better wakeups for obese copd?

This forum made possible through the generous support of SDN members, donors, and sponsors. Thank you.

stephenpatrickd

Full Member
10+ Year Member
Joined
May 5, 2010
Messages
17
Reaction score
4
Hi all,

I've had this experience several times and I'm looking for thoughts on how to improve.

BMI 55, copd, geta, ventilate for low etco2 (30) during the case since I know pco2 is much higher (upsloping capnogram), time to wake up, spontaneous breathing and etco2 is 70 and it takes 15 mins to get co2 off for patient to wakeup.

I would be happy to hear how others handle this.

Thanks!
 
I just go down on the ventilation as I get the gas off and pull tube when they're spontaneously breathing with decent tidal volumes
 
Hi all,

I've had this experience several times and I'm looking for thoughts on how to improve.

BMI 55, copd, geta, ventilate for low etco2 (30) during the case since I know pco2 is much higher (upsloping capnogram), time to wake up, spontaneous breathing and etco2 is 70 and it takes 15 mins to get co2 off for patient to wakeup.

I would be happy to hear how others handle this.

Thanks!
Etc02 in the 70s is pretty high. Are these true hypercapnic severe COPD patients? Not common to see that unless you have a very sick population

Otherwise, keep fully paralyzed which will allow you to use less volatile. No need to go above 0.7-0.8mac, maybe less of you have versed and patient is older.

Use less narcotics maybe

If these patients are baseline hypercapnia, then it's not likely contributing to their sedation of only 60s-70s.

Sometimes folks use less rocuronium, and instead use more narcs and volatile. But with sugammadex, you have instant reversal, so roc is a better alternative instead of additional sedatives
 
What’s the respiratory rate when they’re spontaneous ?
Try head of the bed up or a little reverse trendelenberg…. Just a small angle difference can help the morbidly obese.
maybe try getting the sugamadex in earlier-
 
Etc02 in the 70s is pretty high. Are these true hypercapnic severe COPD patients? Not common to see that unless you have a very sick population

Otherwise, keep fully paralyzed which will allow you to use less volatile. No need to go above 0.7-0.8mac, maybe less of you have versed and patient is older.

Use less narcotics maybe

If these patients are baseline hypercapnia, then it's not likely contributing to their sedation of only 60s-70s.

Sometimes folks use less rocuronium, and instead use more narcs and volatile. But with sugammadex, you have instant reversal, so roc is a better alternative instead of additional sedatives


Agree. Less opioid. More roc, ketamine, precedex.
 
How awake are the patients when you extubate?

Really depends on the patient, case, length of case, amount of narcotics, etc.

But a lot of these patients who are sorta awake and pulling decent volumes or on PSVPro with not too much support and you’re just “waiting” for that ETCO2 to come down, which can take forever…it’s a nice tool for that specific scenario.

Obviously the initial airway degree of difficulty plays a role in this, as well.
 
Unless it was a difficult airway just put in a nasal and/or oral airway and pull the tube if they’re breathing spontaneously.

I’ve never understood why some people like to have their patient’s doing party tricks and flopping all over before pulling the dang tube out.
 
There’s two separate questions you’re asking: 1) getting CO2 off and 2) waking up quickly. An end tidal of 70 is high and may narcotize in the elderly but it’s one number, the question is to think about the clinical course: are they going to be awake and going to ventilate the c02 off or are they going to be narcotized, slumped over in pacu so it gets worse until you get called and have to give narcan, I’ve had this with new crnas.

1) positioning during wake up in the obese helps a lot, in COPDers peep at a minimum of 10, they’re breathing through a tube (hopefully one of your attending has attached an ett to the vent and had you seal your mouth around it and try to breath with no peep and then increasing levels). You’re trying to ventilate, I do pressure support 10/10 right up to the end before going spontaneous with peep, opa to prevent them obstructing if they’re still obstructing

2) faster wake ups: less opioid, low flow anesthesia, +/- propofol infusion for the marathons
 
extubate to bipap routinely
Are you serious??

