Mechanism of action
The active substance is a racemic mixture of L- and D-isomers of hyoscyamine (an ester of the alcohol tropine and tropic acid). By chemical structure, it belongs to tertiary amines. Possessing lipophilic properties, atropine easily crosses histohematic barriers, including the blood-brain barrier (BBB), entering the CNS within 30–60 minutes. The drug carries out a non-selective blockade of $M_1$, $M_2$, and $M_3$ muscarinic receptor subtypes, completely eliminating the physiological influence of the parasympathetic nervous system on organs and tissues.
Pharmacological effects
Blockade of M-cholinoreceptors leads to pronounced systemic reactions:
- Secretion: inhibition of salivary, lacrimal, bronchial, and sweat glands (dry mouth and skin develop).
- Organs of vision: pupillary dilation (mydriasis), increased intraocular pressure, and cycloplegia with impaired near vision.
- CVS: development of tachycardia due to the elimination of the inhibitory effect of the vagus nerve on the heart.
- GI tract and urinary system: decrease in intestinal tone and peristalsis, increased sphincter tone, inhibition of the urinary bladder detrusor.
Indications for use
The drug is used in various clinical situations according to approved dosages:
- Orally prescribed at 0.00025–0.0005 g 1–2 times daily 30–40 minutes before meals.
- Parenterally (s.c.) administered in similar doses (0.00025–0.0005 g).
- Intravenous administration is strictly limited to cases of cholinomimetic poisoning.
- In ophthalmology, 0.5–1% solutions (1–2 drops into the conjunctival sac) or 1% eye ointment are used.
Side effects and contraindications
Adverse reactions are a direct pharmacodynamic continuation of the main action: xerostomia, constipation (obstipation), tachycardia, urination disorders.
Contraindications:
- Glaucoma (due to the ability to increase intraocular pressure).
- Benign prostatic hyperplasia (BPH) (risk of acute urinary retention).
- Tachyarrhythmias and severe cardiovascular pathologies.
- Intestinal atony.
Administration features and poisoning
Overdose leads to acute poisoning with marked dryness of mucous membranes, hyperthermia, tachycardia, and "atropine psychosis" (hallucinations, delirium, motor agitation).
Principles of poisoning treatment:
- Pathogenetic therapy with specific antidotes — administration of anticholinesterase agents that cross the BBB (physostigmine, galantamine).
- Detoxification: gastric lavage with potassium permanganate solution, use of tannin or activated charcoal, hemadsorption, and forced diuresis.
- Symptomatic therapy: management of seizures and agitation with diazepam, respiratory support.
Briefly: answers to topical questions
What symptoms are characteristic of the full-blown clinical picture of acute atropine poisoning?
The full-blown picture of acute atropine poisoning includes peripheral and central disorders. There is severe thirst, dryness of mucous membranes and skin, skin hyperemia, hyperthermia, pronounced tachycardia, extrasystole, risk of myocardial ischemia, headache, dizziness, and urinary retention. In severe poisoning, "atropine psychosis" develops with visual and auditory hallucinations, delirium and severe agitation, seizure syndrome, and in the terminal stage — CNS depression and coma.
- Thermoregulation and secretion disorders — skin hyperemia, hyperthermia.
- Cardiovascular disorders — pronounced tachycardia, extrasystole, risk of myocardial ischemia.
- Psychoneurological disorders — visual and auditory hallucinations, delirium, severe agitation, seizure syndrome.
For what purpose is atropine sulfate included in premedication before surgical interventions?
Atropine sulfate is included in premedication before surgical interventions to achieve several effects. The drug prevents vagal bradycardia due to the blockade of cardiac M2-cholinoceptors, reduces the production of saliva and bronchial secretions, reduces the risk of reflex laryngospasm, and also has an antiemetic effect.
- Prevention of reflex cardiac arrest — prevention of vagal bradycardia due to the blockade of cardiac M2-cholinoceptors.
- Reduction of secretion — reduction of saliva and bronchial secretion production.
- Prevention of complications — reduction of the risk of reflex laryngospasm and antiemetic effect.
How does the pharmacokinetics of atropine differ from quaternary ammonium M-cholinoblockers (e.g., ipratropium bromide)?
Atropine is a tertiary amine and a lipophilic nonpolar compound, therefore it rapidly crosses the blood-brain barrier; it enters the CNS within 30–60 minutes. Ipratropium bromide is a quaternary ammonium compound, has low lipophilicity, and poorly penetrates biological membranes upon topical application. Low systemic absorption of ipratropium upon inhalation administration determines the low severity of systemic side effects.
| Property | Atropine | Ipratropium bromide |
|---|---|---|
| Chemical group | Tertiary amine | Quaternary ammonium compound |
| Lipophilicity | Lipophilic nonpolar compound | Low lipophilicity |
| BBB penetration | Rapidly penetrates | Poorly penetrates biological membranes |
| Systemic absorption upon inhalation administration | Not specified in sources | Low |
What are the indications for intravenous administration of atropine in emergency cardiology?
In emergency cardiology, intravenous administration of atropine is used for bradyarrhythmias and conduction disorders. Indications are sinus bradycardia and atrioventricular block of vagal origin, as well as hemodynamically significant sinus bradycardia or atrioventricular block with an inadequate escape rhythm in acute myocardial infarction.
- Sinus bradycardia — including in acute myocardial infarction or of vagal origin.
- Atrioventricular block — when hemodynamically significant and with an inadequate escape rhythm.
- Criteria from the source — heart rate less than 40 bpm and/or pauses greater than 300 ms.
"Red as a beet, dry as a bone, blind as a bat, mad as a hatter, hot as a hare" is a classic mnemonic for atropine overdose symptoms (skin flushing, dryness, mydriasis/cycloplegia, psychosis, hyperthermia).
Class and exam questions
Why is atropine ineffective in eliminating the increase in skeletal muscle tone induced by neostigmine?
Atropine is an exclusively M-cholinergic receptor blocker, whereas skeletal muscle tone is regulated via N-cholinergic receptors, which the drug does not affect.
What is the main mechanism of atropine penetration into the CNS?
Due to its tertiary amine structure and lipophilic properties, the drug easily crosses the blood-brain barrier and causes central nervous system effects.
What detoxification method is effective in severe atropine poisoning besides gastric lavage?
Active detoxification methods such as hemoperfusion and forced diuresis are used, along with the administration of antidotes (physostigmine).
What else to study on this topic
- Comparative pharmacokinetics of atropine and scopolamine (role of pKa and BBB)
- Pharmacological antagonists of atropine (anticholinesterase agents)
- Synthetic and semi-synthetic analogs of antimuscarinic drugs
- Clinical features of antimuscarinic drugs in ophthalmology
- Pathogenesis and clinical staging of belladonna alkaloid poisoning
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