DrVirgo
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A 30-year-old man comes to the emergency department
complaining of chest palpitations. For the last few hours
he has been light-headed and feels as if his heart is “bursting
out” of his chest. He has had some similar fleeting
episodes of palpitations in the past, but because they have
been transient, he has simply attributed them to stress
and coffee and has not sought emergency medical treatment.
When checking the radial pulse, the physician notes
an irregular, rapid heart rate of approximately 130/min.
The rest of the patient’s vital signs are stable. An electrocardiogram
shows atrial fibrillation with a ventricular rate
as high as 230/min. The QRS complexes appear widened.
An old electrocardiogram obtained 1 year ago as part of a
pre-employment physical examination is available. It
reveals a short PR interval with a strange up-sloping of
the R wave.Which of the following is the most appropriate
treatment for this patient’s arrhythmia?
(A) Digoxin
(B) Emergent electrical cardioversion
(C) Intravenous diltiazem
(D) Metoprolol
(E) Procainamide
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| young_doc
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WPW, avoid A, C, D.
Answer E?
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| robin082006
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E
This is WPW syndrome
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| mjl1717
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aberrant electrical activity with a wave called a delta wave??
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| DrVirgo
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E. Patients with Wolff-Parkinson-
White (WPW) syndrome have an accessory pathway (the
bundle of Kent) that can allow rapid conduction of atrial
impulses to the ventricle. The up-sloping R wave is
termed a delta wave and represents pre-excitation of the
ventricle. This accessory pathway from the atria to the
ventricle also can conduct atrial fibrillation impulses
rapidly, resulting in a very rapid tachycardia. The
increased risk for sudden death in WPW patients is
believed to be secondary to rapid ventricular rates during
atrial tachycardia.Understandably, agents are needed that
directly suppress the extranodal accessory pathway, rather
than just block the AV node, a strategy that is appropriate
for most forms of atrial fibrillation. Indeed, there is concern
that blocking the AV node may increase conduction
through the more rapidly conducting bundle of Kent,
worsening the rapid ventricular response. Procainamide,
flecainide, and propafenone are all reasonable choices to
suppress tissue in the accessory pathway.
Nodal blocking agents, such as digoxin (choice A),
intravenous diltiazem (choice C), or metoprolol
(choice D), are not appropriate choices, as they act
mainly on the AV node.
Emergent cardioversion (choice B) is not necessary if a
patient is hemodynamically stable. Because cardioversion
carries its own risks and morbidity, it should not
be a first-line treatment in a stable patient. If this
patient were unstable, then cardioversion would be
warranted. After this patient is in a normal sinus
rhythm, or at least is rate controlled, radiofrequency
ablation of the accessory bundle should be considered.
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