Extubating to bipap usually means you shouldn't have extubated. Bipap is what the ICU guys use to buy time until they are done with clinic and ready to intubate
 
Are you serious??

Extubating to bipap usually means you shouldn't have extubated. Bipap is what the ICU guys use to buy time until they are done with clinic and ready to intubate
More like when the OR gave a bit too many narcs in an obese, COPD patient and you don't want to reintubate them...

Keep in mind that COPD/OSA patients might "require" a bit higher CO2 to breathe but there's a fine line between that and being narcotized from hypercapnia. Getting them breathing spontaneously early is the way I like to do it. That way they regulate on their own.
 
More like when the OR gave a bit too many narcs in an obese, COPD patient and you don't want to reintubate them...

Keep in mind that COPD/OSA patients might "require" a bit higher CO2 to breathe but there's a fine line between that and being narcotized from hypercapnia. Getting them breathing spontaneously early is the way I like to do it. That way they regulate on their own.
Yea, I was surprised by the "routinely" part

If their respiratory pattern, tidal volume, effort looks appropriate then I am less concerned about a ETCO2 number.

Usually it's the poor respiratory situation first that leads to CO2 elevate and eventually crump
 
“Routinely” in this specific scenario, in this specific population, which I unfortunately encounter relatively often. I mean do we try to avoid this situation? Sure.

But I supervise CRNAs. I often am handed some s*** and these situations are unfortunately not terribly uncommon.

Wasn’t saying that’s my anesthetic plan, but in the scenario the OP described, that’s an option.

Everyone else gave ways to avoid this scenario, I guess I was more speaking on an option to handle that scenario when your encounter it.
 
“Routinely” in this specific scenario, in this specific population, which I unfortunately encounter relatively often. I mean do we try to avoid this situation? Sure.

But I supervise CRNAs. I often am handed some s*** and these situations are unfortunately not terribly uncommon.

Wasn’t saying that’s my anesthetic plan, but in the scenario the OP described, that’s an option.

Everyone else gave ways to avoid this scenario, I guess I was more speaking on an option to handle that scenario when your encounter it.
Ahh gotcha

Makes sense
 
Less narcotics, high peep till the end, reverse trendelenburg for wake up.
Also look at old gases to get an idea of what baseline is.
 
Hi all,

I've had this experience several times and I'm looking for thoughts on how to improve.

BMI 55, copd, geta, ventilate for low etco2 (30) during the case since I know pco2 is much higher (upsloping capnogram), time to wake up, spontaneous breathing and etco2 is 70 and it takes 15 mins to get co2 off for patient to wakeup.

I would be happy to hear how others handle this.

Thanks!
I think my first tip would be not letting the CO2 get to 70 in the first place. I dont let the ETCO2 get that high even if the patient's not breathing.

If their ETCO2 is 50, and their ET anesthetic is 0.0 and they're still not breathing, then they've had too much narcotic or other sedative. That, or you forgot to give sugammadex... or they've had a stroke.
 
Most like some form of spontaneous ventilation early leading up to extubation. I prefer using mechanical ventilation to clear sevoflurane, especially in these patients. Also, I agree with the limited opioid tip from above here. You can always give more quickly if you decide you need to.
 
I use max relaxant, low (.6 to .8) mac with judicious narcotic use. Depends on case. Give last narcs about 20 min before close, turn down or off agent. If they will breathe PSV pro, if not mechanical ventilate until they blow off the agent. (Et around .1 to.3) breathing with adequate tidal volumes and extraterrestrial.
Of course the kind of case matters, open belly vs lap cholesterol etc etc. But this is a general plan.
Hope it helps.
 
Why is everyone focused on the breathing/etco2? Unless the case type caused you to worry about a change in their respiratory mechanics/ability to exchange air, just get the gas off. Unless you over narcotized them, they will breathe.

Agree that narcs can be easily given after the tube is out if necessary. Remember that these patients have an exponentially inversive respiratory response to narcs. Good paper in anesthesiology highlighting this fact a few years ago back.
 
