ECG Response: June 17, 2014 Circulation. 2014;129:2574-2575 doi: 10.1161/CIRCULATIONAHA.114.011134 Circulation is published by the American Heart Association, 7272 Greenville Avenue, Dallas, TX 75231 Copyright © 2014 American Heart Association, Inc. All rights reserved. Print ISSN: 0009-7322. Online ISSN: 1524-4539

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ECG Challenge Response ECG Response: June 17, 2014 ECG Challenge: A 28-year-old man with no known heart disease but a history of occasional palpitations that he states he is able to terminate by performing a Valsalva maneuver presents to the emergency room with an episode of palpitations that did not terminate as usual. When he arrived, he stated that the palpitations had resolved, but while an ECG was being recorded, the symptoms recurred.

There is a regular rhythm at a rate of 160 bpm. However, the QRS complex morphology is not uniform. The first QRS complex (*) is wide and has a broad Q wave in lead I (^). There is a P wave before this complex (+), and the PR interval is short (0.12 second). The QRS complex has a slow or slurred upstroke. This has a morphology suggesting pre-excitation or a Wolff-Parkinson-White pattern. The Q wave in lead I suggests that the pathway is left lateral (ie, a pseudo–lateral wall myocardial infarction pattern). The next 2 QRS complexes are also wide (▲) but are not preceded by a P wave. Their morphology is slightly different from the first QRS complex and they also have a morphology that is slightly different from each other; therefore, these are most likely premature ventricular complexes. Beginning with complex 5, the QRS complex also has a wide duration, but it has a morphology of a typical right bundle-branch block with an RSR′ in lead V1 (→) and broad terminal S waves in leads I, V5, and V6 (←). Also noted are beat-to-beat changes in QRS complex amplitude, especially in leads V1 and V2 (▼, ▼▼). This is called electric or QRS alternans. Causes of electric alternans include a large pericardial effusion or tamponade (resulting from shifting of the position of the heart in the fluid-filled pericardium), acute myocardial infarction, decompensated congestive heart failure, dilated cardiomyopathy, or any rapid supraventricular tachycardia. In all of the conditions listed, except for tamponade, the electrical alternans is the result of beat-to-beat changes in calcium fluxes into the ventricular myocardium. Although no obvious P waves are seen before any of the QRS complexes, there are regular abnormalities noted within the ST (↑), particularly in leads II, III, and aVF. These are P waves; hence, this is a short-RP tachycardia. Etiologies for Correspondence to Philip J. Podrid, MD, West Roxbury VA Hospital, Section of Cardiology, 1400 VFW Pkwy, West Roxbury, MA 02132. E-mail [email protected] (Circulation. 2014;129:2574-2575.) © 2014 American Heart Association, Inc. Circulation is available at

DOI: 10.1161/CIRCULATIONAHA.114.011134

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ECG Challenge Response   2575 a short-RP tachycardia include sinus tachycardia (with a first-degree atrioventricular [AV] block), an ectopic junctional tachycardia, atrial tachycardia, atrial flutter (with 2:1 AV block), AV reentrant tachycardia (AVRT), and AV nodal reentrant tachycardia. Because these waveforms are different from the sinus P waves, this is not sinus tachycardia. The rate of this tachycardia is faster than is usually seen with an ectopic junctional tachycardia. Because a second atrial waveform is not present, atrial flutter is not likely. Therefore, the most likely rhythm is either AVRT or AV nodal reentrant tachycardia. Since the first QRS complex is pre-excited and represents a Wolff-ParkinsonWhite pattern, the most likely etiology is an AVRT, which is the most common arrhythmia occurring in patients with Wolff-Parkinson-White. Although the QRS complex is wide, it has a typical right bundle-branch block morphology and the morphology is different from that of the pre-excited complex. Importantly, the wide QRS complex has a typical right bundle-branch block morphology without any evidence of a delta wave. Therefore, this is an orthodromic AVRT with an associated right bundle-branch block. In this situation, activation of the ventricle is via the normal AV node His-Purkinje pathway, whereas retrograde activation of the atria is via the accessory pathway. With an antedromic AVRT, activation of the ventricle is via the accessory pathway, and retrograde conduction back to the atria is via the normal conduction system (His-Purkinje system and AV node). Therefore, with an antedromic AVRT, the QRS complexes will resemble the pre-excited complexes during sinus rhythm. Also confirming the fact that this is an orthodromic AVRT is the way that the arrhythmia is initiated. Before the AVRT, there are 2 ventricular complexes (▲). The fourth QRS (↓) has a morphology that has features of both the ventricular complexes and the QRS complexes of the AVRT. This is therefore a fusion complex; hence, it represents a third ventricular complex that fuses with the first QRS complex of the AVRT. A fusion complex occurs whenever an impulse coming from above and conducting through the normal AV node His-Purkinje system fuses with an impulse originating within the ventricle. It is not uncommon for ventricular ectopy to initiate an AVRT as a result of retrograde conduction to the atrium via the accessory pathway (which conducts rapidly to the atrium due to the absence of blockade within the AV node) that then antegradely conducts back to the ventricles via the normal AV node His-Purkinje pathway. If the impulse reenters the accessory pathway, an orthodromic AVRT is initiated. Please go to the journal’s Facebook page for more ECG Challenges: Challenges are posted on Tuesdays and Responses on Wednesdays.

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ECG Response: June 17, 2014.

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