Level 3

non-selective Beta Blocker with no intrinsic sympathomimetic activity.

Racemic mixture with S-isomer confers most effects, R-isomer stops T4 to T3 conversion.

PO, IV
PO: May be enterically coated. sustained release 60-160mg. Immediate release 10-80mg.
IV: significantly smaller due to extensive first pass metab - 20mg/5ml.

It produces decreases
in heart rate and cardiac output and myocardial oxygen consumption

- Rapid withdrawal should be avoided as it may precipitate tachycardia, HTN and/or ischaemia.
- Care should be taken when used in conjunction with opioids and halothane and in patients with obstructive airway disease

bioavailabilty - lipid soluble and well absorbed but has a high 1st pass metabolism leading to a bioavailability of 30%

lipid solubility high lipid solubility

90%

4 L/kg

Hepatic via CYP2D6, and CYP1A2 to 4-hydroxypropranolol
(active) and inactive comp

most metabolites are excreted in urine

3-6 hours

Beta Blocker

- Hypertension
- Angina
- essential tremor
- haemodynamically stable oesophaegeal varices
- migraine prophylaxis
- Treatment of choice in thyrotoxicosis as it treats the effects and prevents conversion of T4 to T3.

Beta blockage leads to ↓Gs activity in receptor associated organs and
associated ↓in adenylyl cyclase and intracellular Ca2+.

oral or IV
doses PO up to 320mg, IV 0.5mg - 10mg titrated to effect

Antiarrhythmic –
Vaughan Williams Class II
Beta blocker

- Hypertension
- Angina
- essential tremor
- haemodynamically stable oesophaegeal varices
- migraine prophylaxis
- Treatment of choice in thyrotoxicosis as it treats the eff¬ects and prevents conversion of T4 to T3.

Beta blockage leads to ↓ Gs activity in receptor associated organs and
associated ↓ in adenylyl cyclase and intracellular Ca2+.

oral or IV
doses PO up to 320mg, IV 0.5mg - 10mg titrated to eff¬ect