fentanyl

[taxidriver]

hey y'all. Brand new basic here. Reason i'm posting is because of an experience i had on an ALS rig during clinicals. We responded to the home of an elderly female with abdominal pain, nothing really exciting. Once we started rolling the medic i was in the back with gave the lady fentanyl. After a couple minutes she just crashed. 02 sat was sitting at right around 35% We put her on a NRB and it shot back up to the high 90's in seconds. My question is, if she overdosed on fentanyl and was not breathing how would the non rebreather have been effective in bringing her 02 sat back up? This has been on my mind for a few weeks now.

 

[E tank]

This brings up an issue that gets missed quite a bit. That is the relationship between high-flow O2 administration, SpO2 and hypoventilation. Even for an elderly patient with healthy lungs, it isn't all that difficult to make the sats in the mid to high 90's with a NRM with a RR of 6 or less and an open airway. Ventilation and oxygenation are two different entities. That her sat was in the 90's is great, but I'm guessing her CO2 was heading that way too. On balance, respiratory acidosis is pretty well tolerated in healthy patients, but once comorbidities come into play, it may not be as benign. The bottom line is that 02 sat is a lousy surrogate for hypoventilation and you're better off getting the patient to breath (or actively ventilate them) than flushing their lungs with pure oxygen.

 

[VFlutter]

A good example of this difference in oxygenation vs ventilation is Apnea testing in brain death exams. Patients whom have no respiratory drive are disconnected from the ventilator and placed on a 100% Fio2 T-Piece for extended periods of time and maintain sats completely apneic.

 

[E tank]

A good example of this difference in oxygenation vs ventilation is Apnea testing in brain death exams. Patients whom have no respiratory drive are disconnected from the ventilator and placed on a 100% Fio2 T-Piece for extended periods of time and maintain sats completely apneic.

Right...it's why we spend so much time pre-oxygenating our patients before we intubate them. Leaving O2 cannulae on a patient after paralysis can significantly prolong the safe apneic time during difficult DL, depending on the age and comorbidities of the patient. Its a handy trick.

 

[taxidriver]

Thanks guys, makes sense. Now being a brand new basic I really don't like the idea of putting myself in a position where I'm questioning the actions of someone that's been doing this for years. But overall would you say the call wasn't handled as well as it should have been? It was an obvious overdose yet there was no action to actively ventilate the patient or administer narcan. I know later at the hospital they put her on a narcan drip.

 

[Flying]

Thanks guys, makes sense. Now being a brand new basic I really don't like the idea of putting myself in a position where I'm questioning the actions of someone that's been doing this for years. But overall would you say the call wasn't handled as well as it should have been? It was an obvious overdose yet there was no action to actively ventilate the patient or administer narcan. I know later at the hospital they put her on a narcan drip.

If the person was apneic or hypoventilating, then yes, the BVM should have came out.

 

[CWATT]

@taxidriver - I've been on a real EmCrit binge lately and I'm pretty sure this is where I heard some stats re: pre-oxygenation for intubation. So far as I can remember - the claim was that passive oxygenation in the apanic patient can produce a flow rate of 250ml/min of O2, though only 30ml/min of CO2. This is why they advised a N/C during the intubation procedure and also part of the reason why we're seeing airway management protocols during a cardiac arrest as an OPA and N/C, no BVM, no King, no ET. They also mentioned that a N/C during intubation ca

I'd be willing to bet that the NRB @ 15lpm played a significant role in bringing up that patient's SP02, but as others have mentioned already, that's not to say her CO2 wasn't skyrocketing as well. I

 

[Carlos Danger]

hey y'all. Brand new basic here. Reason i'm posting is because of an experience i had on an ALS rig during clinicals. We responded to the home of an elderly female with abdominal pain, nothing really exciting. Once we started rolling the medic i was in the back with gave the lady fentanyl. After a couple minutes she just crashed. 02 sat was sitting at right around 35% We put her on a NRB and it shot back up to the high 90's in seconds. My question is, if she overdosed on fentanyl and was not breathing how would the non rebreather have been effective in bringing her 02 sat back up? This has been on my mind for a few weeks now.

If her Sp02 really did go up to the high 90's within "seconds" of placing a NRB, then I'm going to go out on a limb here and suggest that her Sp02 was never that low to begin with (pulse oximetry is notoriously inaccurate below about 80%), and/or her hypoxemia was related more to passive airway obstruction than to hypoventilation, and that airway obstruction was relieved after the NRB was placed. My point is, she probably was breathing, which would explain why the medic did not ventilate her, and which makes a NRB perfectly appropriate.

