Monday, July 9, 2012

ECG Interpretation Review #48 (Chest Pain - STEMI - 1st Degree - 2nd Degree AV Block - Infero-lateral - 2-to-1 - Wraparound)

The 12-lead ECG shown in Figure 1 was obtained from 50-year-old woman with “chest tightness”.
  • What two major conclusions should be reached regarding ECG interpretation of this tracing? 
Figure 1 – 12-lead ECG from a 50-year-old woman with chest tightness. (Reproduced from ECG-2014-ePub). – NOTE – Enlarge by clicking on Figures – Right-Click to open in a separate window.
INTERPRETATION: The two conclusions to be reached are: i) that there is a large acute evolving STEMI (ST-Elevation-Myocardial Infarction) in progress; and ii) there is 2nd degree AV block. It may be easiest to first interpret the changes of acute MI:
  • The QRS complex is narrow.
  • The axis is normal.
  • There is no chamber enlargement.
  • Q Waves/R Wave Progression: Q waves are present in each of the inferior leads (II,III,aVF). After a small (but definitely present) initial r wave in lead V1 – there is loss-of-R-wave – with a probable QS in V2 and a definite QS (with notch in downslope of S wave) by lead V3. Abnormal Q waves persist in leads V4-thru-V6.
  • ST-T Wave Changes: There is marked ST elevation in each of the inferior leads. In addition – there is ST segment coving and elevation that appears to begin in lead V2, and persist through to lead V6. T wave inversion (sometimes marked) is seen in each of the leads with ST elevation.
  • Reciprocal Changes – are seen in leads I and aVL. These reciprocal changes entail not only ST depression in lead aVL – but also T wave peaking (which is the “mirror-image” of the deep inferior symmetric T wave inversion).
An extra P wave appears to be hiding in the tail portion of each QRS complex on this tracing (Figure 2). This extra P wave is most evident in lead II (RED arrows in Figure 2) – but it is also seen in other leads (BLUE arrows).
  • The underlying atrial rhythm is rapid (~140/minute) and regular.
  • The PR interval preceding each QRS complex is fixed (albeit prolonged to 0.26 second). Thus, every-other-P-wave is conducting – and the rhythm is 2nd degree AV block with 2:1 AV conduction.
Figure 2 – Addition of red and blue arrows to Figure 1 – revealing 2:1 AV conduction in the underlying rhythm (See text).
IMPRESSION:  The ECG in Figure 1 suggests a large acutely evolving STEMI involving inferior, anterior and lateral precordial lead areas. Large Q waves have already developed in anterior leads (loss or r between V1-to-V2 – and QS in V2,V3). ST segment coving and elevation persists in these anterior lead areas – though ST elevation is not as marked as it is in inferior leads.
  • Whether the extensive pattern of injury seen indicates acute occlusion of a large dominant circumflex artery vs an LAD (Left Anterior Descending) artery with “wraparound” (an LAD that also supplies the inferior wall) vs some combination of lesions (perhaps with collateralization affecting distribution) – is uncertain. What is certain – is that an extremely large infarction with AV block is acutely evolving.
We define the type of AV conduction disturbance seen in Figures 1,2 as 2nd degree AV block with 2:1 AV conduction:
  • In theory – the conduction disturbance could be either Mobitz I (AV Wenckebach) or Mobitz II AV block. The reason we cannot absolutely distinguish between these two possibilities is that one never sees two beats conducted in a row (so that we can’t tell IF the PR interval would lengthen if it did have an opportunity to do so).
  • That said – we strongly suspect the conduction disturbance represents 2nd degree AV block, Mobitz Type I (Wenckebach) – because: i) Mobitz I is far more common than Mobitz II – especially in the setting of acute inferior MI when there is also 1st degree AV block for conducting beats; and  ii) the QRS complex is narrow (as it almost always is with Mobitz I – vs QRS widening that is usually seen with Mobitz II).
  • PEARL: It would be easy to overlook 2:1 AV block in this tracing. Awareness that various forms of AV Wenckebach commonly occur with acute inferior MI should increase your index of suspicion that this conduction disturbance may be “in hiding” whenever ST segment elevation is marked – and you either see: i) a pattern of grouped beating; or ii) a longer-than-expected PR interval preceding those beats that are conducting (as seen here). Use of calipers may prove invaluable for confirming your suspicion.
BOTTOM LINE: Acute reperfusion is urgently needed for this patient.

NOTE: - Relevant PDFs on ECG features in this case


  1. I love it thanks, The Wraparound can you produce a PIC? Or did i over look? If in-front of my face, i over look. I always do.


    My friend.

  2. Hi Mario. I'm working on a web page that will illustrate this - but haven't yet finished with the picture... But think of the LAD (left anterior descending) coronary artery as supplying the anterior wall as it flows down the front (anterior wall) of the heart. In some patients, that vessel is longer - such that it not only reaches the very tip (apex) of the heart - but wraps around underneath to also supply a portion of the inferior wall. Thus, with a "wraparound LAD" - occlusion may lead to ST elevation not only over anterior leads (V2,V3,V4) - but also over the inferior leads (II,III,aVF).

  3. Hello Doc, sorry to bother, but i got a question regarding some ecg rhythms i saw today for one individual. This person had a first degree av block, with PR interval of about 0.24, when he woke up this morning his PR interval had jumped to 0.40, and stayed thereabouts for most of the morning, By the afternoon his PR interval had started shortening, at the end of the day his pr interval was 0.18 i.e it could no longer be plausibly called a 1st degree block. I was wondering if there was an interpretation for these sort of ecg changes, especially if it happens in a cyclical manner. Is this some sort of AV dissociation that is not written about in books or what do you think is going on here?

    Thanks in advance

  4. Hi James. I can't think of an explanation for what you describe with dramatically changing PR intervals - unless there is a changing P-to-QRS relationship ... I'm afraid I would need to see the actual rhythm strips in order to be able to comment more on this .... IF you have them - you could send to - Ken

  5. I was off today, so i couldn't get a hold of the strips, but i'll see if they are still available at work tomorrow, and i'll email them if they are available. Thanks for your response.

  6. In the figure 2, in lead I, the first and the third blue arrows, im my opinion should be put on the first hump of T wave.
    The interval between P waves, appears, im my opinion slightly different.

    1. So SORRY for my delay in responding! You are absolutely correct. Excellent observation on your part. The RED arrows in simultaneously recorded lead II do reflect the correct spatial relationship.

  7. If proximal wraparound occlusion , simultaneous ischemia of high lateral wall and inferior wall cancel each other , as lead III is opposing forces to aVL .
    which lead will be elevated more in this situation? aVL or lead III, Can they be isoelectric in this situation.
    What about other leads I,II,aVF ?
    How differentiate between Proximal Wraparound LAD Vs Mid ?

  8. Hello Mostafa. The answers to many of your questions are, "maybe", "hard to say" and "it depends" ... A very proximal "wraparound" may be a lethal lesion (ie, = proximal LAD + inferior infarction equivalent ... ). The point that I believe you are realizing with your thoughtful questions is that what one sees on the ECG is the "net effect" of everything that is going on (ie, there may at times be things going on that partially or more than that "cancel" each other out). Much of the time — the clinical scenario + assessment of the entire "Gestalt" of the 12-lead will lead to the correct diagnosis (facilitated IF there are also prior tracings to compare to) — but your questions are not things that have any fixed "rules" that I know of ...