Beta blockers competitively antagonise beta adrenoceptors throughout the body including the heart, peripheral vasculature, bronchi, pancreas, uterus, kidney, brain and liver. They are used in a range of cardiovascular conditions, including ischaemic heart disease (stable angina, post–myocardial infarction), heart failure, arrhythmias and hypertension.

Beta blockers are also used in the prevention of migraine, although their precise mechanism of action is unknown. Propranolol, atenolol and metoprolol appear to be equally effective in migraine prophylaxis.

Propranolol is used to treat the motor effects of antipsychotic-induced akathisia and prominent sympathetic symptoms of acute anxiety disorder and social phobia (social anxiety disorder). It does not directly influence the psychic aspects of anxiety.

Beta blockers reduce blood pressure by reducing cardiac output without a reflex increase in peripheral vascular resistance; they also exert effects on the central nervous system to reduce blood pressure and reduce renin secretion. Beta blockers reduce myocardial oxygen demand by lowering heart rate, blood pressure and cardiac filling pressure, which contributes to the benefits seen in angina.

There is considerable heterogeneity within the class, and not all beta blockers are suitable for use across all cardiovascular conditions. This may be reflected in their marketed indications.

Beta blockers competitively antagonise beta adrenoceptors. Beta adrenoceptors are further characterised as beta1 and beta2 subtypes. Beta1-selective beta blockers (atenolol, metoprolol, bisoprolol) have a higher affinity for beta1 adrenoceptors in the heart, with less effect on beta2 adrenoceptors in the bronchi and peripheral vasculature. However, beta1 selectivity is relative and does not confer complete protection against the adverse effects of beta2 blockade. This is the reason for the absolute and relative contraindications noted below.

Oxprenolol and pindolol have intrinsic sympathomimetic activity (ISA) and cause less bradycardia for a given effect on blood pressure, and are less likely to alter lipid profiles than other beta blockers.

Labetalol and carvedilol block both alpha and beta adrenoceptors, which provides additional arteriolar vasodilating action. Labetalol has a higher ratio of alpha1 blockade to beta blockade than carvedilol (but still relatively low) and may be more prone to produce hypotension. Bisoprolol does not have significant vasodilating properties. Carvedilol, bisoprolol, and controlled release metoprolol succinate have similar efficacy in heart failure.

Esmolol and sotalol are commonly, but not exclusively, used for the treatment of cardiac arrhythmias. In addition to beta blockade, sotalol has class III antiarrhythmic effects Sotalol accumulates in renal impairment, so consider decreasing the dosing frequency. Esmolol has a very short duration of action and is only available in a parenteral form.

Asthma remains a contraindication to the use of any of the beta blockers. Peripheral vascular disease is not an absolute contraindication to beta1-selective beta blockers (atenolol, metoprolol, bisoprolol), but caution is required in patients with severe disease. Nonselective beta blockers (eg propranolol) should be strictly avoided in patients with either asthma or peripheral vascular disease.

Atenolol and sotalol are excreted by the kidney, and dosage reduction may be required in patients with impaired renal function.

Metoprolol and propranolol are metabolised by the cytochrome P450 enzyme system, with potential clinically significant interactions.

Abrupt withdrawal of beta blockers can cause a rebound phenomenon that may exacerbate angina and cause rebound hypertension, myocardial infarction or ventricular arrhythmias. Reduce the dose of beta blockers gradually over 8 to 14 days

Important adverse effects of beta blockers include nausea, bronchospasm, dyspnoea, lethargy, depression, exacerbation of Raynaud's syndrome, claudication, cold extremities, heart failure, heart block, hypotension, decreased exercise tolerance, occasional central nervous system symptoms including insomnia and nightmares, and alteration of lipid metabolism, which is possibly less marked with beta1-selective drugs and those with intrinsic sympathomimetic activity (ISA). Beta blockers can predispose to hypoglycaemia, and prolong or delay recovery response to hypoglycaemia in patients with diabetes treated with insulin. Some signs of hypoglycaemia, such as tachycardia and tremors, may be blunted by beta blockers, but other signs such as hunger, irritability and nausea may be unaffected, and sweating can even be increased