fentanyl

@taxidriver - what interventions were performed other than pain management?
 
Plus SpO2 doesn't react that fast; sometimes it will show good #'s up to 30-45 seconds even though the patient isn't breathing. Poor numbers just as long after they start breathing again.
Put a sensor on yourself and hold your breath as long as you can.

Not the waveform but the actual %
 
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.

A good rule of thumb to follow is that pain is a secondary problem to perfusion. Avoid opiates in lethargic, hypotensive patients.
 
Plus SpO2 doesn't react that fast; sometimes it will show good #'s up to 30-45 seconds even though the patient isn't breathing. Poor numbers just as long after they start breathing again.
Put a sensor on yourself and hold your breath as long as you can.

Not the waveform but the actual %

But understand that it is your functional residual capacity that evens out your oxygenation between breath and periods of apnea. It is why pre-oxygenation is a "thing". When you hold your breath, the oxygen in that big breath diffuses into the blood, followed by the oxygen in the functional residual capacity of the lung.

There may be a couple of beat delay in a sat reading change, but that's all it is. You see the real saturation in real time for all practical purposes when you have a good pleth/perfusion.
 
The theory about the hemorrhage is a very real possibility. She looked textbook shocky. Due to the extremely short transport time I believe the medics sort of had the make them comfortable and transport them mentality so the only real intervention was the NRB when she tanked.
 
A good rule of thumb is to withhold pain medication or other non-vital treatments with the potential to harm until you have a solid picture of what is going on and how you'll affect that patient. Pain isn't fun, but it's better than some alternatives. A good assessment supports good decision-making and helps avert negative outcomes, regardless if the trip is ten seconds or forty minutes.
 
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.

You weren't taking the blood pressure on the same arm the SpO2 probe was on were you? Because that's what I get out of the above and would explain the sudden drop in perceived hypoxemia.
 
You weren't taking the blood pressure on the same arm the SpO2 probe was on were you? Because that's what I get out of the above and would explain the sudden drop in perceived hypoxemia.

But being unresponsive to painful stimuli wouldn't be explained by the BP cuff. Really sick old people to not tolerate CNS depressants very well at all.
 
But being unresponsive to painful stimuli wouldn't be explained by the BP cuff. Really sick old people to not tolerate CNS depressants very well at all.


I'm not saying she wasn't hypoxemic or that this was an appropriate use of anelgesia, but I am saying that it's unlikely for a pulse-ox probe to read 35% as well with a spontaneously breathing patient.
 
New to the forum, so I apologize for the late response. In my opinion it is hard to fully understand what happens to our pts even when we are sitting right next to them, none the less reading it on a forum. Sounds like the medic that administered the meds should have asked a few more questions about post-op meds, resp hx, etc etc. I did want to share this piece of information that I learned about one week ago after asking for 100 mcg of Fentanyl for a 113 kg pt with bi-lat wrist fx and lt ankle fx. The receiving ER Doc denied the orders for 100 mcg and ordered 50 mcg of Fentanyl. I was curious as to why the Doc cut the order in half since the pt was well with in the correct dose range. He advised that "yes she was within the correct 1mcg/kg dose range, but with a 40 min tx time he likes to play it safe with a small dose of Fentanyl to start with and if the pt is not managed with 50 mcg then more can be given if vitals can sustain". The ER Doc advised me about Rigid Chest Syndrome with Fentanyl. I've looked it up but not in full detail yet, I'm not saying that your pt experienced RCS but it is something to look up and understand if giving Fentanyl.
 
Fentanyl induced chest wall regidity is not very common at all in low doses and there are very few reported cases. A low dose is considered 1mcg/kg.

It is seen more common in higher doses (+30mcg/kg). I’ve administered 100mcg of Fentanyl many many times and have never had any chest wall rigidity. I have also never seen any hemodynamic changes or really any changes in patient vitals.
 
