Cases reported "Tachycardia"

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1/245. acebutolol-induced ventricular tachycardia reversed with sodium bicarbonate.

    BACKGROUND: acebutolol is a unique beta blocker that possesses cardioselectivity, partial agonist activity, and membrane stabilizing activity. sodium bicarbonate is used to reverse the cardiotoxic effects of other drugs with membrane stabilizing activity. There have been no reported cases of acebutolol-induced ventricular dysrhythmias treated successfully with bolus sodium bicarbonate. CASE PRESENTATION: A 48-year-old man ingested approximately 6.4 g of acebutolol with ethanol (blood ethanol 61 mmol/L). There were no other coingestants identified. One hour after presentation, the patient had a cardiac arrest with the monitor showing ventricular tachycardia. sodium bicarbonate 50 mEq intravenous push converted the patient to sinus rhythm and the blood pressure improved to 129/90 mm Hg. CONCLUSION: This case demonstrates a temporal relationship between bolus sodium bicarbonate administration and the termination of acebutolol-induced ventricular tachycardia.
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2/245. Treatment of the bradycardia-tachycardia syndrome with permanent demand pacing.

    The bradycardia-tachycardia syndrome (paroxysmal supraventricular tachycardia alternating with sinus bradycardia and episodes of sinus node arrest) has previously presented a complicated therapeutic dilemma when excitatory and suppressive drugs have been utilized. A patient with this syndrome successfully treated with a permanent ventricular transvenous demand pacemaker is presented. Various aspects of this syndrome as well as facets of diagnosis and treatment have been reviewed and discussed. Significant underlying cardiac disease was ruled out in this patient by the usual diagnostic methods including left heart catheterization and coronary angiography. An interesting possibility of the relationship of vagal stimulation secondary to hiatus hernia as an etiologic factor in this syndrome has been discussed. The opinion is expressed that the currently preferred method of treatment is the insertion of a permanent transvenous pacemaker alone or in conjunction with antiarrhythmic drugs, preferably digitalis and propranolol.
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3/245. Severe gamma-hydroxybutyrate withdrawal: a case report and literature review.

    We report a case of gamma-hydroxybutyrate (GHB) withdrawal resulting in severe agitation, mental status changes, elevated blood pressure, and tachycardia hours after stopping chronic use of GHB. The patient admitted to substantial GHB abuse on a daily basis for 2.5 years. Previous attempts at cessation reportedly resulted in diaphoresis, tremors, and agitation. The patient's symptoms, negative polypharmacy history, and negative urine and blood toxicological analysis for alcohol, benzodiazepines, sedative-hypnotics, or other substances suggested the diagnosis of GHB withdrawal. Later analysis of a patient drug sample confirmed the presence of GHB. The patient required 507 mg of lorazepam and 120 mg of diazepam over 90 h to control agitation. This is one of the few reported cases of GHB withdrawal and one of the most severe. Given the increasing use of GHB, more cases of severe GHB withdrawal should be anticipated.
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4/245. Clinical and pharmacological profile in a clenbuterol epidemic poisoning of contaminated beef meat in italy.

    Long-acting beta adrenergic agonists, such as clenbuterol accumulate in the liver, but not meat of treated farm animals, and result in epidemic poisonings in consumers. We describe an outbreak of poisoning in 15 people, following the consumption of meat. Clinical symptoms (distal tremors, palpitations, headache, tachipnoea-dyspnoea, and also moderate hyperglycaemia, hypokalemia and leucocytosis) were seen in nine hospitalised patients, starting about 0.5-3 h after poisoning, and disappearing within 3-5 days later. clenbuterol was found in the urine of all the symptomatic patients, at higher levels than pharmacokinetic computing (mean level 28 ng/ml, 36 h after ingestion), based on the levels found in the meat (1140-1480 ng/g edible tissue). Thus, epidemic poisoning can be produced following the consumption of contaminated meat. The need for a better definition of pharmaco- and toxico-kinetics, not only for drugs ingested as parent drug, but also when ingested as residues with animal tissues, is recommended.
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5/245. Gamma-hydroxybutyrate withdrawal syndrome.

