Bradycardia nerve agent exposure

Anticholinesterase effects of nerve agent exposure can be characterized as muscarinic, nicotinic, or CNS. Muscarinic effects occur in the parasympathetic system and, depending on the amount absorbed, can be expressed as conjunctival congestion, miosis, ciliary spasm, nasal discharge, increased bronchial secretion, bronchoconstriction, anorexia, emesis, abdominal cramps, sweating, diarrhea, salivation, bradycardia, and hypotension. Nicotinic effects are those that... 

Nerve agent exposure may cause bradycardia due to vagal stimulation or it may often cause the reverse tachycardia due to fright and hypoxia and adrenergic stimulation secondary to ganglionic stimulation. Bradyarrhythmias such as first-, second-, or third-degree heart block may also occur. Blood pressure may also be elevated because of adrenergic stimulation, but it is usually normal until the terminal decline. 

There may be bradycardia or tachycardia (both can occur following nerve agent exposure together with hyper- or hypotension). 

Exposure to acutely toxic concentrations of nerve agents can result in excessive bronchial, salivary, ocular and intestinal secretions, sweating, miosis, bronchospasm, intestinal hypermotility, bradycardia, muscle fasciculations, twitching, weakness, paralysis, loss of consciousness, convulsions, depression of the central respiratory drive, and death (Grob and Harvey, 1953 Grob, 1956 Marrs, 2007 Sidell, 1997 Yanagisawa et al, 2006 many others). Minimal effects observed at low vapor concentrations... 

Miosis may also occur as a systemic feature, although more usually it follows direct exposure. This explains why, for example, modest dermal exposure may produce systemic features but not miosis. Abdominal pain, nausea and vomiting, involuntary micturition and defecation, muscle weakness and fasciculation, tremor, restlessness, ataxia and convulsions may follow dermal exposure, inhalation or ingestion of a nerve agent. Bradycardia, tachycardia and hypertension may occur, dependent on whether muscarinic or nicotinic effects predominate. If exposure is substantial, death may occur from respiratory failure within minutes, whereas mild or moderately exposed individuals usually recover completely, although EEG abnormalities have been reported in those severely exposed to sarin in Japan (Murata etal., 1997 Sekijima et al., 1997). 

Nerve agents are organophosphates (OPs). Acute exposure to OPs can cause muscarinic, nicotinic, and CNS signs. Muscarinic effects include salivation, lac-rimation, urination, dyspnea, diarrhea, and emesis (SLUDDE), along with miosis, bradycardia, hypotension, and bronchoconstriction. Nicotinic effects include... 

Riot control agents such as CN are those that cause disabling physiological effects when they come into contact with the eyes or skin, or when inhaled. They have the capacity to cause intense sensory irritation of the skin and mucous membranes of the eye and respiratory tract. They are peripheral sensory irritants that pharmacologically interact with sensory nerve receptors in skin and mucosal surfaces at the site of contamination resulting in local pain and discomfort sensations with associated reflexes. The reflex associated with the inhalation exposure of irritants is the Kratschmer reflex. This reflex causes apnea, bradycardia, and a biphasic fall and rise in aortic blood pressure. 

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