Atropine administration

Cardiovascular sysfe/jj-increase in pulse rate (most pronounced with atropine administration)... 

Nerve agent intoxication requires rapid decontamination to prevent further absorption by the patient and to prevent exposure to others, ventilation when necessary, administration of antidotes, as well as supportive therapy. Skin decontamination is not necessary with exposure to vapor alone, but clothing should be removed to get rid of any trapped vapor. With nerve agents, there can be high airway resistance due to bronchoconstric-tion and secretions, and initial ventilation is often difficult. The restriction will decrease with atropine administration. Copious secretions which maybe thickened by atropine also impede ventilatory actions and will require frequent suctioning. For inhalation exposure to nerve agents, ventilation support is essential. 

Systemically administered atropine may also cause mydriasis and raise lOP in patients with open-angle glaucoma. After intramuscular injection of 0.6 mg atropine, three of eight patients developed 0.5- to 1.5-mm mydriasis. A mean increase of 0.8 cm in the near point of accommodation after atropine administration was also reported. 

Atropine is the classic anticholinergic bronchodila-tor. It antagonizes acetylcholine, resulting in reduced intracellular cyclic guanosine monophosphate (cGMP) and smooth muscle relaxation. In horses, the therapeutic index of atropine is narrow and the duration of action is short (0.5-2.0 h). Adverse systemic effects associated with parenteral atropine administration include mydriasis, ileus, dry mucous membranes, blurred vision, excitement and tachycardia. Atropine is not suitable for routine administration to horses with recurrent airway obstruction. 

Patients with respiratory compromise should receive tracheal intubation, with suctioning for excessive bronchial secretions. If the patient s condition precludes intubation, a surgical airway is necessary. Apneic patients require immediate administration of antidotes, including atropine. Some patients will exhibit resistance to ventilation because of bronchial constriction and spasm. This resistance lessons after atropine administration. In some cases, ventilation will not be possible without prior antidote administration (9). 

The reversal of neuromuscular blockade usually involves the administration of an AChE inhibitor, which increases circulating acetylcholine and reduces the effects of competitive blockade. Atropine administration decreases the systemic effects of acetylcholine produced by the cholinesterase inhibitor, without affecting the blockade reversal (because atropine does not affect skeletal muscle in normal therapeutic doses). 

Finkelstein etai. (1989) performed a noncontrolled prospective study of severe OP poisoning, in this study of 53 adult patients, atropine 2 mg by intravenous bolu.s, followed by the same dose at intervals of 10 min or more, was administered and the dose was adjusted as necessary to control tracheobronchial secretions and bronchospasm. All 53 patients w ere mechanically ventilated and obidoxime wa.s also given. Although it is not po.ssiblc to quantify any beneficial effect from atropine administration alone, atropine appeared to counteract the muscarinic features. 

In another study,81 the EEG of a subject who was severely intoxicated with sarin was recorded after the loss of consciousness but before the onset of convulsions. The recording showed marked slowing of activity, with bursts of high-voltage, 5-Hz waves in the temporofrontal leads. These waves persisted for 6 days despite atropine administration. 

Transient arrhythmias occur after nerve agent intoxication and after atropine administration in a normal individual. However, the irregularities generally terminate after the onset of atropine-induced sinus tachycardia (see discussion of cardiac effects, above). 

Give atropine, 0.5-2 mg IV initially (see p 412), repeated frequently as needed. Large cumulative doses of atropine (up to 100 mg or more) may occasionally be required in severe cases. The most clinically important indication for continued atropine administration is persistent wheezing or bron-chorrhea. Note Atropine will reverse muscarinic but not nicotinic effects. 

John H, Mikler J, Worek F, Thiermann H (2012) Application of an enantioselective LC-ESI MS/MS procedure to determine R- and S-hyoscyamine following intravenous atropine administration in swine. Drug Test Anal 4 (Copyright (C) 2012 American Chemical Society (ACS). All Rights Reserved.) 194-198. doi 10.1002/dta.338... 

Our laboratory has recently investigated the reflex effects of carotid sinus hypertension on the coronary circulation (Ito and Feigl, 1984a). The carotid sinuses were vascularly isolated and perfused with a servo controlled pressure pump. The aortic depressor nerves were cut bilaterally to prevent aortic arch baroreceptor reflexes from buffering carotid sinus reflexes. The left main coronary artery was perfused at constant pressure, and the ventricles were paced at a constant rate following the production of heart block in a closed-chest preparation. Aortic pressure was stabilized with a pressure reservoir and propranolol was administered to block reflex sympathetic effects to the myocardium. Step increases in carotid sinus pressure resulted in graded reflex coronary vasodilation accompanied by increases in coronary sinus oxygen tension. Atropine administration demonstrated that the major portion of the reflex vasodilation was due to parasympathetic activation. These results indicate that parasympathetic coronary vasodilation is part of the carotid sinus baroreceptor reflex. 

Rhinorrhoea generally does not merit atropine administration, unless it is severe and interferes with the patient management. 

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