Cases reported "Heart Block"

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1/254. Pacemaker Wenckebach phenomenon due to antiarrhythmic drug toxicity.

    Two patients with intractable ventricular arrhythmia were managed with ventricular pacing and antiarrhythmic drugs. Toxic levels of these drugs results in unusual conduction disturbances at the level of Purkinje ventricular junction which caused pacemaker Wenckebach phenomenon and marked QRS prolongation. Sodium bicarbonate and sodium lactate infusion improved the conduction velocity probably by hyperpolarizing the membrane and reversed the conduction disturbance.
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ranking = 1
keywords = toxicity
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2/254. Single-lead VDD pacemaker implantation via persistent left superior vena cava: an improved technique and a new modality.

    Persistent left superior vena cava (PLSVC), which occurs in approximately 0.5% of the general population, may complicate pacemaker implantation by making lead insertion into the right ventricle more difficult and increasing lead instability when the transvenous approach is attempted. We describe our experience with four PLSVC patients with pacemakers. We developed an open J-loop technique in which the stylet tip is directed toward the orifice of the tricuspid valve anteroinferiorly. The lead was implanted into the right ventricular apex without difficulty. Three of our patients had high-degree atrioventricular block and received VVI pacemakers with the new technique. One patient with complete atrioventricular block received a single-lead VDD pacemaker by means of the same technique, with the paired electrodes positioned in the lower right atrium. Excellent results were obtained on exercise tolerance testing, 24-hour Holter monitoring, and echocardiographically determined systolic and diastolic function. This improved technique can simplify pacemaker implantation in patients with PLSVC. The VDD device is a new way to maintain systolic and diastolic function and is an appropriate option in patients with high-degree atrioventricular block and PLSVC who require pacemaker implantation.
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ranking = 273.76079752312
keywords = lead
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3/254. Inappropriate shocks delivered by implantable cardiac defibrillators during oversensing of activity of diaphagmatic muscle.

    Two cases are reported (both men, one 72 and one 54 years old) of inappropriate shocks delivered by an implantable cardiac defibrillator (ICD) device, which oversensed the myopotentials induced by deep breathing and Valsalva manoeuvre. No damage to leads was associated with the oversensing of myopotentials. The mechanism of the inappropriate shocks was determined using real time electrograms. Modification of the duration of ventricular detection and decrease in sensitivity made it possible to avoid the oversensing of myopotentials and to deliver ICD treatment.
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ranking = 34.22009969039
keywords = lead
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4/254. nicorandil, a potassium channel opener, abolished torsades de pointes in a patient with complete atrioventricular block.

    TdP is a serious complication of AV block. We report a case of complete AV block with QT prolongation who had bouts of TdP resistant to lidocaine and isoproterenol. Temporary pacing could not be performed, because insertion of a pacing lead triggered TdP that deteriorated into ventricular fibrillation. nicorandil, a potassium channel opener, shortened the QT interval and abolished TdP. This may suggest that potassium channel opening drugs are clinically effective against TdP associated with bradycardia-dependent QT prolongation.
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ranking = 34.22009969039
keywords = lead
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5/254. First-degree atrioventricular block in alprazolam overdose reversed by flumazenil.

    This report describes a case of alprazolam overdose associated with marked first-degree atrioventricular block reversed by flumazenil. Animal and human evidence suggests activity of certain benzodiazepines at peripheral benzodiazepine receptors in the myocardium and elsewhere. Myocardial benzodiazepine receptor ligands appear to affect calcium-channel activity, which may explain the clinical findings. benzodiazepines may behave like weak calcium-channel blockers. This case raises the possibility of a potential role for flumazenil as an adjunct in the management of calcium-channel blocker toxicity.
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ranking = 0.25
keywords = toxicity
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6/254. Complete heart block as a rare complication of treatment with chloroquine.

