her was 0.23 it peaked 5 hours later at 0.51 and then went back down to 0.23 within 12 hours. Not sure what this means.

She frankly doesn't look as good as I left the hospital. I gave my colleague a heads up tonite cuz I've got a bad feeling that she is going to crump tonite. I also told the ICU team to call us early rather than later since she is a tough tube.

So you Critical care gurus. Help a dumb pain guy out and try to explain to me what all of this means? How would you approach this woman if you were called to the unit tonite and had to stick a tube in her. Give me your approach...what vent settings...what sedation...etc. And no I don't think that you can go the direct DL route. You may be able to intubate a pregnant fireant but this woman ain;t going to let it happen.

 

[urge]

So, who gets a PA catheter?
Only the ones with an Echo showing "clinically" significant pulm hypertension?

I wouldn't do that, bru. Pulm HTN increases your risk of PA rupture. I would rather stay away. Plus, what info is it going to tell you? High PA pressure? You already know that. CO sucks? You already know that. Mixed venous low? You already know that. I would consider a PA if I was confused as to what is wrong with the pt. It's pretty clear in this scenario.

I would have placed an awake a-line and be more generous on induction. I think the OP got all worked up with the pulm htn and came up with some weird anesthetic plan, ie crap induction with no a-line.

My pt could have crashed too. There is so much you can do.

 

[ucsfgaspain]

So try to answer a multitude of questions in other posters responses. Noyac, I had no frickin idea that she was that acidotic prior to the case. She was out of the unit and all her other gasses in the unit looked Okay. They had pulled all her invasive monitoring the day before and she was transferred to the floor.

She eyeballed sick but not SICK. I'm sure you guys that have been out in the real world know what I mean. I honestly don't know why I had that apprehensive feeling before I induced her. It was just one of those feelings.

You guys are totally right about doing the case as a MAC would have been a wise choice in view of what happened. But I am somewhat of a realist here and I know myself pretty well. My MAC's are like my college drinking. I always tell myself that I'll only drink a little. You know half a shot no more. But inevitably, I end up praying to the porcelain God after downing about 20 shots of JD I've found that I am just tempted by propfol and Ketamine when the patient is squirming that I end up doiing a GA without a tube. It's not right...it's a character weakness but that's how I am.

Peace.

Keep the banter going cuz I love this discussion.

 

[ucsfgaspain]

Damn I did forget to add one detail that urge reminded me of with his comments/criticism. I did have remi going on intubation. But when **** started hitting the fan, I turned it off. I had started it at I believe 0.3 ug/k/m. You know it's hard to remember to post everything when things are going nuts.

 

[urge]

So you Critical care gurus. Help a dumb pain guy out and try to explain to me what all of this means? How would you approach this woman if you were called to the unit tonite and had to stick a tube in her. Give me your approach...what vent settings...what sedation...etc. And no I don't think that you can go the direct DL route. You may be able to intubate a pregnant fireant but this woman ain;t going to let it happen.

A couple of versed, sux, lido. Use the intubating LMA you used before. Be prepared to start an epi drip and to do cpr.

 

[Noyac]

My guess she was acidotic because she had acute RV failure secondary to Positive pressure ventilation and hypoxia.
Her cardiac output was probably very low for a while until they started her on epinephrine.

Exactly!

She was under perfused with a base deficit of -14.

 

[urge]

remi going on intubation. at I believe 0.3 ug/k/m.

People get really hypotensive from that. I always have a neo drip ready.


I had a little scare happen to me not too long ago. Got called to the room at the end of a case. CRNA is bagging like crazy. Sat is reading 85%, bp cuff 50/20, ekg bunch of pvc's but not horrible, ETCo2 20's. Take a listen- distant BS on left, not much on right. I pull ett back just in case...doesn't make much sense....but just in case.... BS still the same. I'm not sure if the pt has a tension pneumo causing all this and I'm not feeling adventurous to stick a needle. So I call for an xray while I'm pushing 320 mcgs of neo. Wait a little bit but the neo doen not seem to anything. Bp is now 40/15. Crack open the epi and give ~50mcgs, then another 50. Sat comes up to 90's Bp to 70/40 and HR 120's. Bring up the BP some more with some vasopressin. Get an A-line, ABG(resp acidosis only)and cxr done (normal btw). Pt is waking up by now since I had stopped everything. Anesthetist wants to put him back down. Me: "Are you ****ting me?" Pt is looking good by now. I ask him if he feels ok and if he would like the tube out. Extubate the pt. Does well. gets discharged the next day.

What the hell happened there? I don't know. Why did the bp go so low? Why was the sat low too? I know that fixing the bp fixed everything.

 

[Noyac]

I wouldn't do that, bru. Pulm HTN increases your risk of PA rupture. I would rather stay away.

