Chapter 12 Wolff-Parkinson-White Preexcitation Patterns
This chapter is a bridge between the first part of the book dealing primarily with abnormal QRS-T patterns and the second part on arrhythmias. Preexcitation patterns, especially the Wolff-Parkinson-White (WPW) pattern, may be mistaken for bundle branch blocks, hypertrophy, or myocardial infarction (MI) and are also an important substrate for supraventricular tachycardias. Even beginning clinicians need to be familiar with this finding, still a relatively common cause of referral to cardiologists.
The WPW pattern is a distinctive and important ECG abnormality caused by preexcitation of the ventricles. Normally the electrical stimulus travels to the ventricles from the atria via the atrioventricular (AV) junction. The physiologic lag of conduction through the AV junction results in the normal PR interval of 0.12 to 0.2 sec. Consider the consequences of having an extra pathway between the atria and ventricles that would bypass the AV junction and preexcite the ventricles. This situation is exactly what occurs with the WPW pattern: an atrioventricular bypass tract connects the atria and ventricles, circumventing the AV junction (Fig. 12-1).
Figure 12-1 Anatomy of the ECG pattern of the Wolff-Parkinson-White (WPW) preexcitation pattern. In a small percentage of people an accessory fiber (atrioventricular bypass tract) connects the atria and ventricles. (The consequences of this abnormal, extra conduction path are discussed in the text.)
Bypass tracts (also called accessory pathways) represent persistent abnormal connections that form and fail to disappear during fetal development of the heart in certain individuals. These abnormal conduction pathways, composed of bands of heart muscle tissue, are located in the area around the mitral or tricuspid valves (AV rings) or interventricular septum. An AV bypass tract is sometimes referred to as a bundle of Kent.
1. The QRS complex is widened, giving the superficial appearance of a bundle branch block pattern. However, the wide QRS is caused not by a delay in ventricular depolarization but by early stimulation of the ventricles. The T wave is also usually opposite in polarity to the wide QRS in any lead, similar to what is seen with bundle branch blocks (“secondary T wave inversions”).
Figure 12-3 Notice the characteristic triad of the Wolff-Parkinson-White (WPW) pattern: wide QRS complexes, short PR intervals, and delta waves (arrows) that are negative in some leads (e.g., II, III, and aVR) and positive in others (aVL and V2 to V6). The Q waves in leads II, III, and aVF are the result of abnormal ventricular conduction (negative delta waves) rather than an inferior myocardial infarction. This pattern is consistent with a bypass tract inserting into the posterior region of the ventricles (possibly posteroseptal in this case).
Figure 12-4 Another example of Wolff-Parkinson-White (WPW) pattern with the triad of wide QRS complexes, short PR intervals, and delta waves (arrows). The finding of negative delta waves that are predominantly negative in lead V1 and positive in the lateral leads is consistent with a bypass tract inserting into the free wall of the right ventricle. This pattern simulates a left bundle branch block pattern.
The QRS complex in sinus rhythm with WPW pattern is the result of the competition (fusion) between signals going down the normal conduction system and down the bypass tract. The signal going down the bypass tract usually reaches the ventricles first, while the signal going down the normal conduction system gets delayed in the AV node. The early activation of the ventricles results in a shorter than normal PR interval. Slow conduction through the ventricular muscle from the bypass tract insertion site is responsible for the initial QRS slurring (delta wave). Once the signal going down the normal conduction system passes the AV node, this activation wave “catches up” with the preexcitation wave by spreading quickly through the His-Purkinje system and activating the rest of the ventricles in the usual way. This competitive mechanism produces the relatively narrow second part of the QRS complex. The degree of preexcitation (amount of the ventricles activated through the bypass tract) therefore is dependent on the speed of AV nodal conduction—the longer the delay in the AV node, the larger portion of the ventricles that is activated through the bypass tract and the longer the delta wave is.