New to the forum, so I apologize for the late response. In my opinion it is hard to fully understand what happens to our pts even when we are sitting right next to them, none the less reading it on a forum. Sounds like the medic that administered the meds should have asked a few more questions about post-op meds, resp hx, etc etc. I did want to share this piece of information that I learned about one week ago after asking for 100 mcg of Fentanyl for a 113 kg pt with bi-lat wrist fx and lt ankle fx. The receiving ER Doc denied the orders for 100 mcg and ordered 50 mcg of Fentanyl. I was curious as to why the Doc cut the order in half since the pt was well with in the correct dose range. He advised that "yes she was within the correct 1mcg/kg dose range, but with a 40 min tx time he likes to play it safe with a small dose of Fentanyl to start with and if the pt is not managed with 50 mcg then more can be given if vitals can sustain". The ER Doc advised me about Rigid Chest Syndrome with Fentanyl. I've looked it up but not in full detail yet, I'm not saying that your pt experienced RCS but it is something to look up and understand if giving Fentanyl.

Unlikely that your patient would not have tolerated a 100 mcg bolus, but I can see wanting to titrate by 50's. Intolerance to the narcotic because of a history of untreated obstructive sleep apnea (sounds like he might have been at risk because of his weight) is more of a concern than a "rigid chest". I have to say that I give fentanyl by the fluid half ounce to ounce at a time and I'm not sure I've ever seen a rigid chest from it. I've had a difficult time mask ventilating because of the relaxation of the airway that occurs with resolution after paralysis, but I can't say for sure if it was ever due to chest wall rigidity from fentanyl.
 
I've had a difficult time mask ventilating because of the relaxation of the airway that occurs with resolution after paralysis, but I can't say for sure if it was ever due to chest wall rigidity from fentanyl.

I wonder how many people think they've seen rigid chest but actually just weren't doing a good job ventilating.
 
I wonder how many people think they've seen rigid chest but actually just weren't doing a good job ventilating.

About the same number that can't ventilate after a whack of propofol....The rigid chest thing came from somewhere....It probably is a "thing", but it isn't nearly as common as folks invoking the warning of the the dreaded "wooden chest" syndrome, I'm sure.
 
So I've been reading through Costanzo's Physiology (4th ed.) and came across something that rang a bell. They state for a person at rest, the O2 consumption rate is 250ml O2/min (p.209) which is identical to the passive flow rate of oxygen Rich Levitan describes.

So there's the hard numbers folks. I know a lot of people have commented with anecdotal evidence, but it's nice to be able to point to a source and say 'this is why'. Now don't get me wrong - there's still whatever underlying pathology and it's metabolic effect on oxygen demand, but that can also be counteracted with supplimental O2 in form of a high-flow N/C.
 
So I've been reading through Costanzo's Physiology (4th ed.) and came across something that rang a bell. They state for a person at rest, the O2 consumption rate is 250ml O2/min (p.209) which is identical to the passive flow rate of oxygen Rich Levitan describes.

So there's the hard numbers folks. I know a lot of people have commented with anecdotal evidence, but it's nice to be able to point to a source and say 'this is why'. Now don't get me wrong - there's still whatever underlying pathology and it's metabolic effect on oxygen demand, but that can also be counteracted with supplimental O2 in form of a high-flow N/C.

Unless you get passive airway obstruction, which is very common in these scenarios.
 
Unless you get passive airway obstruction, which is very common in these scenarios.

Perhaps I need to clarify what I'm implying when I'm talking about this stuff. I'm simply talking about the physiology of apnic oxygenation DURING the lyringoscopy procedure.
 
So I've been reading through Costanzo's Physiology (4th ed.) and came across something that rang a bell. They state for a person at rest, the O2 consumption rate is 250ml O2/min (p.209) which is identical to the passive flow rate of oxygen Rich Levitan describes.

So there's the hard numbers folks. I know a lot of people have commented with anecdotal evidence, but it's nice to be able to point to a source and say 'this is why'. Now don't get me wrong - there's still whatever underlying pathology and it's metabolic effect on oxygen demand, but that can also be counteracted with supplimental O2 in form of a high-flow N/C.

So, just for clarity, even with a completely healthy patient with no airway obstruction who was apneic and whose O2 consumption was 250 ml/min, giving that much O2 would not be sufficient for oxygenation as measured by SpO2. In order for adequate O2 saturation and delivery to occur, there has to be some oxygen left in the blood coming back to the lungs.

Even breathing room air with a minute ventilation of 5-6 lpm, we breath over a liter of O2 per minute and normal room air sats run 92 to 99.
 
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.
I kind of agree with Remi on this one. I don't know it all but I want to say there's a chance of an inaccurate reading as I have also heard it can give false readings below 80. Another common misshaping is placement, or connection. The matter of seconds is the only thing that confused me.
 
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