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Junctional tachycardia

A tachycardia made up of three or more Premature Junctional Beats. Junctional Tachycardia is usually caused by the AV node taking over as the dominant pacemaker due to enhanced automaticity. As in junctional escape beats the atria are retrogradely depolarized, resulting in inverted P waves that can occur after the QRS complex. [Pg.94]


Abnormal initiation of electrical impulses occurs as a result of abnormal automaticity. If the automaticity of the SA node increases, this results in an increased rate of generation of impulses and a rapid heart rate (sinus tachycardia). If other cardiac fibers become abnormally automatic, such that the rate of initiation of spontaneous impulses exceeds that of the SA node, other types of tachyarrhythmias may occur. Many cardiac fibers possess the capability for automaticity, including the atrial tissue, the AV node, the Purkinje fibers, and the ventricular tissue. In addition, fibers with the capability of initiating and conducting electrical impulses are present in the pulmonary veins. Abnormal atrial automaticity may result in premature atrial contractions or may precipitate atrial tachycardia or atrial fibrillation (AF) abnormal AV nodal automaticity may result in junctional tachycardia (the AV node is also sometimes referred to as the AV junction). Abnormal automaticity in the ventricles may result in ventricular premature depolarizations (VPDs) or may precipitate ventricular tachycardia (VT) or ventricular fibrillation (VF). In addition, abnormal automaticity originating from the pulmonary veins is a precipitant of AF. [Pg.110]

A-V junctional escape rhythms, junctional tachycardia atrial rhythms with slowed A-V conduction or A-V block... [Pg.338]

The most commonly reported cardiac signs of toxicity are dysrhythmias, such as ventricular ectopic depolarization, second- and third-degree heart block, junctional tachycardia, atrial tachycardia with block, ventricular tachycardia, sinoatrial block, and sinus arrest. [Pg.361]

The electrocardiographic effects of cardiac glycoside toxicity in 688 patients have been reviewed in the context of three cases of digoxin toxicity (49). The three cases featured bidirectional tachycardia in a 50-year-old man with a plasma digoxin concentration of 3.7 ng/ml, junctional tachycardia in a 59-year-old man with a plasma digoxin concentration of 4.3 ng/ml, and complete heart block in a 90-year-old woman whose postmortem digoxin concentration was 5.0 ng/ml. [Pg.650]

Barold SS, Hayes DL. Non-paroxysmal junctional tachycardia with type 1 exit block. Heart 2002 88(3) 288. [Pg.667]

A 67-year-old woman took about 7 g of procainamide and developed nausea, vomiting, lethargy, a junctional tachycardia, hypotension, and oliguria (61). She was treated with hemodialysis. [Pg.2926]

Amiodarone is indicated for the suppression and prevention of documented life-threatening, recurrent, ventricular tachycardia or fibrillation when other agents have failed. Amiodarone is also used in the management of supraventricular tachyarrhythmias including paroxysmal atrial fibrillation and atrial flutter, ectopic or multifocal atrial tachycardia, junctional tachycardia, and paroxysmal reentrant supraventricular tachycardia when other agents have failed to suppress or prevent their recurrence. Amiodarone has also been used to treat wide-complex tachycardia of uncertain mechanism. [Pg.98]

First degree, second degree (Mobitz type I), third degree AV junctional escape rhythms, junctional tachycardia Atrial arrhythmias with slowed AV conduction or AV block Particularly paroxysmal atrial tachycardia with AV block Sinus bradycardia... [Pg.244]

Junctional tachycardia originates in, or close to, the AV node. Beats are 160-250/minute, which may be paroxysmal. [Pg.481]

B. With chronic intoxication, visual disturbances, weakness, sinus bradycardia, atrial fibrillation with slowed ventricular response rate or junctional escape rhythm, and ventricular arrhythmias (ventricular bigeminy or trigeminy, ventricular tachycardia, bidirectional tachycardia, and ventricular fibrillation) are common. Accelerated junctional tachycardia and paroxysmal atrial tachycardia with block are frequently seen. Hypokalemia and hypomagnesemia from chronic diuretic use may be evident and appear to worsen the tachyarrhythmias. [Pg.156]

If a patient is over-digitalised, signs of toxicity will occur, which may include loss of appetite, nausea and vomiting, and bradycardia. These symptoms are often used as clinical indicators of toxicity, and a pulse rate of less than 60 bpm is usually considered to be an indication of over-treatment. Note that paroxysmal atrial tachycardia with AV block and junctional tachycardia can also occur as a result of digitalis toxicity. Other symptoms inelude visual disturbances, headache, drowsiness and occasionally diarrhoea. Death may result from cardiac arrhythmias. Patients treated for eardiac arrhythmias can therefore demonstrate arrhythmias when they are both under- as well as over-digitalised. [Pg.903]

Monitor cardiac rhythm tor frequent PJCs may indicate junctional irritability and can lead to more serious arrhythmia such as junctional tachycardia. [Pg.51]

For recurrent junctional tachycardia, possibly ablation therapy followed by permanent pacemaker insertion... [Pg.57]

It symptomatic with paroxysmal onset of junctional tachycardia ... [Pg.57]

Not considered junctional tachycardia because rate is below 100 beats/minute. [Pg.91]


See other pages where Junctional tachycardia is mentioned: [Pg.7]    [Pg.8]    [Pg.324]    [Pg.1257]    [Pg.323]    [Pg.202]    [Pg.596]    [Pg.312]    [Pg.332]    [Pg.5]    [Pg.56]    [Pg.57]    [Pg.94]    [Pg.83]    [Pg.93]    [Pg.93]    [Pg.93]    [Pg.95]    [Pg.280]   
See also in sourсe #XX -- [ Pg.110 ]

See also in sourсe #XX -- [ Pg.48 ]

See also in sourсe #XX -- [ Pg.93 ]

See also in sourсe #XX -- [ Pg.93 , Pg.94 ]




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