Beta Blockers
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Beta blockers are competitive inhibitors of beta-adrenergic receptors. There are many kinds of vary half lives and lipid solubility.
They are used mainly as anti-arrhythmic agents, but are also commonly used as secondary prevention in myocardial infarction, and as anti-hypertensives.
They are also used to treat glaucoma as they reduce aqueous humour secretion.


  • AFoften first line in acute AF. Bisoprolol, atenolol or metoprolol may be used orally, or if IV is required, metoprolol (NB much smaller doses than orally!) or the short acting esmolol are useful
  • Heart Failureusing beta blockers in heart failure due to systolic dysfunction reduces mortality and hospital admission. Carvedilol, metoprolol and bisoprolol are recommended. However, initiation of therapy should be cautious, and is usually started in patients after an acute episode, when signs of fluid retention have resolved, but before discharge from hospital.
    • When used in conjunction with an ACE-inhibitor, beneficial effects are increased. ACE-inhibitor therapy should be started first.
  • Anginahighly effective at reducing symptoms but there is no evidence to suggest they reduce mortality or improve outcomes. All patients with stable angina should be on long-term beta blocker therapy, and cardioselective agents – such as atenolol or metoprolol are recommended
  • MI – secondary prevention – all patients with an MI (including ST elevation and non-ST elevation) should be started on a beta blocker to reduce the risk of short term complications and improve long-term survival.
  • Hypertensionmost guideline now only suggest to use if other methods have been unsuccessful, and to use in conjunction with other agents
  • Migrainepropranolol is often used as a regular medication and reduces the frequency of attacks.



  • Limit the action of the sympathetic nervous system and the fight or flight response
  • Beta-blockers bind to beta-adrenergic receptors, and prevent the action of endogenous catecholamines, adrenaline and noradrenaline
  • Beta-blockade causes a reduction in the circulation of intracellular cAMP. This, in turn reduces the flow of sodium and calcium across the cell membrane, which reduces cardiac contractility and suppresses cardiac pacemakers, particularly the AV node, reducing heart rate
  • There are three types of beta receptors, β1, β2, and β3.
    • β1 are mainly in the heart
    • β2 are mainly in the heart and the bronchial and peripheral vascular smooth muscle
    • β3 are in the heart and adipose tissue
  • Beta-blockers can generally be divided into cardioselective  – mainly β1 activity – e.g. metoprolol, atenolol and noncardioselective – which have β1 and β2 activity e.g. propranolol
  • Antihypertensive effects of beta blockers are not well understood buy may be reduced to a combination of reduced heart rate, reduced contraction strength, and reduced secretion of rennin by the kidney
  • Anti-anginal effects occur due to the reduced workload on the heart induced by reducing rate and contractility.
  • Effects on glucose and lipid metabolismcaused by non-selective agents. These can impair gluconeogenesis and decrease insulin release


Normal Physiology

  • Beta receptors, when stimulated, have a positive inotropic (increase the contractility of the heart) and chronotropic (increase the heart rate) effect
  • Thus, when blocked, the heart is slowed, and strength of contractions reduced
  • However, beta blockers have minimal effects on resting heart function in healthy individuals, and instead, block the effects of the sympathetic nervous system, aka the fight or flight response


Absorption and bioavailability

  • Most beta-blockers are well absorbed and peak concentrations occur about 1-3 hours after ingestion
  • The half lives of beta-blockers are variable, but most have a half life of 3-10 hours. Esmolol is notable as being particularly short acting, it has a half life of about 10 minutes. Nadolol has a half life of about 24 hours.



  • Most are metabolised by the liver, and in particular by the cytochrome P450 enzyme. Genetic variability of expression of the enzyme accounts for most of the variability of duration of half-life seen in patient with beta blockers
  • Liver disease can prolong half life
  • A notable exception is Nadolol with is excreted unchanged in the kidneys. Renal disease may further prolong its long 24-hour half life


Adverse Effects

  • Bradycardia
  • Hypotension
  • Orthostatic hypotension
  • Bronchospasm
  • Cold extremities
  • Fatigue
  • Dizziness
  • Alternation of glucose and lipid metabolism due to effects on the liver
  • Heartblock



  • Bradycardia
  • First degree AV node block
  • Peripheral vascular diseaseuse with caution – can cause peripheral vasospasm. Should also be avoided in Raynaud’s phenomenon for the same reason
  • Poorly controlled asthma – can cause bronchospasm. Consider the use of beta1-selective beta-blockers in anyone with asthma (e.g. metoprolol)
  • Pregnancyavoid atenolol as can cause fetal growth retardation. Labetolol and oxprenolol are likely safe



Look out for:

  • Bradycardia
  • Hypotension
  • Prolonged QRS
  • Ventricular arrhythmias (particularly with propranolol and acebutolol)
  • Rarer features:

As well as general acute management, as you would of any other sick patient, get an ECG, and consider giving IV glucagon, which is considered to be the ‘antidote’. Usually a 5mg bolus is given, and if BP does not increase, a further 5mg can be given after 10 minutes.
Consider giving prophylactic antiemetic (e.g. ondansetron) as IV glucagon often causes vomiting.
The evidence for glucagon is not very strong. There are lots of case reports, but not proper controlled trials.


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Dr Tom Leach

Dr Tom Leach MBChB DCH EMCert(ACEM) FRACGP currently works as a GP and an Emergency Department CMO in Australia. He is also a Clinical Associate Lecturer at the Australian National University, and is studying for a Masters of Sports Medicine at the University of Queensland. After graduating from his medical degree at the University of Manchester in 2011, Tom completed his Foundation Training at Bolton Royal Hospital, before moving to Australia in 2013. He started almostadoctor whilst a third year medical student in 2009. Read full bio

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