ECG Challenge: A 79-year-old man with a history of hypertension and coronary artery disease presents to the emergency department with a history of palpitations, lightheadedness, and shortness of breath. On physical examination, his pulse is rapid, his blood pressure is 100/60 mm Hg, and there are bilateral rales one-third the way up the lung fields. A portable chest x-ray confirms the presence of vascular congestion and heart failure. An ECG is obtained (ECG A). It is compared with a previous ECG (ECG B).
ECG A shows a regular rhythm with a rate of 210 bpm. The QRS complex is wide (0.14 s) and there is an extreme left axis between –30° and –90° (positive QRS complex in lead I and negative in leads II and aVF). Although the morphology resembles a right bundle-branch block with an RR′ in lead V1, the morphology is not typical. There are subtle differences in the QRS complex morphology, particularly evident in lead aVL (↓,↑). The QT/QTc intervals are prolonged (280/510 ms) but are normal when the prolonged QRS complex duration is considered (240/440 ms). There are no obvious P waves seen before or after any of the QRS complexes. However, there are occasional prominent positive waveforms seen associated with some but not all of the QRS complexes (v). In addition, there are subtle changes in the ST-T waves (^). These features are consistent with a diagnosis of ventricular tachycardia.
ECG B is the baseline ECG for this patient. The rhythm is regular, although there are occasional premature complexes (↓,↑) that are wide (0.14 s). The narrow and regular QRS complexes have a rate of 54 bpm. There are P waves (+) before each of these complexes. Hence, this is a sinus bradycardia. The QRS complex duration is normal (0.08 s) and the QRS complex has a normal morphology. The axis is normal between 0° and +90° (positive QRS complex in leads I and aVF). The QT/QTc intervals are normal (420/400 ms). The wide and premature QRS complexes have different morphologies (↓,↑) and there is no P wave before them. These are premature ventricular complexes. Because the premature ventricular complexes have 2 different morphologies, they are termed multifocal. The premature ventricular beats are not associated with a pause, and they are not altering the PP interval (↔); hence, they are termed interpolated premature ventricular complexes. Importantly, the QRS morphology of one of the premature ventricular complexes (↓) is identical to the QRS morphology of the tachycardia seen in ECG A, confirming that the rhythm in ECG A is indeed ventricular tachycardia. Although there is a P wave before each of the narrow QRS complexes (+), the PR intervals (┌┐) are not constant and 2 different PR intervals can be seen. The PR intervals of the QRS complexes following the premature ventricular complex is longer (0.26 s) than the PR intervals of all the other QRS complexes (0.20 s). The longer PR interval following the premature ventricular complex is a result of retrograde concealed conduction, which is often seen when the premature ventricular complex is interpolated. Most commonly, the premature ventricular complex results in retrograde impulse conduction into the AV node, rendering it totally refractory. If the next on-time sinus impulse arrives at the AV node while it is still refractory, it is not conducted through the AV node, whereas the subsequent sinus impulse conducts through normally. Thus, there is a pause after the premature ventricular complex, and the PP interval surrounding the premature complex is twice the sinus interval. This is termed a full compensatory pause. However, if the premature ventricular impulse fails to conduct through the entire AV node, but only conducts partially through it (ie, it is concealed), it renders the AV node only partially refractory. In this situation, the subsequent on time sinus impulse is able to conduct through the AV node, but at a slower rate, accounting for the longer PR interval.
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- © 2015 American Heart Association, Inc.