β-blockers are competitive (often highly selective) antagonists of β-adrenoreceptors. They are sub-classified into into selective and non-selective agents:

  • Selective (β1 antagonism) (BEAM)
    • Bisoprolol
    • Esmolol
    • Atenolol
    • Metoprolol
  • Non-selective (β1 and β2 antagonism)
    • Propranolol
    • Sotalol
    • Timolol
  • Non-selective (β & α antagonism)
    • Carvedilol
    • Labetalol


  • Cardio
    • Angina
    • Arhythmia
      • Rate-control in AF
      • Paroxysmal SVT
      • Sinus tachycardia from ↑ catecholamines
    • Cardiac Failure
    • Secondary prevention for MI
  • Vascular
    • Hypertension (2nd line)
      Also useful for aggressive control of BP.
    • Hypotensive anaesthesia
    • Attenuate hypertensive response to laryngoscopy
  • Non-CVS
    • Thyrotoxicosis
    • Glaucoma (topically)
    • Anxiety
    • Migraine prophylaxis

Common Features

Property Action
Kinetics Variability primarily due to lipid solubility. Poor lipid solubility confers poor gut absorption and minimises need for hepatic metabolism. Lipid soluble agents will have CNS effects and be excreted in breast milk.
Respiratory Bronchospasm.
CVS ↓ Inotropy, ↓ HR, ↓ MVO2, ↓ BP, ↑ SVR2 effect), worsen arrhythmia.
CNS Tiredness, nightmares, and sleep disturbance with lipid soluble agents. ↓ IOP.
Metabolic ↓ Insulin release and blunted hypoglycaemic response (β2 effect).
Interactions Contraindicated with cardioselective Ca2+ channel blockers. due to extreme ↓ HR & ↓ inotropy.

Comparison of Beta Blockers

Property Esmolol Metoprolol Atenolol Propranolol Labetalol
Class Cardioselective Cardioselective Cardioselective β non-selective Non-selective β & selective α1
Ratio of β:α antagonism is 3:1 after PO and 7:1 after IV administration
Uses Short-term treatment of tachyarrhythmia and HTN MI, HTN, migraine, thyrotoxicosis HTN, angina, tachyarrhythmias, acute MI HTN, Angina, dysrhythmia, essential tremor, anxiety HOCM, phaeochromocytoma, migraine, oesophageal varices HTN, MI
Presentation Clear, colourless solution Clear, colourless solution, 50mg Tablet. 25/50/100mg tablets, syrup, colourless solution. Tablets and solution at Tablets and solution at
Route of Administration IV PO/IV PO/IV PO/IV PO/IV
Dosing 50-200μ IV: 1mg boluses PO: 12.5-100mg BD PO: 50-100mg daily IV: 2.5mg IV up to 10mg PO: 10-100mg BD/TDS IV: 1mg boluses titrated to response PO: 100-800mg BD
IV: 10-20mg IV bolus, followed by 20-80mg Q30min up to 300mg. Alternatively by infusion at 1-2mg.min-1
Absorption IV only 50% bioavailability, improves with regular use 45% PO bioavailability 30% bioavailability Highly variable bioavailability: 10-80%
Distribution 60% protein bound 20% protein bound. Lipid soluble 5% protein bound 95% protein bound 50% protein bound
Metabolism RBC esterases to an inactive metabolite and methyl alcohol. t1/2 of 10 minutes Hepatic with genetic variability in t1/2 of active metabolites Minimal metabolism - dose reduce in renal failure Hepatic to active and inactive metabolites Considerable hepatic first pass metabolism with inactive metabolites
Elimination Renal elimination of active drug Renal elimination of metabolites Renal elimination of inactive metabolites
CVS Venous irritant SVR, ↓ BP. Does not tend to ↓ HR or ↓ CO when given acutely.
CNS Orthostatic dizziness


  1. Leslie RA, Johnson EK, Goodwin APL. Dr Podcast Scripts for the Primary FRCA. Cambridge University Press. 2011.
  2. Peck TE, Hill SA. Pharmacology for Anaesthesia and Intensive Care. 4th Ed. Cambridge University Press. 2014.
  3. Smith S, Scarth E, Sasada M. Drugs in Anaesthesia and Intensive Care. 4th Ed. Oxford University Press. 2011.
  4. MacCarthy EP, Bloomfield SS. Labetalol: a review of its pharmacology, pharmacokinetics, clinical uses and adverse effects. Pharmacotherapy. 1983. Jul-Aug;3(4):193-219.
Last updated 2019-07-18

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