So don't wedge it. Once you get the PA just advance 2 cm's and stop.

I really can't believe we are talking about swaning a lymph node bx case.

 

[Noyac]

Noyac, I had no frickin idea that she was that acidotic prior to the case.

I wasn't saying that you did. I'm sure you would have sent her back to where she came from had you known.

 

[Arch Guillotti]

A couple of thoughts:

I would not put an LMA in this lady.

We induce, paralyze and provide positive pressure ventilation to folks in the heart rooms at times w/PA HTN. They don't have CV collapse that I have ever seen. They do have a preinduction aline and a CT anesthesiologist though.

I know of a case where the pt. also had pulmonary hypertension and was scheduled for a larger procedure that would require GETA. Was a young guy but pretty sick overall w/ESRD and ischemic cardiomyopathy (EF in 40% range or so). PASP around 50 or so. General anesthesia was induced and unfortunately the NURSES (CRNA/SRNA) mucked around with the airway a bit, couldn't intubate and not great ventilation. So some hypercarbia and acidosis probably ensued. Probably not too much unless you have one foot in the grave and the other on a banana peel like this poor sap. In this case there was no pre-induction art line (in hindsight obviously a poor decision). He spiralled downward, the other foot slipped off the banana peel and he arrested. CPR and multiple boluses of epinephrine were required to resusciate him. Fortunately he made it out of the OR and lived to be neurologically intact though he did have some residual CV problems (heart block I think).

Anyways we all know pulm htn is nothing to fool around with. Does it mean a preinduction CCO SWAN, heck no. It does mean TIGHT control of all the variables we can control and maybe even an art line even for a simple lil ol case like a bx.

 

[Noyac]

I love the discourse that everyone is having on this. So I went and visited her again today amazed at how she survived my anesthetic. I'm not sure what is going on with this lady. Now she's been in the unit day 3 since the incident. She is not intubated. She doesn't look as good as yesterday. Now someone explain to me what these gasses could possibly mean. On CPAP with an FIO2 of .4. 7.36/23/78/-11. When they took her off CPAP and ran her on FM I believe although they labeled the FIO2 as 1.0 so maybe a non rebreather the ABG showed 7.29/33/177/-10. Why is this woman still acidotic. I talked to the ICU team and they have no idea.

I just looked up her labs from home and I do see a couple things that may be helpful. Remembering from my internal medicine days I calculated her gap and she's got a NON-Gap Acidosis. Her creatinine has bumped up a lot int he last two days. She went from 0.86 prior to her "come to jesus moment" in the OR. To her last creatinine this a.m. of 1.68. That I know is not good. So is the acidosis due to RTA? She is going into renal failure right. That can't be good since her mortality risk has just increased dramatically right?

Her troponins bumped a little. Her troponin before my meeting her was 0.17. The one after my meeting her was 0.23 it peaked 5 hours later at 0.51 and then went back down to 0.23 within 12 hours. Not sure what this means.

She frankly doesn't look as good as I left the hospital. I gave my colleague a heads up tonite cuz I've got a bad feeling that she is going to crump tonite. I also told the ICU team to call us early rather than later since she is a tough tube.

So you Critical care gurus. Help a dumb pain guy out and try to explain to me what all of this means? How would you approach this woman if you were called to the unit tonite and had to stick a tube in her. Give me your approach...what vent settings...what sedation...etc. And no I don't think that you can go the direct DL route. You may be able to intubate a pregnant fireant but this woman ain;t going to let it happen.

I believe her cardiac issue is still unresolved. She is still not perfusing. How are the CCU guys treating her? With O2? Any cardiac help for her? Milrinone sounds great to me and whatever other med you like.

As far as crumping tonight. Either tube her awake now b/4 it happens or bring a glidescope and a LMA (you already know the LMA works) when they call.

 

[ucsfgaspain]

Hye Noyac,

When I wrote my response to you...I did not at all take offense to your comments. I realized after I reread my response that it could be read as snipey. That's totally not how it was meant to be. I'm a laid back norcal guy. Hope that no offense was taken b/c none was meant.

BTW how could I be mad at fellow backcountry boarder?

P.S. what's your set up? I wished I lived in Colorado (right?) I'm stuck schlepping to Lake Tahoe or doing the yearly Vail thing.

 

[militarymd]

This thread is worse than Internal Medicine rounds.

 

[ucsfgaspain]

In terms of ICU and what they are doing. They are seriously just letting her just hang out in the unit. She's got no central access ...let alone a PA line. She's only got my aline in her and my foot IV. Hemodynamically she is currently in the 110's and BP are 130/80's.

The lady is a really sweet lady which means that she's got nothing but badness headed for her. God just did not mean for nice people to live long. I think that there should be a new ASA class. ASA 6 for nice people, cuz if you are nice you are f*cked.

