Is atropine less anticholinergic?

Atropine's Anticholinergic Properties

Atropine is a potent anticholinergic agent that exerts strong parasympatholytic activity by competitively antagonizing muscarinic acetylcholine receptors. 1

Mechanism of Action

• Atropine functions as an antimuscarinic agent by antagonizing the muscarine-like actions of acetylcholine and other choline esters 1
• It inhibits muscarinic actions of acetylcholine on structures innervated by postganglionic cholinergic nerves and on smooth muscles that respond to endogenous acetylcholine 1
• The primary mechanism is a competitive antagonism at muscarinic receptors, which can be overcome by increasing acetylcholine concentration at receptor sites 1

Anticholinergic Effects

• Atropine exerts potent and prolonged effects on heart, intestine, and bronchial muscle compared to other anticholinergic agents 1
• It produces significant parasympathetic inhibition that may initially be preceded by a transient phase of stimulation, particularly on the heart 1
• Small doses first slow the heart rate before characteristic tachycardia develops due to vagal control paralysis 1
• Adequate doses of atropine abolish various types of reflex vagal cardiac slowing or asystole 1

Clinical Applications

• Atropine is the first-line drug for acute symptomatic bradycardia, particularly in sinus bradycardia with associated reduced cardiac output and signs of peripheral hypoperfusion 2
• It is particularly useful for treating symptomatic sinus bradycardia within 6 hours of onset of acute myocardial infarction symptoms 2
• The recommended dosage for bradycardia is 0.5 mg intravenously, repeated if needed every 5 minutes to a total dose of no more than 2 mg 2
• For ventricular asystole, the recommended dose is 1 mg intravenously, repeated in 5 minutes if asystole persists 2

Precautions and Side Effects

• Doses less than 0.5 mg may paradoxically result in further slowing of the heart rate due to parasympathomimetic response 2, 3
• Atropine should be used with caution in acute myocardial infarction because parasympathetic tone has a protective effect against ventricular fibrillation and myocardial infarct extension 2
• Atropine is ineffective in patients who have undergone cardiac transplantation without evidence of autonomic reinnervation 2, 3
• Avoid relying on atropine in type II second-degree or third-degree AV block with a new wide-QRS complex where the block is likely in non-nodal tissue 2

Comparison with Other Anticholinergics

• Anticholinergic agents like ipratropium and oxitropium have a slower onset of action (30-90 minutes) compared to β2-agonists (minutes) 2
• Anticholinergic agents are more effective in COPD than in asthma 2
• No evidence has been found of tolerance to anticholinergic drugs during chronic therapy, unlike with β2-agonists 2
• Anticholinergic agents have fewer adverse effects compared to β2-agonists, which may cause a fall in PaO2 due to pulmonary vascular effects 2

Special Considerations

• Atropine is rapidly distributed throughout the body after injection, with exercise increasing its absorption due to increased muscle perfusion 1
• The pharmacokinetics of atropine is nonlinear after intravenous administration 1
• Atropine's onset of action after IV administration is within 3 minutes, with maximum effect observed within this timeframe 3
• Systemic absorption can occur even with topical administration, such as ophthalmic drops, potentially resulting in anticholinergic toxidrome symptoms 4

In conclusion, atropine is not less anticholinergic; it is actually one of the more potent anticholinergic agents available, with strong effects on heart rate, bronchial smooth muscle, and other parasympathetically innervated tissues.