The Electrocardiogram in Wolff-Parkinson-White Syndrome
Part I: The Non-arrhythmic ECG
By William J. Brady, MD
In 1930, Wolff, Parkinson, and White described the "combination of bundle-branch block, abnormally short PR interval, and paroxysms of tachycardia occurring in young, healthy patients with normal hearts."1 This syndrome, termed the Wolff-Parkinson-White (WPW) syndrome, is a form of ventricular pre-excitation involving an accessory conduction pathway that creates a direct electrical connection between the atria and ventricles. Most patients with the ability to conduct with pre-excitation will remain asymptomatic throughout their lives. In those patients experiencing symptoms, the tachyarrhythmias responsible for the unpleasant sensations include supraventricular tachycardia, wide QRS complex tachycardia, atrial fibrillation, and ventricular fibrillation. (Arrhythmia presentations will be discussed in Part II of this special feature, which will appear in the next issue.)
In the normal heart, electrical impulses originate in the sinus node located in the right atrium and spread throughout atrial tissue, eventually arriving at the atrioventricular (AV) node. Within the AV node, physiological slowing of the impulse occurs, followed by conduction through the His-bundle and bundle branches to the ventricular muscle. In WPW, atrial impulses may bypass the AV node and His-Purkinje system; these impulses directly activate the ventricular myocardium. (See Figure 1.)
As such, pre-excitation means that a supraventricular impulse conducted over the accessory pathway (AP) may arrive at the ventricular myocardium significantly earlier than the same impulse conducted through the traditional, appropriate pathway—the AV node. The resultant ventricular depolarization is then a summation of the two impulses traveling through both the AV node and the AP. In WPW, however, the impulse may be conducted only through the AV node, only through the bypass tract, or simultaneously through AV node and bypass tract. The more the bypass tract contributes to the conduction of a given impulse, the wider the QRS complex.
The definition of WPW relies on the following electrocardiographic features: 1) a PR interval less than 0.12 seconds with a normal P wave; 2) a slurring and slow rising of the initial segment of the QRS complex (the delta wave); 3) a widened QRS complex with a total duration greater than 0.11-0.12 seconds in duration; and 4) secondary repolarization changes reflected in ST segment/T wave changes that generally are directed opposite (discordant) to the major delta wave and QRS complex.2 (See Figure 2 and Table 1.)
The PR interval is shortened because the impulse progressing down the AP is not subjected to the physiological slowing which occurs in the AV node. Thus, the ventricular myocardium is activated by two separate pathways, resulting in a fused, or widened, QRS complex. The initial part of the complex, the delta wave, is the key to recognizing WPW. The delta wave represents aberrant activation through the AP, while the terminal portion of the QRS represents normal activation through the His-Purkinje system from impulses traveling through both the AV node and the AP. The delta wave is generally 0.02-0.07 seconds in duration; while theoretically it should be evident in all leads, the realities of vector physics render it difficult to see in various leads in some cases. If the delta wave is negative, it may mimic a pathologic Q wave, and thus represent a pseudoinfarction pattern. A large positive delta wave in V1 resembles that seen with true posterior infarction, right ventricular hypertrophy, or right bundle-branch block; indeed, it is in the differential diagnosis of R wave amplitude greater than S wave amplitude in lead V1.3
In the majority of cases, the APs are characterized by very rapid, nondecremental, anterograde/retrograde conduction. Conduction is "nondecremental" in that the AP itself does not reduce the number of impulses transmitted to the ventricles (a significant difference when compared to the AV node, which is able to conduct a fixed number of impulses to the ventricles per unit time). Conduction is "anterograde/retrograde" regarding the direction the impulse follows in the AP. An AP may be described as "concealed" such "concealment" occurs when a pathway only carries an impulse in retrograde fashion. These pathways are "silent" in that the resting 12-lead ECG is normal—a normal PR interval, a normal QRS complex, and an absence of the delta wave. Pre-excitation may occur intermittently, depending upon a range of factors including cardioactive medication use, physiological stressors with catecholamine release, co-development of cardiac pathology, and normal aging.
Dr. Brady, Associate Professor of Emergency Medicine and Internal Medicine, Residency Director and Vice Chair, Emergency Medicine, University of Virginia, Charlottesville, is on the Editorial Board of Emergency Medicine Alert.
References
1. Wolff L, et al. Bundle-branch block with short PR interval in healthy young people prone to paroxysmal tachy-cardia. Am Heart J 1930;5:685-704.
2. Willems JL, et al. Criteria for intraventricular conduction disturbances and pre-excitation. Am J Cardiol 1985; 5:1261-1275.
3. Surawicz B, et al. Chou’s Electrocardiography in Clinical Practice. 5th ed. Philadelphia:W.B. Saunders Co.; 2001.
In 1930, Wolff, Parkinson, and White described the combination of bundle-branch block, abnormally short PR interval, and paroxysms of tachycardia occurring in young, healthy patients with normal hearts.
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