Nervous system toxicity bradycardia

As little as 0.1 mg of clonidine has produced toxicity in children determination of adult toxicity is based on observation as there is no milligram per kilogram toxic dose established. Clonidine levels are not clinically useful. Toxicity can result from ingestion of used clonidine transdermal patches as residual clonidine remains after full therapeutic use. Symptoms generally begin within 30-90 min and include hypotension, central nervous system depression, bradycardia, and... 

Clinical signs and symptoms of toxicity are related to the overstimulation of muscarinic, nicotinic, and central nervous system receptors in the nervous system. Muscarinic receptors are those activated by the alkaloid drug muscarine. These receptors are under the control of the parasympathetic nervous system, and their hyperactivity results in respiratory and gastrointestinal dysfunction, incontinence, salivation, bradycardia, miosis, and sweating. Nicotinic receptors are those activated by nicotine. Hyperactivity of these receptors results in muscle fasciculations even greater stimulation results in blockade and muscle paralysis (Lefkowitz et al. 1996 Tafliri and Roberts 1987). Hyperactivity of central nervous system receptors results in the frank neurological signs of confusion, ataxia, dizziness, incoordination, and slurred speech, which are manifestations of acute intoxication. Muscarine and nicotine are not... 

Acute toxicity can arise from overdosage or intestinal or renal disease. The main symptoms of magnesium toxicity are neuromuscular (paralysis) and cardiac (electrocardiographic changes, hypotension, bradycardia, heart block). In more severe cases there will be nervous system or respiratory depression, hypomotility of the bowel, muscle paralysis, and hyporeflexia. 

The primary clinical effects observed in beta blocker toxicity are cardiovascular in nature. Direct cardiac effects include bradycardia (sinus, atrioventricular node, and ventricular), all degrees of atrioventricular block, bundle branch blocks, and asystole. Ventricular arrhythmias may occur secondary to bradycardia. Torsades de pointes has been associated with chronic toxicity from sotalol. Hypotension occurs and is due to decreased cardiac output and/or vasodilation. Central nervous system effects of these drugs including lethargy, coma, and seizures are secondary to the cardiovascular toxicities. Seizures and coma may be secondary to hypoglycemia. Bronchospasm can occur secondary to beta-2 blockade. Hypoglycemia and hyperkalemia can occur. 

The toxic effects of illicit fentanyl derivatives include rapid onset respiratory and central nervous system depression. Patients often present comatose and apneic. Other signs and symptoms consistent with opioid intoxication such as bradycardia, hypotension, miosis, and decreased gastrointestinal motility also occur. 

Ranitidine is generally well tolerated in therapeutic doses. Ranitidine has less central nervous system (CNS) penetration, endocrine effects, and cardiovascular effects than cimetidine. Reported CNS effects associated with ranitidine include hallucinations, depression, delirium, headaches, dystonia, and choreoathetosis. Cardiac arrest during infusion, bradycardia, and progressive AV block with syncope have been reported in association with ranitidine. Abnormal liver enzymes, interstitial nephritis, parotitis, leukopenia, granulocytopenia, thrombocytopenia, pancytopenia, eosinophilia, vasculitis, dermatitis, toxic epidermal necrolysis, sexual impotence, gynecomastia, and polymyositis have also been reported in association with ranitidine therapy. 

In addition to phocomelias, other teratogenic effects include eye and ear abnormalities, esophageal and duodenal atresias, and defects in internal organs such as the heart and kidneys. Congenital defects of the kidneys and nervous system may persist throughout life. Very large doses taken with ethanol have been associated with transient hypotension. Bradycardia has been rarely reported with therapeutic use. Acute toxicity appears infrequent. 

Circulatory depression with bradycardia and hypotension can occur with either intravenous (70, 71 ), or oral therapy (69 ). Patients who have already received ligno-caine appear more likely to develop cardiovascular or central nervous system side effects, presumably as a result of summation of toxic effects (71 ). 

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