What is the first-line treatment for addressing acute severe beta-blocker toxicity?

In cases of acute severe beta-blocker toxicity, the first-line treatment focuses on addressing the underlying pathophysiological effects of beta-blockade, which often manifest as bradycardia and hypotension. While atropine can be used to manage bradycardia by increasing heart rate, it is not typically considered the most effective or reliable initial treatment in severe cases.

The management of beta-blocker toxicity is more effectively handled with a continuous glucagon infusion. Glucagon serves a dual purpose: it can increase heart rate and myocardial contractility by activating adenylate cyclase and raising cyclic AMP levels. This mechanism bypasses the beta-receptor blockade and could significantly improve hemodynamic status in patients experiencing severe bradycardia or lowered cardiac output due to beta-blocker toxicity.

Although calcium can help in cases of calcium channel blocker toxicity and has some role in myocardial function, it does not address the unique aspects of beta-blocker toxicity that glucagon does. Similarly, while high-dose insulin can be beneficial in certain types of overdoses, particularly with calcium channel blockers, it is not the first-line treatment for beta-blocker toxicity and may also not provide immediate benefit compared to glucagon.

Thus, the selection of glucagon as the appropriate