Passive oxygenation when a patient is apneic works, but I don't see it converting profound hypoxemia to normoxemia in a matter of seconds in an elderly (reduced diffusing capacity), apneic (and therefore presumably somewhat atelectatic) patient who also presumably has some impaired cardiac output as a result of a fentanyl overdose.

 

[taxidriver]

@taxidriver - I've been on a real EmCrit binge lately and I'm pretty sure this is where I heard some stats re: pre-oxygenation for intubation. So far as I can remember - the claim was that passive oxygenation in the apanic patient can produce a flow rate of 250ml/min of O2, though only 30ml/min of CO2. This is why they advised a N/C during the intubation procedure and also part of the reason why we're seeing airway management protocols during a cardiac arrest as an OPA and N/C, no BVM, no King, no ET. They also mentioned that a N/C during intubation ca

I'd be willing to bet that the NRB @ 15lpm played a significant role in bringing up that patient's SP02, but as others have mentioned already, that's not to say her CO2 wasn't skyrocketing as well. I

I'm kind of struggling to understand how a N/C could be enough to guarantee the patient is getting enough oxygen. Obviously there would be a big C02 build up and I can't imagine that being good for the patient even thought I haven't gone through capnography. One of the things drilled into me is that if the patient isn't able to produce adequate respitations by themselves then you ventilate for them.

 

[taxidriver]

If her Sp02 really did go up to the high 90's within "seconds" of placing a NRB, then I'm going to go out on a limb here and suggest that her Sp02 was never that low to begin with (pulse oximetry is notoriously inaccurate below about 80%), and/or her hypoxemia was related more to passive airway obstruction than to hypoventilation, and that airway obstruction was relieved after the NRB was placed. My point is, she probably was breathing, which would explain why the medic did not ventilate her, and which makes a NRB perfectly appropriate.

Passive oxygenation when a patient is apneic works, but I don't see it converting profound hypoxemia to normoxemia in a matter of seconds in an elderly (reduced diffusing capacity), apneic (and therefore presumably somewhat atelectatic) patient who also presumably has some impaired cardiac output as a result of a fentanyl overdose.

Could be that her o2 wasn't really that low but I was resting her arm on my leg trying to get a blood pressure and her arm just flopped and she was out like a light. No amount of painful stimuli could get her to respond, I'm guessing it was significantly lower than normal.

 

[Carlos Danger]

I'm kind of struggling to understand how a N/C could be enough to guarantee the patient is getting enough oxygen. Obviously there would be a big C02 build up and I can't imagine that being good for the patient even thought I haven't gone through capnography. One of the things drilled into me is that if the patient isn't able to produce adequate respitations by themselves then you ventilate for them.

As long as no airway obstruction exits, oxygen will passively flow from the pharynx, though the glottis, down the trachea and into the lungs, where it diffuses across the alveocapillary membrane into the blood. The big problem with relying on this technique is that passive airway obstruction is very common when patients are supine. Also, atelectasis and other pulmonary pathology can keep this technique from working well.

You are right, it isn't that good for the patient to be apneic for a long time, even if the Sp02 does remain normal. C02 builds up in the blood and pH falls and causes all sort of bad things to happen.

However, for a short period of time, it is fine. It's much better to be hypercarbic with a good Sp02 than it is to be hypercarbic with a low Sp02. Low levels of oxygen kills much quicker than high levels of C02.

 

[taxidriver]

As long as no airway obstruction exits, oxygen will passively flow from the pharynx, though the glottis, down the trachea and into the lungs, where it diffuses across the alveocapillary membrane into the blood. The big problem with relying on this technique is that passive airway obstruction is very common when patients are supine. Also, atelectasis and other pulmonary pathology can keep this technique from working well.

You are right, it isn't that good for the patient to be apneic for a long time, even if the Sp02 does remain normal. C02 builds up in the blood and pH falls and causes all sort of bad things to happen.

However, for a short period of time, it is fine. It's much better to be hypercarbic with a good Sp02 than it is to be hypercarbic with a low Sp02. Low levels of oxygen kills much quicker than high levels of C02.

Makes perfect sense, thanks!

 

[CWATT]

@taxidriver - I did some digging. It was EmCrit episode #70 called Airway Management. I understand you're a Basic, but there is some GREAT info and visuals here that will help you understand effective airway positioning.

