| Class | Beta blocker |
|---|---|
| Chemistry |
aryloxypropanolamine |
| Routes of administration |
Oral or IV |
| Absorption |
50% oral bioavailability |
| Solubility |
pKa 9.7, poor lipid solubility |
| Distribution |
VOD 2.8-4.8 L/kg; only 12% 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 |
Selective β1 receptor blocker |
| Mechanism of action |
By binding to Gs-protein coupled β1 receptors, blocks cAMP synthesis |
| Clinical effects |
β1 effects: decreased heart rate, cdecreased contractility, decreased blood pressure, lower myocardial oxygen demand and increased diastolci coronary fillng, and decreased arrhythmogenicity. |
| Literature reference |
Oliver et al (2019) |
| CICM details of understanding | Not specifically listed in the CICM syllabus |
| Mentioned around Deranged Physiology | |
| Related SAQs |