Tachycardia phosphates

Other Glass III Antiarrhythmic Agents. Clofihum phosphate is a benzene-butanaminium derivative that has highly specific Class III antiarrhythmic activity. It is orahy active, has a rapid onset of action, and a reasonably long duration of antiarrhythmic activity. In preliminary clinical studies, clofihum has shown efficacy against spontaneous ventricular tachycardias (69). 

In a fatal human exposure, a worker engaged in emptying metal gas cylinders of methyl mercaptan was found comatose at the work site he developed expiratory wheezes, elevated blood pressure, tachycardia, and marked rigidity of extremities. Methemoglobinemia and severe hemolytic anemia developed with hematuria and proteinuria but were brief in duration deep coma persisted until death due to pulmonary embolus 28 days after exposure. It was determined that the individual was deficient in erythrocyte glucose-6-phosphate dehydrogenase, which was the likely cause of the hemolysis and formation of methemoglobin. 

Vitamin B1 (thiamine) has the active form, thiamine pyrophosphate. It is a cofactor of enzymes catalyzing the conversion of pyruvate to acetyl CoA, a-ketoglutarate to succinyl CoA, and the transketolase reactions in the pentose phosphate pathway. A deficiency of thiamine causes beriberi, with symptoms of tachycardia, vomiting, and convulsions. In Wernicke-Korsakoff syndrome (most common in alcoholics), individuals suffer from apa thy, loss of memory, and eye movements. There is no known toxicity for this vitamin. 

A 35-year-old woman taking disopyramide phosphate modified-release capsules 150 mg qds was given azithromycin 500 mg initially and 250mg/day thereafter (36). In 11 days she developed malaise, light-headedness, and urinary retention. After the insertion of a urinary catheter she developed a monomorphic ventricular tachycardia with left bundle branch block. She was successfully cardioverted and the electrocardiogram... 

Chelation therapy is usually the treatment of choice. Both CaNai-EDTA (calcium disodium salt of ethylenediaminetetraacetic acid) and British Antilewisite compound (BAL 2,3-dimercaptopropanol) are commonly used to remove lead from the body. Both are administered via intramuscular injection. BAL binds lead to sulfhydral groups and chelates metal from both inside and outside the cellular space. Lead removal through the bile and urine is increased within 30 min of administration. BAL is the common choice when there is known toxicity to the kidney, but it is contraindicated if there is liver failure or glucose-6-phosphate dehydrogenase deficiency. BAL treatment has produced a number of adverse reactions, including nausea, vomiting, tachycardia, and fever. 

Disopyramide phosphate is recommended orally as a prophylaxis of either unifocal or multifocal premature ventricular contractions and ventricular tachycardia. It also exhibits both anticholinergic and local anaesthetic properties. 

An otherwise healthy 32-year-old woman received prilocaine 60 mg for removal of a gluteal abscess and developed symptoms of suspected methemoglobinemia, with dizziness, fever, and headache 1 hour after surgery and peripheral cyanosis and tachycardia 3 hours later [75 ]. She was given 5 ml of methylthioninium chloride 1% and her symptoms resolved within 30 minutes. Erythrocyte glucose-6-phosphate-dehydrogenase activity was normal. 

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