A 69-year-old woman with a history of coronary artery disease and atrial fibrillation for which she is taking sotalol presents to her primary care physician for a routine physical examination. Her physical examination is normal, but her pulse is noted to be irregular, and an ECG is obtained (ECG A). It is compared with her previous ECG (ECG B).
ECG A shows a rhythm that is irregular, but there is a pattern, with many of the RR intervals the same; thus, the rhythm is regularly irregular. The first 2 QRS complexes (*) have a P wave before them (+) with a stable PR interval (0.26 s). The P wave is positive in leads I and II. These are likely 2 sequential sinus complexes with a first-degree AV block (prolonged AV conduction), and they have a rate of 64 beats per minute. The QRS complexes are wide (0.16 s). There is a pattern of a right bundle-branch block with a broad terminal S wave in lead I (←). The axis cannot be accurately established, because there is no sinus complex in lead aVF; however, it is a leftward axis (and likely a left anterior fascicular block), because the QRS complex is positive in lead I and negative in lead II. The QT/QTc intervals are normal (400/415 ms). P waves can be seen thereafter (v), and they are occurring with a stable PP interval (└┘) and a rate of 64 beats per minute. These P waves are positive in leads aVF and V4 through V6; therefore, there is an underlying normal sinus rhythm. However, there is no relationship between the P waves and the QRS complex, that is, there is AV dissociation. The QRS complexes are regular at a rate of 110 beats per minute (bpm). AV dissociation may be attributed to either complete heart block, in which the atrial rate is faster than the rate of the QRS complexes, or an accelerated lower pacemaker, in which the atrial rate is slower than the rate of the QRS complexes. Therefore, this is an accelerated lower pacemaker. The QRS complexes are wide (0.12 s) but not as wide as the initial sinus complexes. In addition, they have a morphology that is different from the sinus complexes. Hence, these are ventricular complexes, and, hence, this is ventricular tachycardia. On occasion, ventricular complexes are narrower than the supraventricular complexes, and this happens if the ventricular focus or re-entrant circuit is located close to one of the distal bundles. The 12th QRS complex (↓) is also preceded by a P wave (^), and the QRS morphology is identical to the first 2 sinus complexes; therefore, this represents intermittent capture and it is termed a Dressler beat or complex. There is a terminal broad S wave (→) consistent with a right bundle-branch block morphology.
ECG B shows a regularly irregular rhythm as a result of several premature complexes (^) associated with a short RR interval (all of which are the same). The longer RR intervals are also the same. There are 2 different QRS complex morphologies. Complexes 1, 3, 5, 6, 8, 9, and 11 (*) are wide (0.16 s) and have a right bundle-branch block morphology with an RSR' in lead V1 (→) and a broad terminal S wave in leads I and V5 through V6 (←). These QRS complex have a preceding P wave (+) with a stable PR interval (0.26 s). The P waves are positive in leads I, II, aVF, and V4 through V6. The bpm rate is 66. Hence, this is a normal sinus rhythm. The P waves are identical to those seen in ECG A, and the QRS complex duration and morphology are also the same as the sinus complexes seen in ECG A. It is now obvious that there is an extreme left axis between –30° and –90° (positive QRS complex in lead I and negative in leads II and aVF). The 2 causes for an extreme left axis are an inferior wall myocardial infarction (with a deep Q wave in leads II and aVF) or a left anterior fascicular block with an rS morphology in leads II and aVF. Hence, this is a left anterior fascicular block. The presence of a left anterior fascicular block and a right bundle-branch block is termed bifascicular block or disease. There is also a prolonged PR interval (first-degree AV block or prolonged AV conduction), and this is often termed trifascicular block or disease. However, this diagnosis cannot be established unless the cause for the first-degree AV block (prolonged AV conduction) is known, that is, conduction delay in the AV node or in the remaining fascicle (ie, left posterior fascicle). The premature complexes have a different morphology compared with the sinus complex, and they are premature ventricular complexes occurring in a bigeminal (every other QRS complex is a premature ventricular complex) and trigeminal pattern (every third QRS complex is a premature ventricular complex). Importantly, the premature ventricular complexes have the same morphology as the abnormal QRS complexes in ECG A, confirming that the rhythm in ECG A is ventricular tachycardia.
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- © 2014 American Heart Association, Inc.