Excessive b-receptor blockade predictably decreases inotropy, chronotropy, and metabolic effects that are expected from subunit stimulation, resulting in hallmark bradycardia and hypotension.

Other mechanisms may contribute to b-blocker toxicity. Several b-blocker drugs antagonize myocardial sodium channels (IabJe...169-1) in a manner similar to the effects of quinidine or cyclic antidepressants. Impedance of sodium entry slows phase zero of the action potential, resulting in prolonged QRS duration and myocardial depression. Thus, patients may present with wide-complex bradycardia.

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