Cases reported "Bradycardia"

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1/163. bradycardia during citalopram treatment: a case report.

    The authors report the case of a 47-year-old depressive woman treated with citalopram 20 mg day-1 for 3 months who presented a marked sinus bradycardia (34 beats/min) 11 days after the citalopram dose was increased to 40 mg day-1. The bradycardia was clinically asymptomatic and disappeared within 24 h after citalopram was stopped. citalopram blood levels were in the usual therapeutic range.
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2/163. Pseudo second degree atrioventricular block with bradycardia. Successful treatment with quinidine.

    Pseudo second degree atrioventricular block resulting from blocked His premature beats was successfully treated with quinidine. The diagnosis was proved by His bundle electrogam which showed both blocked and conducted His premature beats. The blocked His prematures produced second degree atrioventricular block by making the atrioventricular junction refractory. quinidine abolished both conducted and blocked His extrasystoles. There has been no recurrence of arrhythmia during a one-year follow-up.
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3/163. Ictal bradycardia in a patient with a hypothalamic hamartoma: a stereo-EEG study.

    Little is known about bradycardia and cardiac asystole which occur during partial epileptic seizures, especially whether they relate to ictal involvement of well-defined cortical areas. Several reports based on simultaneous electrocardiographic and intracranial depth electroencephalographic monitoring have shown that either the fronto-orbital cortex or the amygdalohippocampal complex could be responsible for such cardiac variations. We performed stereo-EEG recordings in a patient with refractory localization-related epilepsy associated with a hypothalamic hamartoma. We found that other cortical areas, such as the frontocentral region and the temporal neocortex, can contribute to the genesis of ictal bradyarrhythmia. Second, the lesion per se, although located within the hypothalamus, is not involved with this phenomenon.
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keywords = complex
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4/163. Familial association of congenital left heart abnormalities and sustained fetal arrhythmia.

    hypoplastic left heart syndrome (HLHS) is the most common cause of death from heart disease in the first week of life. There are reports about familial concordance by presumed morphogenetic mechanisms of abnormal embryonic blood flow with phenotypes of varying severity. The risk of having a child with a left heart lesion after a previously affected child may be as high as 5% to 12%. We present case reports from four families in which sustained fetal arrhythmia (three ectopic atrial tachycardias and one severe bradycardia due to excessive ectopic atrial beats) was demonstrated. Within these four families a close relative of the mother (a previous child, a brother, or a nephew) had severe left heart abnormality (three with HLHS and one with severe aortic valve stenosis). The association of sustained fetal arrhythmia of ectopic atrial origin and severe left heart abnormalities could be expected to occur by chance in a very low percentage of cases. We conclude that sustained fetal atrial ectopic arrhythmia is a congenital abnormality and should be considered as a risk factor for inherited congenital heart abnormalities.
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5/163. The effect of maternal hypothermia on the fetal heart rate.

    Fetal bradycardia is a recognized response to maternal hypothermia but has not previously been reported in conjunction with diabetes. A 30-year-old insulin-dependent diabetic was admitted at 35 weeks gestation for control of her diabetes. She developed maternal hypothermia and hypoglycemia and the fetal heart rate fell to 100 beats per minute (b.p.m.). However, the fetal heart rate gradually returned to normal after rewarming the patient.
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6/163. bradycardia and asystole with the use of vagus nerve stimulation for the treatment of epilepsy: a rare complication of intraoperative device testing.

    PURPOSES: A 56-year-old man with mild mental retardation, right congenital hemiparesis, and refractory partial seizures was referred for vagus nerve stimulation (VNS). methods: Routine lead diagnostic testing during the surgical procedure (1.0 mA, 20 Hz, and 500 micros, for approximately 17 s) resulted, during the initial two stimulations, in a bradycardia of approximately 30 beats/min. A third attempt led to transient asystole that required atropine and brief cardiopulmonary resuscitation. RESULTS: The procedure was immediately terminated, the device removed, and the patient recovered completely. A postoperative cardiologic evaluation, including an ECG, 24-h Holter monitor, echocardiogram, and a tilt-table test, was normal. CONCLUSIONS: Possible mechanisms for the bradycardia/asystole include stimulation of cervical cardiac branches of the vagus nerve either by collateral current spread or directly by inadvertent placement of the electrodes on one of these branches; improper plugging of the electrodes into the pulse generator, resulting in erratic varying intensity of stimulation; reverse polarity; and idiosyncratic-type reaction in a hypersusceptible individual. The manufacturer reports the occurrence rate in approximately 3,500 implants for this intraoperative event to be approximately one in 875 cases or 0.1%.
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7/163. 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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ranking = 0.25839766021203
keywords = supraventricular
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8/163. Using ultrasound to determine external pacer capture.

    Transcutaneous cardiac pacing is a temporary treatment of hemodynamically unstable bradycardias. However, the rhythmic skeletal muscle contractions that occur during external pacing can make it difficult to assess the hemodynamic status of the patient. We report a case of using bedside ultrasound to assess the effectiveness of transcutaneous pacer capture.
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ranking = 0.0046063390918358
keywords = contraction
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9/163. Hemodynamic during a postexertional asystolia in a healthy athlete: a case study.

    Hemodynamic events leading to spontaneous postexertional vasovagal syncope are not completely understood because of the lack of beat-to-beat data. We report a case study of a young athlete who undergoes a syncopal episode during the recovery period following a maximal cycle-ergometer test. The episode was monitored by an impedance cardiograph which can gather noninvasively beat-to-beat the flow of heart rate (HR), stroke volume (SV), cardiac output (CO), diastolic filling rate (SV/DT), and myocardial contractility index (PEP/LVET). The most important findings of this report are the dramatic reduction of SV/DT preceding the syncope, the increment of SV together with the reduction of HR preceding and following the syncope, the prompt recovery of CO values after the syncopal episode despite the bradycardia, and the reduction of PEP/LVET after the syncope. This report confirms the importance of active recovery immediately after strenuous exercise and supports the hypothesis that the reduction of SV/DT in the presence of an inotropic stimulation can trigger the vasovagal reaction.
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10/163. Fetal and neonatal arrhythmia in one of the twins--a case history.

    There are a lot of publications about fetal arrhythmia in singletons, but up to now there are no published data about fetal arrhythmia in multiple pregnancies. In the present study a case history of fetal and neonatal arrhythmia in one of twins from two mothers treated with betamimetic agents due to imminent preterm labor is reported and discussed. A first case with fetal bradycardia due to complete A-V block had congenital cordis abnormalities (VSD and PFO). The second case with prenatal detected extrasystoles had normal heart anatomy. digoxin was administered to the mother, in the aim to treat fetal arrhythmia without success, because the baby had postnatal bradycardia. After hospitalisation in cardiology Department the described cases were successfully treated. In both cases the second twins were without neonatal arrhythmia and with no structural heart abnormalities. We summarise that in situation of detection fetal arrhythmia the complexity of the problems experienced may warrant early referral to a tertiary centre where the overall management of the mother, fetus and neonate, may be undertaken.
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keywords = complex
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