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Atropine Sulfate

Atropini sulfas

For medical students2 min readUpdated 2026-10-10

Atropini sulfas is a naturally occurring plant alkaloid and the classic non-selective muscarinic receptor antagonist. It blocks the effects of the parasympathetic nervous system, producing a wide spectrum of peripheral and central nervous system effects.

Pharmacological classAutonomic nervous system agents (anticholinergic)

Molecular targetsNon-selective competitive antagonism of M1, M2, and M3 muscarinic receptors

FormulationsPowder, tablets 0.5 mg, 0.1% injection solution, 1% eye drops, 1% ophthalmic ointment

PharmacokineticsElimination half-life (T1/2) is approximately 2 hours

Maximal dosesSingle oral maximum dose 1 mg, daily maximum oral dose 3 mg

Mechanism of Action

Atropine is a racemic mixture of the L- and D-isomers of hyoscyamine (an ester of tropic acid and the base tropine). Chemically, it is a tertiary amine. Due to its high lipophilicity, atropine readily crosses biological barriers, including the blood-brain barrier (BBB), entering the central nervous system within 30 to 60 minutes. The drug acts as a competitive, non-selective antagonist at $M_1$, $M_2$, and $M_3$ muscarinic receptors, completely eliminating the physiological influence of the parasympathetic nervous system on target organs and tissues.

Pharmacological Effects

Muscarinic receptor blockade results in prominent systemic manifestations:

Secretions: Inhibition of salivary, lacrimal, bronchial, and sweat glands, leading to dry mouth (xerostomia) and dry skin.
Eye: Pupil dilation (mydriasis), elevated intraocular pressure, and cycloplegia (paralysis of accommodation leading to blurred near vision).
Cardiovascular system: Tachycardia due to the removal of vagal tone on the sinoatrial node.
Gastrointestinal and urinary tracts: Reduced smooth muscle tone and peristalsis, increased sphincter tone, and relaxation of the detrusor muscle of the urinary bladder.

Indications

Atropine is utilized in various clinical scenarios according to established dosing guidelines:

Oral administration: 0.25–0.5 mg 1–2 times daily, 30–40 minutes before meals.
Parenteral administration (subcutaneous): 0.25–0.5 mg.
Intravenous administration is strictly reserved for cholinergic agonist poisoning (e.g., organophosphate poisoning).
Ophthalmology: 0.5–1% solutions (1–2 drops into the conjunctival sac) or 1% ophthalmic ointment for cycloplegia and mydriasis.

Adverse Effects and Contraindications

Adverse effects represent an extension of the drug's primary pharmacodynamic properties: xerostomia, constipation (obstipation), tachycardia, and urinary retention.

Contraindications:

Glaucoma (due to the risk of precipitating or worsening acute angle-closure via increased intraocular pressure).
Benign prostatic hyperplasia (BPH) (risk of acute urinary retention).
Tachyarrhythmias and severe cardiovascular disease.
Gastrointestinal atonia.

Clinical Considerations and Overtoxicity

Overdose results in acute anticholinergic toxicity characterized by severe mucosal dryness, hyperthermia, tachycardia, and "atropine psychosis" (hallucinations, delirium, agitation).

Management of Overdose:

Pathogenetic therapy with specific antidotes: centrally acting reversible acetylcholinesterase inhibitors such as physostigmine or galantamine.
Decontamination: gastric lavage (with potassium permanganate solution), administration of activated charcoal, hemoperfusion, and forced diuresis.
Symptomatic therapy: control of seizures and agitation with diazepam, and respiratory support.

Mnemonic

"Red as a beet, dry as a bone, blind as a bat, mad as a hatter, hot as a hare" — the classic USMLE mnemonic for anticholinergic toxicity symptoms (flushed skin, anhydrosis/dryness, mydriasis/loss of accommodation, psychosis, and hyperthermia/fever).

Frequently asked questions

What symptoms characterize the full clinical picture of acute atropine poisoning?

The full presentation of acute atropine poisoning involves both peripheral and central manifestations. Typical findings include intense thirst, mucosal and cutaneous dryness, skin flushing (hyperemia), hyperthermia, marked sinus tachycardia, extrasystoles, risk of myocardial ischemia, headache, dizziness, and urinary retention. Severe toxicity leads to "atropine psychosis" with visual and auditory hallucinations, delirium, severe psychomotor agitation, seizures, and in terminal stages, CNS depression and coma.

Thermoregulatory and secretory disturbances — cutaneous flushing, hyperthermia, anhidrosis.
Cardiovascular manifestations — prominent tachycardia, extrasystoles, myocardial ischemia risk.
Neuropsychiatric manifestations — visual and auditory hallucinations, delirium, agitation, seizures.

For what purposes is atropine sulfate included in preoperative premedication regimens?

Atropine sulfate is included in surgical premedication to achieve several goals: it prevents vagally mediated reflex bradycardia by blocking cardiac $M_2$ receptors, decreases salivary and bronchial secretions to reduce the risk of reflex laryngospasm, and provides antiemetic effects.

Prevention of reflex cardiac arrest — blockade of cardiac $M_2$ receptors prevents vagal bradycardia.
Reduction of secretions — decreases saliva and respiratory tract secretions.
Complication prophylaxis — lowers the risk of reflex laryngospasm.

How does the pharmacokinetics of atropine differ from quaternary ammonium antimuscarinics (e.g., ipratropium bromide)?

Atropine is a tertiary amine and a lipophilic uncharged compound, allowing it to rapidly cross the blood-brain barrier within 30–60 minutes. Ipratropium bromide is a quaternary ammonium compound with low lipophilicity, preventing it from readily crossing biological membranes. Low systemic absorption of inhaled ipratropium minimizes systemic side effects.

Property	Atropine	Ipratropium Bromide
Chemical class	Tertiary amine	Quaternary ammonium compound
Lipophilicity	Lipophilic, non-polar compound	Low lipophilicity
BBB penetration	Rapid penetration	Poor penetration across biological membranes
Systemic absorption via inhalation	Not applicable	Low

What are the indications for intravenous atropine administration in emergency cardiology?

In emergency cardiology, intravenous atropine is indicated for symptomatic bradyarrhythmias and conduction blocks. Indications include sinus bradycardia of vagal origin, or hemodynamically significant sinus bradycardia and atrioventricular (AV) block with an inadequate escape rhythm during an acute myocardial infarction.

Sinus bradycardia — including post-myocardial infarction or vagally induced.
Atrioventricular block — when hemodynamically significant with an inadequate escape rhythm.
Clinical thresholds — heart rate below 40 bpm and/or pauses greater than 300 ms.

Why is atropine ineffective at reversing skeletal muscle hypertonia induced by neostigmine?

Atropine is an antagonist exclusively for muscarinic receptors (M-receptors), whereas skeletal muscle tone is regulated via nicotinic receptors (N-receptors at the neuromuscular junction), which atropine does not affect.

What is the primary mechanism by which atropine enters the CNS?

Because of its tertiary amine structure and high lipophilicity, atropine readily crosses the blood-brain barrier to produce central nervous system effects.

What active decontamination methods are used in severe atropine poisoning alongside gastric lavage?

Active detoxification modalities include hemoperfusion and forced diuresis, as well as the administration of specific antidotes such as physostigmine.

Go deeper

Comparative pharmacokinetics of atropine and scopolamine (role of pKa and the BBB)
Pharmacological antagonists of atropine (anticholinesterase agents)
Synthetic and semi-synthetic analogs of muscarinic antagonists
Ophthalmic applications of antimuscarinics
Pathogenesis and clinical staging of belladonna alkaloid poisoning