Cases reported "Tachycardia, Sinus"

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1/27. Laboratory confirmation of scopolamine co-intoxication in patients using tainted heroin.

    BACKGROUND: First described in 1995, at least 325 patients with a history of heroin use have since required emergency medical evaluation in several eastern US cities, because of an anticholinergic toxidrome following use of heroin. This co-intoxication has been alleged to result from an atropine-like compound. We report the clinical findings and laboratory analysis of one of several individuals who presented to our Emergency Department during this epidemic. CASE REPORT: A 23-year-old male was one of 3 patients brought to the Emergency Department due to agitated behavior after insufflating heroin. Following physical and chemical restraint, vital signs were pulse 134 bpm, BP 160/90 mm Hg, RR 24/min, and T 37.3 degrees C. physical examination was remarkable for dilated pupils 8-9 mm without nystagmus, along with dry mouth, decreased bowel sounds, and flushed dry skin. A bladder catheter was placed and 500 mL of urine was obtained. Electrocardiogram revealed sinus tachycardia only. Additional sedation was required for 12 hours until normal mental status returned. A small sample of the "heroin" used was obtained and analyzed. Scopolamine was confirmed by gas chromatography-mass spectrometry. Further evidence of scopolamine intoxication was supported by identifying scopolamine in the urine of this patient. CONCLUSION: gas chromatography-mass spectrometry revealed scopolamine to be the cause of anticholinergic findings in a patient following use of tainted heroin. It is unclear whether scopolamine is an adulterant or contaminant in this heroin. patients with anticholinergic findings following use of heroin may be co-intoxicated with scopolamine.
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2/27. Evidence of sinoatrial block as a curative mechanism in radiofrequency current ablation of inappropriate sinus tachycardia.

    Inappropriate sinus tachycardia is a nonparoxysmal tachycardia characterized by high resting heart rates and a disproportionate response to activity. Sinus node modification with radiofrequency current has been used successfully as treatment for this arrhythmia. However, the electrophysiologic mechanisms leading to successful modification are not yet fully elucidated. We report a case of a patient with drug-resistant inappropriate sinus tachycardia in whom successful treatment of the arrhythmia was achieved by documented sinoatrial exit block induced by radiofrequency current applications.
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ranking = 1718.0278937245
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3/27. theophylline toxicokinetics in premature newborns.

    BACKGROUND: While cytochrome P4501A2 is the primary pathway for theophylline (aminophylline ethylenediamine) metabolism in adults, it is developmentally immature in the newborn. OBJECTIVE: To report the developmental differences in theophylline toxicokinetics of neonates. DESIGN: Case series. Three premature neonates received inadvertent intravenous overdoses of theophylline for apnea of prematurity while in newborn intensive care. Maximum serum concentrations ranged from 55 to 123 mg/L. theophylline-derived caffeine levels plateaued at 8.4 to 13 mg/L and did not decline during the sampling period. All newborns experienced sinus tachycardia and agitation. Sequential theophylline and caffeine serum levels were obtained periodically for 62 to 100 hours. In contrast to older children and adults, in whom theophylline disposition follows zero-order kinetics at high concentrations, a monoexponential function best described theophylline elimination in the premature newborn, with half-lives ranging from 24.7 to 36.5 hours and estimated clearance from 0.02 to 0.05 L/kg per hour. These values are consistent with those previously reported in neonates. All patients were treated with supportive care without invasive procedures. No seizures or apparent sequelae occurred. CONCLUSION: Developmental differences in the balance between nonrenal (ie, metabolic) and renal elimination pathways produce the unique toxicokinetics of theophylline in the neonate.
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4/27. clenbuterol ingestion causing prolonged tachycardia, hypokalemia, and hypophosphatemia with confirmation by quantitative levels.

    BACKGROUND: clenbuterol is a long acting beta2-adrenergic agonist used in the treatment of pulmonary disorders. Acute clenbuterol toxicity resembles that of other beta2-adrenergic agonists. Most previously reported cases of clenbuterol toxicity describe patients who ate livestock illicitly treated with clenbuterol. CASE REPORT: We report a case of human clenbuterol toxicity confirmed and correlated with qualitative and quantitative serum clenbuterol assays. This poisoned patient, a 28-year-old woman, developed sustained sinus tachycardia at 140/min, hypokalemia (2.4 mEq/L, 2.4 mmol/L), hypophosphatemia (0.9 mg/dL, 0.29 mmol/L), and hypomagnesemia (1.52 mg/dL, 0.76 mmol/L) after ingesting a reportedly small quantity of clenbuterol. The patient received repeated doses of metoprolol to treat her cardiovascular stimulation and potassium chloride to treat her hypokalemia. She remained symptomatic for more than 20 hours after the ingestion. Analysis by enzyme-linked immunosorbent assay and liquid chromatography/mass spectrometry revealed a serum clenbuterol concentration of 2.93 mcg/L 3 hours after the ingestion and an undetectable serum concentration 20 hours after ingestion. It is noteworthy that at a serum concentration below the limit of detection by liquid chromatography/mass spectrometry, the patient remained symptomatic. Acute clenbuterol toxicity is rarely reported following illicit use in humans, and this is the first such case to provide confirmatory toxicological analysis.
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5/27. Lactic acidosis associated with the usual theophylline dose in a patient with asthma.

