High respiratory rate at the end of neuro case

[Foodie]

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50-something, relatively thin lady, breathing at 29-32 RR with TV in 250-350 ml at the end of a 6-hr craniotomy for aneurysm despite having 200 mcg of sufentanil on board. Yes, you read that right. Total of 200 mcg SUfent was given, with 100 mcg given at the end in small doses in an attempt to titrate down her RR. No matter how much sufent I gave her, the RR wouldn't budge. Well, it did go from 32 to 29. Pupils were normal, in fact they were 3mm in diameter, equal. As she breathed out the gas, TV climbed up to 400's while RR remained the same. Her EtCO2 was in range of 28-32 while she was breathing on her own. Not tachycardic, SBP in 110's without pressors or vasodilators. Because she was not responsive to even a rather stimulating jaw thrust (she was extubated deep - no airway issues, minimal aspiration risk) , we gave her 40 mcg of naloxone. She did wake up about 5 min after, very slowly. Transported to neuro ICU on non rebreather and monitors. Started moving spontaneously when we arrived there, following commands, just drowsy.Checked on her an hour later, and she was talking and moving all extremities, and completely comfortable. No neuro deficits. Of note, the only symptoms she had from her aneurysm was a mild headache.

SSEP, EEG, and motors were monitored throughout the case without any issues. We were running sevo (MAC < 0.6), propofol at 50 mcg/kg/min, and sufentanil @ 0.05 mcg/kg/hr. Sufent gtt was turned off about 30 min before skin closure. EtCO2 was maintained around 27 on vent during the case, and as I menioned above, she maintained her EtCO2 between 28 and 32 near the end of case on her own.

I know I gave her a lot of narc, and really, after I gave her 50 mcg of sufent at the end of the case, I was curious to see what she would do if I gave her more (hence the high total amount). Even started a new IV thinking that maybe her IV had infiltrated (though it was running in the arm I could see, and confirmed that it was drawing blood well). Yet even before naloxone her MV remained high and her pupils were far from constriction. How is it possible that she did not develop respiratory depression despite the high narc dose?? My attending attributed it to her pre-op high anxiety level and high concentration of catecholamines in her system.

But she was barely tachcardic with her HR in 70's to 90's. She does have a medical history of hypertension but was only on diltiazem and Accupril. Told me that she tried a betablocker in the past but it was discontinued because of adverse side effects.

Wondering what other thoughts are out there. My first thought was that I had a bad batch of sufent, since the access was working just fine. Or whatever the surgeons did in her brain.

 

[jetproppilot]

50-something, relatively thin lady, breathing at 29-32 RR with TV in 250-350 ml at the end of a 6-hr craniotomy for aneurysm despite having 200 mcg of sufentanil on board. Yes, you read that right. Total of 200 mcg SUfent was given, with 100 mcg given at the end in small doses in an attempt to titrate down her RR. No matter how much sufent I gave her, the RR wouldn't budge. Well, it did go from 32 to 29. Pupils were normal, in fact they were 3mm in diameter, equal. As she breathed out the gas, TV climbed up to 400's while RR remained the same. Her EtCO2 was in range of 28-32 while she was breathing on her own. Not tachycardic, SBP in 110's without pressors or vasodilators. Because she was not responsive to even a rather stimulating jaw thrust (she was extubated deep - no airway issues, minimal aspiration risk) , we gave her 40 mcg of naloxone. She did wake up about 5 min after, very slowly. Transported to neuro ICU on non rebreather and monitors. Started moving spontaneously when we arrived there, following commands, just drowsy.Checked on her an hour later, and she was talking and moving all extremities, and completely comfortable. No neuro deficits. Of note, the only symptoms she had from her aneurysm was a mild headache.

SSEP, EEG, and motors were monitored throughout the case without any issues. We were running sevo (MAC < 0.6), propofol at 50 mcg/kg/min, and sufentanil @ 0.05 mcg/kg/hr. Sufent gtt was turned off about 30 min before skin closure. EtCO2 was maintained around 27 on vent during the case, and as I menioned above, she maintained her EtCO2 between 28 and 32 near the end of case on her own.

I know I gave her a lot of narc, and really, after I gave her 50 mcg of sufent at the end of the case, I was curious to see what she would do if I gave her more (hence the high total amount). Even started a new IV thinking that maybe her IV had infiltrated (though it was running in the arm I could see, and confirmed that it was drawing blood well). Yet even before naloxone her MV remained high and her pupils were far from constriction. How is it possible that she did not develop respiratory depression despite the high narc dose?? My attending attributed it to her pre-op high anxiety level and high concentration of catecholamines in her system.

