ECG Challenge: A 72-year-old man with a history of hypertension treated with atenolol and hydrochlorothiazide presents with acute renal failure resulting from a urinary tract obstruction from prostatic hypertrophy. On presentation, his heart rate is noted to be slow, and an ECG is obtained (ECG A). After admission to the hospital, an ECG is repeated (ECG B).
ECG A shows a regular rhythm at a rate of 42 bpm. The QRS complex duration is normal (0.08 second), and there is a normal morphology. The axis is extremely leftward between −30° and −90° (positive QRS complex in lead I and negative a complex in leads II and aVF). There are 2 reasons for an extreme left axis: 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 as an rS morphology in leads II and aVF). The QRS complexes in leads II and aVF have an rS morphology; hence, this is a left anterior fascicular block. There is a tall R wave in lead V2 (←) that is attributable to early transition or counterclockwise rotation of the axis in the horizontal plane. This is established by imagining the heart as it is viewed from under the diaphragm. With counterclockwise rotation, left ventricular forces develop early in the precordial leads, producing the tall R wave in V2. The QT/QTc intervals are normal (440/370 milliseconds). There is a P wave before each QRS complex (+) with a constant PR interval (0.20 second). The P wave is positive in leads I, II, aVF, and V4 through V6. Hence, there is an underlying sinus rhythm. A second P wave (*), with the same morphology as the P wave before the QRS complex, is seen after each QRS complex, and it is nonconducted; that is, it is not followed by a QRS complex. The PP interval is constant (└┘) at a rate of 85 bpm. Therefore, there is a second-degree atrioventricular block (defined as an occasional nonconducted P wave) with a pattern of 2:1 atrioventricular conduction or atrioventricular block. The 2:1 atrioventricular nodal block may be either Mobitz type I (Wenckebach) or Mobitz type II. The only way to establish the pathogenesis is by a change in the pattern of conduction, that is, 2 sequentially conducted P waves or the development of complete (or third-degree) atrioventricular block. If with 2 sequentially conducted P waves the PR interval becomes longer, this is Mobitz type I; if the PR intervals are the same, this is Mobitz II. If with complete (third-degree) atrioventricular block there is an escape junctional rhythm, then the 2:1 atrioventricular block is Mobitz type I; if the escape rhythm is ventricular, then the 2:1 atrioventricular block is Mobitz type II.
In ECG B rhythm is irregular, but there is a pattern, and it appears to be group beating, that is, 2 complexes and a pause. All of the long intervals (1.4 seconds) are the same, and the short intervals (0.92 second) are the same. Thus, the rhythm is regularly irregular. The average rate is 54 bpm. The QRS complexes have the same width, morphology, and axis as seen in ECG A. The QT/QTc intervals are the same. There is a P wave before each QRS complex, and the P wave is positive in leads I, II, aVF, and V4 through V6. Hence, there is an underlying sinus rhythm, and the PP interval is constant (┌┐) with a rate of 75 bpm. The PR interval is not constant because the PR interval of the first of the 2 QRS complexes is 0.20 second, whereas the PR interval of the second of the 2 QRS complexes (^) is longer (0.32 second). After the second QRS complex, there is an on-time but nonconducted P wave (*), which accounts for the pause or long RR interval. Therefore, there are 2 sequentially conducted P waves that have a pattern of 3:2 Wenckebach or Mobitz type I. Therefore, the 2:1 atrioventricular block in ECG A is Mobitz type I with the atrioventricular block within the atrioventricular node.
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- © 2016 American Heart Association, Inc.