Pharmacology. Atropine and glycopyrrolate competitively block the action of acetylcholine at muscarinic receptors. Desired therapeutic effects for treating poisoning include decreased secretions from salivary and other glands, decreased bronchorrhea and wheezing, decreased intestinal secretion and peristalsis, increased heart rate, and enhanced atrioventricular conduction.

1. 
   

   Atropine is a naturally occurring tertiary amine that crosses the blood-brain barrier and has significant structural and functional similarity to scopolamine, homatropine, and ipratropium. The elimination half-life of atropine is 2–4 hours (longer in children), with approximately 50% excreted unchanged in urine.

   
   
2. 
   

   Glycopyrrolate is a synthetic quaternary amine that crosses the blood-brain barrier poorly and is less likely than atropine to cause altered mental status or tachycardia. It has approximately twice the potency of atropine. Glycopyrrolate is excreted unchanged primarily in the bile and urine.

   
   
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   Note: These drugs do not reverse the effects of excess acetylcholine at nicotinic receptors of the neuromuscular junctions, ganglia of the parasympathetic and sympathetic nervous system, and CNS.

Indications

1. 
   

   Correction of bronchorrhea and excessive oral and GI tract secretions associated with cholinesterase inhibitor (eg, organophosphate and carbamate insecticide) intoxication. Glycopyrrolate may be especially useful in managing peripheral muscarinic symptoms in cholinesterase inhibitor poisoning. Although glycopyrrolate will not reverse CNS toxicity associated with cholinesterase inhibitor poisoning, it also will not cause the CNS side effects seen with large doses of atropine, which are difficult to distinguish from the toxic effects of cholinesterase inhibitors.

   
   
2. 
   

   Acceleration of the rate of sinus node firing and atrioventricular (AV) nodal conduction velocity in the presence of drug-induced AV conduction impairment (eg, caused by digitalis, beta blockers, calcium antagonists, organophosphorus or carbamate insecticides, or physostigmine).

   
   
3. 
   

   Reversal of central (by atropine) and peripheral (by atropine and glycopyrrolate) muscarinic symptoms in patients with intoxication by Clitocybe or Inocybe mushroom species.

   
   
4. 
   

   When neostigmine or pyridostigmine is used to reverse nondepolarizing neuromuscular blockade, glycopyrrolate is the preferred agent to block unwanted muscarinic effects (see “Neuromuscular Blockers”).

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