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  1. 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 the urine.

    3. 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.

  2. Indications

    1. Correction of bronchorrhea and excessive oral and GI tract secretions associated with cholinesterase inhibitor (eg, organophosphorus 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 cardiac glycosides, beta-adrenergic blocking agents, calcium channel 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 either neostigmine or pyridostigmine is used to reverse nondepolarizing neuromuscular blockade, glycopyrrolate is the preferred agent to block unwanted muscarinic effects (see "Neuromuscular Blockers").

  3. Contraindications. All these contraindications are relative, and in some clinical situations benefit exceeds possible harm.

    1. Patients with hypertension, tachyarrhythmias, thyrotoxicosis, congestive heart failure, coronary artery disease, valvular heart disease, or other illnesses, who might not tolerate a rapid heart rate. Note: Patients with cholinesterase inhibitor poisoning are often tachycardic, but antimuscarinics may still be given because they can improve oxygenation, thereby reducing catecholamine release associated with hypoxia; glycopyrrolate may be less likely than atropine to cause excessive tachycardia.

    2. Angle-closure glaucoma, in which papillary dilation may increase intraocular pressure (may be used safely if the patient is being treated with a miotic agent).

    3. Partial or complete obstructive uropathy.

    4. Myasthenia gravis.

    5. Obstructive diseases of the GI tract, severe ulcerative colitis, bacterial infections of the GI tract.

  4. Adverse effects

    1. Adverse effects include dry mouth, blurred vision, cycloplegia and mydriasis, palpitations, tachycardia, aggravation of angina, congestive heart failure (CHF), and constipation. Urinary retention is common, and a Foley catheter may be needed. Duration of effects may be prolonged (several hours). Additionally, CNS antimuscarinic toxicity (delirium) ...

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