Formulary
Atropine: Uses, Dosing, Side Effects and Indian Brand Names
Atropine is the prototype muscarinic antagonist used for symptomatic bradycardia, organophosphorus poisoning antidote, and pre-anaesthetic medication. It blocks parasympathetic effects to produce tachycardia, mydriasis, bronchodilation, and reduced secretions.
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Atropine: Uses, Dosing, Side Effects and Indian Brand Names
Atropine is the prototype muscarinic antagonist used for symptomatic bradycardia, organophosphorus poisoning antidote, and pre-anaesthetic medication. It blocks parasympathetic effects to produce tachycardia, mydriasis, bronchodilation, and reduced secretions.
NEET PG High-Yield: Atropine is the antidote for ORGANOPHOSPHORUS poisoning -- endpoint of atropinisation is DRYING OF SECRETIONS (not heart rate or pupil size). Pralidoxime (2-PAM) must be given within 24 hours before AChE 'ageing' becomes irreversible. Atropine is first-line for symptomatic bradycardia (0.5 mg IV). CONTRAINDICATED in narrow-angle glaucoma (acute angle closure crisis). The mnemonic for anticholinergic toxidrome: 'hot as a hare, blind as a bat, dry as a bone, red as a beet, mad as a hatter.'
Clinical overview
Atropine is the prototype antimuscarinic drug and one of the oldest drugs in pharmacology, derived from the plant Atropa belladonna (deadly nightshade). It has been used medicinally for over a century and remains indispensable in modern medicine. Its three most important clinical applications are: (1) treatment of symptomatic bradycardia (first-line per ACLS guidelines), (2) antidote for organophosphorus (OP) poisoning (the most common cause of poisoning-related deaths in rural India), and (3) pre-anaesthetic medication (reduces secretions and prevents vagal reflexes during intubation). In organophosphorus poisoning, atropine counteracts the muscarinic effects of acetylcholine excess (bradycardia, bronchospasm, bronchorrhoea, salivation, lacrimation, urination, defecation -- SLUDGE syndrome). Large doses may be needed (up to hundreds of milligrams in severe cases), titrated to the endpoint of drying of bronchial secretions (NOT heart rate or pupil size). Pralidoxime (2-PAM) must be given concurrently to reactivate the inhibited acetylcholinesterase before ageing occurs. In ophthalmology, atropine eye drops are used for cycloplegic refraction in children and for the treatment of anterior uveitis (prevents posterior synechiae). Atropine is also emerging as a treatment for myopia progression in children (low-dose 0.01-0.05% atropine eye drops).
Pharmacological class
Atropine belongs to the Muscarinic receptor antagonist (anticholinergic; belladonna alkaloid) class. Atropine competitively and reversibly blocks muscarinic acetylcholine receptors (M1-M5 subtypes) at neuroeffector junctions of parasympathetic nerves and at some central synapses. By blocking parasympathetic (vagal) input, it allows sympathetic tone to predominate, producing: tachycardia (M2 blockade on SA node), mydriasis and cycloplegia (M3 blockade on iris sphincter and ciliary muscle), bronchodilation (M3 blockade on bronchial smooth muscle), reduced secretions (salivary, bronchial, GI), and reduced GI motility.
Indian brand names and formulations
Available as: Atropine Sulphate Injection IP (Various manufacturers), Tropicamet (Sun Pharma) [eye drops -- tropicamide, shorter acting], Atropine Eye Drops IP (Various manufacturers), Bellafolin (Lupin).
Injection: 0.6 mg/mL (1 mL ampoule), 1 mg/mL (1 mL ampoule). Eye drops: 0.5%, 1% (cycloplegic), 0.01% (myopia control). Tablets: 0.6 mg (rare oral use). Pre-filled auto-injectors for military use (atropine + pralidoxime combination).
Regulatory status
Atropine is classified under Schedule H in India under the Drugs and Cosmetics Act, 1940. Schedule H prescription drug. Must be available in all emergency departments, ICUs, and operation theatres. Essential in rural India where organophosphorus poisoning is common. NLEM 2022 listed.
Indications
- Symptomatic bradycardia (first-line per ACLS guidelines)
- Organophosphorus and carbamate poisoning (antidote -- muscarinic antagonism)
- Pre-anaesthetic medication (reduces secretions, prevents vagal reflexes)
- Cycloplegic refraction in children (ophthalmology -- 1% eye drops)
- Anterior uveitis (mydriatic to prevent posterior synechiae)
- Myopia control in children (low-dose 0.01-0.05% eye drops -- emerging indication)
- Mushroom poisoning (muscarinic type -- Inocybe, Clitocybe species)
- Cardiac arrest -- asystole and PEA (per ACLS -- use is declining)
Dosing
Bradycardia: 0.5 mg IV every 3-5 minutes (max 3 mg total). OP poisoning: 1-2 mg IV bolus, then double the dose every 5-10 minutes until secretions dry (atropinisation endpoint: dry lungs, HR >80, pupils dilate). Massive OP poisoning may require 50-100+ mg in 24 hours. Pre-anaesthetic: 0.4-0.6 mg IM/IV 30-60 minutes before surgery. Cycloplegic refraction: 1% eye drops TDS for 3 days before examination. Myopia control: 0.01% eye drops once nightly. Children (bradycardia): 0.02 mg/kg IV (min 0.1 mg, max 0.5 mg per dose).
