What Is Preexcitation?

In the last chapter, we discussed what happens when conduction from the atria to the ventricles is delayed or blocked. This chapter presents the other side of the coin: what happens when the electrical current is conducted to the ventricles more quickly than usual.

How can such a thing happen?

With normal conduction, the major delay between the atria and the ventricles is in the atrioventricular (AV) node, where the wave of depolarization is held up for about 0.1 second, long enough for the atria to contract and empty their content of circulating blood into the ventricles. In the preexcitation syndromes, there are accessory pathways by which the current can bypass the AV node and thus arrive at the ventricles without the delay and often ahead of time.

A number of different accessory pathways have been discovered. Probably fewer than 1% of individuals possess one of these pathways. There is a decided male preponderance. Accessory pathways may occur in normal healthy hearts as an isolated finding, or they may occur in conjunction with mitral valve prolapse, hypertrophic cardiomyopathies, and various congenital disorders.

The most important preexcitation syndrome is Wolff–Parkinson–White (WPW). It is easily diagnosed on the EKG. In WPW, the accessory conduction pathway acts as a short circuit, allowing the atrial wave of depolarization to bypass the AV node and activate the ventricles prematurely.

Wolff–Parkinson–White

In WPW, the bypass pathway is a discrete aberrant conducting pathway that connects the atria and ventricles. It can be left sided (connecting the left atrium and left ventricle) or right sided (connecting the right atrium and right ventricle).

Premature ventricular depolarization through the accessory pathway causes two things to happen on the EKG:

1. The PR interval, representing the time from the start of atrial depolarization to the start of ventricular depolarization, is shortened. The specific criterion for diagnosis is a PR interval less than 0.12 seconds.
   
2. The QRS complex is widened to more than 0.1 second by the presence of what is called a delta wave. Unlike bundle branch block, in which the QRS complex is widened because of delayed ventricular activation, in WPW it is widened because of premature activation. The QRS complex in WPW actually represents a combination beat: most of the ventricular myocardium is activated through the normal conduction pathways, but a small region is depolarized early through the accessory pathway. This small region of myocardium that is depolarized early gives the QRS complex a characteristic slurred initial upstroke called a delta wave. A true delta wave may be seen in only a few leads, so scan the entire EKG.

A Short PR Interval Without a Delta Wave

Even more common than WPW is the presence of a short PR interval without an accompanying delta wave. No single anatomic pathway has been consistently identified to explain this finding, and it is probably the result of a variety of structural abnormalities. Some patients may have a small bypass pathway within or very close to the AV node. Others may simply have an AV node that conducts more rapidly than normal.

Why Do We Care About Preexcitation?

In many individuals with WPW, preexcitation poses few, if any, clinical problems. However, preexcitation does predispose to various tachyarrhythmias. It is estimated that 50% to 70% of individuals with WPW experience at least one supraventricular arrhythmia. These patients may then develop symptoms such as palpitations, shortness of breath, and so on. The presence of both the classic EKG abnormalities and symptoms is referred to as WPW syndrome.

The two tachyarrhythmias most often seen in WPW are a supraventricular tachycardia and atrial fibrillation.

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