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A 40-year-old male presents to the ED after a syncopal episode. In his past medical history he relates a history of frequent debilitating “dizzy spells”. After reviewing his ECG your interpretation/advice is:
 
(May choose more than one)
alt
 
A. This could represent a posterior infarction
B. Wolff-Parkinson-White (WPW) syndrome
C. Significantly wide Q-waves in Leads III, avF suggestive of inferior infarction
D. Meets the voltage criteria of LVH
E. Short PR interval, but otherwise does not satisfy the criteria of WPW
F. Incomplete LBBB
G. Lown-Ganong-Levine Syndrome
H. None of the above
 
See next page for diagnosis and discussion
{mospagebreak title=Diagnosis}
General discussion 
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This tracing is an example of a classic Wolff-Parkinson-White Syndrome (WPW).  The general category of the pre-excitation syndrome (of which WPW is an example) is a result of a congenital (vestige of fetal tissue) abnormality of the electrical system of the heart. In particular, the person with WPW has inherited an extra electrical connection accessory pathway that short circuits the AV
node. You will recall that the AV node is the primary reason for the long duration of the PR interval (normal range = 0.12 – 0.20 sec). This is a direct result of the extremely slow conduction across the AV node. There are several variants on the theme, but for the sake of example let us consider the specific case of WPW and the Bundle of Kent. This accessory pathway results in a premature
excitation of the ventricles and so it follows that the PR interval is shortened, i.e. PR < 0.12 sec.
The Bundle of Kent is composed of myocardial tissue and its electrical conduction is slow, nevertheless much more rapid than the conduction velocity across the AV node. 
 
Regarding the normal heart, the atria and ventricles are electrically insulated from each other and are connected only by the AV node and Bundle of HIS. In WPW, the ventricular depolarization (beginning
of the QRS complex) will occur earlier than that of the normal QRS complex. Then after a standard time delay while traversing the AV node, the electrical signal will enter the Bundle of HIS and propagate to the Purkinje cells in the usual manner (this generates a fusion beat). It is therefore
clear that the latter portion of the QRS complex will remain less distorted (normal waveshape).

Teaching point #1
Because of the early depolarization (preexcitation) of the ventricles, it follows that the duration of the QRS complex will be widened. QRS duration > 0.10 sec. Thus the appearance of an inferior infarction.
 
Teaching point #2
When the pre-excitation depolarization wavefront rejoins the normal pathway wavefront, there is a sudden change in direction (instantaneous slope change) in the QRS waveform. The portion of the
signal preceding this slope change represents the depolarization of the pre-excited tissue.  This waveform typically takes on a peculiar characteristic low-slope, ramp shape and is called the DELTA wave. Please know that the DELTA wave may not be apparent in all the leads and certainly might be positive or negative. I have magnified lead avF and Lead V6 and labeled the DELTA wave as
“negative” and “positive” respectively. It is clear that the direction of the DELTA wave will depend upon the origin and terminal position of the accessory pathway.
 
In Summary: The Triad of WPW
1. QRS duration > 0.10 sec.
2. PR < 0.12 sec.
3. Presence of DELTA waves.
Seek and you will find
If one measures a short PR interval on the ECG, one should “think” WPW and proceed to look for the presence of the other two criteria. It is no trite statement to say that if you do not look for the WPW, you will never find it.
Did you know?
1. WPW has been categorized by some as either Type A or Type B according to the appearance of the Delta wave.
    Type A: Positive Delta wave in all precordial leads
    Type B: Negative Delta wave in Leads V1, V2

2. When treating tachyarrhythmias associated with WPW, you most often do not use traditional agents such as calcium channel blockers, beta blockers, digitalis, adenosine, and amiodarone. These agents
potentially might paradoxically worsen the condition and degenerate to ventricular tachycardia, ventricular fibrillation and death.

3. If medical treatment is considered: 
    Use Procainimide or amiodarone infusion if…antidromic tachycardia (regular wide complex)
    Use adenosine if…orthodromic (regular narrow complex)
    Atrial fibrillation (wide complex)…consider procainimide or amiodarone but synchronized        
    cardioversion is recommended..

4. Tachyarrhythmias associated with the WPW might be transient and self-limiting, or they might be sustained and require treatment. Depending on hemodynamic status, the patient might be asymptomatic or experience dizziness, syncope or the rhythm can degenerate to ventricular
tachycardia, ventricular fibrillation and sudden death.

5. Location (origin to termination) of accessory pathway in order of occurance:
(insert picture)
Origin Termination
Left atrium Free wall left ventricle
Atrial septum Ventricular septum
Right atrium Free right ventricle

6. Mimics of the WPW:  The WPW syndrome is often referred to as the “great imposter”. It will often mimic the following (pseudopatterns):
    1. Old MI
    2. Acute MI
    3. Ischemia
    4. LVH
    5   . RVH
    6. LBBB
    7. RBBB
    8. Posterior Infarction
 

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