Level 1

anticholinergic activity

onset / duration rapid / 1-2 hours

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

Crosses BBB and placenta

Antimuscarinic

- Treatment of bradycardia
- Counter muscarinic effects of anticholinesterase agents
- Treatment of organophosphate poisoning
- Tetanus
- Treatment of occulocardiac reflex crises

Prototypical tertiary alkaloid

Racemic mixture but only L-atropine is active
Clear, colourless solution for injection (0.5 or 0.6mg/ml)

Competitive antagonism of acetylcholine at muscarinic receptors. Little effect on nicotinic receptors except in high doses.

- Painful IM
- Dry mouth
- Central anticholinergic syndrome in the elderly
- Hyperpyrexia in children (inhibition of sweating)
- Urinary retention
- Glaucoma from ocular (but not intravenous or intramuscular)
administration.

Rapidly absorbed orally but bioavailability is 10-25%

50% PB

Vd 2-4L/kg.

Hydrolyzed in liver and tissues to tropine and tropic acid

94% excreted in urine in 24 hours

T1/2 is 2.5hours

Onset in 2-4 min, duration of up to 3 hours

Muscarinic antagonist

used to antagonize muscarinic e¬ffects produced by AChE drugs, Mx of intraop bradycardia during GA, or Rx and Dx of Organophosphate
poisoning.
Ophthal: to induce mydriasis and cycloplegia to aid
examination

anticholinergic activity is primarily due to the L enantiomer although it is presented as a racemic mixture.

IV.
Although previously available in oral formulations, it is only available for topical application to the eye.

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

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

IV

50%

1-2 L/kg rapidly distributed from central compartment

extensively metabolised by liver esterases

urine (fraction unchanged)

h 2-3 hours

IV. doses 15-70 mcg/kg