 

[jetproppilot]

I really can't believe we are talking about swaning a lymph node bx case.

HAHAHAHAHAHAHAHAHAHAHAHA

Thats a good point.

But she probably shouldda hadda swan a while ago, especially if the medicine guys are still scatching their heads.

 

[jwk]

Where's zip when you need him?

Versed, O2, local, cut, end of story.

Regards, JWK (doing his feeble zippy impersonation)

OH - and PS to Jeff05 - these cases, whether GA or MAC, are done every day in non-academic non-cardiac surgery hospitals without a cardiovascular anesthesiologist or swan in sight.

 

[Noyac]

Where's zip when you need him?

Versed, O2, local, cut, end of story.

Regards, JWK (doing his feeble zippy impersonation)

He's probably mowing lawns with the long days and the grass growing like weeds down in Florida.





Did I imagine it or did he say he had a side job?

 

[huktonfonix]

People get really hypotensive from that. I always have a neo drip ready.


I had a little scare happen to me not too long ago. Got called to the room at the end of a case. CRNA is bagging like crazy. Sat is reading 85%, bp cuff 50/20, ekg bunch of pvc's but not horrible, ETCo2 20's. Take a listen- distant BS on left, not much on right. I pull ett back just in case...doesn't make much sense....but just in case.... BS still the same. I'm not sure if the pt has a tension pneumo causing all this and I'm not feeling adventurous to stick a needle. So I call for an xray while I'm pushing 320 mcgs of neo. Wait a little bit but the neo doen not seem to anything. Bp is now 40/15. Crack open the epi and give ~50mcgs, then another 50. Sat comes up to 90's Bp to 70/40 and HR 120's. Bring up the BP some more with some vasopressin. Get an A-line, ABG(resp acidosis only)and cxr done (normal btw). Pt is waking up by now since I had stopped everything. Anesthetist wants to put him back down. Me: "Are you ****ting me?" Pt is looking good by now. I ask him if he feels ok and if he would like the tube out. Extubate the pt. Does well. gets discharged the next day.

What the hell happened there? I don't know. Why did the bp go so low? Why was the sat low too? I know that fixing the bp fixed everything.

? anaphylaxis. Doesnt seem to fit the absolute clinical picture, but always a possibility.

 

[Planktonmd]

A couple of thoughts:

I would not put an LMA in this lady.

Why not???

 

[ecCA1]

I assume that whoever wrote that they'd use "nitrous" mean "nitric oxide." While the sympathetic discharge would help someone with pericardial effusion filling limitations, the increase in PVR wouldn't be a good idea for this person.

 

[Bertelman]

I assume that whoever wrote that they'd use "nitrous" mean "nitric oxide." While the sympathetic discharge would help someone with pericardial effusion filling limitations, the increase in PVR wouldn't be a good idea for this person.

I didnt' see anyone else mention nitrous.

Jeff05 mentioned nitric.

 

[amyl]

about the LMA: LOL with OSA, etc. (suggesting she is overweight, suggesting GERD even if undiagnosed) is exactly the kind of patient that wouldn't tolerate aspiration. an LMA is not the worst idea in the world but i would much rather use regional or local and be skimpy on the versed as well.

 

[Planktonmd]

about the LMA: LOL with OSA, etc. (suggesting she is overweight, suggesting GERD even if undiagnosed) is exactly the kind of patient that wouldn't tolerate aspiration. an LMA is not the worst idea in the world but i would much rather use regional or local and be skimpy on the versed as well.

Yes,
It's probably better to avoid any airway instrumentation in this patient (actually in every patient).
But, if you are going to put her to sleep anyway, then an LMA is a superior option to an ETT because it causes less hemodynamic changes and you will need less anesthesia which means you are less likely to kill the patient.
Those assumptions about over weight people having more aspiration risk with an LMA are not supported by any evidence, and even if they are true that remote risk of aspiration is probably better than the inevitable hemodynamic compromise an ETT would cause to this patient.

 

[militarymd]

Exactly!

She was under perfused with a base deficit of -14.

Although you're right in this particular case....a base deficit does not necessarily equate hypoperfusion.

Hyperchloremic acidosis (non anion gap acidosis) can give you LARGE base deficits.

In ARF..(with anion gap acidosis) you can have LARGE base deficits without hypoperfusion.

 

[Noyac]

Although you're right in this particular case....a base deficit does not necessarily equate hypoperfusion.

Hyperchloremic acidosis (non anion gap acidosis) can give you LARGE base deficits.

In ARF..(with anion gap acidosis) you can have LARGE base deficits without hypoperfusion.

Absolutely!

But this case is hypoperfusion until proved otherwise in my book.

And now that her perfusion deficit has been going on for so long the kidneys are failing and the picture gets even worse.