But she was barely tachcardic with her HR in 70's to 90's. She does have a medical history of hypertension but was only on diltiazem and Accupril. Told me that she tried a betablocker in the past but it was discontinued because of adverse side effects.

Wondering what other thoughts are out there. My first thought was that I had a bad batch of sufent, since the access was working just fine. Or whatever the surgeons did in her brain.

200 mikes of sufent is not a lot for a 6 hour case.

 

[Foodie]

So it is not uncommon to wake up drowsy, comfortable with high MV (secondary to high RR) after getting 100 mcg of sufent in the last 30 min of a neuro case, on top of 100 mcg on board? Most often once sufent gtt (0.05 mcg/kg/hr) is turned off about 45 min prior to skin closure, patients begin breathing at rates between 8-12.

 

[Dhanwanthari]

WAG'ing (wild ***** guessing) here... but getting off the reservation.

How about chest wall rigidity from the massive amt of sufenta.... causing dec. Tv and a compensatory inc in RR?

Probably not... but throwing it in the circle....

 

[btbam]

200 mikes of sufent is not a lot for a 6 hour case.

200 mcgs of sufent = 2 mg of fent, you wouldn't consider that a lot for a non-cardiac case?

 

[scotchnwater]

Had the anuerysm already ruptured and you were doing damage control, or was this a clipping? I've seen a lot of people with primary respiratory alkalosis simply with the best-guess for the etiology being "brain badness".

Although I agree that it is puzzling regarding the minimal response to significant amount of opiates bolused towards the end of the case (and I share your skepticism that it could be solely attributable to 'pre-op anxiety').

 

[Idiopathic]

i do remi for cranis, they tend not to hurt as bad as you think they will afterwards and you dont have to guess when they are going to be able to finish closing.

my differential would be:

1) pharmacy error
2) IV error
3) patient tolerance, maybe unknown to you

if she had tight head then you could have been dealing with something else, but it sounds like she was fine there.

on an unrelated note, we would not have left the operating room until she was following commands or had established her expected baseline, whatever that was going to be. its easier to go to scanner from the OR than from the unit.

 

[epidural man]

50-something, relatively thin lady, breathing at 29-32 RR with TV in 250-350 ml at the end of a 6-hr craniotomy for aneurysm despite having 200 mcg of sufentanil on board. Yes, you read that right. Total of 200 mcg SUfent was given, with 100 mcg given at the end in small doses in an attempt to titrate down her RR. No matter how much sufent I gave her, the RR wouldn't budge. Well, it did go from 32 to 29. Pupils were normal, in fact they were 3mm in diameter, equal. As she breathed out the gas, TV climbed up to 400's while RR remained the same. Her EtCO2 was in range of 28-32 while she was breathing on her own. Not tachycardic, SBP in 110's without pressors or vasodilators. Because she was not responsive to even a rather stimulating jaw thrust (she was extubated deep - no airway issues, minimal aspiration risk) , we gave her 40 mcg of naloxone. She did wake up about 5 min after, very slowly. Transported to neuro ICU on non rebreather and monitors. Started moving spontaneously when we arrived there, following commands, just drowsy.Checked on her an hour later, and she was talking and moving all extremities, and completely comfortable. No neuro deficits. Of note, the only symptoms she had from her aneurysm was a mild headache.

SSEP, EEG, and motors were monitored throughout the case without any issues. We were running sevo (MAC < 0.6), propofol at 50 mcg/kg/min, and sufentanil @ 0.05 mcg/kg/hr. Sufent gtt was turned off about 30 min before skin closure. EtCO2 was maintained around 27 on vent during the case, and as I menioned above, she maintained her EtCO2 between 28 and 32 near the end of case on her own.

I know I gave her a lot of narc, and really, after I gave her 50 mcg of sufent at the end of the case, I was curious to see what she would do if I gave her more (hence the high total amount). Even started a new IV thinking that maybe her IV had infiltrated (though it was running in the arm I could see, and confirmed that it was drawing blood well). Yet even before naloxone her MV remained high and her pupils were far from constriction. How is it possible that she did not develop respiratory depression despite the high narc dose?? My attending attributed it to her pre-op high anxiety level and high concentration of catecholamines in her system.

But she was barely tachcardic with her HR in 70's to 90's. She does have a medical history of hypertension but was only on diltiazem and Accupril. Told me that she tried a betablocker in the past but it was discontinued because of adverse side effects.

