Friday, December 27, 2013

Is this Left Bundle Branch Block? Is there STEMI?

A male 1 ppd smoker in his 50's with no prior cardiac history called 911 because the chest pain and left arm pain, with SOB and diaphoresis,  He callled because the pain was not going away with antacids after 8 hours.

Here is the prehospital ECG (time zero), reportedly recorded with chest pain, but this is not certain:

The first tracing is limb leads:
 The second tracing is precordial leads:
What is going on?????








This was shown to me as a case of "new left bundle branch block (LBBB)."  Is it?







If you notice, there are no P-waves before each QRS.  It is not a supraventricular rhythm and thus it is not LBBB.  If it were LBBB, there would have to be a supraventricular rhythm conducted down the Purkinje system, but blocked at the left bundle.  It would have a P-wave (if not another supraventricular origin) and it would also have a monophasic R-wave in I and aVL, which it does not.

Is it Ventricular Tachycardia?  No.  To be VT, it would have to have a rate of at least 100.  Because the rate is so slow, it is very unlikely to be a re-entrant rhythm (VT is re-entrant).  It is far more likely to be an automatic rhythm (spontaneous depolarization of the cells, initiated by slow rise in intracellular potential, followed by a rapid upstroke when the potential reaches the triggerreshold).

A ventricular automatic rhythm is usually a ventricular "escape," which escapes because there is no faster supraventricular rhythm.  But in this case, the ventricular automatic rhythm is faster than the sinus, and thus it is called Accelerated Idioventricular Rhythm (AIVR)AIVR is associated with reperfusion of STEMI.

P-waves

Notice also there are inverted (previously wrote upright) P-waves buried in each QRS Are they simply going the same rate as the QRS, by chance?  Possibly.  More likely, the preceding QRS is resetting (capturing) the sinus node by retrograde conduction.   Because the accelerated idioventricular rhythm is faster (almost 100) than the sinus rhythm, the sinus rhythm never takes over.

ST segments

Do ST segment rules for AIVR follow the same Sgarbossa Rule (or Smith Modified Sgarbossa Rule) as for LBBB and, as we believe, for Paced Rhythm?  --I believe they do.

In this case, there is concordant ST elevation in lead V4.  There is no proportionally excessive discordant ST elevation or ST depression anywhere.

But that one lead (V4)with concordant ST elevation is diagnostic.

Concordant T-waves

Furthermore, a concordant T-wave is very specific for MI as diagnosed by biomarkers (see Sgarbossa's study).  There are concordant T-waves in several leads, especially V4-V6.

The patient arrived in the ED and had this ECG recorded 16 minutes after the first:
Now there is sinus bradycardia.  There are prominent Q-waves in V1-V3, diagnostic of infarction.  There is little evidence of acute infarction on this ECG: only some minimal ST elevation in V1 and V2, which could be due to old MI (though the patient has no history of MI) AND some mild ST depression in V5 and V6, suggesting ischemia.  ST elevation in V1 and V2, combined with ST depression in V5 and V6 are suggestive of acute septal STEMI.


At 42 minutes, this ECG was recorded:
AIVR again, but with 2 P-waves that came a bit early: one of them was too late to affect the QRS, the second came early enough to result in conduction to the ventricle and a normal QRS.  The concordant ST elevation in V4 is much less prominent.

The AIVR with Q-waves, minimal ST elevation, and the decrease in STE in V4 suggest that this is a subacute STEMI that began at the time of the chest pain 8 hours prior and has now perhaps reperfused spontaneously.  It may re-occlude at any moment and the patient should go immediately to the cath lab.

The initial troponin I was 28 ng/mL, consistent with subacute STEMI.  At cath, the LAD was 100% occluded.  It was opened and stented.

Peak cTnI was 462 ng/mL.  Post cath echo had an EF of 35-40%.

Lessons:

1. AIVR looks like LBBB
2. AIVR is strongly associated with STEMI, often as a reperfusion dysrhythmia.
3. The rules of appropriate discordance, and the modified Sgarbossa rules for diagnosis of STEMI in LBBBB probably apply to AIVR
4. The sinus node can be captured by ventricular rhythms, then fire and manifest as anterograde P-waves in the midst of the QRS.


9 comments:

  1. Interesting case. The p wave is negative and conducted retrograde from the ventricle. In the final ECG this can be seen in the lead II rhythm strip. On the left there is no p wave seen initially due to isorhythmic dissociation. On the right the negative p wave is seen in the ST segment.

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    1. This comment has been removed by the author.

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    2. MJ,
      I'm looking again and you are right! I will fix it.
      Thanks,
      Steve

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  2. Hello dr. Smith,

    Interesting post! I was wondering why you think there is STE elevation in v4 in the prehospital EKG. The j-point does not seem to be elevated compared to the baseline.
    Kind regards and thanks for your time,
    Emil

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    Replies
    1. Emil,
      I think you are not finding the J-point accurately. It is a bit later than you might think. Look closely. The true J-point is elevated.
      Thanks for your comment/question!
      Steve

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  3. Dr. Smith,
    It was my understanding that the distance the impulse had to travel in a retrograde fashion from the ventricle was not sufficient enough to reset the sinus node, which is why PVC's are followed by compensatory pauses. Is this not the case?

    I just thought that the inverted P waves buried at the end of the QRS's were just retrograde activation from the ventricles, not actually sinus P waves. Was I wrong?

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    Replies
    1. Jesse,
      You were right. I was wrong. You'll see that in answer to MJ above, I corrected the post. They are indeed retrograde P-waves.
      Thanks,
      Steve Smith

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  4. great clue to STEMI... IF pci not available, would you give thrombolytics ?

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