Reentry

• For anatomically-determined re-entry such as Wolf-Parkinson-White syndrome (WPW) drugs the arrhythmia can be resolved by blocking action potential (AP) propagation. (In WPW syndrome, an accessory conduction pathway, linking atria and ventricles and bypassing the atrioventricular node, is the structure responsible for the arrhythmia)

• In WPW-based arrhythmias, blocking conduction through the AV node may be clinically effective.

  • Drugs that prolong nodal refractoriness and slow conduction include: Ca²⁺ channel blockers, beta-adrenergic blockers, or digitalis glycosides.

  • For functional (non-anatomical) reentrant circuits, prolongation of refractoriness is the electrophysiological change most likely to terminate the reentry arrhythmia.

• Prolongation of tissue refractoriness can be accomplished by those antiarrhythmic drugs that block Na⁺ channels.

  • Sodium channel blockers reduces the percentage of recovered channels (following inactivation by depolarization) at any given membrane potential.

  • Examples of antiarrhythmic drugs classified as sodium channel blockers include lidocaine, quinidine, and tocainide.

  • "Although any type of arrhythmia can occur in a patient with WPW, the two most common are CMTs (circus
    movement tachycardias) and atrial fibrillation (AFib). CMT is the more common arrhythmia of the two

    • Treatment of CMTs associated with WPW is similar to treating PSVT

    • In a stable patient, adenosine (6 mg rapid IV push; if unsuccessful, 12 mg rapid IV push) should be the first-line treatment in any regular tachycardia, regardless of whether the complex is wide or narrow

  • Treatment of AFib associated with WPW is necessarily different than for a patient with a normal heart. AFib is an irregular rhythm as opposed to the regular rhythm seen in CMTs.

    • The basic treatment principle in WPW AFib is to prolong the anterograde refractory period of the accessory pathway relative to the AV node. This slows the rate of impulse transmission through the accessory pathway and, thus, the ventricular rate.

    • If AFib were treated in the conventional manner by drugs that prolong the refractory period of the AV node (eg, calcium channel blockers, beta-blockers, digoxin), the rate of transmission through the accessory pathway likely would increase, with a corresponding increase in ventricular rate. This could have disastrous consequences, possibly causing the arrhythmia to deteriorate into V fib.

    • Procainamide (17 mg/kg IV infusion, not to exceed 50 mg/min; hold for hypotension or 50% QRS widening) blocks the accessory pathway, but it has the added effect of increasing transmission through the AV node. Thus, although procainamide may control the AFib rate through the accessory pathway, it may create a potentially dangerous conventional AFib that may require treatment with other medications. Prompt cardioversion of patients with WPW and AFib is recommended.

    • Medical management may be a viable option in some patients, but it may have unpredictable results. Note that cardioversion is always the treatment of choice in unstable patients."----*From emedicine (http://www.emedicine.com/EMERG/topic644.htm) Authored by Mel Herbert, MD, MBBS, Assistant Professor of Medicine and Nursing, Department of Emergency Medicine, Olive View-University of California at Los Angeles Medical Center

Category: Pharmacology Notes