Cases reported "Bradycardia"

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1/8. Profound sinus bradycardia after intravenous nicardipine.

    IMPLICATIONS: nicardipine-induced bradycardia has been reported in experimental animals but not in clinical patients. We report a clinical case of unexpected bradycardia caused by nicardipine. The mechanism of this bradycardia was not clear, and depression of sympathetic tone by epidural anesthesia, hypothermia, and paroxysmal atrial fibrillation might have been contributory.
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keywords = animal
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2/8. Toad venom poisoning: resemblance to digoxin toxicity and therapeutic implications.

    A healthy man developed gastrointestinal symptoms after ingesting purported aphrodisiac pills. He had severe unrelenting bradycardia, hyperkalaemia, and acidosis. He rapidly developed severe life threatening cardiac arrhythmias and died after a few hours. He was found to have positive serum digoxin concentrations, although he was not taking digoxin. Toad venom poisoning is similar to digitalis toxicity and carries a high mortality. Cardiac glycoside poisoning can occur from ingestion of various plants and animal toxins, and the venom gland of cane toad (bufo marinus) contains large quantities of cardiac glycosides. Toad venom, a constituent of an aphrodisiac, was considered responsible for the development of clinical manifestations and death in this patient. digoxin specific Fab fragment has been reported to be beneficial in the treatment of toad venom poisoning. This report alerts physicians to the need to be aware of a new community toxic exposure, as prompt treatment with digoxin specific Fab fragment may be life saving. The treatment approach to patients with suspected toad venom poisoning is described.
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keywords = animal
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3/8. Near-fatal amitraz intoxication: the overlooked pesticide.

    Amitraz is commonly used in agricultural industries throughout the world as a farm-animal insecticide. Despite its widespread use, amitraz intoxication is extremely rare and mainly occurs through accidental ingestion by young children. Severe, life-threatening amitraz intoxication in adults is very rarely recognized and reported. Described herein is a previously healthy 54-year-old patient who accidentally ingested a mouthful of liquid amitraz concentrate, and rapidly developed life-threatening clonidine-like overdose syndrome, manifested as nausea, vomiting, hypotension, bradycardia, bradypnoea, and deep coma. Supportive treatment, including mechanical ventilation, and atropine administration resulted in full recovery within 48 hr. Very few cases of near-fatal amitraz poisoning in adults have been described in the medical literature, leading to low awareness of physicians in general practice to the potential toxicity of amitraz. As a consequence, cases of amitraz poisoning are not recognised and therefore erroneously treated as the much more commonly recognized organophosphate and carbamate intoxication. In our discussion, we review the clinical and laboratory manifestations of amitraz poisoning, including clinical hints that aid in the recognition of this often-overlooked diagnosis. Differentiation of amitraz intoxication from the much more commonly seen pesticide-related organophosphate and carbamate intoxication is of utmost importance, in order to avoid erroneous, unnecessary, and often dangerous treatment.
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keywords = animal
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4/8. Systemic toxicity after an ocular exposure to xylazine hydrochloride.

    There are limited reports of human overdose with the animal tranquilizer, xylazine hydrochloride. The reported effects include hypotension, bradycardia, and respiratory depression. Ocular exposures to xylazine have not been previously reported. A 38-year-old man arrived in the Emergency Department, reporting the accidental irrigation of both eyes with approximately 8 mL of xylazine (100 mg/mL) 30 min before arrival. The patient was asymptomatic. The eyes were copiously irrigated with isotonic crystalloid. Two hours after the exposure, the patient developed sinus bradycardia (40-50 beats/min), hypotension (90/60 mm Hg), and a decreased level of consciousness. The patient was admitted for observation, during which the bradycardia and hypotension were noted to persist. He remained otherwise asymptomatic. The symptoms resolved without intervention, other than i.v. fluids, approximately 25 h after the exposure. The patient was discharged home. This case demonstrates that ocular exposure to xylazine can cause systemic central nervous system and cardiovascular effects.
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keywords = animal
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5/8. Transient bradycardia during vespid venom immunotherapy.