Wondering what other thoughts are out there. My first thought was that I had a bad batch of sufent, since the access was working just fine. Or whatever the surgeons did in her brain.

Funny your attending tried to give an explaination. Sometimes weird stuff happens with no explanation.

I have seen this a couple of times. One time I was doing a case under LMA in a young healthy guy, he had a respiratory rate of +35, despite opioids making absolutely no difference. Once the anesthetic gas came off, his rate returned to normal.

Remember, anesthetic gas increases respiratory rate and decreases tidal volume - and it isn't so hard to imagine that everyone's receptor physiology is different, and in some, the anesthetic gas effects those brain centers different - and it overides the CO2 centers that opioids act on.

By the way, chest wall rigidity is a myth - a farse, at least based on the best evidence in the literature today. That has been shown pretty clearly in novel and cleverly done studies.

Ask around your house of greatness to see if any of your attendings know what I am talking about. Hint - difficulty breathing isn't from a stiff chest - what else could it be?

 

[dhb]

By the way, chest wall rigidity is a myth - a farse, at least based on the best evidence in the literature today. That has been shown pretty clearly in novel and cleverly done studies.

I found a study from 1983 that already showed this quite well.

 

[sevoflurane]

i do remi for cranis....

I'm with you. Turn it off towards the end of the case and work in some fent or narcotic du jour titrated to resp. rate keeping in mind that high Co2 is going to increase ICP in a tight vault.

A neuro exam is something the neurosurgeons are going to want pretty quickly, if not immediately. Having them follow commands before leaving the OR = good anesthetic care, IMHO.

Of course... some crani's are just not going to be able to do this post-op.

 

[Dhanwanthari]

By the way, chest wall rigidity is a myth - a farse, at least based on the best evidence in the literature today. That has been shown pretty clearly in novel and cleverly done studies.

Hint - difficulty breathing isn't from a stiff chest - what else could it be?

really? thanks for dispelling the myth... it is still taught by some of our attendings...

To the point that I've had attendings state they don't push as much opioid on induction when working with CA-1's if they think the patient wont be an easy mask to begin with due to "chest wall rigidity." Amazing how this stuff perpetuates... and even changes practice.

as for other causes, highly multifactorial... inc. airway resistance/compliance issues from atelectasis, alveolar collapse, breathing through a tube/straw (smaller diameter airway).

then there is splinting, and the respiratory depressing effects of opioids, and always must consider residual NMB.... the era in which the chest wall rigidity myth evolved was during the long-acting NMB days... right?

 

[dhb]

the era in which the chest wall rigidity myth evolved was during the long-acting NMB days... right?

right, but not for the rest of your hypothesis

 

[Mman]

I'm with you. Turn it off towards the end of the case and work in some fent or narcotic du jour titrated to resp. rate keeping in mind that high Co2 is going to increase ICP in a tight vault.

A neuro exam is something the neurosurgeons are going to want pretty quickly, if not immediately. Having them follow commands before leaving the OR = good anesthetic care, IMHO.

Of course... some crani's are just not going to be able to do this post-op.

Forget turning it off towards the end of the case. I keep it running until the case is done (or at least dressing going on). Keep the remi running while you get the volatile or propofol out of their system (that takes a lot longer) and they will wake up pronto when you cut off the remi. You can usually time it out so they are opening their eyes and following commands as the dressing is finishing.

I don't like to give any longer acting narcotics until after extubating because it just slows down the wake up, and like you said crani's don't hurt.

Neurosurgeons love the quickly wide awake patients in the OR that they can establish a baseline exam with.

 

[Idiopathic]

i wake my carotids/thyroids up on remi and its nice, i would do the same with cranis

 

[Arch Guillotti]

To the point that I've had attendings state they don't push as much opioid on induction when working with CA-1's if they think the patient wont be an easy mask to begin with due to "chest wall rigidity." Amazing how this stuff perpetuates... and even changes practice.

This is silly and I am glad you recognize it as such. If chest wall rigidity existed, pushing relaxant right after the narcotic and induction agent would fix it anyway.

 

[fakin' the funk]

I like Scotch's "brain badness," and Epidural's rapid/shallow volatile explanations the best.

As far as dispelling the myth of chestwall rigidity, before we go patting each other on the back can we have some actual references instead of just Epidural's passing comment about some studies?

FWIW, my attending say something to the effect of, "if you're going to give a lot of narcotic, give relaxant too so that they won't get rigid"

 

[epidural man]

I like Scotch's "brain badness," and Epidural's rapid/shallow volatile explanations the best.

