Bradycardia physostigmine effects

In the heart, the effects on the parasympathetic limb predominate. Thus, cholinesterase inhibitors such as edrophonium, physostigmine, or neostigmine mimic the effects of vagal nerve activation on the heart. Negative chronotropic, dromotropic, and inotropic effects are produced, and cardiac output falls. The fall in cardiac output is attributable to bradycardia, decreased atrial contractility, and some reduction in ventricular contractility. The latter effect occurs as a result of prejunctional inhibition of norepinephrine release as well as inhibition of postjunctional cellular sympathetic effects. 

Physostigmine Suggested for antimuscarinic anticholinergic agents not for tricyclic antidepressants Adult dose is 0.5-1 mg IV slowly. The effects are transient (30-60 minutes), and the lowest effective dose may be repeated when symptoms return. May cause bradycardia, increased bronchial secretions, seizures. Have atropine ready to reverse excess effects. Do not use for tricyclic antidepressant overdose. 

Adverse effects The effects of physostigmine on the CNS may lead to convulsions when high doses are used. Bradycardia may also occur. Inhibition of acetylcholinesterase at the skeletal neuromuscular junction causes the accumulation of acetylcholine and ultimately results in paralysis of skeletal muscle. However, these effects are rarely seen with therapeutic doses. 

Physostigmine has the potential for induction of seizure activity. In addition, the increase in cholinergic activity does not significantly affect the bradycardia caused by the quinidine-like effects of tricyclics. 

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