ECG Challenge: A 47-year-old woman with a history of palpitations that occur after exercise presents to an emergency department with palpitations that have persisted for several hours. An ECG (A) is obtained. Several minutes later the palpitations abruptly stop and an ECG (B) is repeated.
ECG A shows a regular rhythm at a rate of 120 bpm. The QRS complex duration is increased (0.12 s) and there is a morphology consistent with a right bundle-branch block with a tall an RR′ wave in V1 (←) and a broad terminal S wave in leads I and V5 to V6 (→). The axis is extremely leftward between –30° and –90° (positive QRS complex in lead I and negative complex in leads II and aVF). There are 2 causes for an extreme left axis; that is, an old inferior wall myocardial infarction (which has a deep initial Q wave in leads II and aVF) or a left anterior fascicular block (which has an rS morphology in leads II and aVF). Because the QRS complexes in leads II and aVF have an rS morphology, this is a left anterior fascicular block. The QT/QTc intervals are prolonged (360 ms/510 ms) but are normal when corrected for the wide QRS complex duration (340 ms/480 ms). There is a P wave seen before each QRS complex (+), most obvious in leads I, II, aVF, and V5 to V6. The P waves are positive in these leads, consistent with a sinus mechanism. The PR interval is constant, although prolonged (0.26 s). This represents a first-degree atrioventricular (AV) conduction delay (or first-degree AV block. Therefore, it appears that this is a sinus tachycardia with a first-degree AV conduction delay (first-degree AV block).
After the palpitations stopped, ECG B shows a regular rhythm at a rate of 85 bpm. There are 2 premature complexes (*). The QRS complex duration is normal and there is a normal morphology. The axis is normal between 0° and +90° (positive QRS complex in leads I and aVF) and the QT/QTc intervals are normal (340 ms/400 ms). There is flattening of the ST segment (↑) in leads I, aVL, and V5 to V6, which are nonspecific changes. There is a P wave (+) before each QRS complex with a constant PR interval (0.20 s). The P wave is positive in leads I, II, aVF, and V4 through V6. Hence, this is a normal sinus rhythm. The 2 premature QRS complexes (*) have the same morphology as the sinus complexes; they are both preceded by a P wave (^), but the P wave is different than the sinus P wave. These are premature atrial complexes. Although ECG A appears to show a sinus tachycardia with a first-degree AV conduction delay, ECG B shows a normal sinus rhythm with a PR interval that is shorter (0.20 s) than the PR interval during the tachycardia (0.26 s). The PR interval stays the same or shortens with sinus tachycardia. Sinus tachycardia is attributable to enhanced sympathetic tone or increased catecholamines, which results in more rapid impulse conduction through the AV node and, hence, a shortening of the PR interval. Therefore, a longer PR interval with a faster heart rate is not consistent with a sinus mechanism, but is consistent with an atrial tachycardia. With an atrial tachycardia, which is not the result of enhanced sympathetic tone, there is generally a slowing of conduction through the AV node (and, hence, a longer PR interval) as a result of decremental AV conduction. When the AV node is stimulated at a more rapid rate (in the absence of sympathetic stimulation), conduction through the node is slower. In addition, the P waves seen in ECG A are different than those seen with sinus rhythm (ECG B). Therefore, the rhythm in ECG A is an atrial tachycardia. Last, the QRS complex during the atrial tachycardia has a right bundle-branch block morphology and a left anterior fascicular block, whereas these features are not seen during normal sinus rhythm. Hence, these conduction abnormalities are rate-related changes.
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- © 2016 American Heart Association, Inc.