Beta-Blocker Poisoning



Normal Physiology
  • Cardiovascular: β1-receptors:
    • ATP converted to cAMP by adenyl cyclase with stimulation of β-receptors
    • cAMP activates protein kinase, which phosphorylates proteins of the sarcoplasmic reticulum
    • Sarcoplasmic reticulum releases calcium
    • Excitation–contraction coupling occurs
  • Effects of β-blockers:
    • Cardiovascular:
      • Decreased excitation/contraction
      • Membrane stabilizing activity
      • Sodium channel blockade causes a prolongation of the QRS complex (with some agents)
      • Prolongation of QTc interval leading to ventricular dysrhythmias (with some agents)
      • Intrinsic sympathomimetic activity
      • Partial agonist properties (with some agents)
    • Neurologic:
      • CNS effects with the lipophilic agents (propranolol, metoprolol, labetalol)

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