ECG Challenge: A 67-year-old man with a history of chronic obstructive pulmonary disease and hypertension, presented to his physician 2 months ago with complaints of palpitations. He was noted to be in atrial fibrillation. He was begun on anticoagulation. After 1 month of anticoagulation his physician began therapy with sotalol as therapy of the arrhythmia. He returned for a follow-up visit 1 week later.
The initial portion of the ECG shows a rhythm that is irregularly irregular without any evidence for organized atrial activity. The average rate is about 160 bpm. Hence the rhythm is atrial fibrillation. The QRS complexes have a normal duration (0.08 sec) and a normal morphology, although there is low voltage, defined as a QRS complex amplitude <5 mm in each limb lead. The QT/QTc intervals are normal (260/425 ms). In the second half of the ECG the rhythm becomes fairly regular, although some longer RR intervals are noted. However, these longer intervals have the same duration; the rhythm is therefore regularly irregular. The ventricular rate is 260 bpm, although the longer RR intervals are at a rate of 130 bpm. Distinct atrial waveforms can be seen, primarily in V1 (v). All these wave forms are uniform in morphology, interval, and amplitude, and they are regular at a rate of 260 bpm. Hence the rhythm is now atrial flutter with 1:1 conduction (because the atrial flutter rate is the same as the ventricular rate). The longer RR intervals are attributable to 2:1 AV conduction because distinct flutter waves can also be seen in leads V5 and V6 (^) during the longer RR interval. Several of the QRS complexes at the beginning of the atrial flutter (+) are wider (0.12 sec), and they have a right bundle-branch block morphology with a tall broad R wave in lead V1. Although these widened QRS complexes might be rate related aberration, it can be seen that there are other RR intervals with same short duration (┌┐) that are not associated with a right bundle-branch block aberrancy. Hence the aberrancy is not rate related. Noted is the fact that these wide QRS complexes follow a long (↔)–short (└┘) cycle. This is consistent with the Ashman phenomenon. Unlike rate-related aberration, which is generally the result of an abnormality of conduction through the bundles (often as the result of some disease process), the Ashman phenomenon is a normal physiological change in His-Purkinje refractoriness that is related to rate. When the heart rate is slower (longer RR interval) His Purkinje refractoriness lengthens, whereas with a faster heart rate (shorter RR interval) His Purkinje refractoriness shortens. When there is an abrupt change in heart rate, going from slower (long RR interval) to faster (short RR interval), His Purkinje refractoriness does not adapt immediately and hence 1 or several QRS complexes will be conducted with aberration. Most often the aberrancy is a right bundle-branch block, likely because the right bundle branch has a longer refractory period compared with the left bundle.
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- © 2014 American Heart Association, Inc.