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For cases of -blocker poisoning where symptomatic bradycardia and hypotension are present, high-dose glucagon is considered the first-line antidote. Poisoning by -blockers or CCBs usually produces hypotension and bradycardia, which may be refractory to standard resuscitation measures.
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Health-system pharmacists should be aware that when these drugs are used as antidotes, higher than normal dosing is needed.Ĭonclusion. For cases of CCB poisoning where cardiotoxicity is evident, first-line therapy is a combination of calcium and epinephrine high-dose insulin with supplemental dextrose and potassium therapy (HDIDK) is reserved for refractory cases. Traditionally, antidotes for CCB overdose have included calcium, glucagon, adrenergic drugs, and amrinone. However, in -blocker poisoning where symptomatic bradycardia and hypotension are present, high-dose glucagon is considered the first-line antidote. Therapies include -agonists, glucagon, and phosphodiesterase inhibitors. Poisoning by CCBs is characterized by cardiovascular toxicity with hypotension and conduction disturbances, including sinus bradycardia and varying degrees of atrioventricular block. The common feature of -blocker toxicity is excessive blockade of the -receptors resulting in bradycardia and hypotension. In overdose, -blockers and CCBs have similar presentation and treatment overlaps and are often refractory to standard resuscitation measures. Beta-blockers and CCBs represent the most important classes of cardiovascular drugs. Overdoses with cardiovascular drugs are associated with significant morbidity and mortality. The toxic effects and treatment of -adrenergic blocker and calcium-channel blocker (CCB) overdose are reviewed.