- Mechanism of Action
- Clinical Uses & Dosing
- Overdose and Central Anticholinergic Syndrome
Glycopyrrolate combines reversibly (competitve antagonism) with muscarinic cholinergic receptors, and thus prevents access of the neurotransmitter acetylcholine to these sites. It is termed an anticholinergic.
IV Administration: onset of action 2-3 minutes; duration of action 30-60 minutes.
Glycopyrrolate, in contrast to atropine and scopolamine, is a non-lipid soluble quaternary amine, and hence does NOT cross the blood-brain barrier. It has minimal CNS effects such as sedation or delerium, and thus makes it a wise choice for use in the elderly, and when treating peripheral effects of physostigmine.
- Determining the "Correct" Patient Weight to use for Drug Calculations
In Combination with Anticholinesterase Drugs:
- -to prevent parasympathomimetic effects that occur with edrophonium, neostigmine, and pyridostigmine.
- -typical dosing with neostigmine (Click on Link)
- -usually supplied as 200 mcg/ml.
- Antisialagogue Effect
- -Glycopyrrolate is twice as potent as atropine for inhibiting salivation (see table above)
- -starting dose Adult: 0.2mg (200 mcg)
- Treatment of Reflex-Mediated Bradycardia
- -Glycopyrrolate is less potent than atropine for treating an intraoperative bradycardia, particularly that resulting from increased parasympathetic nervous system activity.
- -Dose is 7 to 35 ug/kg IV (70kg adult= 0.5-2 mg)
- -Increases the heart rate by blocking the effects of acetylcholine on the sinoatrial node -Equivalent doses of glycopyrrolate produce similar increases in heart rate compared to atropine, but the onset of effect is slower than after the administration of atropine (Bevan et al., 1992).
- -EKG effect is to shorten the P-R interval.