Anticholinergics

Anticholinergics is a topic covered in the Washington Manual of Medical Therapeutics.

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General Principles

Anticholinergic effects are primarily due to blockade of muscarinic receptors (i.e., antimuscarinic effects) and, therefore, mainly affect parasympathetic functions.

Epidemiology

Anticholinergic poisoning occurs either from intentional ingestion of certain plants or over-the-counter medications (e.g., Jimson weed, diphenhydramine)1 or from accidental overdosing (e.g., medical noncompliance, polypharmaceutical regimens).2

Etiology

Drugs and medications with anticholinergic effects include the following:

  • Anticholinergics: Atropine, scopolamine, benztropine, glycopyrrolate, ipratropium
  • Antihistamines: Diphenhydramine, promethazine, doxylamine
  • Antipsychotics: Chlorpromazine, clozapine, olanzapine, quetiapine
  • Antidepressants: Amitriptyline, nortriptyline, imipramine, desipramine
  • Antiparkinson drugs: Benztropine, trihexyphenidyl
  • Mydriatics: Cyclopentolate, homatropine, tropicamide
  • Muscle relaxants: Cyclobenzaprine
  • Plants: Belladonna, Jimson weed, Amanita mushrooms

Pathophysiology

  • Blockade of muscarinic receptors (i.e., parasympathetic autonomic nervous system [ANS], except for the sympathetically innervated sweat glands) leads to the so-called anticholinergic toxidrome.
  • Tachycardia is one of the main symptoms in anticholinergic poisoning. Vagal blockade of cardiac muscarinic receptors leads to unopposed sympathetic stimulation of the myocardium.
  • Some anticholinergic drugs can also cross the blood–brain barrier and interact with muscarinic receptors in the cortex and subcortical regions of the brain causing anticholinergic CNS manifestations.

Associated Conditions

  • Antihistamines and cyclic antidepressants also block sodium channels and cause additional cardiac symptoms such as dysrhythmias and QRS prolongations.
  • Potassium channel blockade may result in QTc prolongation and TdP.

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