| Class | Beta blocker |
|---|---|
| Chemistry |
aryloxypropanolamine |
| Routes of administration |
Oral or IV |
| Absorption |
25% oral bioavailability |
| Solubility |
pKa 9.3, 50% fairly lipid-soluble |
| Distribution |
VOD 3-16 L/kg; 50% protein bound |
| Metabolism |
Mainly hepatic clearance |
| Elimination |
minimal renal excretion; half-life 3-4 hrs |
| Time course of action |
Clinical effects persist for longer than the half life would suggest, because they are mainly determined by drug-receptor affinity |
| Target receptor |
Nonselective β1 and β2 receptor blocker, with some anti-α1 effects and some sodium channel blocker (membrane stabilising) effects |
| Mechanism of action |
By binding to Gs-protein coupled β1 and β2 receptors, blocks cAMP synthesis |
| Clinical effects |
β1 effects: decreased heart rate, decreased contractility, decreased blood pressure, lower myocardial oxygen demand and increased diastolci coronary fillng, and decreased arrhythmogenicity. β2 effects: increased peripheral vascular resistance, bronchospasm, decreased insulin release, increased bladder and uterine tone α1 effects: afterload reduction, vasodilation Membrane-stabilising (sodium channel blocker) effect |
| Literature reference |
Oliver et al (2019) |
| CICM details of understanding | Level 2 |
| Mentioned around Deranged Physiology | |
| Related SAQs |
Question 5 from the first paper of 2022 (labetalol vs. esmolol) |