Why paralytics are not reversed in some OR cases?

[icu2crna]

In my ICU we recover our pt after OR. I have noticed in some pts paralytics are not reversed. Is there any specific reason it's not done?

[wtbcrna, MSN, DNP, CRNA]

Paralytics are not truly reversed, but given an competitive antagonist to antagonize the paralytic until the paralytic has effectively been eliminated from the body. The "reversal" has lots of side-effects. Assuming there has been enough half-lives for the paralytic and the patient has shown they can pull adequate tidal volumes then it is sometimes acceptable not to give a "reversal". It is a personal choice based on the anesthesia provider.

I sometimes do not use a reversal agent after giving a paralytic, but there is a lot of criteria that I use when I do not reverse patients. There is also a least one large retrospective study that concluded that blindly reversing all patients increased of respiratory depression events post operatively.

[icu2crna]

Thanks for the explanation.

[KPHIL71]

The most commonly used reversal drug is Neostigmine. Neostigmine is not a direct competitive antagonist. A competitive antagonist is a drug that competes for a binding site. Neostigmine does not compete at the specific site of action and is therefore by definition not a direct competitive antagonist. Neostigmine (reversal agent) is a reversable acetylcholinesterase inhibitor. Acetylcholinesterase is an enzyme which breaks down acetylcholine at the neuromuscular junction. So if you block enough acetylcholinesterases, acetylcholine will flood the neuromuscluar junction and out-compete paralytic for available binding sites.

First if your patient has 4/4 twitches then only ~75% of their Nm receptors are blocked. What in hell does this mean? Without getting into too much detail it means that your patient can initiate their own breaths and they may be able to move. So when I'm emerging someone and if they have met all my extubation criteria without reversal I will extubate.

The reasons for not administering reversal are many. Remember. . . neostigmine is a drug. All drugs have potential negative side effects. The problem with neostigmine it isn't selective. It has cholinergic effects at both the Nm junction (intended target) and also in the heart (uninteded target) and in the lungs (unintended target). Most of the time we give reversal coupled with an antcholinergic drug like glycopyrrulate or atropine to counter the bradycardic effects. Unfortunately in pts with reactive airway disease such as COPD or asthma, reversal agents can cause increased secretions (bad) and bronchospasms (really bad).

Well that is all I got right now. Have to get back to my DNP online classes.

thanks

[icu2crna]

The most commonly used reversal drug is Neostigmine. Neostigmine is not a direct competitive antagonist. A competitive antagonist is a drug that competes for a binding site. Neostigmine does not compete at the specific site of action and is therefore by definition not a direct competitive antagonist. Neostigmine (reversal agent) is a reversable acetylcholinesterase inhibitor. Acetylcholinesterase is an enzyme which breaks down acetylcholine at the neuromuscular junction. So if you block enough acetylcholinesterases, acetylcholine will flood the neuromuscluar junction and out-compete paralytic for available binding sites.

First if your patient has 4/4 twitches then only ~75% of their Nm receptors are blocked. What in hell does this mean? Without getting into too much detail it means that your patient can initiate their own breaths and they may be able to move. So when I'm emerging someone and if they have met all my extubation criteria without reversal I will extubate.

The reasons for not administering reversal are many. Remember. . . neostigmine is a drug. All drugs have potential negative side effects. The problem with neostigmine it isn't selective. It has cholinergic effects at both the Nm junction (intended target) and also in the heart (uninteded target) and in the lungs (unintended target). Most of the time we give reversal coupled with an antcholinergic drug like glycopyrrulate or atropine to counter the bradycardic effects. Unfortunately in pts with reactive airway disease such as COPD or asthma, reversal agents can cause increased secretions (bad) and bronchospasms (really bad).

Well that is all I got right now. Have to get back to my DNP online classes.

thanks

Thanks.

[Trauma1RN]

Because it's a Friday at 3:30pm and the MDA wants to go home...