Glycopyrrolate

[cfdavid]

Do you guys use it more as an antisialagogue, and/or mixed with neostigmine to counter the excessive Ach availability post neostigmine, in order to mitigate the muscarinic effects on the heart of all the Ach??

At our institution, Robinul is always mixed with neostigmine in the cases I've been in on. And, the above latter explanation is what the residents gave me.

However, my book (Miller's Basics...) just mentions it as a useful antisialagogue preop for certain cases (bronchoscopies and elective surgeries).

Any thoughts?

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[Planktonmd]

Do you guys use it more as an antisialagogue, and/or mixed with neostigmine to counter the excessive Ach availability post neostigmine, in order to mitigate the muscarinic effects on the heart of all the Ach??

At our institution, Robinul is always mixed with neostigmine in the cases I've been in on. And, the above latter explanation is what the residents gave me.

However, my book (Miller's Basics...) just mentions it as a useful antisialagogue preop for certain cases (bronchoscopies and elective surgeries).

Any thoughts?

Glycopyrolate is (as you probably know) a quaternary amine anti muscarinic agent.
This means it has anti muscarinic properties (like Atropine) but it does not cross the blood brain barrier because of the quatertnary structure (unlike atropine and scopolamine that get to the brain and cause sedation and delirium in the elderly).
Glycopyrolate tends to have less anticholinergic effect on the heart than Atropine so although it produces tachycardia, it is less pronounced.
In anesthesia we use this medication as you mentioned mixed with cholinesterase inhibitors to reduce the undesirable muscarinic effects (Bradycardia, salivation, intestinal cramps, vomiting...) and it is used also as our anticholinergic of choice for mild bradycardia or any vagal reaction.
It is a very good anti sialogogue and we use it very frequently for that indication as well.

 

[cfdavid]

Glycopyrolate is (as you probably know) a quaternary amine anti muscarinic agent.
This means it has anti muscarinic properties (like Atropine) but it does not cross the blood brain barrier because of the quatertnary structure (unlike atropine and scopolamine that get to the brain and cause sedation and delirium in the elderly).
Glycopyrolate tends to have less anticholinergic effect on the heart than Atropine so although it produces tachycardia, it is less pronounced.
In anesthesia we use this medication as you mentioned mixed with cholinesterase inhibitors to reduce the undesirable muscarinic effects (Bradycardia, salivation, intestinal cramps, vomiting...) and it is used also as our anticholinergic of choice for mild bradycardia or any vagal reaction.
It is a very good anti sialogogue and we use it very frequently for that indication as well.

Thanks Plank. Nice explanation/clarification.

 

[coprolalia]

It also has to do with duration of action.

Glycopyrrolate has a slower onset but sticks around longer. For example, you can "reverse" NMB with edrophonium. In that instance, you mix it with atropine. This is more to do with the fact that edrophonium has a faster onset (and shorter duration) of action, as does atropine. Although, I have rarely seen this done (I think once during residency).

Also, the antisialorrhea dose of glyco is typically much lower (0.1-0.2 mg), and you definitely don't get as much tachycardia with that low dose. You will if see much more tachycardia when you "fully" reverse someone (i.e. someone weighing greater than 70kg who gets the 5mg/1mg combo neo/glyco dose).

-copro

 

[proman]

I don't mix the two because I normally give 0.2mg less of glyco than dictated (except in marginal people). I think that was a tip posted a while ago here.

I rarely use it to dry people out, occassionally use it to counter high vagal tone (like peritoneal manipulation etc).

 

[nutmegs]

It also has to do with duration of action.

Glycopyrrolate has a slower onset but sticks around longer. For example, you can "reverse" NMB with edrophonium. In that instance, you mix it with atropine. This is more to do with the fact that edrophonium has a faster onset (and shorter duration) of action, as does atropine. Although, I have rarely seen this done (I think once during residency).

Also, the antisialorrhea dose of glyco is typically much lower (0.1-0.2 mg), and you definitely don't get as much tachycardia with that low dose. You will if see much more tachycardia when you "fully" reverse someone (i.e. someone weighing greater than 70kg who gets the 5mg/1mg combo neo/glyco dose).

-copro

What if you "fully" reverse them but just give an appropriate dose of glyco to counteract the bradycardia? I don't "mix" syringes just for this reason, and rarely have tachycardia. Or code browns, for that matter...

 

[coprolalia]

What if you "fully" reverse them but just give an appropriate dose of glyco to counteract the bradycardia? I don't "mix" syringes just for this reason, and rarely have tachycardia. Or code browns, for that matter...

Yeah, I suppose you could do that. I wouldn't suggest trying that in little kids, though.

