|Reviewed by Dr Patricia Clarkson, Dr Jon Skinner, Brenda Hughes, Cherry Olsen, Lijla Brkic|
|Caffeine||An increase in propranolol dose may be required. No clear evidence for this|
|Chlorpromazine||Possible hypotension. (Both drugs inhibit hepatic metabolism of each other)|
|Digoxin||May lead to bradycardia|
|Insulin||Potential for severe, prolonged hypoglycaemia (reported in adult diabetics ).|
|Phenobarbitone||May require increase in propranolol dose. (Increase in metabolism and clearance may occur)|
|Rifampicin||May require increase in propranolol dose. (Increase in hepatic metabolism)|
|Theophylline||Increase in theophylline levels possible|
|Thyroid hormones||Altered levels of triodothyronine, T3 and thyroxine may occur – monitor.|
|Flecainide||Possible additive negative inotropic effect. Cardiac depression may occur|
|Verapamil||Contraindicated in combination with a beta-blocker (negative inotropic effect)|
Propranolol is a non-selective beta-blocker acting on both β1 (mainly heart) and β2 (bronchial tissue) receptors. Blockade of β2 receptors may result in bronchospasm in some patients. Propranolol has membrane stabilising properties in high doses. It does not have intrinsic sympathomimetic activity (ISA). It exhibits a negative inotropic effect.
Propranolol is almost completely absorbed from the GI tract (adults) and there is significant first pass metabolism and hepatic tissue binding with up to 90% of an oral dose being eliminated. At least one metabolite shows biological activity but the effect on overall activity is unknown. Metabolites and a small amount of unchanged propranolol are excreted in the urine. Propranolol is highly protein-bound (80-95%). It is widely distributed throughout the body with highest levels occurring in the lungs, kidney, brain and heart.