Cases reported "Bradycardia"

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1/82. A case of sinus arrest and vagal overactivity during REM sleep.

    A young man presented with tachycardia and faintness after an episode of influenza. He underwent 24-h heart rate recordings, each of which documented episodes of sinus arrest lasting up to 7.2 seconds. All episodes occurred in the second half of the night and were always accompanied by severe bradycardia. Cardiac function tests failed to disclose anything abnormal. Two polysomnographic recordings demonstrated that the sinus arrests occurred during REM sleep. Power spectral analysis of heart rate variability showed that during the second half of the night there was an abnormal prevalence of vagal activity, particularly during REM sleep stages, presumably responsible for the bradycardia and fall in blood pressure. We speculate that the episodes of sinus arrest are linked to a central mechanism that triggers the autonomic imbalance during REM sleep.
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2/82. Hormonal and cardiovascular reflex assessment in a female patient with pure autonomic failure.

    We report the case of a 72-year-old female with pure autonomic failure, a rare entity, whose diagnosis of autonomic dysfunction was determined with a series of complementary tests. For approximately 2 years, the patient has been experiencing dizziness and a tendency to fall, a significant weight loss, generalized weakness, dysphagia, intestinal constipation, blurred vision, dry mouth, and changes in her voice. She underwent clinical assessment and laboratory tests (biochemical tests, chest X-ray, digestive endoscopy, colonoscopy, chest computed tomography, abdomen and pelvis computed tomography, abdominal ultrasound, and ambulatory blood pressure monitoring). Measurements of catecholamine and plasmatic renin activity were performed at rest and after physical exercise. Finally the patient underwent physiological and pharmacological autonomic tests that better diagnosed dysautonomia.
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3/82. death due to bioterrorism-related inhalational anthrax: report of 2 patients.

    On October 9, 2001, a letter containing anthrax spores was mailed from new jersey to washington, DC. The letter was processed at a major postal facility in washington, DC, and opened in the Senate's Hart Office Building on October 15. Between October 19 and October 26, there were 5 cases of inhalational anthrax among postal workers who were employed at that major facility or who handled bulk mail originating from that facility. The cases of 2 postal workers who died of inhalational anthrax are reported here. Both patients had nonspecific prodromal illnesses. One patient developed predominantly gastrointestinal symptoms, including nausea, vomiting, and abdominal pain. The other patient had a "flulike" illness associated with myalgias and malaise. Both patients ultimately developed dyspnea, retrosternal chest pressure, and respiratory failure requiring mechanical ventilation. leukocytosis and hemoconcentration were noted in both cases prior to death. Both patients had evidence of mediastinitis and extensive pulmonary infiltrates late in their course of illness. The durations of illness were 7 days and 5 days from onset of symptoms to death; both patients died within 24 hours of hospitalization. Without a clinician's high index of suspicion, the diagnosis of inhalational anthrax is difficult during nonspecific prodromal illness. Clinicians have an urgent need for prompt communication of vital epidemiologic information that could focus their diagnostic evaluation. Rapid diagnostic assays to distinguish more common infectious processes from agents of bioterrorism also could improve management strategies.
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4/82. Asymptomatic bradycardia associated with amisulpride.

    Well-known adverse effects of amisulpride include nausea, insomnia or tiredness, gastrointestinal, extrapyramidal and endocrine symptoms. Cardiac disorders, however, appear to be an extremely rare complication of the drug. Only a few case reports on this complication have been published so far, which deal with QT prolongation, hypotension, hypertension and palpitations. bradycardia has not yet been mentioned. Here, we will report on a case of asymptomatic bradycardia that developed subsequent to therapeutic doses of amisulpride in a 25-year-old male patient with chronic paranoid-hallucinatory schizophrenia. The patient had been rehospitalized for an acute exacerbation of the psychosis. When the patient failed to respond at the beginning of hospitalization, the treatment was changed from clozapine to amisulpride. After a complete switchover to amisulpride, the patient's ECG showed sinus bradycardia and QT prolongation. When the daily dose of amisulpride was reduced from 800 mg/d to 600 mg/d, the patient's ECG quickly normalized (including blood pressure and pulse rate) within a few days. The patient did not report any cardiovascular-related complaints. Since the cardiovascular-specific diagnostics did not yield any indicative results, bradycardia may be a rare complication of amisulpride treatment.
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5/82. citalopram-induced bradycardia and presyncope.

