Atrial fibrillation in the setting of Wolff-Parkinson-White syndrome can be quite dangerous! This is an occasion where giving the wrong drugs (i.e., adenosine or a calcium channel blocker) can be a big mistake! For reasons that are not completely clear these drugs are believed to “facilitate conduction across the accessory pathway”.
The ECG in AF/WPW is quite unique. It shows an irregular, polymorphic tachycardia without turning of the points. That’s how it can be distinguished from polymorphic VT or torsades de pointes. Procainamide or ibutilide may be the only appropriate medications for these patients. Hemodynamically unstable patients should receive synchronized electrical cardioversion.
Narrow complex: Treat similar to SVT
Wide complex: treat with procainamide or cardioversion.
· DO NOT give: adenosine, verapamil, diltiazem, digoxin, beta blocker or amio. Due to the presence of accessory pathway blocking down the AV node, may cause the accessory pathway to become the primary driver of conduction.
· Treated with IV procainamide if clinically stable. Dose is 15-16 mg/kg given at a rate no faster than 50 mg/min.
· If unstable: Immediate DC cardioversion
Wolff-Parkinson-White syndrome is a relatively uncommon congenital heart defect. A large percentage of WPW patients will present a tachyarrythmia. Of this subgroup of patients, 20 percent will have atrial fibrillation.
Atrial fibrillation in WPW is particularly dangerous because the normal rate-limiting function of the AV node is bypassed with an accessory tract.
Treatment with AV nodal blocking drugs e.g. adenosine, calcium-channel blockers, beta-blockers may increase conduction via the accessory pathway with a resultant increase in ventricular rate and possible degeneration into VT or VF.
AF in WPW – it looks similar to polymorphic VT but lacks the undulating baseline seen in torsades de pointes.
Cardiac Rhythms associated with WPW: Sinus Rhythm, Reentrant Paroxysmal SVT (80% of arrhythmias in WPW), Antidromic AVRT: Impulses travel anterograde down the AP and retrograde through the AV node. Rare, occurs in less than 5% of patients with WPW, Atrial fibrillation with WPW (a subset of orthodromic AVRT): 20% to 30% of patients with WPW will also have atrial fibrillation.
A myriad of other tachyarrhythmias may occur in WPW syndrome. Far less common than orthodromic AVRT, antidromic AVRT may also occur at an incidence of 5% of WPW patients. Procainamide, a class 1A antiarrhythmic medication that acts by inhibiting cardiac myocyte sodium channels, is an appropriate medical treatment option in otherwise stable antidromic AVRT patients, though electrical cardioversion stands as another reasonable treatment option. Rarely, WPW may lead to sudden cardiac death (SCD) due to atrial fibrillation and subsequent ventricular tachycardia and ventricular fibrillation,
The differential diagnosis of irregularly irregular WCT is essentially limited to three main dysrhythmias. Dr. Littmann calls these FBI: Fast, Broad, and Irregular:
Afib with LBBB
Afib with RBBB
Afib with WPW
EKG shows a wide complex tachycardia rhythm. If team gives AV nodal blocking agents, the pt will devolve into a VF rhythm, and the pt will become nonresponsive. If team administers procainamide, pt will go into a rate controlled rhythm that reveals WPW and should then be placed on a procainamide drip.
Orthodromic SVT in WPW can be treated much like any other SVT (adenosine, vagal manoeuvres etc), whereas in antidromic SVT many of the usual drugs are contraindicated. AF is disturbingly common in WPW- 10 to 30% of patients will have it at some point.
As you begin to coach her through vagal maneuvers and reach for your adenosine she advises you ‘I have something called Wolff-Parkinson-White – does that change anything?’ You think maybe it does, but you’re not sure...
Atrial fibrillation with Wolff Parkinson White (WPW)
Irregularly irregular tachycardia
Changing QRS morphologies (as opposed to AF with a bundle branch block, which will be monomorphic)
Rate 250-300 bpm
Wide complex tachycardia in WPW must be treated with procainamide or electrical cardioversion and AV nodal blockade avoided. This is because the pathway is probably going retrograde through the AV node (antidromic rhythm creates wide complex) and blocking the AV node could send the pathway to a completely unchecked alternative route around it.
It is imperative to recognize AF with WPW, as incorrect treatment with AV nodal blocking agents can be fatal. Blocking the AV node in these patients will result in preferential use of the accessory pathway. Rates may exceed 300 or 400 bpm and are at extreme risk for degeneration into ventricular fibrillation (VF).
Atrial fibrillation in the setting of Wolff-Parkinson-White syndrome can be quite dangerous! This is an occasion where giving the wrong drugs (i.e., adenosine or a calcium channel blocker) can be a big mistake! For reasons that are not completely clear these drugs are believed to “facilitate conduction across the accessory pathway”
It’s worth remembering that the same potential thromboembolitic complications apply to these patients as for any other patient presenting with atrial fibrillation or atrial flutter.