Cases reported "Tachycardia"

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1/133. 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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2/133. electrocardiography in the patient with the wolff-parkinson-white syndrome: diagnostic and initial therapeutic issues.

    The wolff-parkinson-white syndrome (WPW), estimated to occur in approximately 0.1% to 3% of the general population, is a form of ventricular preexcitation involving an accessory conduction pathway. The definition of WPW relies on the following electrocardiographic features: (1) a PR interval less than 0.12 seconds (2) with a slurring of the initial segment of the QRS complex, known as a delta wave, (3) a QRS complex widening with a total duration greater than 0.12 seconds, and (4) secondary repolarization changes reflected in ST segment-T wave changes that are generally directed opposite (discordant) to the major delta wave and QRS complex changes. The accessory pathway bypasses the atrioventricular (AV) node, creating a direct electrical connection between the atria and ventricles. The majority of patients with preexcitation syndromes remain asymptomatic throughout their lives. When symptoms do occur they are usually secondary to tachyarrhythmias; the importance of recognizing this syndrome is that these patients may be at risk to develop a variety of supraventricular tachyarrhythmias which cause disabling symptoms and, in the extreme, sudden cardiac death. The tachyarrhythmias encountered in the WPW patient include paroxysmal supraventricular tachycardia (both the narrow QRS and wide QRS complex varieties), atrial fibrillation, atrial flutter, and ventricular fibrillation. Diagnostic and urgent, initial therapeutic issues based on initial electrocardiographic information are presented via 5 illustrative cases.
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3/133. The diagnosis or ventricular tachycardia with ventriculo-atrial conduction.

    A 57 year old man developed recurrent tachycardia with QRS complexes of 0.13 second in duration at a rate of 140 beats per minute. Inverted P waves appeared to follow each QRS complex in the electrocardiographic leads II, III and aVF. The differentiation between ventricular tachycardia with1 : 1 V-A conduction and supraventricular tachycardia with aberrant ventricular conduction was difficult to make from the surface electrocardiogram. This differentiation is important for selection of appropriate therapy. The diagnosis of ventricular tachycardia with 1 : 1 V-A conduction was clearly established in this case on simultaneous recording of surface electrocardiogram, His bundle electrogram and high right atrial electrogram.
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4/133. Bidirectional tachycardia a study of five cases.

    Five patients with bidirectional tachycardia due to digitalis toxicity associated with severe organic heart disease were studied. The origin of the abnormal rhythm was established with the aid of His bundle recordings in three cases and by indirect clues in the others two. In three cases the origin of bidirectional tachycardia was suprahisian while in two patients it was infrahisian. In one patient the transition from junctional to ventricular tachycardia could be observed. Bidirectional tachycardia appears to be a complex arrhythmia in which similar electrocardiographic configuration can be due to different mechanism. digitalis toxicity was often a causal factor.
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5/133. lidocaine-induced conduction disturbance in patients with systemic hyperkalemia.

    We report 2 cases in which lidocaine, given for wide-complex tachycardia in the presence of hyperkalemia, precipitated profound conduction disturbance and asystole. The electrophysiologic effects of hyperkalemia and its interaction with lidocaine are reviewed. In patients with known hyperkalemia and wide-complex tachycardia, treatment should be directed at hyperkalemia, rather than following treatment algorithms for wide-complex tachycardia.
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6/133. Concealed accessory pathway with long conduction times and incremental properties: a case report.

    Concealed AP with Slow and Incremental Conduction. We report a peculiar form of permanent junctional reciprocating tachycardia that occurs only during daytime and physical activity. ECG obtained during tachycardia showed an unusual progressive shortening of the ventriculoatrial (VA) interval that was maximal at the first complex and shortest at the last one before block occurred, always at the accessory pathway level. This phenomenon has not been previously described and appears to be a reverse type of Wenckebach block. It was observed during salvos of spontaneous tachycardia and could be reproduced by right ventricular pacing. The accessory pathway was ablated successfully at the right posteroseptal region, close to the coronary sinus ostium. After ablation, there was no VA conduction, and tachycardia did not recur during a 9-month follow-up period.
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7/133. 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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8/133. Post exertional broad complex tachycardia in a normotensive patient: a rare presentation of phaeochromocytoma.

    Phaeochromocytomas are rare cause of secondary hypertension with significant morbidity and mortality, if left untreated. Paroxysms with hypertension are considered as "textbook" presentations but atypical forms represent considerable diagnostic challenge. We report an unusual association between phaeochromocyotoma and post-exertional malignant arrhythmia in a normotensive subject.
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9/133. 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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10/133. Wide complex tachycardia and congenital heart disease.

    We present a patient with congenital heart disease and haemodynamically poorly tolerated wide QRS tachycardia. Differential diagnosis and therapy are discussed. After the patient underwent heart transplantation, and the substrates for ECG abnormalities and arrhythmias were demonstrated in the explanted heart.
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