Wolff-Parkinson-White Syndrome WPW

Named after the discoverers of the syndrome, WPW is caused by a foetal abnormality resulting in an additional pathway between the atria and the ventricles. As discussed earlier the atria and ventricles are electrically isolated by the atrioventricular ring. Electrical impulses pass from atria to ventricle by the AV node and the His bundle into the ventricles, hi WPW an extra accessory pathway exists between the atria and ventricles (Fig. 6.26). This pathway is called the Brmdle of Kent . The electrical impulse can now travel through the AV node in the normal way and through the accessory pathway. 

Because there is no AV node to slow the impulse in the accessory pathway the PR interval is short. The impulse is then slower to activate the ventricles as it is not passing through the normal conduction system. This leads to the formation of a delta wave (Fig. 6.27) on the ECG. The short PR interval and delta wave are the key ECG featiues of this syndrome (Eig. 6.28). 

The impulse can also travel back up to the atria via the accessory pathway and create a sustained tachycardia. WPW normally occurs in the young and adults aged 20-35 years of age. Most people with this condition seek medical attention due to the frequent occurrence of Supra Ventricular tachyarrhythmias. 

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Prophylaxis in reentrant nodal and atrial tachycardias—not Wolff-Parkinson-White syndrome (WPW). Avoid in VT, as may progress to VF. In digitalis toxicity, can 4 delayed after-depolarization. 

Ventricular rhythms originating in the left ventricle Posterior Myocardial Infarction (MI) Wolff-Parkinson-White syndrome (WPW) Dextrocardia... 

EF, ejection fraction CHF, chronic heart failure WPW, Wolff-Parkinson-White syndrome DC, direct current. 

WNL within normal limits WPW Wolff-Parkinson-White syndrome... 

Class Ic Ventricular tachycardia Tachycardia associated with the Wolff-Parkinson-White (WPW) syndrome AV-nodal re-entry tachycardia... 

Primary indications for the use of quinidine include (1) abolition of premature complexes that have an atrial, A-V junctional, or ventricular origin (2) restoration of normal sinus rhythm in atrial flutter and atrial fibrillation after controlling the ventricular rate with digitahs (3) maintenance of normal sinus rhythm after electrical conversion of atrial arrhythmias (4) prophylaxis against arrhythmias associated with electrical countershock (5) termination of ventricular tachycardia and (6) suppression of repetitive tachycardia associated with Wolff-Parkinson-White (WPW) syndrome. 

Contraindications are hypotension, cardiogenic shock, marked bradycardia, second or third degree AV-block, Wolff-Parkinson-White (WPW) syndrome, wide complex tachycardia, VT and uncompensated heart failure. 

Flecainide slows conduction in all cardiac cells including the anomalous pathways responsible for the Wolff-Parkinson-White (WPW) syndrome. Together with encainide and moricizine, it underwent clinical trials to establish if suppression of asymptomatic premature beats with antiarrhythmic drugs would reduce the risk of death from arrhythmia after myocardial infarction. The study was terminated after preliminary analysis of 1727 patients revealed that mortality in the groups treated with flecainide or encainide was 7.7% compared with 3.0% in controls. The most likely explanation for the result was the induction of lethal ventricular arrhythmias possibly due to ischaemia by flecainide and encainide, i.e. a proarrhythmic effect. In the light of these findings the indications for flecainide are restricted to patients with no evidence of structural heart disease. The most common indication, indeed where it is the drug of choice, is atrioventricular re-entrant tachycardia, such as AV nodal tachycardia or in the tachycardias associated with the WPW syndrome or similar conditions with anomalous pathways. This should be as a prelude to definitive treatment with radiofrequency ablation. Flecainide may also be useful in patients with paroxysmal atrial fibrillation. 

Patients with Wolff-Parkinson-White (WPW) syndrome may have several different tachycardias that are treated acutely by different strategies orthodromic reentry (adenosine), antidromic reentry (adenosine or procainamide), and atrial fibrillation (procainamide or amiodarone). AV nodal blocking drugs are contraindicated with WPW syndrome and atrial fibrillation. 

Keep in mind that it may be difficult to differentiate between bundle-branch block and Wolff-Parkinson-White (WPW) syndrome. Whenever you spot what seems to be bundle-branch block, check for WPW syndrome as well. 

Wolff-Parkinson-White (WPW) syndrome is a common type of preexcitation syndrome, an abnormal condition in which electrical impulses enter the ventricles from the atria using an accessory pathway that bypasses the atrioventricular (AV) junction. This results in a short PR intenral and a wide QRS complex with an initial slurring of the upward slope of the QRS complex, called a delta wave. Because the delta wave prolongs the QRS complex, it may be confused with a bundle-branch block. 

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