ECG Challenge: A 66-year-old woman with a history of diabetes mellitus, hyperlipidemia, and rheumatoid arthritis presents to her primary care physician with complaints of intermittent lightheadedness. She has not experienced syncope. With the lightheadedness, she has noted her heart rate to be slow, often at ≈40 bpm. She denies any other cardiac symptoms. While in the office, she has a sudden onset of lightheadedness, and an ECG is obtained.
There is a regular rhythm at a rate of 32 bpm. The QRS complex has a normal duration (0.08 second) and a normal morphology. The axis is extremely leftward between −30° and −90° (positive QRS complex in lead I and negative QRS complex in leads II and aVF with an rS morphology). Causes of an extreme left axis include an inferior wall myocardial infarction in which there is a deep Q wave in leads II and aVF or a left anterior fascicular block in which there is an rS morphology in leads II and aVF. This is a left anterior fascicular block. The QT/QTc intervals are normal (460/340 milliseconds). P waves are seen before each QRS complex (+), with a stable PR interval of 0.40 second. The P wave is positive in leads I, II, aVF, and V4 through V6. This represents a sinus rhythm with a first-degree atrioventricular (AV) block or prolonged AV conduction. A second sinus P wave is seen after each QRS complex (*); it is not followed by a QRS complex and hence is nonconducted. The presence of an occasional on time but not conducted P wave defines a second-degree AV block, and because every other P wave is nonconducted, this represents a 2:1 AV block or AV conduction. The second-degree AV block may be either Mobitz type I or Wenckebach, which is attributable to a conduction abnormality in the AV node, or Mobitz type II, which is attributable to a conduction abnormality within the His-Purkinje system. When there is a continuous pattern of 2:1 AV block, the block may be Mobitz type I or II. The etiology can only be established if there is a change in the pattern of conduction, ie two sequentially conducted P waves (if PR interval stable it is Mobitz II, if PR interval lengthens it is Mobitz I) or the development of complete heart block (escape junctional rhythm it is Mobitz I, escape ventricular rhythm it is Mobtiz II). It can be seen that the PP interval is not constant, but there is a repeating pattern such that the PP interval surrounding the QRS complex is slightly shorter (↔, 0.80 sec) than the PP interval without a QRS complex (└┘, 0.96 sec). This is called ventriculophasic arrhythmia. Proposed mechanisms include enhanced sinus node artery pulsatile blood flow with ventricular contraction that increased the automaticity of the sinus node, stretch of the right atrium and sinus node with ventricular contraction that augments sinus node automaticity, and changes in baroreceptor output resulting from the stroke volume caused by ventricular contraction.
- © 2013 American Heart Association, Inc.