ECG Challenge: A 74-year-old man with a history of chronic obstructive pulmonary disease, prostate cancer (treated with surgery), and hypertension, which is being treated with an angiotensin-converting enzyme inhibitor and a β-blocker, presents to the emergency department with concerns of palpitations that had been present for several hours. He initially felt that the palpitations were the result of his albuterol inhaler, but the symptoms persisted for several hours and prompted him to come to the emergency department. On presentation, his respiratory status was stable and his blood pressure was 130/78 mm Hg. Heart sounds were regular, but he had a rapid heart rate. An ECG was obtained (A). The patient underwent urgent cardioversion after which a second ECG (B) was obtained.
There is a regular wide complex tachycardia with a rate of 138 bpm. The QRS complexes have a duration of 0.14 s. Although the QRS complexes resemble a right bundle-branch block with a tall R wave in lead V1 (→), and deep S waves in leads I and V6 (←), as well, the morphology is not typical for a right bundle-branch block. In addition, the axis is indeterminate between –90° and ±180° (negative QRS complex in leads I and aVF). Also noted is 1 on-time QRS complex (^), which has a morphology that is very different from all of the other QRS complexes (+). The QT/QTc intervals are prolonged (340/515 ms and 300/455 ms when the prolonged QRS complex duration is considered). There are no P waves before any of the QRS complexes. However, there are intermittent or irregular notches on the T waves, best seen in the rhythm strip (↓), and other nonconsistent irregularities of the ST-T waves (↑), as well. A wide QRS complex with an indeterminate axis is seen when there is direct myocardial activation, as with a paced rhythm (specifically biventricular pacing), Wolff-Parkinson-White pattern, or a ventricular complex. There are no pacing stimuli seen, and, hence, this is not a paced rhythm. There is no evidence for preexcitation attributable to Wolff-Parkinson-White. Therefore, the cause of the rhythm based on the unusual QRS complex morphology and the indeterminate axis is ventricular tachycardia. Further support for ventricular tachycardia is the variability of the QRS complex morphology and the nonconsistent irregularities of the ST-T waves. Some of these irregularities may reflect superimposed P waves that are dissociated from the QRS complexes.
The second ECG (B) is the baseline ECG for this patient, obtained after cardioversion. There is a regular rhythm at a rate of 76 bpm. There is a P wave before each QRS complex (+) with a stable PR interval (0.18 s). The P waves are positive in leads I, II, aVF, and V4 through V6. This is a normal sinus rhythm. The P wave is all negative in lead V1 and has a notching in leads II and aVF; these findings are consistent with a left atrial abnormality or hypertrophy. The QRS complexes have a normal duration (0.10 s) and a normal morphology, although there is poor R-wave progression from V1 through V3, which is consistent with clockwise rotation of the electric axis in the horizontal plane. This is established by imagining the heart as if viewed from under the diaphragm. With clockwise rotation, the appearance of left ventricular forces is delayed and they develop later in the precordial leads. The axis is very leftward between –30° and –90° (positive QRS complex in lead I and negative QRS complex in leads II and aVF). The 2 causes for an extreme left axis include an old inferior wall myocardial infarction in which there is a deep Q wave or a left anterior fascicular block in which there is an rS morphology, which is seen in this case; therefore, this is a left anterior fascicular block. There are ST-T–wave abnormalities seen in leads I, aVL, and V4 to V5 (^). The QT/QTc intervals are normal (340/380 ms).
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- © 2015 American Heart Association, Inc.