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Atropine is a tropane alkaloid and anticholinergic medication used to treat certain types of nerve agent and pesticide poisonings as well as some types of slow heart rate, and to decrease saliva production during surgery. [6] It is typically given intravenously or by injection into a muscle. [6]
Acetylcholine hyperpolarizes the sinoatrial node; this is overcome by MRAs, and thus they increase the heart rate. If atropine is given by intramuscular or subcutaneous injection, it causes initial bradycardia. This is because when administered intramuscularly or subcutaneously atropine acts on presynaptic M1 receptors (autoreceptors).
Atropine is often used as a first line treatment of a third-degree heart block in the presence of a narrow QRS which indicates a nodal block, but, may have little to no effect in an infra-nodal block. [11] Atropine works by reducing vagal stimulation through the AV node but will not be effective in those who have had a previous heart transplant ...
Sinus bradycardia due to a hypersensitive vagus nerve; Organophosphate based nerve agent poisoning, such as VX, sarin, tabun, and soman (atropine is favoured in conjunction with an oxime, usually pralidoxime) [6] [7]
Chemical structure of atropine. Patients with bradycardia are treated with atropine. [4] Atropine is a muscarinic antagonist, which can obstruct the muscarinic receptor and acetylcholine cannot bind to the receptor for sustaining transmission of nerve signals to the heart through the parasympathetic nervous system. This allows an increase in ...
The typical dose is 1.5 mg/kg IV given three minutes prior to intubation. [34] Atropine may also be used as a premedication agent in pediatrics to prevent bradycardia caused by hypoxia, laryngoscopy, and succinylcholine. Atropine is a parasympathetic blocker. The common premedication dose for atropine is 0.01–0.02 mg/kg.
In the 1850s, atropine was used as antispasmodic in asthma treatment and as morphine antidote for its mydriatic effect. [4] Bezold and Bloebaum showed that atropine blocked the effects of vagal stimulation on the heart in 1867. Subsequently in 1872, Heidenhain found its ability to prevent salivary secretion. [6]
Intravenous calcium gluconate (or calcium chloride if a central line is available) and atropine are first-line therapies. If the time of the overdose is known and presentation is within two hours of ingestion , activated charcoal , gastric lavage , and polyethylene glycol may be used to decontaminate the gut.
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