Cases reported "Bradycardia"

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1/20. 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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2/20. Severe bradycardia and bradypnea following vaginal oocyte retrieval: a possible toxic effect of paracervical mepivacaine.

    We report a case of a patient with a history of heart conduction disease, symptom-free and without treatment in the last years, who experienced a severe cardiac complication associated with in vitro fertilization (IVF) with vaginal oocyte retrieval (VOR). Eighty-five minutes after the VOR a severe bradycardia and bradypnea occurred, requiring an emergency application of a pacemaker. Presumably the condition occurred because of a toxic effect of the 400 mg of mepivacaine administered paracervically. It is concluded that in the paracervical anesthesia in the IVF cycles the therapeutic range should be scrupulously followed in patients with heart condition.
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3/20. Apparent bradycardia-dependent sinoatrial block associated with respiration.

    In our previous patients, apparent bradycardia-dependent block has been shown in the atrioventricular (AV) junction and in the accessory pathway. It was suggested that these previous cases were not of true bradycardia-dependent block; namely, that, as a result of periodic increases in vagal tone associated with respiration, conductivity in the AV junction or in the accessory pathway was depressed to a greater degree than automaticity in the sinus node. In the present article, 3 patients with frequent sinoatrial (SA) block were reported. In 1 patient, sinus escape-capture bigeminy caused by SA block was found. In these present patients, when the sinus cycle lengthened, SA block occurred. The purpose of the present article is to show that the patients have apparent bradycardia-dependent SA block, namely, not true bradycardia-dependent SA block. In all patients, the respiration curve was recorded simultaneously with the electrocardiogram. In all patients, during inspiration, the sinus cycle gradually shortened; on the other hand, during expiration, the sinus cycle gradually lengthened, and then a sinus impulse was blocked in the SA junction. These findings suggested that increased vagal tone during expiration depressed conductivity in the SA junction to a greater degree than automaticity in the sinus node.
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4/20. Mechanism of bradycardia-dependent appearance of manifest extrasystoles in concealed bigeminy. A theoretical model derived from the concepts of longitudinal dissociation and multilevel block in the reentrant pathway of extrasystoles.

    A case of bradycardia-dependent appearance of manifest extrasystoles in concealed bigeminy is presented. To explain the mechanism of such bradycardia-dependent appearance, a theoretical model is derived from the concepts of "longitudinal dissociation" and "multilevel block" in the reentrant pathway of extrasystoles. In the theoretical model, functional longitudinal dissociation divides the reentrant pathway into dual pathways F and S. When manifest extrasystoles are not found for a long time, alternate sinus impulses pass through both pathways F and S, but become concealed extrasystoles because of insufficient conduction delay in the pathways. The other alternate sinus impulses are blocked in the pathways; in pathway F, the impulses are blocked at the entrance, while in pathway S, the impulses are blocked at a more distal level. When sinus cycles gradually lengthen, one of such alternate sinus impulses passes through the entrance of pathway F and, traveling very slowly, is blocked at a more distal level. The next sinus impulse is blocked at the entrance of pathway F; namely, 3:2 Wenckebach block occurs at the entrance of pathway F. Thus this sinus impulse enters only pathway S and passes through pathway S with enough conduction delay to become a manifest reentrant extrasystole.
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5/20. Apparent bradycardia-dependent right bundle branch block associated with atypical atrioventricular Wenckebach periodicity as a possible mechanism.

    The Holter monitor electrocardiogram was taken from a 15-year-old male athlete. Intermittent right bundle branch block frequently occurred at rest. When sinus cycles gradually lengthened, sinus impulses were conducted to the ventricles with right bundle branch block (RBBB) in succession. When, thereafter, sinus cycles gradually shortened, sinus impulses were conducted without RBBB. However, it seems that these findings do not show true bradycardia-dependent RBBB. Atypical atrioventricular Wenckebach periodicity was occasionally found in which sudden shift from the period of comparatively short PR intervals to the period of long PR intervals occurred. In the Wenckebach periodicity, when a QRS complex occurs after a much longer pause, RBBB was not found, while when it occurs after a much shorter period, RBBB was found. This suggests that this case may be apparent bradycardia-dependent RBBB, namely, a form of tachycardia-dependent RBBB. This is the first report suggesting apparent bradycardia-dependent bundle branch block associated with gradual lengthening of sinus cycles, as a possible mechanism.
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6/20. tachycardia- and bradycardia-dependent atrioventricular block: observations regarding the mechanism of block.

