The only EKG book. 9th Ed

Chapter 5. Preexcitation Syndromes

In this chapter you will learn:

1

what happens when electrical current is conducted to the ventricles more rapidly than usual

2

what an accessory pathway is

3

that Wolff-Parkinson-White is not the name of a law firm

4

why accessory pathways predispose to arrhythmias

5

about the case of Winston T., a preexcitable personality

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.

Wolff-Parkinson-White (WPW). Current is held up by the normal delay at the AV node but races unimpeded down the accessory pathway. The EKG shows the short PR interval and delta wave.

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.

The PR interval is short, but there is no delta wave.

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.

(A) Supraventricular tachycardia; note the regular rhythm. (B) Atrial fibrillation, with the classic irregularly irregular rhythm.

Supraventricular Tachycardia in WPW

In normal hearts, supraventricular tachycardias usually arise arises through a reentrant mechanism (AV nodal reentrant tachycardia [AVNRT], see page 133). The same is true in WPW. In fact, the presence of an accessory bundle—an alternate pathway of conduction—is the perfect substrate for reentry. Here is how it works.

We have seen how, in WPW, a normal beat generates a QRS complex that is a combination of two waves, one conducted through the accessory pathway and one through the AV node and along the normal pathway of conduction. Although the accessory pathway usually conducts current faster than the AV node, it also tends to have a longer refractory period once it has been depolarized. What happens, then, if a normal sinus impulse is followed abruptly by a premature atrial beat? This premature beat will be conducted normally through the AV node, but the accessory pathway may still be refractory, blocking conduction through the alternate route. The wave of depolarization will then move through the AV node and into the bundle branches and ventricular myocardium. By the time it encounters the accessory pathway on the ventricular side, it may no longer be refractory, and the current can pass back into the atria. It is then free to pass right back down through the AV node, and a self-sustaining, revolving reentrant mechanism has been established. The result is a supraventricular tachycardia. The QRS complex during the arrhythmia is narrow because ventricular depolarization occurs through the normal bundle branches.

The formation of a reentry circuit in WPW. (A) A premature atrial beat sends current down the normal conduction pathways but not through the refractory accessory pathway. (B) Current then circles back through the accessory pathway, which is no longer refractory to conduction, forming a complete reentrant circuit.

Less commonly, the reentrant mechanism circles the other way, that is, down the accessory pathway and back up through the AV node. The result, again, is a supraventricular tachycardia, but now, the QRS complex is wide and bizarre because ventricular depolarization does not occur along the normal bundle branches. This arrhythmia may be indistinguishable from ventricular tachycardia on the EKG.

A second type of reentry circuit in WPW. Current moves antegrade down the accessory pathway and then retrograde through the AV node, establishing an independent revolving circuit.

Wide-complex supraventricular tachycardia in WPW.

Let’s again recall that the “usual” form of supraventricular tachycardia in normal hearts is most often caused by a reentry loop within the AV node and is called AV nodal reentrant tachycardia. Here, in WPW, because the reentrant loop reciprocates between the atria and ventricles, the arrhythmia is more accurately termed AV reciprocating tachycardia (AVRT). Remember back in Chapter 3 (page 132) that we first mentioned this arrhythmia as one of the causes of a sustained supraventricular tachycardia, one that we would discuss later? Well, here it is!

When the tachycardia activates the ventricles in an antegrade manner through the AV node, generating a narrow QRS complex, the arrhythmia is further subcategorized as an orthodromic tachycardia (the prefix ortho conveys the meaning of correct, or orthodox). Reciprocating tachycardias that activate the ventricles through the accessory pathway, generating a wide QRS complex, are subcategorized as antidromic tachycardia.

In 10% to 15% of patients with WPW, there is more than one accessory pathway, permitting the formation of multiple reentry loops as the current passes up and down through the different accessory pathways and the AV node.

So what do you do if a hemodynamically unstable patient shows up in your emergency room with a wide QRS complex tachycardia, and the various techniques we discussed on page 154—don’t help you distinguish ventricular tachycardia from a wide complex supraventricular tachycardia in a patient with WPW? You can’t rely on looking for delta waves—you will almost never see them in a patient with WPW while he or she is experiencing a supraventricular arrhythmia until you restore the patient to normal sinus rhythm. The answer is this: Assume the patient has ventricular tachycardia and proceed to treat it accordingly. Ventricular tachycardia is much more common and can be lethal.

Atrial Fibrillation in WPW

Atrial fibrillation, the other arrhythmia commonly seen in WPW, can be particularly devastating. The accessory pathway can act as a free conduit for the chaotic atrial activity. Without the AV node to act as a barrier between the atria and ventricles, ventricular rates can rise as high as 300 beats per minute! The precise rate will depend on the refractory period of the accessory pathway. The QRS complexes will often show varying morphology, as some are triggered via normal conduction through the AV node and others via conduction through the accessory pathway. This very rapid atrial fibrillation has been known to induce ventricular fibrillation, because of the lack of normal filtering by the AV node. Fortunately, atrial fibrillation is rare in WPW, but it must be considered a diagnostic possibility in patients who have been resuscitated from an episode of sudden death or syncope and are found to have preexcitation on their cardiograms.

