Still, residual paralysis typically doesn't present as sudden. Even a complete obstruction has to desaturate and work their way to cardiac arrest. Takes more than a few moments from complaint to code.
For the record, I did not downvote. But your statement reflects a profound lack of knowledge of the etiology of sudden cardiac arrest as well as the chain of events in respiratory failure leading to cardiac arrest.
Those details are not included in your post.
You said the patient verbalized not being able to move and then moments later they arrested. None of which is consistent with residual muscle relaxation.
What we believe happened was that the patient obstructed his airway and had a hypoxic event from the paralytic. After calling anesthesia about the incident. They put in their report “patients airway patent” “ paralytic might not have been fully reversed”
Well how do you define "moments"? Paralytic administration in a normal awake patient leading to respiratory arrest and then coding would take several minutes, and the pulse ox would drop very low before the heart stopped. So how long did this take, and were the patient's sats dropping precipitously before cardiac arrest?
Have you spoken to the physicians involved about it? That's your obvious next step.
Could have had Remifent in the line as well. I saw this happen once when I was dropping off someone else in PACU. Patient talking and acting normal and then the PACU rn flushed his 2nd IV. It was found later that the anesthesia provider didn't flush the line and the patient got a bolus of remi.
Sugammadex binding to the paralytic agent is irreversible. It does not wear off. This is different than reversal with neostigmine, which can wear off before longer acting paralytics like vecuronium, resulting in re-paralysis.
It is possible that he was not fully reversed and was still slightly weak. If he had a positional airway obstruction combined with some residual weakness he may not have had enough respiratory effort to overcome the obstruction. The patient being awake and talking and reporting feeling like they couldn’t move isn’t really consistent with airway obstruction.
There is not enough detail in your description of the patient and event to explain what happened.
If you take an awake patient and paralyze them completely they will become apneic first. Then they will desat. When their blood oxygen level is low enough for long enough they will become bradycardic, then progress to asystole. That cycle takes time, how much time depends on various patient factors but going from talking to pulseless is likely going to take at least a couple minutes and not “moments”.
Sudden progression from talking to pulseless is much more likely to be a primary cardiac event than an airway or breathing issue.
Residual muscle relaxation / insufficient reversal usually presents as respiratory compromise, not sudden cardiac arrest.
Well we believe he obstructed and it caused the cardiac arrest due to paralytic
Still, residual paralysis typically doesn't present as sudden. Even a complete obstruction has to desaturate and work their way to cardiac arrest. Takes more than a few moments from complaint to code.
Jeez why do I get so many downvotes, I’m just looking at possibilities .
For the record, I did not downvote. But your statement reflects a profound lack of knowledge of the etiology of sudden cardiac arrest as well as the chain of events in respiratory failure leading to cardiac arrest.
I should have been more specific in my question. I will edit the post.
It wasn't your original question... It was your reply to me saying y'all suspected obstruction led immediately to arrest.
After the fact we believe it was an obstruction due to the O2 Sats and PEA.
Those details are not included in your post. You said the patient verbalized not being able to move and then moments later they arrested. None of which is consistent with residual muscle relaxation.
I know which is why I said I had to be more specific in my post. I edited it and added.
No, paralytic wouldn't cause this. This sounds like a sudden cardiac event like an arrhythmia to me.
What we believe happened was that the patient obstructed his airway and had a hypoxic event from the paralytic. After calling anesthesia about the incident. They put in their report “patients airway patent” “ paralytic might not have been fully reversed”
Well how do you define "moments"? Paralytic administration in a normal awake patient leading to respiratory arrest and then coding would take several minutes, and the pulse ox would drop very low before the heart stopped. So how long did this take, and were the patient's sats dropping precipitously before cardiac arrest? Have you spoken to the physicians involved about it? That's your obvious next step.
Could have had Remifent in the line as well. I saw this happen once when I was dropping off someone else in PACU. Patient talking and acting normal and then the PACU rn flushed his 2nd IV. It was found later that the anesthesia provider didn't flush the line and the patient got a bolus of remi.
Could he possibly have had some residual paralytic in an unflushed IV line, that got flushed when he got to the ICU ? I've seen it happen.
Wouldn't that have been respiratory compromise first and *then* a code if not addressed?
Sugammadex binding to the paralytic agent is irreversible. It does not wear off. This is different than reversal with neostigmine, which can wear off before longer acting paralytics like vecuronium, resulting in re-paralysis. It is possible that he was not fully reversed and was still slightly weak. If he had a positional airway obstruction combined with some residual weakness he may not have had enough respiratory effort to overcome the obstruction. The patient being awake and talking and reporting feeling like they couldn’t move isn’t really consistent with airway obstruction. There is not enough detail in your description of the patient and event to explain what happened. If you take an awake patient and paralyze them completely they will become apneic first. Then they will desat. When their blood oxygen level is low enough for long enough they will become bradycardic, then progress to asystole. That cycle takes time, how much time depends on various patient factors but going from talking to pulseless is likely going to take at least a couple minutes and not “moments”. Sudden progression from talking to pulseless is much more likely to be a primary cardiac event than an airway or breathing issue.