You know, neurologists give neostigmine without any anticholinergic. I heard a story once about a somewhat infamous case report wherein a neurologist reported "profound bradycardia" following neostigmine administration, and several hypotheses as to why this happened, as reported to some some neurology journal. Apparently, a bunch of anesthesiologists replied in letters to the editor saying, essentially, this was a common thing and the reason why "you guys" don't see it more often is because "you don't have your patients on monitors when you give cholinesterase inhibitors."

If someone could dig that up, that'd be awesome to look at.

-copro

 

[nutmegs]

Yeah, I suppose you could do that. I wouldn't suggest trying that in little kids, though.

You know, neurologists give neostigmine without any anticholinergic. I heard a story once about a somewhat infamous case report wherein a neurologist reported "profound bradycardia" following neostigmine administration, and several hypotheses as to why this happened, as reported to some some neurology journal. Apparently, a bunch of anesthesiologists replied in letters to the editor saying, essentially, this was a common thing and the reason why "you guys" don't see it more often is because "you don't have your patients on monitors when you give cholinesterase inhibitors."

If someone could dig that up, that'd be awesome to look at.

-copro

I've participated in giving unopposed neo in the ICU for a colonic pseudoobstruction. You gotta be REALLY sure first, though... 😉

 

[pgg]

For example, you can "reverse" NMB with edrophonium. In that instance, you mix it with atropine. This is more to do with the fact that edrophonium has a faster onset (and shorter duration) of action, as does atropine. Although, I have rarely seen this done (I think once during residency).

Didn't they take Enlon off the market? Like mivacurium - good drug but no one used it, so no one made money off it, so now you can't get it.

What if you "fully" reverse them but just give an appropriate dose of glyco to counteract the bradycardia? I don't "mix" syringes just for this reason, and rarely have tachycardia. Or code browns, for that matter...

That's what I do - almost never give equal volumes. You don't need much glycopyrrolate to prevent the bad muscarinic effects but of course you need some ...

As local neostigmine legend goes, one of our attendings decided one day to try a neostigmine only reversal because the patient was pretty tachycardic. First words upon awakening ... "I'm gonna be sick" followed by horrible abdominal cramping, gushing eyes/nose, puking, and a massive code brown.

Local neostigmine legend #2 was a surgery intern in the ICU, fresh off a whole week of anesthesia, who wanted to hasten along a patient toward extubation criteria. He thought the patient was weak, so he called upon his newly acquired anesthesia-fu and reversed him with neostigmine (but his fu was weak, and he used no glycopyrrolate) and soon found himself coding an asystolic patient.

 

[Bertelman]

What if you "fully" reverse them but just give an appropriate dose of glyco to counteract the bradycardia? I don't "mix" syringes just for this reason, and rarely have tachycardia. Or code browns, for that matter...

I've tried pushing a couple cc's of neostig, reaching over to draw the glyco in the same 3cc syringe, then chasing with appropriate amount. When certain attending I highly respect saw this, he regaled with stories of profound brady and subsequent code because onset of neostig preceded glyco.

Granted, I think you can do what you describe in a selected patient population, but I'm sufficiently wary to keep them mixed, even if there is always a little less glyco in the syringe. If the onset is a few minutes, you're waaayyy behind the 8-ball by the time the glyco you titrate kicks in.

 

[nutmegs]

I've tried pushing a couple cc's of neostig, reaching over to draw the glyco in the same 3cc syringe, then chasing with appropriate amount. When certain attending I highly respect saw this, he regaled with stories of profound brady and subsequent code because onset of neostig preceded glyco.

Granted, I think you can do what you describe in a selected patient population, but I'm sufficiently wary to keep them mixed, even if there is always a little less glyco in the syringe. If the onset is a few minutes, you're waaayyy behind the 8-ball by the time the glyco you titrate kicks in.

:shrugs: I just push glyco first. that was if there's a problem with the IV, I have tachycardia to deal with, not asystole. either way, it's all good.

 

[Bertelman]

:shrugs: I just push glyco first. that was if there's a problem with the IV, I have tachycardia to deal with, not asystole. either way, it's all good.

I misunderstood your technique. Clearly this wasn't you, but I thought I had read here before about some who push the reversal, then wait to see how bad the brady is before pushing glyco.

 

[nutmegs]

I misunderstood your technique. Clearly this wasn't you, but I thought I had read here before about some who push the reversal, then wait to see how bad the brady is before pushing glyco.

😱😱😱 no sir.

 

[dA pilot]

Sometimes I push neogstigmine to treat tachycardia when I'm worried about giving beta blockers because of hypotension.

 

[Planktonmd]

Sometimes I push neogstigmine to treat tachycardia when I'm worried about giving beta blockers because of hypotension.