    OBJECTIVE: To report a case of symptomatic bradycardia and hypotension that resulted from the therapeutic use of citalopram and to review any previous reports in the literature, from the manufacturer, and the Australian Drug Reaction Advisory Committee (ADRAC). CASE SUMMARY: A 60-year-old white woman who had been taking citalopram 20 mg/d for two weeks presented to the hospital with a heart rate of 39 beats/min, mild hypotension (systolic BP 105 mm Hg), and a normal electrocardiogram (QTc < 440 msec), following a presyncopal episode. The patient was admitted for cardiac monitoring, and citalopram was discontinued. The bradycardia and hypotension resolved in the 48-hour period following cessation of citalopram. No other medical or pharmacologic cause was found for the adverse drug reaction. DISCUSSION: bradycardia has been reported rarely with citalopram in therapeutic doses, but this is the first detailed case with a dose of only 20 mg. The manufacturer reports bradycardia as an infrequent adverse effect (0.1-1%) of citalopram. There have been no reports to ADRAC or to the manufacturer in postmarketing surveillance. There is a case report of asymptomatic bradycardia in a patient whose dose was increased to 40 mg. In the case reported here, there was no QTc prolongation consistent with previous reports. The sinus bradycardia reported more often with therapeutic doses would appear to be distinct to QT abnormalities seen with citalopram overdose. CONCLUSIONS: citalopram should be used with care in the elderly and in persons with a history of heart disease. heart rate and blood pressure should be monitored in the first week of therapy and when doses are modified.
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6/82. Bites by puff-adder (Bitis arietans) in nigeria, and value of antivenom.

    Ten patients bitten by the puff-adder (Bitis arietans) were studied in the North of nigeria. Six showed severe local signs, and four also had evidence of systemic envenoming, including spontaneous bleeding with thrombocytopenia, hypotension, and bradycardia. Two patients died after developing circulatory collapse and renal failure. Antivenom and intravenous fluid restored blood pressure in two hypotensive patients, and antivenom probably prevented the development of local necrosis in four others with massive local swelling. Victims of B arietans who have swelling of more than half the bitten limb or show signs of systemic envenoming should be given at least 80 ml of specific polyvalent antivenom and watched carefully for signs of circulatory collapse. debridement of necrotic tissue may be necessary.
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7/82. Extreme night bradycardia developing after malfunction of a lumboperitoneal shunt.

    CASE REPORT: An 8-year-old boy who was treated for hydrocephalus with lumboperitoneal shunting presented with extreme night bradycardia. RESULTS AND CONCLUSION: The night bradycardia disappeared after shunt revision, suggesting that the probable cause was secondary to long-lasting increased intracranial pressure (ICP). Long-lasting increased ICP is known to be associated with papilledema, but it has rarely been reported to induce night bradycardia in clinical practice. Extreme night bradycardia in this setting is not only a clinical sign of increased ICP but also a possible cause of cardiogenic sudden death, which must be borne in mind in the management of patients with shunted hydrocephalus.
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8/82. Cardioactive steroid poisoning from an herbal cleansing preparation.

    We describe a case of unintentional poisoning from a cardioactive steroid and the subsequent analytic investigation. A 36-year-old woman with no past medical history and taking no conventional medications ingested an herbal preparation marketed for "internal cleansing." Its ingredients were neither known to the patient nor listed on the accompanying literature. The next morning, nausea, vomiting, and weakness developed. In the emergency department, her blood pressure was 110/60 mm Hg, and her pulse rate was 30 beats/min. Her ECG revealed a junctional rhythm at a rate of 30 beats/min and a digitalis effect on the ST segments. After empiric therapy with 10 vials of digoxin-specific Fab (Digibind), her symptoms resolved, and she reverted to a sinus rhythm at a rate of 68 beats/min. Her serum digoxin concentration measured by means of the fluorescence polarization immunoassay (Abbott TDx) was 1.7 ng/mL. Further serum analysis with the Tina Quant digoxin assay, a more digoxin-specific immunoassay, found a concentration of 0.34 ng/mL, and an enzyme immunoassay for digitoxin revealed a concentration of 20 ng/mL (therapeutic range 10 to 30 ng/mL). serum analysis by means of high-performance liquid chromatography revealed the presence of active digitoxin metabolites; the parent compound was not present. When the diagnosis of cardioactive steroid poisoning is suspected clinically, laboratory analysis can confirm the presence of cardioactive steroids by using immunoassays of varying specificity. An empiric dose of 10 vials of digoxin-specific Fab might be beneficial in patients poisoned with an unknown cardioactive steroid.
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9/82. Persistent atrial standstill, report of three cases.

    Three cases, of which two are brothers, of persistent atrial standstill are reported. The diagnosis was made by the lack of P wave in routine 12 leads and right atrial cavity lead, no response of atrium to electrical stimulation and absence of "a" wave in right atrial pressure curve.
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10/82. hypotension and bradycardia in infants after the use of topical brimonidine and beta-blockers.

    Brimonidine is a selective alpha-2 adrenergic agonist used to treat glaucoma. There have been several reports of central nervous system depression after its use in infants. We observed rapid-onset bradycardia and decreased blood pressure in addition to central nervous system depression in 2 infants who received concomitant topical brimonidine and beta-blockers.
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