9.14 SFGH pearls: Bradycardia and med effects!

  • Timolol, though used as an eye drop for glaucoma, does have some systemic absorption and effects and can cause bradycardia and bronchospasm.
  • *Molecular medicine pearl – Why is glucagon the treatment for beta blocker overdose, you might ask? Remember from med school that beta receptors are coupled to G-proteins, which activate cAMP formation from ATP – this process is inhibited beta blockers. Glucagon activates adenylate cyclase at a different site than beta receptors, which causes an increase in cAMP. The cAMP elevation the increases the intracellular calcium pool for release during depolarization to increase contractility.
    • Because of this pathophys, calcium can also be a helpful adjunct in beta blocker toxicity
    • Tachyphylaxis will develop to glucagon, so it cannot be use for prolonged treatment
    • If possible pre-treat with anti-emetics before giving glucagon, as it causes severe nausea and vomiting
    • Rivastigmine is an acetylcholinesterase inhibitor used to treat moderate Alzheimer’s dementia and nausea and vomiting are well-known side effects. It is known to increase vagal tone and can provoke bradycardia and heart block even in patients with no history of conduction disease.

Evernote link here: https://www.evernote.com/shard/s300/sh/df6b660e-708d-44b8-8bd4-28daa9b15364/8b04dbd866562061e298a6448c36e621

Bailey B. Glucagon in beta-blocker and calcium channel blocker overdoses: a systematic review. J Toxicol Clin Toxicol 2003; 41:595.

Lee J. Glucagon use in symptomatic beta blocker overdose. Emerg Med J 2004; 21:755.

Rösler M, Anand R, Cicin-Sain A, et al. Efficacy and safety of rivastigmine in patients with Alzheimer’s disease: international randomised controlled trial. BMJ 1999; 318:633.

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