Wolff-Parkinson-White Syndrome for USMLE

0:02 Hello everyone. In this particular lecture, we will be dealing with cardiology, and our topic of concern for today's lecture is WPW, that is, Wolff-Parkinson-White. There are two different conditions: the first one is only WPW pattern, and the other is WPW syndrome. WPW pattern is nothing but the ECG evidence: if there is any evidence of ventricular pre-excitation complexes on ECG, then that is WPW pattern. However, there is no evidence of arrhythmia, and there are no reported symptoms in the patient. In WPW syndrome, in addition to ECG changes, there will be evidence of arrhythmia and reported symptoms. Regarding the main pathophysiology of WPW syndrome, it is intermittent tachycardia mainly because of an accessory pathway, and this accessory

0:52 pathway is the bundle of Kent. The bundle of Kent is an accessory pathway that bypasses the AV node. If this bundle of Kent bypasses the AV node, then the impulse from the SA node can easily propagate or transmit into the ventricles. So this bundle of Kent bypasses the AV node, and the impulses easily pass from the atria into the ventricles. Sometimes WPW syndrome can be associated with Ebstein anomaly, and this Ebstein anomaly is strongly associated with maternal lithium exposure. Lithium is a mood-stabilizing agent used in bipolar disorders, and use of lithium in the mother increases the risk of having an anomaly in the fetus, and this anomaly is associated with having Wolff-Parkinson-White syndrome.

1:39 There are certain other arrhythmias strongly associated with WPW syndrome, including atrioventricular reciprocating tachycardia (AVRT). 80% of patients with WPW syndrome will have AVRT, around 30% will have atrial fibrillation, and a few people will have atrial flutter. A very rare subset of people will have arrhythmias such as multifocal atrial tachycardia or ventricular fibrillation. ECG findings of WPW syndrome are a high-yield area. The findings are mainly because of the accessory pathway known as the bundle of Kent. Because of this accessory pathway, the AV node has been bypassed. The normal function of the AV node is to create an intrinsic delay in transmission of impulses from the SA node through the AV node into the

2:29 bundle branches and finally into the Purkinje fibers. Because the AV node has been bypassed, the impulse can be transmitted from the atria into the ventricles in a faster manner or at a faster rate. Because of this, the PR interval – which represents the intrinsic delay of the AV node – becomes shortened. If the AV node is stronger, then the PR interval gets longer; if the AV node has been bypassed or is weaker, then the PR interval gets shortened. Here, because of the accessory pathway (the bundle of Kent), the PR interval gets shortened. Additionally, there is something called a delta wave. The delta wave

3:14 is the slurring of the upstroke of the QRS complex. It represents that the impulse has been transmitted through this accessory pathway. Because of all these changes, there will be widening of the QRS complexes. However, this delta wave is not seen in all patients. These are the characteristic ECG findings of WPW syndrome. If WPW syndrome is associated with other arrhythmias like AVRT, atrial fibrillation, or atrial flutter, then the changes of those arrhythmias can also be observed on the ECG. Regarding management of WPW syndrome, it can be categorized into two different ways:

4:00 the first is for acute episode management, and the other is long-term management. Let's first discuss the acute episode. In the acute episode, we assess the hemodynamic stability of the patient. If the patient is hemodynamically unstable, then we perform straightforward electrical cardioversion. However, if the patient is hemodynamically stable, then we look at the ECG. If the patient has wide-complex tachycardia, then we use rhythm control measures; we can perform cardioversion or use drugs like ibutilide. The catch here is that we should avoid AV nodal blocking agents. We should avoid drugs like adenosine, beta-blockers, non-dihydropyridine calcium channel blockers (including verapamil and diltiazem), and digoxin

4:46 because they can precipitate fatal ventricular tachycardia or ventricular fibrillation in those patients. We should also avoid vagal maneuvers for the same reason; vagal maneuvers increase the activity of the AV node because the AV node is highly innervated by the vagus nerve. Whenever we do vagal maneuvers, the AV node gets blocked or activated for longer durations, and the patient can develop fatal ventricular tachycardia or ventricular fibrillation. Regarding other ECG changes: if the patient has a regular narrow-complex tachycardia and is hemodynamically stable, then vagal maneuvers or adenosine can be used. Regarding long-term management of WPW syndrome, we perform risk stratification based on clinical history findings and electrophysiological parameters. Depending on these parameters, we

5:36 stratify the patient as high risk or low risk. For high-risk patients, the only management that has been approved is catheter ablation (radiofrequency ablation) of the accessory pathway. If the patient has been categorized as low risk, then we look at the patient's symptoms. If the patient is asymptomatic, we simply perform observation. However, if the patient is symptomatic, then first-line management is again catheter ablation of this accessory bundle of Kent. Second-line management consists of long-term antiarrhythmics. If there is any structural heart disease, we can use drugs like dofetilide and sotalol. If there is no structural heart disease, we can use drugs like flecainide and propafenone. These are the long-term antiarrhythmic drugs. However, these antiarrhythmic drugs themselves are

6:24 second-line drugs. The first-line management for symptomatic low-risk WPW syndrome is cardiac catheter ablation (radiofrequency ablation) of this accessory bundle of Kent. With this, we conclude Wolff-Parkinson-White syndrome, one of the characteristically high-yield topics. Thank you for your time and attention.