Atropine hypertension caused

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. 

Diphenoxylate is an opiate (schedule V) with antidiarrheal properties. It is usually dispensed with atropine and sold as Lomotil. The atropine is added to discourage the abuse of diphenoxylate by narcotic addicts who are tolerant to massive doses of narcotic but not to the CNS stimulant effects of atropine. Diphenoxylate shonld be used cautiously in patients with obstructive jaundice because of its potential for hepatic coma, and in patients with diarrhea cansed by pseudomembranous colitis because of its potential for toxic megacolon. In addition, it should be used cautiously in the treatment of diarrhea caused by poisoning or by infection by Shigella, Salmonella, and some strains of E. coli because expulsion of intestinal contents may be a protective mechanism. Diphenoxylate should be used with extreme caution in patients with impaired hepatic function, cirrhosis, advanced hepatorenal disease, or abnormal liver function test results, because the drug may precipitate hepatic coma. Because diphenoxylate is structurally related to meperidine, it may cause hypertension when combined with monoamine oxidase inhibitors. As a narcotic, it will augment the CNS depressant effects of alcohol, hypnotic-sedatives, and numerous other drugs, such as neuroleptics or antidepressants that cause sedation. 

Hypotension per se need not be treated, at least initially. Generally the restoration of oxygenation and the increase in heart rate caused by atropine, aided perhaps by the hypertensive effects of 2-PAM Cl, will cause the blood pressure to increase to an... 

A. Patients with hypertension, tachyarrhythmias, thyrotoxicosis, congestive heart failure, coronary artery disease, and other illnesses, who might not tolerate a rapid heart rate. Patients with severe cholinesterase inhibitor poisoning are often tachycardia. Atropine should not be withheld and may lower heart rate (by improving oxygenation). Glycopyrrolate may also be helpful (due to its lessened propensity to cause a tachycardia). 

Phenylephrine causes vasoconstriction, which can raise the blood pressure. Normally this would be limited by a baroreflex mediated by the vagus nerve, but if this cholinergic mechanism is blocked by atropine or other antimuscarinics, the rise in blood pressure is largely uncontrolled. Severe hypertension may occur, and other adverse cardiae events such as acute cardiac failure may follow. 

Well-known symptoms of sarin toxicity include miosis, hypersecretions, bradycardia, and fasciculations. However, the mechanism of organophosphate toxicity seems to involve conflicting actions. For example, mydriasis or miosis, and bradycardia or tachycardia may occur. Acute respiratory insufficiency is the most important cause of immediate death. Early symptoms include (i) tachypnea due to increased airway secretions and bronchospasm (a muscarinic effect), (ii) peripheral respiratory muscle paralysis (a nicotinic effect), and (iii) inhibition of respiratory centers (a CNS effect), all of which lead to severe respiratory deficiency. If left untreated at this stage, death will result. Cardiovascular symptoms may include hypertension or hypotension. Various arrhythmias can also occur, and caution is required when the QT interval is prolonged. In particular, if hypoxemia is present, fatal arrhythmias may occur with intravenous administration of atropine... 

In some species, pharmacological effects other than muscle-relaxation may dominate. Thus, as already seen, the activity of S. erichsonii extracts appears to be due primarily to the presence of diaboline derivatives. Leaf extracts have analgesic properties, while stem-bark extracts have spasmolytic properties and augment the activity of the central nervous system (50). The bark alkaloids of S. glabra are reported to have central rather than peripheral effects (Table 1.4, footnote j). Sublethal doses of aqueous extracts from S. castelnaeana cause hypertension, tachycardia, and slight respiratory stimulation enhancement of the hypertension by atropine and its reduction by hexamethonium (mecamylamine) show that the extract has nicotinic activity. Evidently, the toxicity of the plant must be partly due to the tertiary bases it contains (314). 

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