Treatment

1. No specific treatment is usually required.

2. Treat the underlying disorder.

3. Antiarrhythmic therapy with quinidine or procainamide may be useful if JPCs are frequent, symptomatic, or initiate more serious dysrhythmias.

JUNCTIONAL RHYTHMS Under normal circumstances, the sinus node discharges at a faster rate than the AV junction, so the pacemaker function of the AV junction and all other slower pacemakers is suppressed (overdrive suppression). If sinus node discharges slow or fail to reach the AV junction, then junctional escape beats may occur, usually at a rate between 40 and 60, depending on the level of the pacemaker. Generally, junctional escape beats do not conduct retrograde into the atria, so a QRS complex without a P' wave is usually seen (Fig.„1124:14).

FIG. 24-14. Junctional escape rhythm, rate 42.

Under other circumstances, enhanced junctional automaticity may override the sinus node and produce either an accelerated junctional rhythm (rate 60 to 100) or junctional tachycardia (rate greater than 100). Usually, the enhanced junctional pacemaker ( Fig 24:15) captures both the atria and ventricles.

FIG. 24-15. Accelerated junctiional rhythm, rate 61.

Clinical Significance Junctional escape beats may occur whenever there is a long enough pause in the impulses reaching the AV junction: sinus bradycardia, slow phase of sinus dysrhythmia, AV block, or during the pause following premature beats. Sustained junctional escape rhythms may be seen with congestive heart failure, myocarditis, hypokalemia, or digoxin toxicity. If the ventricular rate is too slow, myocardial or cerebral ischemia may develop.

Accelerated junctional rhythm and junctional tachycardia may occur from digoxin toxicity, acute rheumatic fever, or inferior myocardial infarction. With digoxin toxicity, the rate is usually between 70 and 130. If this rhythm develops in a patient being treated with digoxin for atrial fibrillation, the ECG is characterized by regular QRS complexes superimposed on atrial fibrillatory waves. Regulation of ventricular response during digoxin therapy in a patient with atrial fibrillation should therefore raise the suspicion of digoxin toxicity.

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