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cycloplegia

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cycloplegia

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Phenylephrine is an alpha one adrenergic receptor agonist. The radial muscles of the iris are innervated by neurons with alpha one receptors thus it causes dilation when stimulated. However the ciliary body of the eye (which controls accommodation) is controlled by muscarinic 3 cholinergic receptors. That pathway for accommodation remains unaffected while the iris is dilated so you will not get cycloplegia.

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The purpose of cycloplegia in ocular inflammation is threefold:

1. reduces ocular pain by preventing cilliary body spasm

2. helps to stabilize blood/aqueous barrier

3.reduces area of contact of peripheral iris with anterior lens surface decreasing risk of synechie and possible angle closure.

Much protein is released into the AC by way of cell and flare, this is sticky and and contributes to the lens being bound to the iris. Additionally, the person is highly photophobic, by stabilizing the iris and cilliary body, they are much more comfortable.

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Atropine increases firing of the sinoatrial node (SA) and conduction through the atrioventricular node (AV) of the heart, opposes the actions of the vagus nerve, blocks acetylcholine receptor sites, and decreases bronchial secretions.

In general, atropine lowers the parasympathetic activity of all muscles and glands regulated by the parasympathetic nervous system. This occurs because atropine is a competitive antagonist of the muscarinic acetylcholine receptors (Acetylcholine is the main neurotransmitter used by the parasympathetic nervous system). Therefore, it may cause swallowing difficulties and reduced secretions.

Ophthalmic use

Topical atropine is used as a cycloplegic, to temporarily paralyze the accommodation reflex, and as a mydriatic, to dilate the pupils. Atropine degrades slowly, typically wearing off in 7 to 14 days, so it is generally used as a therapeutic mydriatic, whereas tropicamide (a shorter-acting cholinergic antagonist) or phenylephrine (an α-adrenergic agonist) is preferred as an aid to ophthalmic examination. Atropine induces mydriasis by blocking contraction of the circular pupillary sphincter muscle, which is normally stimulated by acetylcholine release, thereby allowing the radial pupillary dilator muscle to contract and dilate the pupil. Atropine induces cycloplegia by paralyzing the ciliary muscles, whose action inhibits accommodation to allow accurate refraction in children, helps to relieve pain associated with iridocyclitis, and treats ciliary block (malignant) glaucoma. Atropine is contraindicated in patients pre-disposed to narrow angle glaucoma.

Atropine can be given to patients who have direct globe trauma.

Resuscitation

Injections of atropine are used in the treatment of bradycardia (an extremely low heart rate), asystole and pulseless electrical activity (PEA) in cardiac arrest. This works because the main action of the vagus nerve of the parasympathetic system on the heart is to decrease heart rate. Atropine blocks this action and, therefore, may speed up the heart rate. The usual dosage of atropine in bradyasystolic arrest is 0.5 to 1 mg IV push every three to five minutes, up to a maximum dose of 0.04 mg/kg. For symptomatic bradycardia, the usual dosage is 0.5 to 1.0 mg IV push, may repeat every 3 to 5 minutes up to a maximum dose of 3.0 mg[2].

Atropine is also useful in treating second-degree heart block Mobitz Type 1 (Wenckebach block), and also third-degree heart block with a high Purkinje or AV-nodal escape rhythm. It is usually not effective in second-degree heart block Mobitz type 2, and in third-degree heart block with a low Purkinje or ventricular escape rhythm. Atropine is contraindicated in ischemia-induced conduction block, because the drug increases oxygen demand of the AV nodal tissue, thereby aggravating ischemia and the resulting heart block.

One of the main actions of the parasympathetic nervous system is to stimulate the M2 muscarinic receptor in the heart, but atropine inhibits this action.

Secretions and bronchoconstriction

Atropine's actions on the parasympathetic nervous system inhibits salivary, sweat, and mucus glands. This can be useful in treating hyperhidrosis, and can prevent the death rattle of dying patients. Even though atropine has not been officially indicated for either of these purposes by the FDA, it has been used by physicians for these purposes.[3]

Treatment for organophosphate poisoning

Atropine is not an actual antidote for organophosphate poisoning. However, by blocking the action of acetylcholine at muscarinic receptors, atropine also serves as a treatment for poisoning by organophosphate insecticides and nerve gases, such as Tabun (GA), Sarin (GB), Soman (GD) and VX. Troops that are likely to be attacked with chemical weapons often carry autoinjectors with atropine and obidoxime, which can be quickly injected into the thigh. Atropine is often used in conjunction with Pralidoxime chloride.

Atropine is given as a treatment for SLUDGE (Salivation, Lacrimation, Urination, Diaphoresis, Gastrointestinal motility, Emesis) symptoms caused by organophosphate poisoning. Another mnemonic is DUMBBELSS, which stands for Diarrhea, Urination, Miosis, Bradycardia, Bronchoconstriction, Excitation (as of muscle in the form of fasciculations and CNS), Lacrimation, Salivation, and Sweating (only sympathetic innervation using Musc receptors).

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