    antimalarials are well established disease modifying antirheumatic drugs. A rare and underappreciated treatment difficulty is cardiac complication, in particular conduction disturbances. We describe 2 more patients that developed complete heart block after high dose, longterm treatment. Patient 1, a 73-year-old woman with longstanding rheumatoid arthritis, had taken chloroquine (250 mg/day) for 12 years when she developed complete heart block requiring a permanent pacemaker. Patient 2, a 40-year-old woman with discoid lupus erythematosus, was taking chloroquine from 1979 until 1996. Depending on the clinical disease activity, she intermittently increased the dose from 250 to 750 mg/day. In 1994, she developed complete heart block and a permanent pacemaker had to be implanted. Intensive investigations in both cases did not reveal another underlying cause for conduction disturbances; the atrioventricular block was probably due in both cases to chloroquine related cardiac toxicity. This toxicity seems to be restricted to longterm, high dose treatment; however, it should be kept in mind in patients with preexisting conduction disturbances during longterm treatment.
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ranking = 0.5
keywords = toxicity
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7/254. Partial rupture of the tricuspid valve after extraction of permanent pacemaker leads: detection by transesophageal echocardiography.

    Traumatic lesions of the tricuspid valve complicating pacemaker lead extractions appear to be rare. We report two cases of partial rupture of the tricuspid valve, following apparently uneventful extraction of permanent ventricular leads, resulting in severe regurgitation and, in one case, chronic heart failure. TEE was useful to identify the traumatic mechanism of tricuspid regurgitation (TR) and the extent of valvular lesions in these patients. Such etiology should be suspected, and TEE performed, in patients developing TR or heart failure late after lead extraction.
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ranking = 239.54069783273
keywords = lead
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8/254. Wide QRS complex tachycardia: ECG differential diagnosis.

    Wide QRS complex tachycardias (WCT) present significant diagnostic and therapeutic challenges to the emergency physician. WCT may represent a supraventricular tachycardia with aberrant ventricular conduction; alternatively, such a rhythm presentation may be caused by ventricular tachycardia. Other clinical syndromes may also demonstrate WCT, such as tricyclic antidepressant toxicity and hyperkalemia. Patient age and history may assist in rhythm diagnosis, especially when coupled with electrocardiographic (ECG) evidence. Numerous ECG features have been suggested as potential clues to origin of the WCT, including ventricular rate, frontal axis, QRS complex width, and QRS morphology, as well as the presence of other characteristics such as atrioventricular dissociation and fusion/capture beats. Differentiation between ventricular tachycardia and supraventricular tachycardia with aberrant conduction frequently is difficult despite this clinical and electrocardiographic information, particularly in the early stages of evaluation with an unstable patient. When the rhythm diagnosis is in question, resuscitative therapy should be directed toward ventricular tachycardia.
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ranking = 0.25
keywords = toxicity
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9/254. Prominent bifid T waves observed in the QT prolongation caused by complete atrioventricular blockade in a hypokalemic diabetic patient.

    A 63-year-old diabetic man was admitted with general fatigue. Electrocardiogram (ECG) on admission showed complete atrioventricular (AV) blockade associated with prominent bifid T waves. The second component of the bifid T waves was distinguished from U waves by the beat-to-beat varying bifidity and the nadir between the two components located at > or = 1 mm above the isoelectric line. Range of absolute QT interval was 535 to 650 ms. hypokalemia (3.6 mEq/L) was noted at admission. Partial restoration of the potassium level (3.9 mEq/L) prior to temporary ventricular demand pacing obscured the bifid T waves and attenuated the QT prolongation and dispersion to some extent (absolute QT interval ranging 520 to 620 ms). It was concluded that marked bradycardia caused by complete AV blockade (ie, a junctional escaped rhythm at a rate of 42 beats/min), hypokalemia, and underlying diabetes mellitus contributed in concert to the QT prolongation and dispersion leading to the prominent bifid T waves.
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ranking = 34.22009969039
keywords = lead
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10/254. Pseudo A-V block. Part II.

    This vignette demonstrates the importance of analyzing arrhythmias in the context of their particular clinical setting. Analysis and treatment of an arrhythmia without clinical information leads to errors in judgment. Arrhythmias may be interpreted as a didactic exercise that is used in the process of teaching and learning. However, when the question is asked, "How do you treat this arrhythmia?", then all clinical information ambient to the arrhythmia in question has to be available for analysis and judgment.
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ranking = 34.22009969039
keywords = lead
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