Pathophysiology and Management of Self-Poisoning with Beta-Blockers

Abstract

The prognosis of self-poisoning with beta-blockers is excellent, especially if medical management is started immediately but the wide variety of clinical symptoms and proposed treatments complicate the therapeutic strategy. Beta-blockers that are liposoluble or have marked anti-arrhythmic activity are more lethal (e.g. propranolol, sotalol). Similarly, pre-existing cardiac pathology or co-ingestion of psychotropic or cardioactive drugs increases mortality. The first-line symptomatic treatment is administration of atropine and volume-expanding fluids to treat bradycardia and hypotension, respectively. However atropine is often unsuccessful in reversing beta-blocker-induced bradycardia and repeated doses can provoke atropine poisoning. If symptomatic treatment fails, then antidotes should be administered in a precise order: first, high doses of glucagon, followed by isoproterenol, epinephrine, and the new inhibitors of phosphodiesterases. Mechanical ventilation should be started at the same time as pharmacological treatment in cases of severe collapse or prolonged QRS.

KEY WORDS:

• sympatholytics
• adrenergic beta receptor blockaders
• poisoning
• suicide
• glucagon
• isoproterenol
• epinephrine
• inhibitors of phosphodiesterases