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Re-entry tachycardia

Class Ic Ventricular tachycardia Tachycardia associated with the Wolff-Parkinson-White (WPW) syndrome AV-nodal re-entry tachycardia... [Pg.341]

Dofetihde has been used to convert atrial fibrillation and atrial flutter to sinus rhythm, in maintaining sinus rhythm thereafter, in suppressing paroxysmal supraventricular tachycardia, inducible atrioventricular nodal re-entry tachycardia, and inducible sustained ventricular tachycardia, in suppressing the dysrhythmias of the Wolff-Parkinson-White syndrome, and in facilitating conversion of ventricular fibrillation. [Pg.1173]

At 30 weeks of gestation in a 41-year-old woman the fetus had hydrops, ascites, a pericardial effusion, and bilateral hydroceles. A supraventricular tachycardia with 1 1 conduction was treated by giving the mother oral flecainide 150 mg bd. However, during the next few weeks the mother developed evidence of hepatic cholestasis. The dosage of flecainide was reduced to 50 mg bd and the liver damage resolved. The child was born healthy but later required sotalol for a re-entry tachycardia. [Pg.1373]

These slow and fast pathways can exist in different places, such as the SAN, this leads to what is termed SAN re-entry tachycardia (Fig. 6.30). When the pathway is in the AV node, this is termed AV nodal re-entry tachycardia (AVNRT). This form of re-entry tachycardia is the most common (Fig. 6.31) and presents on the ECG with a regular rhythm, fast rate usually above 130 BPM. There may also be retrograde P waves present as the SAN is triggered from below. [Pg.99]

Paroxysmal (re-entry) supraventricular tachycardia (recurrent/ refractory to vagal stimulation or adenosine)... [Pg.7]

Ventricular and supraventricular tachycardia (especially those due to re-entry phenomena), atrial fibrillation and flutter (can convert recent-onset fibrillation or flutter to sinus rhythm) Paroxysmal supraventricular tachycardia, atrial or ventricular premature beats, atrial fibrillation, or flutter (slows ventricular rate)... [Pg.157]

This agent also has some class lA and class II effects. It is effective for the treatment of ventricular and supraventricular tachycardias (AV nodal and accessory pathway re-entry, atrial flutter and fibrillation). Propafenone is useful in converting recent-onset atrial fibrillation or flutter to sinus rhythm, and for terminating paroxysmal supraventricular tachycardia. Its pro-ariythmic and myocardial depressant effects limit its use, especially in patients with poor ventricular function. [Pg.159]

DiMarco JP, Sellers TD, Belardinelli L (1984) Paroxysmal supraventricular tachycardia with Wenckebach block evidence for re-entry within the upperportion of the atrioventricular node. J Am Coll Cardiol 3(6) 1551-1555... [Pg.202]

Class la antiarrhythmic agents block fast sodium channels and prolong the action potential (class III effect), thereby lengthening the effective refractory period. They can cause QT interval prolongation, which may in turn be proarrhythmic, promoting re-entry. In the horse, they are useful for the treatment of a wide variety of arrhythmias, including both supraventricular and ventricular tachycardias. [Pg.195]

Arrhythmias occur within a few seconds after reperfusion, following ischemic periods of 10-30 min long. They start by a spontaneous stimulus in the reperfused zone and change afterward in a re-entry multiple wavelet type of ventricular tachycardia (VT) or ventricular fibrillation (VF). Extremely short action potential, short refractory period and slow conduction are the main contributing factors. Increased hyperpolarization and elevated intracellular calcium that act negatively on gap conductance impair conduction. Unidirectional conduction is favored by the marked heterogeneity in extracellular potassium, action potential and refractory period. The extra stimulus is initiated in the reperfused zone, probably by early (EAD) and late (DAD) afterdepolirizations. [Pg.27]

The only calcium channel blocking drug to have been licensed for the treatment of cardiac arrhythmias is verapamil. Its main uses are in the treatment of supraventricular tachycardia (SVT) and paroxysmal SVT. Because verapamil lengthens the ERP and FRP of the AV node and prolongs AV nodal conduction time [16], it can be used to control the ventricular rate in atrial fibrillation or atrial flutter and it usually terminates re-entry arrhythmias involving the AV node [208, 209], However, intravenous verapamil should not be given to patients who have the Wolff-Parkinson-White syndrome and atrial... [Pg.284]

Class IV anti-arrhythmic drugs usually interfere with calcium conductance such as verapamil hydrochloride. Verapamil inhibits the aetion potential of the upper and middle nodal regions of the heart where the slow inward ealeium-ion-mediated current contributes to depolarisation. This is responsible for the bloekade of slow-ehannel eonduetion in the atrioventricular node. It has been found to inhibit one limb of the re-entry circuit which is assumed to underlie most paroxysmal supraventricular tachycardias, thereby causing the reduction of ventricular rate in atrial flutter and fibrillation. [Pg.367]


See other pages where Re-entry tachycardia is mentioned: [Pg.94]    [Pg.94]    [Pg.7]    [Pg.245]    [Pg.158]    [Pg.159]    [Pg.499]    [Pg.1371]    [Pg.80]    [Pg.42]    [Pg.98]   
See also in sourсe #XX -- [ Pg.93 , Pg.98 ]




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