A 76-year-old man with a history of hypertension and diabetes mellitus presents to the ophthalmology clinic for an evaluation before cataract surgery. Shortly after arriving, he complains of lightheadedness, his pulse is noted to be very rapid, and his blood pressure is 80/50 mm Hg. He is brought urgently to the emergency room where an ECG is obtained. He denies previous cardiac disease, although he states that over the past 2 months he has had similar episodes of episodic lightheadedness. As a result of the rapid tachycardia, he is urgently cardioverted, and after the rhythm is reverted, another ECG is obtained.
ECG A shows a rapid regular tachycardia at a rate of 280 bpm. The QRS complex duration is increased (0.14 second). The axis is rightward between 90° and 180° (negative QRS complex in lead I and positive QRS complex in lead aVF). The QRS complex morphology does not resemble either a left or right bundle-branch block. There is a tall R wave from V1 to V6 (↓), which is positive concordance. Positive concordance is seen whenever there is direct activation of the myocardium, specifically a ventricular complex, paced complex, or Wolff-Parkinson-White syndrome. Although distinct P waves are not obvious, there is variability of the ST-T waves, particularly in lead V1 (^). Some of the irregularities appear to be P waves, and this variability in the presence of (ie, a P wave with some but not all of the QRS complexes) and the relationship between the P waves and QRS complexes indicate atrioventricular dissociation. In addition, there is a marked variability of the QRS complex morphology (*), especially evident in leads V2 and V3. The findings seen on this ECG, that is, atrioventricular dissociation, variability of the QRS complex morphology, and variability in the ST-T waves, are consistent with a diagnosis of ventricular tachycardia. When the heart rate is >260 bpm, the ventricular tachycardia is called ventricular flutter. With a supraventricular tachycardia (sinus, atrial, or atrioventricular nodal) with aberration, the impulse is always conducted to the ventricles via the same pathway (the normal atrioventricular node His-Purkinje system). Thus, all the QRS complexes and ST-T waves are the same. Ventricular tachycardia involves a circuit within the ventricular myocardium; ventricular activation bypasses the normal conduction system; and the direction of impulse conduction and repolarization may be variable. One last feature that is consistent with a ventricular tachycardia is the relationship between the R and S wave in any precordial lead that has an RS complex. An R wave that is narrower than the S wave with a duration <100 milliseconds is consistent with a supraventricular tachycardia with aberration because the initial forces are normal and the terminal forces are prolonged, accounting for the widened QRS complex. When the R wave is wider than the S wave and had a duration of <100msec, then even initial activation is abnormal and this is consistent with a ventricular complex.
After the tachycardia is terminated, there is resumption of a regular rhythm at a rate of 66 bpm (ECG B). There is a P wave (+) before each QRS complex with a stable PR interval (0.20 second). The P wave is positive in leads I, II, aVF, and V4 through V6. Hence, this is a normal sinus rhythm. However, the P wave is negative in leads V1-V2 consistent with a left atrial abnormality or hypertrophy. The QRS complex duration is normal (0.10 second) and has a normal morphology with a QS complex in leads V1 and V2 (↓) that is suggestive of (but not definitely) a chronic anteroseptal myocardial infarction. The axis is normal between 0° and 90° (positive QRS complex in leads I and aVF). There are nonspecific ST-T–wave abnormalities in leads I, aVL, V5, and V6 (^). The QT/QTc intervals are normal (400/420 milliseconds). Comparing the QRS complex during sinus rhythm with those during the tachycardia shows that there is a marked change in morphology and axis.
- © 2013 American Heart Association, Inc.