If they are hypotensive and tachycardic maybe we should find out why before trying to treat the symptom (tachycardia).

 

[cfdavid]

Yeah, I suppose you could do that. I wouldn't suggest trying that in little kids, though.

You know, neurologists give neostigmine without any anticholinergic. I heard a story once about a somewhat infamous case report wherein a neurologist reported "profound bradycardia" following neostigmine administration, and several hypotheses as to why this happened, as reported to some some neurology journal. Apparently, a bunch of anesthesiologists replied in letters to the editor saying, essentially, this was a common thing and the reason why "you guys" don't see it more often is because "you don't have your patients on monitors when you give cholinesterase inhibitors."

If someone could dig that up, that'd be awesome to look at.

-copro

Very interesting. Good point Copro.

 

[cfdavid]

It also has to do with duration of action.

Glycopyrrolate has a slower onset but sticks around longer. For example, you can "reverse" NMB with edrophonium. In that instance, you mix it with atropine. This is more to do with the fact that edrophonium has a faster onset (and shorter duration) of action, as does atropine. Although, I have rarely seen this done (I think once during residency).

Also, the antisialorrhea dose of glyco is typically much lower (0.1-0.2 mg), and you definitely don't get as much tachycardia with that low dose. You will if see much more tachycardia when you "fully" reverse someone (i.e. someone weighing greater than 70kg who gets the 5mg/1mg combo neo/glyco dose).

-copro

In my limited experience, I haven't seen it yet either, but "baby" Miller does mention it along with (I reread/found the correct reference) glycopyrrolate with neostigmine for the purposes we've been discussing....

 

[pgg]

Sometimes I push neogstigmine to treat tachycardia when I'm worried about giving beta blockers because of hypotension.

That's unkind if the patient's awake.

I'm trying to think of a situation where this would be a good idea. Can you elaborate? Some of the things that cause tachycardia & hypotension would be abruptly worsened by giving neostigmine, or at best not helped.

 

[dA pilot]

If they are hypotensive and tachycardic maybe we should find out why before trying to treat the symptom (tachycardia).

Typically physicians do try to find out what is causing the problem before treating the symptom.

An example I was trying to convey was the 85 year old cardiomyopathy lady having a fem pop bypass under a GA whose heart rate is in the 90's with a bp of 100/60. She is having a tough time handling the anesthetic and it could be due to a decreased preload or her cardiomyopathy. The patient does not need muscle relaxation for the case. We can give her fluids or start a vasopressor. Another option to control heart rate is neostigmine. Neostigmine side effect of bradycardia is reliable without much effect on contractility or tone, its available right in your pyxsis. Its effect is in a few minutes and lasts a half hour. I'm not saying it is a drug of choice for any instance, but it can be an option to consider. Most people do use neostigmine at the end of the case with glycopyrolate in varying ratios to control heart rate already. You can think about it as giving reversal during the middle of a case when muscle relaxation is not necessary.

 

[Planktonmd]

The neostigmin to slow heart rate is an old trick that people used in the past to make the numbers look good instead of treating the cause.
An 80 Y/O with cardiomyopathey and dehydration most likely needs that slightly elevated HR to maintain her cardiac output and tissue perfusion.
Now If you added Aortic stenosis to his picture then it might make a bit more sense to worry about the HR and want to treat it aggressively although I would probably use a combination of Beta blocker and a Small dose Phenylephrine to do that.

 

[2ndyear]

Didn't they take Enlon off the market? Like mivacurium - good drug but no one used it, so no one made money off it, so now you can't get it.

Yes, last February. I'm sure you can still get generic edrophonium if you wanted to though. I always thought that the Enlon Plus was a neat idea, kind of. But do you really need a trade name drug for something already very cheap in two different syringes? We actually have a bunch of ampules of Enlon Plus laying around. Ebay? Just think, it will be like Polaroid film. I'm sure someone out there loves to use the stuff!

 

[jetproppilot]

The neostigmin to slow heart rate is an old trick that people used in the past to make the numbers look good instead of treating the cause.
An 80 Y/O with cardiomyopathey and dehydration most likely needs that slightly elevated HR to maintain her cardiac output and tissue perfusion.
Now If you added Aortic stenosis to his picture then it might make a bit more sense to worry about the HR and want to treat it aggressively although I would probably use a combination of Beta blocker and a Small dose Phenylephrine to do that.

I've used neostigmine a few times in the heart room after coming off bypass and a (sinus) tachycardia is occurring despite all other parameters (especially volume, contractility, BP) looking good, and I'm a little concerned about the tachycardia's effect on myocardial oxygen consumption.

Small doses of esmolol is probably a better choice.