Atropine excessive

Atropine acts as an antagonist of acetylcholine at muscarinic receptors, but not at nicotinic receptors. By acting as an antagonist, it can prevent overstimulation of muscarinic receptors by the excessive quantities of acetylcholine remaining in the synaptic cleft when AChE is inhibited. The dose of atropine needs to be carefully controlled because it is toxic. 

Muscarine, an alkaloid from certain species of mushrooms, is a muscarinic receptor agonist. The compound has toxicologic importance muscarine poisoning will produce all of the effects that are associated with an overdose of ACh (e.g., bronchocon strict ion, bradycardia, hypotension, excessive salivary and respiratory secretion, and sweating). Poisoning by muscarine is treated with atropine. 

Goodman s literature review and analysis appears, however, to provide the best available LD50 estimate for atropine, since it is based on the actual outcomes of known doses. He excluded from his analysis the few reported cases in which death occurred after less than 30 mg of atropine (e.g. 3 mg). He assumed that deaths following such low doses were probably the result of complications, including, for example, hyperpyrexia due to an excessively warm environment and/or underlying medical illnesses. 

Give before or after meals, as determined by patient s reaction. Postencephalitic patients (more prone to excessive salivation) may prefer to take it after meals and may, in addition, require small amounts of atropine. If the mouth dries excessively, take before meals, unless it causes nausea. If taken after meals, thirst can be allayed by mint candies, chewing gum, or water. 

Atropine can be useful in patients with carotid sinus syncope. This condition results from excessive activity of afferent neurons whose stretch receptors are in the carotid sinus. By reflex mechanisms, this excessive afferent input to the medulla oblongata causes pronounced bradycardia, which is reversible by atropine. 

Atropine can be used in the differential diagnosis of S-A node dysfunction. If sinus bradycardia is due to extracardiac causes, atropine can generally elicit a tachy-cardic response, whereas it cannot elicit tachycardia if the bradycardia results from intrinsic causes. Under certain conditions, atropine may be useful in the treatment of acute myocardial infarction. Bradycardia frequently occurs after acute myocardial infarction, especially in the first few hours, and this probably results from excessive vagal tone. The increased tone and bradycardia... 

Parenteral overdose produces a cholinergic crisis manifested as abdominal discomfort or cramps, nausea, vomiting, diarrhea, flushing, facial warmth, excessive salivation, diaphoresis, urinary urgency, and blurred vision. If overdose occurs, stop all anticholinergic drugs and immediately administer 0.6-1.2 mg atropine sulfate IM or IV. 

Certain mushrooms, especially those of the genus Inocybe, contain muscarinic alkaloids. Ingestion of these mushrooms causes typical signs of muscarinic excess within 15-30 minutes. These effects can be very uncomfortable but are rarely fatal. Treatment is with atropine, 1-2 mg parenterally. (Amanita muscaria, the first source of muscarine, contains very low concentrations of the alkaloid.)... 

Treatment of acute nicotine poisoning is largely symptom-directed. Muscarinic excess resulting from parasympathetic ganglion stimulation can be controlled with atropine. Central stimulation is usually treated with parenteral anticonvulsants such as diazepam. Neuromuscular blockade is not responsive to pharmacologic treatment and may require mechanical respiration. 

A third approach to protection against excessive acetylcholinesterase inhibition is pretreatment with reversible enzyme inhibitors to prevent binding of the irreversible organophosphate inhibitor. This prophylaxis can be achieved with pyridostigmine but is reserved for situations in which possibly lethal poisoning is anticipated, eg, chemical warfare (see Chapter 7). Simultaneous use of atropine is required to control muscarinic excess. 

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