As far as dispelling the myth of chestwall rigidity, before we go patting each other on the back can we have some actual references instead of just Epidural's passing comment about some studies?

FWIW, my attending say something to the effect of, "if you're going to give a lot of narcotic, give relaxant too so that they won't get rigid"

Sure

Scamman FL: Fentanyl-0 sub 2-N sub 2 O rigidity and pulmonary compliance. Anesth Analg 1983; 62:332-34 (I couldn't get this article, but i think it shows that people with a trach, and LARGE doses of fentanyl had no decrease in pulmonary compliance, compared to people with no trach - suggesting an upper airway issue rather than a muslce rigitidy problem)

Arandia HY, Patil VU: Glottic closure following large doses of fentanyl [Letter]. Anesthesiology 1987; 66:574-5 (some case reports of fiber optically seen upper airway obstruction after large dosses of fentanyl)

Abrams JT, Horrow JC, Bennett JA, Van Riper DF, Storella RJ: Upper airway closure: a primary source of difficult ventilation with sufentanil induction of Anesthesia. Anesth Analg 1996; 83:629-32 (Masked ventilated verses tubed patients after large sufenta dose. Tubed patients much easier to ventilate suggesting upper airway as the cause of decrease in compliance)

The same investigators repeated a similar study (and actually it might be the same patients and they were just fishing for more papers) in Anesthesiology the following year - and they measured pulmonary compliance.
Anesthesiology:
November 1997 - Volume 87 - Issue 5 - p 1070–1074

Anyway, after reading these, it would seem that there might be some muscle rigitidy, but by far the most problematic source is the glottis.

 

[sevoflurane]

Forget turning it off towards the end of the case. I keep it running until the case is done (or at least dressing going on). Keep the remi running while you get the volatile or propofol out of their system (that takes a lot longer) and they will wake up pronto when you cut off the remi. You can usually time it out so they are opening their eyes and following commands as the dressing is finishing.

I don't like to give any longer acting narcotics until after extubating because it just slows down the wake up, and like you said crani's don't hurt.

Neurosurgeons love the quickly wide awake patients in the OR that they can establish a baseline exam with.

I think we are saying the same thing. Propofol gets turned off first. Depending on how long the case has been going and how invasive it is, I may turn it off 15-30 minutes or more in advance (syringe of milk of amnesia on standy).

I use DES for my cranis, at low flows and about .3-.5 Mac.... so it comes off supa fast. Remi comes off last... but I don't keep it unning through extubation. Because of it's metabolism, it is extremely predictable. 25mcgs of fentanyl here and there depending on my respers, heart rate, spontaneous movements, spider sense, etc.

You can get them to open their eyes before the tube comes out as you say. It's all about how you use your brush.

I does not delay my wake ups as everything is pretty much gone by the time I pull the tube. Although it is not the most painful surgery in the world I do like to have some longer acting analgesia on board. These people often come in with nausea, vomiting, head aches, dural irritation, etc.

(I'm sure once the neuro exam is done you titrate in some longer acting analgesics).

Just my style. 😉

 

[Foodie]

Had the anuerysm already ruptured and you were doing damage control, or was this a clipping? I've seen a lot of people with primary respiratory alkalosis simply with the best-guess for the etiology being "brain badness".

Although I agree that it is puzzling regarding the minimal response to significant amount of opiates bolused towards the end of the case (and I share your skepticism that it could be solely attributable to 'pre-op anxiety').

It was a clipping for aneurysm, no rupture.

 

[Planktonmd]

It was a clipping for aneurysm, no rupture.

Any chance you might have lost too much blood and the patient has a metabolic acidosis she is trying to correct with tachypnea?

 

[Foodie]

i do remi for cranis, they tend not to hurt as bad as you think they will afterwards and you dont have to guess when they are going to be able to finish closing.

my differential would be:

1) pharmacy error
2) IV error
3) patient tolerance, maybe unknown to you

if she had tight head then you could have been dealing roth something else, but it sounds like she was fine there.

on an unrelated note, we would not have left the operating room until she was following commands or had established her expected baseline, whatever that was going to be. its easier to go to scanner from the OR than from the unit.

I agree with you. When I'm an attending, my neuro patients are getting remi gtt's intr-op analgesia and a full neuro exam before leaving the OR.

