Tuesday, May 15, 2012

New LBBB after Cardiac Arrest

An elderly man with a history of DM and renal failure had a complaint of back pain, and called 911.  En route, he had a seizure, then lost pulses.  No rhythm was recorded, but he was resuscitated with chest compressions, epi and atropine. Here is his first ECG:

An old ECG had LVH; a different one had IVCD, but there was no LBBB.

First ECG at 1507:
There is sinus with new LBBB.  There is no concordant ST elevation.  There is proportionally excessively discordant ST elevation, or nearly so, in lead V2 (see enlargement below), with a ratio of 4.5/20 = 0.225.  Depending on whether the cutoff is 0.20 or 0.25 (and this does vary in my research), this might represent LAD occlusion.
Excessively discordant ST elevation?  Very suspicious in lead V2.  
The T-wave in V5 is concordant, but this is nonspecific.  

There is a fragmented or notched QRS on the upstroke of the QRS in lead V3, which may be a sign of old infarction.  
This is to be distinguished from Cabrera's sign, which is a notch on the upstroke of the QRS in leads V3-V5.  
There is absence of an r-wave in V4, with fragmentation of the downstroke of the QS-wave.

There are often ST abnormalities after cardiac arrest, usually ST depression.   In the setting of post cardiac arrest, when an ECG is not clearly diagnostic, I always recommend waiting 10-15 minutes for a repeat ECG to see if the findings resolve.

Also, the K was 6.0, and one must entertain the possibility that hyperkalemia is causing this apparent new LBBB, possibly with ST changes. 

At 1502, this was recorded.  There had been no therapy for hyperkalemia:
There is less ST elevation, and more of a normal LBBB, though still with a fragmented QRS.
This ECG was recorded at 1922:
There is yet more resolution

There was no wall motion abnormality.  The peak troponin was only 0.064 ng/ml (99% reference = 0.034), so this was barely elevated, consistent with cardiac arrest but it would be highly unusual to be this low even in a transient STEMI.  But not impossible.

Also, there was no wall motion abnormality the next day.  Of course, with transient STEMI, there might not be any WMA.

I can't prove there was not a transient LAD occlusion.  There might have been.  No cause of the arrest was found.  No cath was done.

Learning point:

1) Post cardiac arrest, the ECG may have transient ST abnormalities.


  1. Could it have been caused by the epi?


  2. Should this patient be treated with IV calcium if he was not on dig for his moderate hyperkalaemia?


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