I also need to correct my numbers. Passive O2 flow rate is 250ml/min and CO2 is 10ml/min (not 30ml/min as I stated earlier). These numbers at at 52:56mins into the video.

(Also, sorry about the fragmented post earlier. No more using my phone to post on EMTLife for me. Lol)

 

[E tank]

Makes perfect sense, thanks!

Could be that her o2 wasn't really that low but I was resting her arm on my leg trying to get a blood pressure and her arm just flopped and she was out like a light. No amount of painful stimuli could get her to respond, I'm guessing it was significantly lower than normal.

People turn pretty blue with a sat like you describe. If she had normal skin color, it might not have been as low as you thought.

 

[RocketMedic]

Distal perfusion, the fitting of the sensor, and the temperature of the skin all matter as well. Were you taking a B/P?

Fentanyl is a very safe drug I've given a lot of. Do you know how much the patient weighed and how much was given? Also, what sort of vitals are we looking at? There's a world of difference between a normotensive, GCS 15 patient getting an initial-and-appropriate dose of 1mcg/kg and scaling up from there and a hypotensive, obtunded patient getting 2-3mcg/kg right off the bat.

 

[E tank]

@taxidriver - I did some digging. It was EmCrit episode #70 called Airway Management. I understand you're a Basic, but there is some GREAT info and visuals here that will help you understand effective airway positioning.

I also need to correct my numbers. Passive O2 flow rate is 250ml/min and CO2 is 10ml/min (not 30ml/min as I stated earlier). These numbers at at 52:56mins into the video.

There is a nuanced note there that I think needs clarification. When he talks about the atmospheric pressure gradient that is produced through passive alveolar diffusion of O2 and CO2 causing 250 mls O2/min to be drawn into the airway, he's not saying that if you just gave 250 mls a minute, the patient would remain oxygenated for an extended period of apnea. They would not. When NC are used in the way he describes, at least 4-6 lpm should be used and the O2 gets to the alveoli through the mass effect of the flowing oxygen and open airway. From there its just a matter of the oxygen moving down its concentration gradient into the blood.

 

[Carlos Danger]

Distal perfusion, the fitting of the sensor, and the temperature of the skin all matter as well. Were you taking a B/P?

Fentanyl is a very safe drug I've given a lot of. Do you know how much the patient weighed and how much was given? Also, what sort of vitals are we looking at? There's a world of difference between a normotensive, GCS 15 patient getting an initial-and-appropriate dose of 1mcg/kg and scaling up from there and a hypotensive, obtunded patient getting 2-3mcg/kg right off the bat.

You do have to keep in mind that elderly patients often don't tolerate opioids well. Old folks have a smaller plasma volume and often reduced plasma protein levels, which together can result in a much higher serum concentration for the same weight-based dose of any highly protein-bound drug, such as fentanyl. They also tend to have reduced hepatic blood flow and reduced enzyme activity (unless they are taking enzyme-inducing medications or alcohol), which can prolong the action of the drug.

 

[rescue1]

Given that the patient apparently lost consciousness for a few seconds, could this have just been a brief syncopal episode? It's not a side effect of fent that I've ever heard of, but a LOC with a brief period of apnea followed by full recovery sounds like syncope to me.

Assuming I understand what happened correctly, of course.

 

[taxidriver]

To add some context. The women had her ovaries removed the day prior and when we showed up she did not look good. Very pale and lethargic. I was there to pretty much watch and observe. There was not a whole lot of effort to get a good history including what medication she was on. This leads me to believe that she might've already been on some sort of opioid for pain medication and when the medic pushed more it caused her to overdose but that's just a theory. We were both unable to ascultate a blood pressure and didn't bother using the lifepak to get one since by the time we both failed to ascultate one we were in front of the hospital. What I believe happened is she OD'd on the pain meds and passed out from hypoxia but was brought back from the NRB through passive oxygenation. When I say "brought back" I mean it loosely. She only made any sort of effort to open her eyes when when spoken to and she could not speak in complete sentences. Overall a pretty weird experience and I wish I had gotten to follow up with the hospital to see what they had to say about it.

 

[VFlutter]

Really? Or she had a massive intraabdominal hemorrhage, tanked her pressure even further after the Fentanyl and lost her pleth wave on the pulse ox. Sounds like she wasn't perfusing her brain.

Recent surgery with high risk of bleeding, pale, lethargic, unable to obtain a blood pressure...doesn't raise any red flags?