A 65-year-old man with a history of obesity and severe chronic obstructive pulmonary disease presents to the emergency room with increasing shortness of breath and a productive cough. A chest x-ray shows changes of chronic obstructive pulmonary disease but no acute pathology. It is felt that he has a chronic obstructive pulmonary disease exacerbation and is begun on antibiotics, steroids, and albuterol inhalers. Several minutes after presenting, his heart rate is noted to increase and become irregular. An ECG is obtained.
The rhythm is irregular as there are several long RR intervals, all of which are the same. Therefore, the rhythm is regularly irregular with group beating and an average rate of 120 bpm. The QRS complexes are narrow (0.08 sec) and have a normal morphology. The axis is about 0° (positive QRS complex in lead I and biphasic in lead aVF). There is downsloping ST segment depression and T wave abnormalities seen in leads I, II, III, aVR (the ST elevation in this lead is actually ST depression), and leads V3 through V6 (^). The J point and downsloping ST changes are consistent with subendocardial ischemia. The QT/QTc intervals are normal (320/450 ms). During each long RR interval there is a P wave seen before the QRS complex (+). The P wave is negative in leads II, III, aVF, and V4 through V6. Hence this is not a sinus P wave. There are P waves seen before the subsequent QRS complexes, most obvious in lead V1 (v) and also V2 where they are notching the T waves (↓). All of the P waves have the same morphology and they have a constant PP interval at a rate of 150 bpm. Therefore, the underlying rhythm is atrial tachycardia. However, the PR intervals are not constant and can be seen to progressively prolong (└┘) from 0.16 sec (the first PR interval after the pause) to 0.30 sec just before the pause. It can be seen that the pause or long RR interval is the result of a P wave that is not followed by a QRS complex (*; ie, it is nonconducted). Therefore this is a second degree AV block (defined as a regular rhythm with an occasional nonconducted P wave) and there is progressive PR interval lengthening with one nonconducted P wave after which the PR interval shortens to its baseline value (ie, 0.16 sec). This defines Mobitz type I or Wenckebach.
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- © 2014 American Heart Association, Inc.