Contraindications
- Narrow-angle glaucoma (mydriasis precipitates acute angle closure -- ABSOLUTE CONTRAINDICATION for systemic and topical ocular use)
- Prostatic hypertrophy with urinary retention (worsens retention)
- Paralytic ileus or intestinal obstruction (reduces motility further)
- Myasthenia gravis (anticholinergic effects can worsen weakness)
- Pyloric stenosis (in neonates -- reduces gastric motility)
- NO contraindication in life-threatening bradycardia or OP poisoning (always give)
Adverse effects
- Tachycardia (most common cardiovascular effect)
- Mydriasis and photophobia (pupil dilation)
- Dry mouth (xerostomia -- salivary gland M3 blockade)
- Blurred vision (cycloplegia -- loss of accommodation)
- Urinary retention (especially in elderly males with BPH)
- Constipation (reduced GI motility)
- Hyperthermia (reduced sweating -- dangerous in children and hot climates)
- CNS effects: confusion, agitation, hallucinations, delirium (antimuscarinic toxidrome -- especially in elderly)
- Flushing ('atropine flush' -- cutaneous vasodilation)
Drug interactions
- Other anticholinergic drugs (TCAs, antihistamines, phenothiazines) -- additive anticholinergic toxicity
- Cholinesterase inhibitors (neostigmine, physostigmine) -- mutual antagonism (physostigmine is used to reverse atropine toxicity)
- Potassium chloride (slow-release) -- anticholinergics slow GI transit, increasing potassium concentration at contact points and risk of GI ulceration
- Pralidoxime -- synergistic in OP poisoning (atropine blocks muscarinic effects; pralidoxime reactivates AChE)
Pregnancy and lactation
Category C. Atropine crosses the placenta. At therapeutic doses, no significant teratogenicity reported. May cause fetal tachycardia. Used when indicated (pre-anaesthetic, emergency bradycardia) during pregnancy and caesarean section. In OP poisoning during pregnancy, atropine must be given regardless -- maternal death is the alternative.
Exam-style clinical scenario
A 35-year-old farmer is brought to the emergency department after ingesting an organophosphorus insecticide. He presents with excessive salivation, lacrimation, urination, defecation (SLUDGE), miosis, bradycardia (HR 40/min), and bronchorrhoea with respiratory distress. What is the emergency management? Answer: (1) ABCs with supplemental oxygen, suction of secretions, (2) IV atropine 2-5 mg bolus, double the dose every 5 minutes until bronchial secretions dry (atropinisation -- the endpoint is DRY LUNGS, NOT heart rate or pupil size), (3) IV pralidoxime (2-PAM) 1-2 g over 15-30 minutes within 24 hours of exposure (reactivates AChE before irreversible ageing), (4) Decontamination: remove clothes, wash skin with soap and water, gastric lavage if <1 hour since ingestion. (5) Atropine infusion 0.5-1 mg/hour may be needed for days. Monitor for intermediate syndrome (days 1-4: proximal muscle weakness, respiratory failure).
Cost in India
INR 5-15 per ampoule (0.6 mg/mL, 1 mL); Eye drops 1%: INR 20-40; Eye drops 0.01% (myopia): INR 200-500
Clinical governance
Author: MedNext Editorial Team. Clinical reviewer: Awaiting clinical review. Jurisdiction: India (Drugs and Cosmetics Act, 1940). Sources: CIMS India, Indian Pharmacopoeia. Publication state: Awaiting clinical review. Correction: Report errors at support@mednext.academy.
Frequently Asked Questions
Why is drying of secretions the endpoint of atropinisation, not heart rate?
In OP poisoning, death occurs from respiratory failure caused by bronchorrhoea (excessive bronchial secretions drowning the lungs) and bronchospasm, not from bradycardia per se. Atropine is titrated to dry the lungs and clear the airway, which is the immediately life-saving effect. Heart rate may increase before secretions are adequately controlled, and pupil dilation is an unreliable indicator of adequate atropinisation. Stopping atropine based on heart rate alone can leave the patient with fatal bronchorrhoea.
What is AChE ageing and why is early pralidoxime important?
After an organophosphorus compound binds to acetylcholinesterase (AChE), the bond initially can be broken by an oxime (pralidoxime), reactivating the enzyme. However, over 24-48 hours (varies by OP compound), one alkyl group is lost from the OP-AChE complex ('ageing'), making the bond irreversible and the enzyme permanently inactivated. New AChE must then be synthesised (takes days to weeks). Therefore, pralidoxime must be given EARLY (within 24 hours, ideally within 6 hours) to be effective.
Why is atropine contraindicated in narrow-angle glaucoma?
Atropine causes mydriasis (pupil dilation) by blocking M3 receptors on the iris sphincter muscle. In patients with narrow anterior chamber angles, mydriasis causes the peripheral iris to bunch up against the trabecular meshwork, physically blocking aqueous humour drainage. This precipitates acute angle-closure glaucoma -- a sudden, severe rise in intraocular pressure causing ocular pain, visual loss, and potential permanent blindness if untreated. Open-angle glaucoma patients can receive atropine safely (the drainage angle is already open and not obstructed by the iris).
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