    Metabolic and electrolyte abnormalities, including hypokalemia, hyperglycemia and lactic acidosis, are associated with theophylline overdose. However, we report an unusual case of sinus tachycardia, lactic acidosis, hypokalemia and hyperglycemia associated with the usual theophylline dose in a patient with asthma. The theophylline dose was 200 mg orally twice daily. Three hours after administration of the third dose, the patient experienced palpitation. An electrocardiogram showed a sinus tachycardia. Arterial blood gas analysis revealed a mixed metabolic acidosis and respiratory alkalosis. serum lactate level was 51 mmol/L (normal 0.7-2.1 mmol/L). biochemistry results were sodium 136 mEq/L, chloride 99 mEq/L, potassium 1.9 mEq/L and glucose 204 mg/dL. Our case suggests that a possibility of theophylline-associated metabolic abnormalities should be considered when an asthmatic patient given the usual theophylline dose presents with lactic acidosis, hypokalemia and hyperglycemia of unknown etiology.
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6/27. hypoglycemia after albuterol overdose in a pediatric patient.

    albuterol overdose can lead to tachycardia, hypotension, tremor, hypokalemia, and hyperglycemia in children. hypoglycemia had been previously reported in only one child. We describe a 3-year-old boy who ingested high-dose albuterol in this report. On arrival to the emergency department, the child was agitated and had noticeable restlessness, sinus tachycardia, mild hypokalemia (3.2 mEq/L), and hyperglycemia (187 mg/dL). Activated charcoal and intravenous hydration were given, and electrocardiogram monitoring was performed. Sinus tachycardia resolved within 4 to 6 hours. hypoglycemia (45 mg/dL) was identified 4 hours after admission. The child recovered uneventfully within 24 hours with glucose replacement. This case suggests that hypoglycemia could be a late complication of acute albuterol overdose; thus, the period of observation should be extended in these cases.
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7/27. Anomalous origin of the left coronary artery with diffuse coronary hypoplasia resulting in sudden death.

    A case of sudden death is reported in a 13-year-old boy due to an acute myocardial infarction and arrhythmias following exertion. On autopsy, he was found to have an anomalous origin of the left coronary artery, an acute angle of takeoff of the left coronary artery, and diffuse hypoplasia of both the left and right coronary arteries. Both arteries had markedly small lumens throughout their course. This report provides the first description of this combination of congenital coronary artery abnormalities resulting in sudden death.
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ranking = 859.01394686226
keywords = rhythm
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8/27. ECG of the month. hypotension, pulmonary edema, and an irregular cardiac rhythm in a 50-year-old woman. Sinus tachycardia, type I (Wenckebach) second degree atrioventricular block, acute inferoposterior myocardial infarct, and anterolateral myocardial infarct of indeterminate age (probably old).

    A 50-year-old woman came to the emergency department because of chest discomfort and dyspnea. She was found to have hypotension, oliguria, and pulmonary edema, i.e., full-blown cardiogenic shock, an irregular rhythm, and no cardiac murmur. The electrocardiogram (ECG) was recorded one lead at a time, and a lead II rhythm strip was mounted above the standard 12 leads (Figure 1).
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ranking = 5154.0836811736
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9/27. Pseudosinus tachycardias originating from left pulmonary veins.

    The case of a 55-year-old man with LV dysfunction in whom the baseline cardiac rhythm falsely mimicked a sinus rhythm (SR) but actually originated from the left superior and inferior pulmonary vein (PV) is reported. The P waves before ablation were flat in leads I and V1, negative in lead aVL, and positive in leads II, III, aVF. After the left superior PV was isolated from the left atrium, another ectopic rhythm newly appeared from the left inferior PV. Interestingly, the LV systolic function improved after the resumption of the SR, thus suggesting that tachycardia-induced cardiomyopathy might be involved in the mechanism of LV systolic disturbance.
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ranking = 2577.0418405868
keywords = rhythm
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10/27. Arrhythmias induced by device antitachycardia therapy due to diagnostic nonspecificity.

    New technology has produced automatic cardioverter-defibrillators capable of delivering antitachycardia pacing, as well as low and high energy shocks and backup bradycardia pacing. These expanded treatment options have led to a wider range of clinical applications for such devices, including the treatment of ventricular tachycardias with longer cycle lengths, which may overlap the cycle lengths of some supraventricular arrhythmias. The diagnostic capability of these devices, although improved, has not advanced sufficiently to ensure reliable discrimination between all supraventricular and ventricular arrhythmias. Two cases are presented in which device-mediated pacing therapy, triggered by supraventricular arrhythmias, induced ventricular tachycardia requiring additional therapeutic intervention. This report illustrates the therapeutic versatility and some of the potential pitfalls, of the recently developed devices and reviews the status of automatic arrhythmia identification technology.
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ranking = 6872.1115748981
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