  • Like
Reactions: pgg
Why is everyone focused on the breathing/etco2? Unless the case type caused you to worry about a change in their respiratory mechanics/ability to exchange air, just get the gas off. Unless you over narcotized them, they will breathe.

Agree that narcs can be easily given after the tube is out if necessary. Remember that these patients have an exponentially inversive respiratory response to narcs. Good paper in anesthesiology highlighting this fact a few years ago back.
You are correct. People are only focused on the ETCO2 in order to say that we shouldn't be focused on it. It's a symptom of the issue, not a cause.

Usually it's residual paralysis/too much narcs that leads to elevated CO2.

Also you don't necessarily need the patient to wake up immediately. You can extubated them while they are still sedated if they are breathing comfortably, pain controlled, no upper airway issues, good spontaneous tidal volumes without accessory muscle use and appropriately npo.

Then head to pacu, watch them for a bit while you chart and then hand off to pacu nurses
 
“Routinely” in this specific scenario, in this specific population, which I unfortunately encounter relatively often. I mean do we try to avoid this situation? Sure.

But I supervise CRNAs. I often am handed some s*** and these situations are unfortunately not terribly uncommon.

Wasn’t saying that’s my anesthetic plan, but in the scenario the OP described, that’s an option.

Everyone else gave ways to avoid this scenario, I guess I was more speaking on an option to handle that scenario when your encounter it.

Well that's your problem kind sir. When your CNRA gives 2mg of Dilaudid during closing to these patients "so they don't wake up in pain", well they aren't going to wake up. Lesson learned: do your own cases. I'm so happy I practice solo in California, this "team model" crap doesn't work.
 
I like to instill a little bit lidocaine down the ETT so they aren't bucking and coughing and taking terrible ineffective breaths
I do this lots… some people will just gag and gag and not breathe well enough. Once I get them spontaneous - drop the cuff, 100 lido down the tube - wait a minute- put the cuff slowly back up. If you’ve gotten the mucosa well they won’t cough when the cuff goes back up.
 
I do this lots… some people will just gag and gag and not breathe well enough. Once I get them spontaneous - drop the cuff, 100 lido down the tube - wait a minute- put the cuff slowly back up. If you’ve gotten the mucosa well they won’t cough when the cuff goes back up.

If u instill down the ETT then u also don't anesthetize mucosa above the vocal cords. Just RLN. So I think it is less likely to cause aspiration issues postop for thr patient compared to spraying RLN, SLN and CNIX
 
Well that's your problem kind sir. When your CNRA gives 2mg of Dilaudid during closing to these patients "so they don't wake up in pain", well they aren't going to wake up. Lesson learned: do your own cases. I'm so happy I practice solo in California, this "team model" crap doesn't work.
Don't forget the 17 "micro" doses of Precedex given throughout the case to "smooth the wakeup" which they aren't going to do because it's easier to replace the LMA with an oral airway and take them obtunded-as-**** to the PACU where a different RN can be present for emergence 35 minutes later.

Its a "balanced" anesthetic!
 
Less narcotics, high peep till the end, reverse trendelenburg for wake up.
Also look at old gases to get an idea of what baseline is.
What's your definition of high PEEP? One of the most common iatrogenic causes of hypoxia I see on a daily basis is high PEEP for obese patients.
 
Don't forget the 17 "micro" doses of Precedex given throughout the case to "smooth the wakeup" which they aren't going to do because it's easier to replace the LMA with an oral airway and take them obtunded-as-**** to the PACU where a different RN can be present for emergence 35 minutes later.

Its a "balanced" anesthetic!
This is the crap that annoys me. I see new residents doing it because there are 5cc sticks in our med cart. I always call them out in it. Is 85yo meemaw really going to wake up like a raging bull??
 
Depends on how obese. I titrate to best compliance. Usually ends up between 8-12. But I’m interested to hear further your rationale

@Ronin786
 
Last edited:
Some COPD patients will not breathe well after being exposed to general anesthesia , period. Even with almost no, or zero, opioid . It’s a pattern you see if you do enough advanced COPD.