    STUDY OBJECTIVE: Gamma-hydroxybutyrate (GHB) withdrawal syndrome is increasingly encountered in emergency departments among patients presenting for health care after discontinuing frequent GHB use. This report describes the characteristics, course, and symptoms of this syndrome. methods: A retrospective review of poison center records identified 7 consecutive cases in which patients reporting excessive GHB use were admitted for symptoms consistent with a sedative withdrawal syndrome. One additional case identified by a medical examiner was brought to our attention. These medical records were reviewed extracting demographic information, reason for presentation and use, concurrent drug use, toxicology screenings, and the onset and duration of clinical signs and symptoms. RESULTS: Eight patients had a prolonged withdrawal course after discontinuing chronic use of GHB. All patients in this series were psychotic and severely agitated, requiring physical restraint and sedation. Cardiovascular effects included mild tachycardia and hypertension. Neurologic effects of prolonged delirium with auditory and visual hallucinations became episodic as the syndrome waned. Diaphoresis, nausea, and vomiting occurred less frequently. The onset of withdrawal symptoms in these patients was rapid (1 to 6 hours after the last dose) and symptoms were prolonged (5 to 15 days). One death occurred on hospital day 13 as withdrawal symptoms were resolving. CONCLUSION: In our patients, severe GHB dependence followed frequent ingestion every 1 to 3 hours around-the-clock. The withdrawal syndrome was accompanied initially by symptoms of anxiety, insomnia, and tremor that developed soon after GHB discontinuation. These initial symptoms may progress to severe delirium with autonomic instability.
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6/245. syncope in patients with atrial flutter during treatment with class Ic antiarrhythmic drugs.

    We describe 2 atrial flutter (AFL) patients with syncope during treatment with class Ic antiarrhythmic drugs. During the syncope, 1:1 atrioventricular (AV) conduction during AFL preceded a wide QRS tachycardia. The class Ic drugs, flecainide and pilsicainide, slowed the atrial rate, resulting in AFL with 1:1 AV conduction, and the width of the QRS complexes became wider during the tachycardia. syncope was abolished after successful radiofrequency catheter ablation of the AFL. These potential proarrhythmic effects of the class Ic drugs should be taken into account in AFL patients, and concomitant use of beta-blocking agents would be critical to prevent proarrhythmias.
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7/245. Rare side-effects of fenofibrate.

    Fibrates are widely prescribed as hypolipidemic drugs and are considered as safe. We report the case of a 69 year-old woman who probably developed a major allergic reaction following a fenofibrate prescription (generic form) of 300 mg per day. Clinical features included asthenia, hyperthermia (40.5 degrees C) and slight muscular pain. Biological abnormalities were mildly elevated muscular enzymes and pancytopenia rapidly developed. All bacteriologic, virologic, immune and radiologic investigations were normal. Evolution was spontaneously favorable with fenofibrate withdrawal. This is the first reported case of major fever and pancytopenia following a fenofibrate prescription. Adverse effects of fenofibrate are briefly reviewed and their usual favorable outcomes following drug removal are outlined.
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8/245. propylthiouracil-induced perinuclear-staining antineutrophil cytoplasmic autoantibody-positive vasculitis in conjunction with pericarditis.

    OBJECTIVE: To describe a case of propylthiouracil-induced vasculitis manifesting with pericarditis. methods: We present the first case report of a woman with hyperthyroidism treated with propylthiouracil in whom a syndrome of pericarditis, fever, and glomerulonephritis developed. Serologic testing and immunologic studies were done, and a pericardial biopsy was performed. RESULTS: A 25-year-old woman with Graves' disease had a febrile illness and evidence of pericarditis, which was confirmed by biopsy. Serologic evaluation revealed the presence of perinuclear-staining antineutrophil cytoplasmic autoantibodies (pANCA) against myeloperoxidase (MPO). propylthiouracil therapy was withdrawn, and she was treated with a 1-month course of prednisone, which alleviated her symptoms. A literature review revealed no prior reports of pericarditis in anti-MPO pANCA-positive vasculitis associated with propylthio- uracil therapy. CONCLUSION: pericarditis may be the initial manifestation of drug-induced vasculitis attributable to propylthio- uracil therapy.
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9/245. Spontaneous right ventricular outflow tract tachycardia in a patient with brugada syndrome.

    We report the case of a 28-year-old man with no structural heart disease, who exhibited clearly augmented ST segment elevation in the right precordial leads, followed by induction of spontaneous right ventricular outflow tract tachycardia with intravenous administration of Class IA antiarrhythmic drugs. The electrophysiologic mechanism of this tachycardia was thought to be triggered activity due to delayed afterdepolarizations. Due to the existence of substrates that were similar to brugada syndrome combined with right ventricular outflow tract tachycardia, this case may represent a subtype of brugada syndrome.
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10/245. Torsade de pointes induced by ajmaline.

    ajmaline, a reserpine derivative, is an effective class I antiarrhythmic agent. Herein we report two cases of ajmaline-induced abnormal QT prolongation accompanied by polymorphic ventricular tachycardia of the torsade de pointes type. Since ajmaline is increasingly used for the acute termination of wide complex tachycardia and as a diagnostic tool after syncope and in patients with idiopathic ventricular tachyarrhythmias, our observations suggest that caution should be exercised with regard to the effects of the drug on the QT interval and its potency to induce proarrhythmia of the torsade de pointes type.
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