Ipratropium bromide

Class Bronchodilator
Chemistry

Quaternary ammonium derivative of atropine

Routes of administration

Nebulised

Absorption

Less than 1% of the inhaled drug dose is absorbed through the bronchial mucosa; minimal oral bioavailability, but because the majority of the administered dose is swallowed 2% of the systemic levels are due to oral absoprtion

Solubility

pKa is 15.3; highly alkaline drug. Insoluble in lipids, but highly soluble in water. Does not pentrate the blood-brain barrier, unlike atropine.

Distribution

VOD is 2.4-4.6 L/kg; about 20% protein-bound

Metabolism

60% is metabolise din the liver into inactive metabolites,and 40% is excreted unchanged in the urine.

Elimination

Half life is similar to atropine (approximately 1.5-3 hours)

Time course of action

Onset is seen within 3-5 minutes of administration, peak response is seen at about 1.5-2 hours, some effect is still seen up to 6 hours after administration.

Target receptor

Non-selective muscarinic receptor antagonist; bronchodilator effect is mainly mediatd by the M3 receptors

Mechanism of action

By blocking the M3 muscarinic receptor, ipratropium prevent the acetylcholine-mediated increase in PIP2 being converted to IP3 and DAG, which lead to calcium release and smooth muscle contraction.  In absence of this stimulus, bronchial smooth muscle runs out of calcium and relaxes.  By a related effect, muscarinic blockade also results in a decrease in bronchial mucus gland secretion.

Clinical effects

Bronchodilation, tachycardia, dry mouth, increased viscosity of airway secretions

Literature reference

Boehringer monograph

CICM details of understanding Level 2
Mentioned around Deranged Physiology
Related SAQs

Question 12 from the first paper of 2019 (vs. salbutamol)