At our institution, we have a neuroanesthesia protocol for us residents to follow that involves sufent, propofol, nicardipine, phenylephrine drips intra-op. The explanation for sufent instead of remi was that most crani patients will wake up comfortably without much hemodynamic instability, although it is obvious to any anesthesiologist that titrating a little longer-acting narc at the end of a procedure will also accomplish the same goal. The patients who were maintained of sufent, too, are able to pass a basic neuro exam in the OR before leaving for the neuro ICU ("raise up 2 fingers in both hands, wiggle your toes"). Of course, they wake up hypercapneic, which is detrimental to their ICP.

 

[Foodie]

Any chance you might have lost too much blood and the patient has a metabolic acidosis she is trying to correct with tachypnea?

That is possible and should have been on my differential in the beginng. It is unlikely in this case, as blood loss was < 200 ml and her preop Hb was >14. Can't remember the exact number.

 

[Foodie]

Lo

Sure

Scamman FL: Fentanyl-0 sub 2-N sub 2 O rigidity and pulmonary compliance. Anesth Analg 1983; 62:332-34 (I couldn't get this article, but i think it shows that people with a trach, and LARGE doses of fentanyl had no decrease in pulmonary compliance, compared to people with no trach - suggesting an upper airway issue rather than a muslce rigitidy problem)

Arandia HY, Patil VU: Glottic closure following large doses of fentanyl [Letter]. Anesthesiology 1987; 66:574-5 (some case reports of fiber optically seen upper airway obstruction after large dosses of fentanyl)

Abrams JT, Horrow JC, Bennett JA, Van Riper DF, Storella RJ: Upper airway closure: a primary source of difficult ventilation with sufentanil induction of Anesthesia. Anesth Analg 1996; 83:629-32 (Masked ventilated verses tubed patients after large sufenta dose. Tubed patients much easier to ventilate suggesting upper airway as the cause of decrease in compliance)

The same investigators repeated a similar study (and actually it might be the same patients and they were just fishing for more papers) in Anesthesiology the following year - and they measured pulmonary compliance.
Anesthesiology:
November 1997 - Volume 87 - Issue 5 - p 1070–1074

Anyway, after reading these, it would seem that there might be some muscle rigitidy, but by far the most problematic source is the glottis.

Awesome. Thank you for taking the time to post these references!

 

[Planktonmd]

That is possible and should have been on my differential in the beginng. It is unlikely in this case, as blood loss was < 200 ml and her preop Hb was >14. Can't remember the exact number.

Yes, with only 200cc of blood loss I wouldn't either consider metabolic acidosis caused by hypovolemia as a differential, but if you had to artificially induce hypotension for a long time for the clipping and as a result created hypo-perfusion and metabolic acidosis that could be a cause of tachypnea while the acidosis is being corrected.
The lack of response to Sufenta is most likely due to opiate use that she did not want to tell you about.

 

[dhb]

Scamman FL: Fentanyl-0 sub 2-N sub 2 O rigidity and pulmonary compliance. Anesth Analg 1983; 62:332-34

that's the one
amazing that people will repeat as nauseum (even on this forum) a myth that was dispelled in a good article from 1983 published in a good journal.
there's also a case report or two on lifting a fentanyl induced laryngospasm with narcan

 

[urge]

that's the one
amazing that people will repeat as nauseum (even on this forum) a myth that was dispelled in a good article from 1983 published in a good journal.
there's also a case report or two on lifting a fentanyl induced laryngospasm with narcan

This is why I love this forum.

Articles like this settle the issue. It's so simple it's ..... irrefutable. 5 patients in each group. That's all you need in life.

 

[Planktonmd]

This is why I love this forum.

Articles like this settle the issue. It's so simple it's ..... irrefutable. 5 patients in each group. That's all you need in life.

How many patients do you need Urge?

 

[urge]

Any chance you might have lost too much blood and the patient has a metabolic acidosis she is trying to correct with tachypnea?

Maybe....

Any chance your attending (or anyone giving you breaks) pocketed 190mcg while you were not looking?

 

[Foodie]

Maybe....

Any chance your attending (or anyone giving you breaks) pocketed 190mcg while you were not looking?

And now I'm left wondering if my attending suspects that I pocketed the said drug since no one gave me a break during the case... (I didn't.)

 

[dhb]

This is why I love this forum.

Articles like this settle the issue. It's so simple it's ..... irrefutable. 5 patients in each group. That's all you need in life.

can tell if you're being serious or ironic? 😕

 

[jetproppilot]

can tell if you're being serious or ironic? 😕

OK I'm THOROUGHLY ENTERTAINED

at this point.

Which is kinda sad.

Could've been a Seinfeld episode