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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 ...