Ventricular preexcitation associated with a short P-R
interval and a wide QRS complex.
Incidence 1 to 3:1000 in a general population.
Unclear, an autosomal dominant inheritance is
suggested by some kindreds. Can be caused by mutation in the gamma-2
regulatory subunit of AMP-activated protein kinase (PRKAG) located on 7q36.
During fetal life, numerous connections link the
atria to the ventricles, but they all disappear before birth except for the
bundle of His. Sometimes, some of the connections do not disappear. This
accessory pathway(s) characterizes the Wolff-Parkinson-White syndrome. An
accessory atrioventricular connection (bundle of Kent) bypasses the
atrioventricular node, and inserts directly into myocardium (consistent with
bypass tracts in Lown-Ganong-Levine syndrome). The accessory bundle may
conduct anteor retrograde. Antegrade conduction causes early commencement
of ventricular depolarization, seen as a delta wave on the ECG. Retrograde
conduction allows a reentry circuit to develop and is a mechanism for
paroxysmal tachycardia generation. The accessory connection may only conduct
in a retrograde direction; therefore a delta wave will not appear on ECG.
Such a tract is described as concealed. In atrial fibrillation, antegrade
conduction along the accessory pathway may result in rapid ventricular rate,
which is poorly tolerated.
History, ECG findings of a short P-R interval, and a
delta wave. Electrophysiology studies to define individual pathway anatomy
and mechanism for dysrhythmia generation.
May be asymptomatic. Symptoms include
palpitations (paroxysmal episodes of supraventricular tachycardia or atrial
fibrillation), shortness of breath, feeding difficulties in infancy, syncope
and chest pain. In infancy, WPW tends to improve in the first year of life
and may be associated with Ebstein anomaly. Sudden death secondary to
dysrhythmia may occur. Type A WPW demonstrates a large R wave in leads V1 and V2.
In type B WPW, the S or QS waves predominate in leads V1 and V2. Supraventricular
tachycardias may be managed by verapamil (potent negative inotrope), beta
blockade, amiodarone, adenosine or cardioversion. Adenosine is said to achieve
cardioversion in up to 87% of narrow complex tachycardias associated with
WPW. Catheter or surgical ablation of pathways or pacemakers may also be
Obtain a history of frequency of
dysrhythmia, and current treatment regimen. Continue antidysrhythmic drugs
perioperatively. Review results of electrophysiology studies if available.
Preoperative ECG mandatory. Pacemaker details if used to control
supraventricular tachycardia (atrial overdrive pacing). Correct any
electrolyte disturbance (sodium, potassium, and magnesium).
Minimize perioperative catecholamine
surges; premedication may be beneficial. Perioperative beta blockade has
been used. Atropine premedication, however, is relatively contraindicated.
Use a technique to minimize risk of hypoxia, hypercarbia, or acidosis, all of
which render cardiac muscle membranes unstable and ectopic depolarization
Enflurane is the volatile agent,
which is probably least likely to induce arrhythmia. Halothane should be
avoided (proarrhythmogenic, myocardial depressant). Desflurane has a
sympathomimetic effect, which is undesirable. Sevoflurane has been used and reported to be
appropriate. Propofol has no effect on ...