@taxidriver - what interventions were performed other than pain management?
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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.
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 %
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.
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.
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.
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.
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.
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.
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.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.