    A case of paroxysmal bradycardia- and tachycardia-dependent atrioventricular (AV) block is described in a patient with right bundle branch block. The His bundle recordings demonstrated the site of the AV block to be distal to the His bundle recording site (probably in the left bundle branch). Whereas AV block distal to the His bundle occurred at an atrial paced cycle length of 700 ms, intact ventriculoatrial (VA) conduction was present up to a ventricular paced cycle length of 400 ms. Resumption of AV conduction was dependent on a critical HH or RH (in case of escapes) interval. These findings suggest that the bradycardia-dependent block is related to a time-dependent decrease in the amplitude of the current intensity of the proximal segment during late diastole. Spontaneous diastolic depolarization during late diastole resulted in impaired anterograde (AV) conduction but facilitated retrograde (VA) conduction. These findings are consistent with experimental "in vitro" observation in the sucrose gap model of AV block.
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7/20. Evaluation and management of a supraventricular tachycardia with a standard bradycardia support pacemaker.

    A standard dual chamber pacemaker with the ability to telemeter intracardiac electrograms and to perform noninvasive electrophysiological studies was implanted in a patient with previously documented complex ventricular arrhythmias treated with amiodarone who later presented with a hypersensitive carotid sinus syndrome and syncope. Subsequently, he developed a supraventricular tachyarrhythmia with an atrial cycle length of 320 ms. Its diagnosis was facilitated by the ability to noninvasively telemeter atrial endocardial electrograms directly from the implanted pacemaker. Its management was aided by utilizing the already implanted bradycardia support pacemaker to stimulate the patient with premature extrastimuli coupled to his intrinsic atrial rhythm (PS1 and S1S2 each 170 ms.) by connecting the pacemaker to an electrophysiological stimulator via the pacemaker programmer. This particular pacemaker was not chosen because of this capability at the time of its original implantation. However, this capability facilitated the patient's evaluation and subsequent management.
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8/20. quinidine-induced long QTU interval and torsade de pointes: role of bradycardia-dependent early afterdepolarizations.

    Right ventricular endocardial monophasic action potential recordings were obtained in a patient with a qunidine-induced long QTU interval and polymorphic ventricular tachycardia of the torsade de pointes type. The recording showed a deflection on phase 3 repolarization characteristic of early afterdepolarization. The early afterdepolarization was synchronous with the U wave in surface electrocardiographic leads and there was a strong correlation between the amplitude of both waves. A strong correlation was also present between the cardiac cycle length and the U wave amplitude with larger amplitudes after longer cycles. Ventricular ectopic beats occurred only after long cycle lengths and seemed to arise close to the peak of the U wave and early afterdepolarization. However, there was no correlation between the amplitude of the U wave or early afterdepolarization and the occurrence of ectopic beats. Rapid ventricular pacing resulted in suppression of the ectopic rhythm associated with suppression of both the U wave and the early afterdepolarization. This case provides the first evidence to suggest that a quinidine-induced long QTU interval and torsade de pointes may be related to bradycardia-dependent early afterdepolarizations, although other factors may be involved in triggering the arrhythmia.
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9/20. Sinoatrial and atrioventricular dysfunction associated with the use of guanabenz acetate.

    guanabenz acetate is an antihypertensive drug that is closely related to clonidine hydrochloride. clonidine is well known to potentiate atrioventricular (AV) node conduction disturbances, but to date that effect has not been attributed to guanabenz. A case of electrocardiographic and electrophysiologic studies in a patient with both sinus and AV node conduction disturbances associated with the use of guanabenz acetate is reported. The sinus cycle length was increased by 50% after guanabenz and the sinus node recovery time was prolonged by 42%. AV block occurred proximal to the His bundle and His-ventricular prolongation of 42% also occurred. This drug should be used cautiously in patients with evidence of sinus or AV node dysfunction.
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10/20. Complete sinoatrial block in two patients with bradycardia-tachycardia syndrome.

    Electrophysiologic studies with recordings of sinus node electrograms were performed in two patients with bradycardia-tachycardia syndrome. In both patients, the rest electrocardiogram showed apparent sinus bradycardia. Patient 1 had frequent paroxysms of atrial tachycardia with long pauses of up to 10 seconds; Patient 2 had paroxysmal atrial flutter and atrial pauses of up to 8 seconds. Multiple, repetitive, low frequency deflections, with a cycle length ranging from 730 to 960 ms in Case 1 and 570 to 750 ms in Case 2, suggestive of sinus node electrograms, were recorded at a critical area at the junction between the superior vena cava and the right atrium. These low frequency deflections had no relation to spontaneous junctional beats or the spontaneous atrial beats that showed high frequency deflections on the atrial electrogram. However, they could be suppressed by spontaneous or paced atrial beats. Pharmacologic interventions in Case 2 showed that the cycle length of the low frequency deflections shortened after administration of isoproterenol and did not change after propranolol or atropine. Thus, complete sinoatrial exit block with intact entrance conduction can occur in patients with bradycardia-tachycardia syndrome. Under such circumstances, the surface electrocardiographic manifestation of sinus bradycardia may not be of sinus origin.
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