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Beta blocker antidote glucagon
Beta blocker antidote glucagon






  • Consider checking acetaminophen and salicylate levels if coingestion is possible.
  • Consider checking TSH, Lyme serology (if no definite history of medication ingestion).
  • Digoxin level, for patients taking digoxin.
  • Chemistries (including Ca, Phos, & Mg).
  • Fingerstick glucose if altered mental status.
  • BBl with sodium channel blockade activity may also cause QRS widening, tall R-waves in aVR, and a Brugada pattern.
  • Any BBl or CCB may cause bradycardia and various heart blocks.
  • History & physical examination (focusing on medication list and access to various substances).
  • Some investigations to consider may include: The differential diagnosis of bradycardia is listed here.Įvaluation will depend on the clinical context.
  • (4) Peripheral vasodilators (betaxolol, bucindolol, carteolol, carvedilol, celiprolol, labetalol, nebivolol) may cause hypotension due partially to peripheral vasodilation.
  • (3) Cardiac potassium channel blockade (acebutolol, sotalol) may prolong the QTc and cause torsade de pointes.
  • Hypotension can be more severe than one would expect, based solely on the degree of bradycardia.
  • (2) Cardiac sodium channel blockade (acebutolol, betaxolol, carvedilol, oxprenolol, pindolol, propranolol) – may cause QRS widening and monomorphic VT.
  • (1) Lipophilic agents (e.g., propranolol) are more likely to enter the brain and cause delirium or seizure.
  • Higher doses: will affect heart as well (vasodilation combined with bradycardia).
  • Lower doses: can cause a primarily vasodilatory shock state (hypotension with reflex tachycardia).
  • However, at high doses they lose selectivity for the vasculature and suppress the myocardium.
  • Dihydropyridine CCBs (e.g., nifedipine, isradipine, amlodipine, felodipine, nimodipine) initially cause vasodilation.
  • Presentation is marked by early development of hypotension and bradycardia.
  • Nondihydropyridine CCBs (verapamil and diltiazem): Cause myocardial suppression more than vasodilation.
  • Neurologic: Delirium, seizure, coma (may result from brain hypoperfusion, or may be due to lipophilic beta-blockers see below).
  • beta blocker antidote glucagon

    💡 In an undefined intoxication with bradycardia and hypotension, the glucose may provide a clue pointing to either CCB or BBl intoxication.CCB poisoning usually causes hyperglycemia, whereas BBl poisoning may cause hypoglycemia.Cardiovascular: Bradycardia, hypotension, and shock are common.Extended-release formulations or sotalol may present later, with deterioration occurring within 24 hours.

    beta blocker antidote glucagon beta blocker antidote glucagon

    Ingestion of immediate-release formulations should cause clinical deterioration within ~6-8 hours.Onset of symptoms depends on the medication and formulation:.Other issues that may require treatment.








    Beta blocker antidote glucagon