Wolff-Parkinson-White Syndrome Pathophysiology, Pre-Excitation and AVRT, Animation

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  • Published on:  7/9/2018
  • (USMLE topics, cardiology) Mechanism of tachycardia in WPW patients.
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    Voice by Sue Stern
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    Wolff-Parkinson-White, or WPW, syndrome is a congenital heart disease characterized by presence of an ABnormal electrical CONNECTION between the atria and ventricles of the heart. WPW typical symptom is an abnormally FAST heart rate, or TACHYCARDIA.
    In normal conduction, electrical signals are initiated in the SA node, and travel throughout the atria before they reach the AV node. The AV node is the GATEWAY to the ventricles. It DELAYS the passage of electrical impulses to the ventricles to ensure that the atria have ejected all the blood into the ventricles before the ventricles contract. This REFRACTORY property of the AV node is essential in LIMITING electrical activities that reach the ventricles. In situations where the ATRIAL rate is EXCESSIVELY high, such as during atrial fibrillation or atrial flutter, the AV node BLOCKS most of the impulses from passing to the ventricles, keeping the heart rate under control.
    In WPW, there is an ADDITIONAL connection between the atria and the ventricles, called the ACCESSORY pathway, or bundle of Kent. This pathway is essentially a patch of conductive tissue that provides a SHORTCUT to the ventricles, BYPASSING the AV node. It allows PART of electrical impulses to arrive to the ventricles SOONER, causing a so-called “PRE-excitation”. This can be seen as a SHORTENED PR interval on an ECG. Because part of the ventricles depolarize EARLIER, ventricular depolarization develops in a more GRADUAL fashion and lasts LONGER, resulting in a SLURRING slow rise of the initial portion of the QRS complex, known as DELTA wave, and QRS prolongation.
    To note, however, that the presence of an accessory pathway ALONE does NOT cause tachycardia. In fact, most people with a WPW pathway NEVER develop any symptoms. They are said to have a WPW PATTERN, as opposed to WPW SYNDROME in symptomatic patients.
    There are 2 mechanisms by which tachycardia can happen in WPW:
    - Most commonly, tachycardia develops when electrical impulses travel DOWN one pathway, either the normal or accessory, then BACK UP via the OTHER, creating a SELF-perpetuating LOOP, or a RE-ENTRANT circuit. The frequency of this loop determines heart rate and CAN be very fast, ranging from 150 to 250 beats per minute. This is known as Atrioventricular Re-entry Tachycardia, or AVRT. AVRT can be orthodromic or antidromic depending on the direction of the loop.
    - Another scenario is when WPW patients ALSO suffer from Atrial Fibrillation. In this condition, the atria contract at a VERY HIGH rate but most of the electrical impulses do NOT make it through the AV node to the ventricles. This is where a WPW pathway can have a detrimental effect. It provides a BYPASS to let MORE impulses reach the ventricles, causing a FASTER heart rate that could potentially be fatal.
    The severity of WPW tachycardia depends on how FAST the accessory pathway is able to conduct. This varies from person to person and can be evaluated in a procedure called Programmed Electrical Stimulation, in which the atria are stimulated to produce progressively HIGHER rates and the atrial-to-ventricular conduction ratio is monitored. Patients are at high risk of developing LETHAL tachycardia if their accessory pathway CONTINUES to conduct at 1-to-1 ratio with dangerously high atrial rates. High-risk patients are usually treated with catheter ablation to destroy the conductive tissue of the accessory pathway.
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