ECG Challenge: A 54-year-old college professor presents to the university health services with complaints of palpitations that began after an aerobics class and have persisted for >1 hour. She states that she has had palpitations in the past, although they have been self-terminating after several minutes. Her physical examination is normal except for a pulse rate that is regular at 148 bpm. An ECG (ECG A) is obtained. An intervention (carotid sinus pressure) is performed while the ECG (ECG B) is recorded, and the heart rate slows.
ECG A shows a regular rhythm at a rate of 148 bpm. The QRS complex has a normal duration (0.08 second) and a normal morphology. The axis is normal between 0° and +90° (positive QRS complexes in leads I and aVF). The QT/QTc intervals are normal (280/440 milliseconds). There is increased QRS complex amplitude or voltage with an S wave in lead V2 of 33 mm ([) and an R wave in lead V5 of 18 mm (]). The SV2+RV5=51 mm meets 1 of the criteria for left ventricular hypertrophy (ie, SV2+RV5 ≥35 mm). There are ST-T wave changes in leads I, II, aVL, aVF, and V3 through V6 (^). These changes may be related to left ventricular hypertrophy (repolarization abnormalities that are consistent with subendocardial ischemia) or the rapid ventricular rate (and the development of subendocardial ischemia). No obvious P waves are seen before or after any of the QRS complexes. However, there is a small positive waveform superimposed on the terminal portion of the QRS complex, best seen in lead V1 (↓). This may represent an R’, or it may be a superimposed P wave. Regardless of whether this is a superimposed P wave, the rhythm is called a no-RP tachycardia because no definitive P wave is seen. The most likely cause of this type of tachycardia is a typical atrioventricular nodal re-entrant tachycardia.
ECG B, recorded during carotid sinus pressure, shows the termination of this tachycardia. The first 6 QRS complexes are regular at a rate of 148 bpm. The QRS complexes have the same duration, morphology, axis, and QT/QTc intervals as the QRS complexes in ECG A. This is a no-RP tachycardia, and it is identical to the arrhythmia seen in ECG A. The tachycardia terminates abruptly after the sixth QRS complex. The first complex after the arrhythmia terminates (complex 7) has a P wave before it (*). The 10th QRS complex is premature and has the same P-wave morphology (*) and PR interval as complex 7. These are therefore atrial in origin. The remaining QRS complexes (complexes 8, 9, and 11–16) are regular at a rate of 95 bpm. There is a P wave before each of these complexes (+) with a stable PR interval (0.16 second), and the P wave has a different morphology than the P waves with complexes 7 and 10. These are sinus complexes. The QRS complexes during the tachycardia have an R’ (↓), which is not present in the sinus complexes. This confirms that this is likely a P wave superimposed on the QRS complex. The tachycardia therefore terminates with a nonconducted P wave (v), which is the mode of termination of arrhythmias that are generated by the atrioventricular node or requires the atrioventricular node as part of a re-entrant circuit (ie, ectopic junctional tachycardia, atrioventricular nodal re-entrant tachycardia, or atrioventricular re-entrant tachycardia). Retrograde atrial activity has occurred before the termination of the arrhythmia. This confirms the fact that the tachycardia in ECG A is a typical atrioventricular nodal re-entrant tachycardia, which is the most common arrhythmia, associated with no distinct or definitive P wave before or after the QRS complex. Atrioventricular nodal re-entrant tachycardia is the result of dual AV nodal pathways, ie, a slow pathway with a short refractory period or time for recovery and a fast pathway with a long refractory period or time for recovery. With a typical atrioventricular nodal tachycardia antegrade conduction to the ventricles is via the slow pathway while retroconduction back to the atria is via the fast pathway. As a result there is simultaneous atrial and ventricular activation and hence no obvious P waves before or after the QRS complex. In this case the retrograde P wave is simultaneous but superimposed at the end of the QRS complex.
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- © 2015 American Heart Association, Inc.