ECG Challenge: A 22-year-old graduate student presents to student health because of palpitations that have been present for ≈2 hours. They occurred after she was jogging. She states that she has had similar palpitations in the past, but they were usually of a briefer duration. An ECG (ECG A) is obtained during the palpitations. Adenosine is administered, and this terminates the arrhythmia. A second ECG (ECG B) is obtained thereafter.
ECG A: The rhythm is regular at a rate of 190 bpm. The QRS-complex duration is normal (0.08 s), and there is a normal morphology and axis between 0° and +90° (positive QRS complex in leads I and aVF). The QRS amplitude is increased, with an S wave in lead V2 that is 20 mm (]) and an R wave in lead V6 that is 30 mm ([) (total=50 mm). Although this meets 1 of the criteria for left ventricular hypertrophy (ie, SV2+RV6≥45 mm in a subject <45 years of age), the QRS-complex amplitude or voltage is likely normal in this young healthy woman who is likely thin and has no lung disease. ST-segment depression is noted in leads II, aVF, and V3 to V6 (^). These are likely related to the rapid rate, although subendocardial ischemia should be considered. The QT/QTc intervals are normal (240/430 ms). There are no obvious P waves seen before or after any of the QRS complexes. However, there is notching (that appears to be negative) of the ST segment, seen best in leads III, aVF, and V6 (). There is also a positive waveform at the end of the QRS complex in lead aVL (). These notches are P waves and therefore this is a short RP tachycardia. Causes for a short RP tachycardia include sinus tachycardia, atrial tachycardia, ectopic junctional tachycardia, atrial flutter, typical atrioventricular nodal tachycardia, or an atrioventricular tachycardia. However, the cause for this tachycardia cannot be definitively established.
ECG B: After the tachycardia has been terminated by adenosine, there is a regular rhythm at a rate of 76 bpm. The QRS-complex duration is increased (0.14 s), and the morphology does not resemble either a typical right or left bundle-branch block. Indeed, the upstroke of the QRS complex is slurred (), and there is positive concordance (ie, tall R wave) across the precordium (→). This is abnormal and is not seen with normal conduction through the His-Purkinje system, but rather reflects direct myocardial activation, as seen with a paced complex, ventricular complex, or preexcited complex. There is a P wave before each QRS complex (+), and the P wave is positive in leads I, II, aVF, and V4 to V6. Hence, there is an underlying normal sinus rhythm. The PR interval is constant; however, it is short (0.12 s). The short PR interval and the widened QRS complex are characteristic of a Wolff-Parkinson-White pattern. The slurred upstroke is known as a delta wave. There are diffuse ST-T–wave abnormalities (^). However, because initial myocardial activation occurs via the accessory pathway and not the normal His-Purkinje system, abnormalities of the left ventricle cannot be reliably established on the ECG. Therefore, the ST-T–wave changes are related to preexcitation and not a primary problem of the myocardium. Because this patient has Wolff-Parkinson-White, the narrow QRS complex tachycardia seen in ECG 11A is termed orthodromic atrioventricular reentrant tachycardia. In this situation, antegrade activation of the ventricles is via the normal AV node His-Purkinje system, whereas the retrograde conduction back to the atria is via the accessory pathway.
- © 2013 American Heart Association, Inc.