Beta blockers competitively antagonize beta-adrenergic receptors. They differ in beta-1 selectivity, intrinsic sympathomimetic activity, membrane-stabilizing activity, vasodilating properties, lipid solubility and duration of action.

Beta-1 blockade decreases heart rate, contractility, atrioventricular conduction and renin release. Beta-2 blockade can cause bronchoconstriction and reduces glycogenolysis and tremor; chronic cardiac beta blockade also limits maladaptive sympathetic stimulation.

Examples include propranolol, nadolol and timolol as nonselective agents; metoprolol, bisoprolol, atenolol and esmolol as beta-1 selective agents; and carvedilol, labetalol and nebivolol as vasodilating beta blockers.

Uses include ischaemic heart disease, selected tachyarrhythmias, chronic HFrEF with evidence-based agents, hypertension with compelling indications, aortic syndromes, migraine prevention, essential tremor, portal hypertension, glaucoma and symptomatic thyrotoxicosis.

Bradycardia, fatigue, exercise intolerance, hypotension, sexual dysfunction and sleep disturbance may occur. Nonselective drugs can cause bronchospasm and can delay recovery from hypoglycaemia; overdose may cause shock, conduction block, seizures or hypoglycaemia.

Major cautions include severe bradycardia, advanced heart block, cardiogenic shock and acute decompensated heart failure. Nonselective agents are generally avoided in active asthma, and chronic therapy should not be withdrawn suddenly.