Two examples of atrial fibrillation in WPW. The ventricular rate is extremely fast.

Mapping the aberrant pathways in patients with WPW can be accomplished with an electrophysiology study (EPS) and has become routine in patients who are symptomatic, for example, those with a history of syncope or those who have documented arrhythmias. During the mapping procedure, the aberrant pathway can be ablated, thereby resolving the problem.

Patients with WPW have an increased risk of sudden cardiac death, but this is only very rarely its first manifestation, allowing time for successful clinical intervention before an episode of sudden death can occur. The overall prognosis today for patients with WPW is excellent.

Patients with a short PR interval without a delta wave may also have an increased risk of tachyarrhythmias. The risk, however, appears to be exceedingly small, and there is no evidence that these patients are at increased risk of sudden cardiac death. Patients with a short PR interval without delta waves and who have had at least one tachyarrhythmia are said to have Lown-Ganong- Levine syndrome.

If you get one take home lesson from this chapter, it is this: Always look for a short PR interval and a delta wave on the EKG of any patient who presents with a history suggestive of a tachyarrhythmia, for example, palpitations or syncope. And look at all 12 leads; you may only see clear-cut delta waves in some of them.

SUMMARY

Preexcitation

The diagnosis of preexcitation is made by looking for a short PR interval.

Criteria for WPW

1. PR interval less than 0.12 seconds

2. Wide QRS complexes

3. Delta wave seen in some leads

Arrhythmias commonly seen include the following:

1. AV reciprocating tachycardia—narrow QRS complexes (orthodromic tachycardia) are more common than wide ones (antidromic tachycardia).

2. Atrial fibrillation—can be very rapid and rarely can lead to ventricular fibrillation.

Differential Diagnosis of Wide Complex Tachycardias

1. Ventricular tachycardia

2. A supraventricular tachycardia with aberrant conduction (e.g., supraventricular tachycardia with underlying bundle branch block); often rate-related, appearing only with fast heart rates

3. AV reciprocating tachycardia (antidromic tachycardia) in a patient with preexcitation

4. Paced rhythms

When you see what appears to be a wide complex tachycardia and you did not run the EKG yourself—for example, if you are looking at the tracing on a hospital monitor—make sure you are not seeing an artifact caused by the patient’s activity; it could be caused by something as simple as brushing one’s teeth!

Because the presence of an accessory pathway in WPW alters the vectors of current flow to at least some degree, you cannot assess axis or amplitude with any precision, and hence, any attempt to determine the presence of ventricular hypertrophy or bundle branch block is bound to be unreliable.

CASE 9.

Winston T., a young biochemical engineer, is brought to the emergency room by his wife. During dinner, he became lightheaded and nauseated (not an uncommon event during dinner at the Winston household, but the severity of the symptoms prompted concern).

In the emergency room, Winston denies any chest pain or shortness of breath.

The medical student who is the first to examine him has seen just enough patients to feel overconfident in his diagnostic abilities. Tired and overworked, he listens to Winston’s story and is ready to send Winston home with a diagnosis of food poisoning when an astute nurse takes the trouble to put a hand on Winston’s pulse and discovers it is extremely rapid. An EKG reveals the following:

Distraught by his carelessness, the medical student becomes somewhat pallid himself. The emergency room doctor takes over, notes the patient’s rapid, regular pulse, glances at the rhythm strip and immediately orders a dose of intravenous adenosine. The tachycardia breaks at once, and the new rhythm strip looks like this:

Can you match the emergency room doctor’s heady acumen with erudition of your own and figure out exactly what has happened?

Of course you can! Winston has WPW. This is readily apparent from the second EKG, which reveals the characteristic short PR interval, delta wave, and prolonged QRS complex. The initial strip shows the typical narrow QRS complex AV reciprocating tachycardia that can occur in these individuals. The rapid tachycardia was responsible for Winston’s symptoms, not his undercooked Cornish game hen.

Intravenous adenosine, a potent AV node blocking agent with a half-life of less than 10 seconds, is extremely effective at breaking reentrant tachycardias that involve the AV node. This was Winston’s first attack, and because most patients with WPW have only infrequent episodes of tachycardia, chronic antiarrhythmic therapy is not indicated at this time.

As for what became of the medical student, he learned from his humiliating experience and went on to become a model of thoroughness and efficiency, eventually graduating at the top of his class. He also has never forgotten the first rule of medicine: always take the vital signs. There is good reason why they are called “vital.”



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