Low doses (2mcg/kg) act centrally and may augment vagal outflow, ↓ HR
Normal 15-70mcg/kg also acts on periph muscarinic receptors blocking the action of the vagal nerve and ↑ HR & pupil size whilst ↓ secretory gland activity. cholinergic poisoning to ↓ bronchorrhoea& bronchoconstriction. Other eff¬ects: ↓ tone in the gut, bile
ducts, and contractions in the ureter and bladder

competitive antagonism at peripheral muscarinic receptors. More potent antagonism than atropine. Minimal anti-nicotinic effects, but more than atropine

CVS
- In low doses may produce a bradycardia (Bezold-Jarisch reflex, partial agonist at M2) followed by tachycardia (usual effect
- Cardiac output is increased with little effect on blood pressure
- Decreases AVN conduction time and may promote arrhythmias

Resp
- Bronchodilation with increase in physiological dead space
- Bronchial secretions decrease
- RR increased
- Decreased laryngospasm has been reported

CNS
- Central depression or excitation may occur (anticholinergic syndrome)- characterized by hallucinations, agitation, confusion, dysarthria, ataxia, delirium
- Has antiemetic and antiparkinsonian effects

GIT
- Decreased salivation
- Decreased GIT motility
- Antispasmodic in biliary tree
- Decreased LOS tone

GU- Tone and peristalsis in urinary tract decreased

Metabolic/other
- Sweating inhibited (children may develop pyrexia)
- BMR increased
- Suppresses ADH release

CVS: Tachycardia. Little effect on BP. Less arrhythmias than atropine. Vagolytic effects last 2-3 hours.

CNS: Does not cross BBB. No effect on pupils.

Resp: Bronchodilator. May increase dead space. Decreased bronchial secretions.

Renal: Difficulty micturition

GIT: Decreased salivation (8 hours). Decreased LOS.

Other: Inhibition of sweating but generally no effect on body temperature.

Rapidly absorbed from the gastrointestinal tract with oral bioavailability about 10-25%. After intramuscular administration, peak concentration is reached at about 30 minutes. Intravenous administration bypasses absorption.

poor oral absorption F 5%

Crosses BBB and placenta

Rapid redistribution (90% disappears from plasma at 5 min)
- Crosses placenta
- Does not cross BBB

Approximately 50% protein-bound in plasma.

1-2 L/kg rapidly distributed from central compartment

Vd 0.2-0.6L/Kg

Hepatic metabolism to several metabolites; enzymatic hydrolysis contributes importantly to elimination.

Limited

Predominantly urinary; approximately 30–50% of a dose may be excreted unchanged.

85% urine, 15% bile (80% unchanged)

Plasma half-life approximately 2–3 hours after parenteral administration.

T1/2 of 1 hour

Although less pronounced than scopolamine (hyoscine) high doses and overdosage of atropine may cause a central anticholinergic syndrome characterised by
excitement, hallucinations and hyperpyrexia. In overdosage this leads to coma,
respiratory depression and death

- Tachycardia
- Dry mouth
- Urinary retention
- Inhibition of sweating

Tertiary alkaloid supplied as a racemic mixture. Antimuscarinic activity is predominantly due to the L-enantiomer.

Quaternary amine derivative of atropine

Muscarinic antagonist

Antimuscarinic

Treatment of bradycardia, antagonism of muscarinic effects from anticholinesterase drugs, treatment of organophosphate poisoning, management of oculocardiac reflex crises, and ophthalmic mydriasis or cycloplegia. Tetanus is also listed in the legacy source.

- Protect against antimuscaranic effects when Acetylcholinesterase inhibitor used
- Treatment of bradycardia
- Hyperhydrosis
- Symptom control in palliative care

anticholinergic activity

Level 1

Level 2

onset / duration rapid / 1-2 hours

Clear, colourless atropine sulfate solution for injection. The referenced text lists 0.5-0.6 mg/mL and 3 mg in 10 mL preparations, with 0.6 mg tablets also described.

Clear solution for injection or in combination with neostigmine

Intramuscular or intravenous administration: 0.015-0.02 mg/kg in the referenced text. Adult oral dose 0.2-0.6 mg. A total dose of about 3 mg is described for complete vagal blockade in adults.