My approach to these is very little gas and dense paralysis. At the end mostly apneic oxygenation with a high PEEP to prevent desaturation until they have an acceptable respiratory rate. Still have to extubate to bipap even with these measures sometimes.
 
What's your definition of high PEEP? One of the most common iatrogenic causes of hypoxia I see on a daily basis is high PEEP for obese patients.
Interesting can you explain this a little more in terms of physiology and how the peep is causing hypoxia
 
Seriously?
Get off your high horse...it's not peep, its 'too high' peep which is a relative category and it's only in particular contexts. If you can't nuance the question, just say so or nothing.
 
Interesting can you explain this a little more in terms of physiology and how the peep is causing hypoxia
Alveolar filling diseases, such as pneumonia and acute respiratory distress syndrome (ARDS), cause significant gas exchange abnormalities and, in particular, right-to-left intrapulmonary shunt. When a significant fraction of the cardiac output passes through unventilated alveoli (the shunt fraction), the PaO<sub>2</sub> does not improve significantly with application of increased FiO<sub>2</sub> and other strategies are necessary to correct arterial hypoxemia. The most commonly used initial tactic in such situations is to increase PEEP. When used in diffuse alveolar filling processes such as ARDS, PEEP reduces the shunt fraction and improves PaO<sub>2</sub> by increasing lung volume and opening or “recruiting” atelectatic alveoli. When used in focal processes, such as lobar pneumonia, however, PEEP can paradoxically worsen oxygenation by two mechanisms. First, increased PEEP causes overdistention of normal alveoli in regions not affected by the focal process. This causes an increase in capillary resistance in those regions, which redistributes blood flow to other regions, thereby worsening ventilation–perfusion ratios and arterial hypoxemia. Second, PEEP increases intrathoracic pressure, particularly when used in focal processes. This decreases venous return and cardiac output with subsequent adverse effects on systemic blood pressure and tissue oxygen delivery. When oxygen delivery decreases, tissue oxygen extraction increases, leading to a fall in central and mixed venous oxygen content and saturation, which, in the presence of significant shunt, further worsens arterial oxygenation.
 
Depends on how obese. I titrate to best compliance. Usually ends up between 8-12. But I’m interested to hear further your rationale

@Ronin786

Interesting can you explain this a little more in terms of physiology and how the peep is causing hypoxia
Ultimately, obese lungs are still overall normally compliant and the obstructive/restrictive component of their obesity is only limited to a certain portion of the lung (mainly the base and posterior portions when supine). Similarly with aggressive insufflation. It takes an immense amount of PEEP to actually inflate these collapsed alveoli and so the PEEP you add with the vent ultimately only gets reflected on the non-affected, normal compliance alveoli that are already carrying the bulk of the oxygenation.

High PEEP in obese patients = alveoli collapsed by weight that remain collapsed and normal alveoli that are now overdistended = pulse ox go boop.

I've seen patients die due to this misunderstanding. It's also the ultimate boss move to find the BMI 55 patient on 100% FiO2 and high PEEP (sometimes as "low" as ~14) and fix their hypoxia by dropping the PEEP down to more normal ranges. Also head up helps.
 
Ultimately, obese lungs are still overall normally compliant and the obstructive/restrictive component of their obesity is only limited to a certain portion of the lung (mainly the base and posterior portions when supine). Similarly with aggressive insufflation. It takes an immense amount of PEEP to actually inflate these collapsed alveoli and so the PEEP you add with the vent ultimately only gets reflected on the non-affected, normal compliance alveoli that are already carrying the bulk of the oxygenation.

High PEEP in obese patients = alveoli collapsed by weight that remain collapsed and normal alveoli that are now overdistended = pulse ox go boop.

I've seen patients die due to this misunderstanding. It's also the ultimate boss move to find the BMI 55 patient on 100% FiO2 and high PEEP (sometimes as "low" as ~14) and fix their hypoxia by dropping the PEEP down to more normal ranges. Also head up helps.
yes I agree mostly. But I find titrating to compliance (when it’s the chest wall that’s the problem) stops you from overdoing it
 
Top