Bradycardia caused

Respiratory Effects. Pulmonary edema was reported in humans dying from acute methyl parathion (Wofatox) intoxication (Fazekas 1971). Edema was found in a man who died 2 hours after intoxication, and, in other cases, edema was found in others who died as long as 9 days after exposure. Broncho-constriction and hypersecretion of bronchial glands (bronchorrhea) are primary muscarinic effects of methyl parathion. The broncoconstriction, bronchorrhea, and bradycardia caused by methyl parathion are strongly conducive to pulmonary edema. 

Succinylcholine may cause tachycardia, cardiac arrhythmias, and hypertension, which is brought about by stimulation of the sympathetic ganglia. It may also provoke bradycardia, caused by stimulation of muscarinic receptor sites in the sinus node of the heart. This effect is more pronounced following a second dose of succinylcholine. The bradycardia may be blocked by thiopental, atropine, and ganglionic blocking agents. 

Loss of consciousness due to marked bradycardia caused by severe hyperkalemia has been described in an 85-year-old woman who took loxoprofen for several days and long-term imidapril, an ACE inhibitor. The combination of an NSAID with an ACE inhibitor can produce serious adverse effects in high-risk patients (5). 

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. 

Raymond-Hamet (172) observed that hordenine, like nicotine, provokes a contracture and then a relaxation of the small intestine. It causes a liberation of adrenaline from the adrenal medulla which can be detected by several physiological methods, as for instance by adrenal-jugular anastomoses. Large doses of hordenine abolish the effects of vagal stimulation and those of nicotine on the heart, on the arterial pressure, and on the small gut in situ, but it does not modify the bradycardia caused by acetylcholine, nor the hypertensor effects of adrenaline. 

Tubocurarine can block bradycardia caused by phenylephrine but has no effect on bradycardia caused by neostigmine. Explain The SMll Keeper Answer appears at the end of the chapter. 

Reduction of secretions and vagal reflexes Muscarinic antagonists, usually hyoscine, are used to prevent salivation and bronchial secretions and, more importantly, to proteci the heart from arrhythmias, particularly bradycardia caused by halothane, propofol, suxamethonium and neostigmine. Hyoscine is also iiniiemeiic and produces some amnesia. 

DDD (R) AV synchrony is maintained for patients with sinus node and AV node disease. Reqnues two leads More complex Bradycardia caused by sinus node disease or AV node disease... 

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