Wednesday, June 15, 2011

The development of an inferior-posterior STEMI, from prehospital to hospital

For other cases of inferior hyperacute T-wave click here and here.
For more on lead aVL, click here and here.  Also use labels on the right sidebar.

A 65 yo woman called 911 for pain in her upper back (between the shoulder blades) and in the left shoulder and left biceps, and some "mild chest pressure" elicited by the medics.  Exam was normal. All but the back pain resolved with nitroglycerine

Medics recorded 6 prehospital ECGs.  Below are 3 of them:

There are hyperacute T-waves in II, III, and aVF.  Note T-wave inversion in aVL, which is the earliest finding in acute inferior STEMI, as well as in V2, suggesting posterior wall involvement

No significant change

Now there is clear ST elevation in inferior leads.  T-wave inversions in aVL and V2 have evolved to ST depression.  
They arrived in the ED at 1503.  BP was 116/70.  CXR and cardiac and aortic ultrasound were done to look for any evidence of aortic dissection.  All were normal except for a possible inferior wall motion abnormality.

In the ED, the following ECGs were recorded. 
ST segments have almost normalized. Hyperacute Ts are less prominent, as is T inversion.  There is probably some spontaneous reperfusion of the infarct-related artery.  The computer noticed only some "minimal" ST depression.
Inferior ST elevation is more obvious, with 1 mm in II and III, but T-waves have normalized.  ST depression in V2 is clearly abnormal.  Computer did not read MI.
Now the most obvious findings are ST depression in aVL and V2
Cardiology was consulted.  Again, a cardiology fellow opined that this was not a STEMI, and went to talk with the interventionalist. 

A posterior ECG was recorded:
Only aVL was of great concern.  There is no posterior ST elevation.
The interventionalist was very concerned and activated the cath lab.  The patient was taken to the cath lab.  The proximal RCA was 100% occluded.  It was stented.  Door to balloon time was 62 minutes.  Peak troponin I was 5.15 ng/ml.

T-waves and ST segments are back to normal


  1. Dear Smith
    can you explain why there is STD in V2 without STE in post leads? just mean that there is ischemia in anterior wall? without post leads, how can we different they? Thanks

    1. Looking at this, I'm not sure that the "posterior ECG" really was posterior, as the QRS looks exactly the same as the previous. However, to answer your question in more general terms: the posterior leads must record electrical activiity through a lot of lung tissue (air), which is a good insulator. This diminishes the voltage. Freqently, posterior lead give a false sense of security. So I always recomment that, if you diagnose posterior MI on the regular 12-lead, do NOT change your mind based on absence of STE in posterior leads. And remember that the "criteria" for posterior leads is 0.5 mm, not 1 mm, and to especially evaluate in the context of proportionality to the QRS.


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