AV JUNCTIONAL RHYTHM DISTURBANCES



If suprajunctional pacemakers fail, a junctional escape rhythm may emerge at a rate of 35 to 60 beats per minute. The junctional escape rhythm is usually fairly regular, but the rate may increase gradually when the escape rhythm first begins (warm-up phenomenon). A junctional rhythm may be associated with retrograde P waves for each QRS complex, or AV dissociation may be present.

Premature junctional complexes arise from the AV junction. A retrograde P wave is usually pres­ent but may be prevented by a sinus P wave. They usually do not require therapy. A regular junctional rhythm with a rate ex­ceeding 60 beats per minute (usually between 70 and 130 per minute) is considered an accelerated junctional rhythm or nonparoxysmal AV junc­tional tachycardia. The gradual onset and ter­mination account for the term nonparoxysmal and may imply that the mechanism of the tachycardia is increased automaticity. Retrograde activation of the atria or AV dissociation may be present. Non­paroxysmal AV junctional tachycardia occurs most commonly in patients with underlying heart disease, such as inferior myocardial infarction, myocarditis, and acute rheumatic fever, or after open heart surgery. The most common cause is digitalis excess. Therapy is directed toward the underlying etiological factor.

Paroxysmal supraventricular tachycardias (PS VT) are regular tachycardias that occur and ter­minate suddenly. They are due to a variety of mechanisms, the most common of which are atrio­ventricular (AV) nodal re-entry (approximately 60 per cent of cases) and AV re-entry using a con­cealed accessory bypass tract (approximately 30 per cent of cases). Sinus nodal re-entry, intra-atrial re­entry, and automatic atrial tachycardias account for the remaining PSVT’s.

AVnodaJ re-entry is characterized by narrow QRS complexes (unless functional aberration has oc­curred), sudden onset and termination, and regular rates, usually between 150 and 250 beats per minute. Carotid sinus massage may slow the tachy­cardia slightly, and if termination occurs, it is abrupt. AV nodal re-entry commonly occurs in pa­tients with no organic heart disease. Symptoms vary according to the rate of the tachycardia and the presence of organic heart disease. In some pa­tients, rest, reassurance, and sedation may abort an attack. Vagal maneuvers including Valsalva, carotid sinus massage, and gagging may terminate the tachycardias and should be repeated after each pharmacological intervention. Intravenous vera­pamil, 5 to 10 mg, terminates AV nodal re-entry after about two minutes in over 90 per cent of cases and is the treatment of choice should vagal maneuvers fail. Edrophonium chloride, a short-acting cholinesterase inhibitor, may also termi­nate AV nodal re-entry and is administered in a total dose of 10 mg IV after a 1-mg test dose. Ed­rophonium should be used cautiously in patients who have hypotension or bronchospastic lung disease. Intravenous propranolol may be given (see Table 8-2) but must be used cautiously in patients with heart failure or chronic lung disease. Intravenous digoxin may also be used, but its onset of action is longer. If the patient is experi­encing hemodynamic compromise, DC cardio­version with low energies is effective. Atrial or ven­tricular pacing also may restore sinus rhythm. In some patients, type I antiarrhythmic agents such as procainamide, quinidine, and disopyramide may be required to terminate AV nodal re-entry, but these drugs are used more often to prevent recurrences. Vasopressors (e.g., phenylephrine or metaraminol) may terminate AV nodal re-entry by inducing reflex vagal stimulation but are not com­monly used. Digitalis is usually the initial drug choice for chronic therapy. If unsuccessful, ver­apamil, propranolol, or quinidine may be added. For some hard-to-control patients, antitachycar-dia pacemaker implantation or surgery may be considered.

PSVT may be caused by re-entry utilizing a re­trograde concealed accessory pathway. The pres­ence of the accessory pathway is not evident dur­ing sinus rhythm because antegrade conduction is not present, and therefore the ECG manifesta­tions of the Wolff-Parkinson-White syndrome are not evident. However, the mechanism of tachy­cardia is the same as that in most patients with the Wolff-Parkinson-White syndrome, that is, an­tegrade conduction over the AV node and retro­grade conduction over the accessory pathway. Since it takes a relatively long time for the im­pulse to travel through the ventricular tissue to the accessory pathway and back to the atrium, the retrograde P wave during this form of tachycardia occurs after completion of the QRS complex, usu­ally in the ST segment or early T wave. In dis­tinction, patients with AV nodal re-entrant tach­ycardias usually have their retrograde P wave inscribed during or just after the QRS complex, although longer retrograde conduction intervals can occur in AV nodal re-entry. Tachycardia rates tend to be somewhat faster than those in AV nodal re-entry (2:200 per minute), but a great deal of ov­erlap exists. Vagal maneuvers, verapamil, digi­talis, and propranolol are acceptable choices for prompt termination. Chronic therapy often in­volves combinations of drugs that prolong acces­sory pathway conduction time and refractoriness (for example, quinidine, procainamide, and di­sopyramide) and drugs affecting AV nodal con­duction.