Non-selective Beta-Blockers (Propranolol, Timolol)

1701

Summary

Propranolol and timolol are nonselective beta blockers with both beta 1 and beta 2 blocking activity. Blocking of beta-1 receptors reduces cardiac output by slowing down the heart rate and reducing contractility, while beta-2 blockade has minor positive effects and mainly leads to a host of side effects.  These drugs are used for a variety of cardiovascular conditions, including hypertension, angina, and arrhythmia, and heart failure. Common side effects as a result of beta-2 blockade are asthma and COPD exacerbation, as well as hypoglycemia. 

Key Points

  • Nonselective Beta-Blockers
    • Drug Names
      • Propranolol
      • Timolol
      • Nadolol
      • Pindolol
    • Mechanism of Action:
      • Non-selective (beta-1 = beta-2)
        • Beta 1 Blockade → Decreased HR (Chronotropy and Dromotropy) and Stroke Volume (Inotropy) → Decreased Cardiac Output
        • Beta 2 Blockade → Bronchoconstriction, Vasoconstriction
    • Clinical use
      • Decreases myocardial oxygen demand
        • Angina Pectoris
        • Myocardial Infarction
      • Decreased Contractility
        • HCM
          • Decreased contractility decreases the Left Ventricular Outflow Obstruction
      • Decreased AV Nodal Conduction
        • Supraventricular Tachycardia
          • Decreased Dromotropy → Ventricle receives signals more slowly → Rate Control
      • Decreased Renin Release
        • Heart Failure
          • Decreased Renin → Less RAAS-mediated fluid retention → Less Congestion in Body
    • Adverse Effects
      • Erectile Dysfunction, Cardiovascular (Bradycardia, AV Block, CHF), CNS (seizures, sleep alterations)
      • Asthma/COPD Exacerbation
      • Hypoglycemia (Mictlan)
        • AV Block caused by decreased dromotropy, will present with elongated PR Interval (will be discussed alongside Decreased AV Nodal Conduction, does not need separate symbol)
        • Asthma/COPD exacerbation caused by bronchoconstriction
        • Hypoglycemia caused by beta 2 antagonism, leading to decreased hepatic glycogenolysis/gluconeogenesis and also masking of autonomic symptoms of hypoglycemia