Please email me with any suggestion at Seger, MD The blood pressure was subsequently stabilised by continuous glucagon infusion with the aid of an insulin-dextrose drip. I am interested in any questions you would like answered in the Question of the Week. This question prepared by: Cosby Arnold MD, UT Emergency Medicine Resident "Treatment of poisoning caused by beta-adrenergic and calcium-channel blockers." Am J Health Syst Pharm 63(19): 1828-1835. Goldfrank's toxicologic emergencies 9th edition (McGraw-Hill Education, New York, 2011). "Calcium channel antagonist and beta-blocker overdose: antidotes and adjunct therapies." Br J Clin Pharmacol 81(3): 453-461. Current definitive treatment for these patients involves intravenous glucagon therapy, and as such, glucagon is considered both a first-line treatment and an. "Pharmacology, pathophysiology and management of calcium channel blocker and beta-blocker toxicity." Toxicol Rev 23(4): 223-238. Glucagon may also be considered in other cases of drug-induced bradycardia.ĭeWitt, C.R. Current definitive treatment for these patients involves intravenous glucagon therapy, and as such, glucagon is considered both a first-line treatment and an antidote in cases of symptomatic. Glucagon has a short half-life and the bolus should be followed by a continuous infusion at 3-5 mg/hr. Symptomatic beta blocker overdose is a relatively uncommon, but potentially life-threatening condition (Sheppard, 2006 Health Protection Agency, 2010). Giving the bolus more quickly increases risk for vomiting. We recommend giving glucagon as a 10 mg bolus over 10 minutes. Glucagon binding to these receptors results in increased adenylyl cyclase activity independent of β-receptor activity. Similar to β-receptors, cardiac glucagon receptors are coupled to Gs proteins. Glucagon, a polypeptide counterregulatory hormone secreted from the pancreatic α-cells, bypasses β-receptors to exert inotropic and chonotropic cardiac effects. β1-receptor antagonism results in decreased calcium entry and, subsequently, decreased inotropy and chronotropy. These receptors normally act through a second messenger system (Gs proteins*) to activate adenyl cyclase (AC) and increase cyclic AMP (cAMP), which results in the influx of intracellular calcium through L-type calcium channels. Beta blockers competitively inhibit myocardial β1 receptors. Implications for the Pharmacist The doses of glucagon necessary for the management of -blocker or CCB toxicity are much higher than those typically used to induce hyperglycemic or antispasmodic.