ACLS: Atropine: Not Just a Treatment for a Broken Heart...

September 13, 2018

Welcome to another installment of the #antidoteseries !!


Most learn in nursing school that Atropine is a treatment for symptomatic bradycardia, but did you also know it plays an equally large role as an antidote!? That’s right, Atropine is an anticholinergic…remember the rhyme anyone?


“Can't see, can't pee, can't spit, can't shit”! In other words, they dry you out, causing blurred vision, urinary retention, cotton mouth and constipation.


Atropine is also a competitive antagonist of the muscarinic acetylcholine receptors found in smooth and cardiac muscle, secretory tissue, and the Central Nervous System. Because acetylcholine is the main neurotransmitter used in the parasympathetic nervous system, it is considered an anti-parasympathetic drug, resulting in reduction of vagal tone, increased automaticity of the SA node and increased AV conduction. But we aren’t talking about its cardiac use today, what we care about is its effects on drying secretions and blocking acetylcholine receptors.


You see Atropine is used to treat both Organophosphate and Nerve agent poisoning! In fact ask soldiers that served in certain areas of the middle east and they will tell you they carried Atropine Autoinjector pens!

Poisonings by organhosphates, whether accidental (used commonly in the U.S. as an insecticide by farmers) or in war (in the from of Sarin, VX, and other nerve gases) work by inhibiting acetylcholinesterase, the enzyme responsible for breaking down acetylcholine. Thus acetylcholine builds up in the brain resulting in overstimulation, constricted pupils, involuntary urination, copious bronchial secretions and convulsions. This eventually leads to death, most commonly from asphyxiation.

Atropine saves the day in these cases by blocking the acetylcholine receptors. So even though the nerve agent still inhibits the break down, and there is an overabundance of acetylcholine in the brain, it is unable to bind to receptor sites, and thus no life threatening symptoms arise.

There is no set dose for this type of treatment as it depends on both physiologic and chemical factors. Often a loading dose of 2-6 mg is given intramuscularly dependent on severity of symptoms. IM is preferred to IV as this will ensure the drug circulates longer and inhibits the binding of acetylcholine while the nerve agent is still active. Atropine must be continuously given until bronchial secretions stop, indicating the build up of acetylcholine in the brain has evened out.

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