    A woman developed generalized symptoms of hypersensitivity when she was stung requiring treatment with adrenalin. Intradermal venom skin tests showed immediate hypersensitivity to yellow hornet and white-faced hornet thus fulfilling the criteria to receive appropriate venom immunotherapy. During the course of modified rush immunotherapy with yellow hornet and white-faced hornet venoms, she developed transient but progressive bradycardia necessitating interruption of the venom immunotherapy. Transient bradycardia recurred when venom immunotherapy was resumed but it was possible to reach a maintenance dose of 100 micrograms protein for each venom. bradycardia has been reported to be induced in experimental animals by oriental hornet venom as well as other venoms, through a direct cholinergic action. It appears that a similar effect may occur in man in susceptible individuals during venom immunotherapy.
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keywords = animal
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6/8. Insect repellent (N,N-diethyl-m-toluamide) cardiovascular toxicity in an adult.

    OBJECTIVE: To describe a case of N,N-diethyl-m-toluamide (deet)-induced cardiovascular toxicity in an adult and reviews other cases that have been reported in the published literature. Human and animal data available on deet pharmacokinetics are reviewed and factors that predispose an individual to deet toxicity are identified. DATA SOURCES: Case report information was obtained through personal contact with the patient during hospitalization and by telephone, and also from the patient's medical records. Computerized literature searches were conducted with the following systems to obtain medical literature on deet toxicity: TOXLINE, International Pharmaceutical abstracts, and medline. Index Medicus was searched manually. STUDY SELECTION: All reported cases of deet toxicity in children and adults were reviewed. DATA EXTRACTION: case reports were evaluated for the quantity of the deet exposure (topical or oral), the clinical manifestations of the exposure, and the outcome of the exposure. DATA SYNTHESIS: This case is similar in some aspects to those already in the literature; however, very few cases of deet toxicity in adults have been reported. Cardiovascular toxicity in humans related to deet application has not been previously reported in the published medical literature. deet exposure (topical or oral) results in a highly variable clinical course. Whether the outcome is death or recovery without sequelae is difficult to predict. CONCLUSIONS: Adults, as well as children, are at risk for toxicity from insect repellents. The use of highly concentrated deet-containing insect repellents should be avoided to reduce the risk of toxicity in both children and adults. The consequences of deet toxicity are variable and unpredictable.
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keywords = animal
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7/8. Profound reflex bradycardia produced by transient hypoxia or hypercapnia in man.

    A quadraplegic patient was able to breathe adequately for the first 3 days after his cervical spinal cord was transected by a bullet. However, for several days thereafter spontaneous ventilation became inadequate, most likely due to edema of the cord, and mechanical ventilation was required. When the ventilator was disconnected for required tracheal aspiration, before there was any tracheal stimulation, profound bradycardia, hypotension and syncope occurred within a few seconds. The bradycardia could be diminished by atropine and its onset delayed by prior ventilation with oxygen. Because of the rapid onset of the hemodynamic changes and their correlation with relatively small changes in PaO2 and PaCO2, it is suggested that this vagally mediated bradycardia represents the primary cardiac reflex response to peripheral chemoreceptor stimulation, which, although extensively studied in experimental animals, has not before been described in man. Just as in animals, it seems likely that the inability to hyperventilate permitted the primary cardiac reflex to occur rather than the usual response of tachycardia to chemoreceptor stimulation which is prepotent with spontaneous ventilation. An understanding of this reflex was important in the clinical mangement of this patient.
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keywords = animal
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8/8. bradycardia in toluene poisoning.

    BACKGROUND: Tachyarrhythmias are the classical manifestation of toluene cardiotoxicity. The presumed mechanism is sensitization of the myocardium to the potential arrhythmogenic effect of endogenous catecholamines, occasionally resulting in fatality. Bradyarrhythmias have been repeatedly shown in animal models, but have been reported only once in a human. case reports: Two patients with toluene intoxication presented with severe sinus bradycardia. One patient had also atrial-ventricular dissociation. In both cases cardiac rhythm returned to normal within several hours. CONCLUSION: We suggest that the spectrum of cardiotoxic symptoms associated with toluene intoxication in humans includes bradyarrhythmias as well as tachyarryhthmias.
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keywords = animal
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