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Ventricular preexcitation syndrome.

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Accelerated Atrioventricular Nodal Conduction; Enhanced Atrioventricular Nodal Conduction Syndrome; Short PR/Normal QRS Syndrome; Short PR/Narrow QRS Syndrome.

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Occurrence of frequent paroxysms of tachycardia in patients with short PR interval was described by A. Clerc in 1938, but B. Lown, W.F. Ganong, and S.A. Levine gave it their eponym in 1952.

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Ventricular preexcitation syndrome (other types include Wolff-Parkinson-White syndrome via Kent fibers and preexcitation via Mahaim fibers).

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0.5% of the overall adult population. Retrospective analysis has suggested that paroxysmal supraventricular tachycardia occurs in approximately 9.5% of patients with short PR and normal QRS duration.

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Unknown. A familial occurrence has been suggested.

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Atriofascicular tracts (called James fibers) completely or partially bypass the atrioventricular node, resulting in a short PR interval (<0.12 seconds). These tracts insert into the bundle of His or its branches; thus, the ventricles are depolarized in a normal sequence and the QRS complex appears normal on ECG (no delta wave as in Wolff-Parkinson-White syndrome). Paroxysmal tachycardias classically arise from reentry through the bypass tract. Direct atrioventricular connections have been suggested to be part of the syndrome; such connections could allow tachycardias to develop as a result of antegrade, rather than retrograde, conduction.

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History; ECG; short PR interval with normal QRS complex; electrophysiologic studies.

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Patients may remain asymptomatic. Episodes of paroxysmal palpitation (atrial flutter, supraventricular tachycardia) may be associated with shortness of breath, signs of ventricular failure, and syncope. Investigations include ECG and electrophysiologic studies to define the site of accessory conducting tissue and the individual mechanism for tachycardia generation. The tachycardia is usually a narrow complex, but functional right bundle or left bundle branch block may cause a wide complex tachycardia. Several drugs may be used in the management of the condition, including adenosine (acutely), verapamil, beta blocker, procainamide, amiodarone, or digitalis. However, verapamil and digoxin are contraindicated for treatment of atrial fibrillation or flutter in these patients because they might accelerate conduction through the bypass tract and induce ventricular fibrillation. Surgical or catheter pathway ablation or pacemakers (overdrive pacing) may be used.

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Obtain a history of the frequency of dysrhythmias and the current treatment regimen. Continue antidysrhythmic drugs perioperatively. In case of chronic amiodarone therapy, check thyroid function and exclude pulmonary fibrosis. Review the results of electrophysiologic studies if available. Preoperative ECG mandatory. Data regarding pacemaker if overdrive pacing is being used to control supraventricular tachycardias. Correct any electrolyte disturbance (sodium, potassium, and magnesium).

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Minimize perioperative catecholamine surges. Premedication may be beneficial. Atropine is relatively contraindicated. Hypoxia, hypercarbia, or acidosis must be prevented because all these complications render cardiac muscle membranes unstable and ectopic depolarization more likely.

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Same as for Wolff-Parkinson-White syndrome. Enflurane is the volatile agent that probably is least likely to induce arrhythmia. Halothane is contraindicated (proarrhythmogenic, myocardial depressant). Isoflurane and sevoflurane have been used without problem in patients with Wolff-Parkinson-White syndrome. Desflurane has a sympathomimetic effect that is undesirable. Because propofol has no effect on the refractory period of normal and accessory tissue, it is useful for electrophysiologic studies and ablation procedures. Pancuronium is relatively contraindicated. Extreme care if administering a beta blocker to a patient already taking verapamil (may precipitate extreme bradycardia or heart block); in case of need, esmolol probably is the perioperative beta blocker ...

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