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Acute Anterior-lateral M.I. With Right Bundle Branch Block and Left Posterior Fascicular Block

Thu, 08/21/2014 - 11:45 -- Dawn

This ECG was obtained from a patient who suffered an occlusion of the left main coronary artery.  ST elevation is seen in Leads V1 through V6, as well as I and aVL.  This is an indicator that the circumflex artery is included in this M.I., and the occlusion is above the bifurcation of the LM and the circ.  The patient also has a right bundle branch block and a left posterior fascicular block.  This bi-fascicular block can be a dangerous complication of acute M.I., as two of the three main bundle branches are no longer functional.

The ECG shows typical ST depression, probably reciprocal to the elevation, in the inferior leads.

The right bundle branch block is diagnosed by the following criteria:  1) Wide QRS;  2) Supraventricular rhythm; and 3) rSR' pattern in V1 with Rs with a wide little s wave in Leads I and V6.

The left posterior fascicular block is diagnosed by right axis deviation and by ruling out other causes of right axis deviation.  In RAD, Lead III will have a taller positive ( R ) wave than Lead II, and a negative Lead I.

This type of occlusion is often called the "Widow Maker", and requires very rapid intervention to restore blood flow and prevent complicatons.  If there is good news, it is that there are no pathological Q waves, which would indicate necrosis, and this patient was taken quickly to a full-service cardiac center with interventional cath labs and open heart surgery available.

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Comments

ekgpress@mac.com's picture
 
Interesting case and tracing. I'll make the following comments to supplement those by Dawn.
  • LMain (Left Main coronary artery) occlusions are rare. This is because true left main occlusion (100%)  usually results in very rapid demise of the patient (before they can get to the hospital). I would especially in this case not expect this patient to survive for long with acute left main occlusion because of obvious extent of damage (diffuse ST elevation) in association with presumably new bifascicular block involving the RBBB and LPHB.
  • I was surprised to learn that the lesion in this case is acute left main occlusion  because typically in those rare instances in which this occurs and an ECG is obtained  there is significant ST elevation in lead aVR (that is usually greater than the amount of ST elevation in lead V1). In contrast  with proximal LAD (Left Anterior Descending) occlusion  ST elevation in lead V1 tends to be more than in aVR. The right-sided unique viewing perspective of lead aVR assesses the basal part of the interventricular septum  so that ischemia of the septum (as occurs with very proximal lesions) produces a vector that points superiorly. I see no ST elevation in aVR in this tracing.
  • There ARE some "pathologic" Q waves already present on this tracing. Note in lead V1  that instead of the typical rSR' of RBBB  there is a small-but-fairly-wide Q wave (QR pattern). You can drop a vertical line down from the onset of this Q in V1  and it coincides with the onset of the QRS complex in lead V2.
  • In addition  there are tiny-but-real q waves in leads II and aVF  that in association with a small but disproportionately wide Q wave in lead III are real and probably pathologic. Perhaps there is some component of "LAD wraparound" (in which the LAD continues beyond the apex to 'wrap around' and supply a portion of the inferior wall of the left ventricle as well).
  • Extensive anterior involvement should be obvious in this case not only from the marked precordial ST elevation - but from extension to involve leads I and aVL.
  • Of note  is the marked inferior reciprocal ST depression (especially in leads III and aVF). Mid-LAD occlusions do not always have reciprocal inferior ST depression (or when present it is subtle). It is primarily proximal LAD or left main lesions that manifest reciprocal inferior ST depression. Note that the J-point is down more than 3mm in lead III.
  • In general  the significance of conduction defects depend on the company they keep. That is, many patients with longstanding bifascicular block (RBBB/LAHB) never evolve to need a pacemaker. In contrast  new occurrence of a conduction defect in association with acute stemi is always worrisome. Of the 2 hemiblocks  LAHB is far more common than LPHB. This is because the left posterior hemifascicle is much thicker and dually innervated by the left and right coronary arteries. We recognize LPHB because the straight portion of QRS descent in lead I is steep. Our focus is on the initial part of the descent  not on the last part of the expected S wave in lead I. So  the occurrence of RBBB/LPHB with the diffuse ST elevation, reciprocal changes and evolving Q waves seen here are clearly ominous. Hopefully transfer of this patient to a full service cardiac center was in time.
For those wanting more on determination of the "culprit artery" with acute STEMI  Please check out this pdf (excerpted from my ECG-2014-ePub CLICK HERE TO DOWNLOAD. The part on distinction between LMain vs proximal LAD occlusion is covered in Sections 10.24, 10.25.
  • NOTE: For more on distinction between LMain disease vs LMain occlusion — Please See Section 09.40 in our pdf on Using Lead aVR (from my ECG-2014-ePub).
  • This case is linked to my ECG Blog #103 

Submitted by Dawn on

Agree with Ken about location of lesion. I don't believe I ever saw the cath on this patient, but is was reported to me as a "left main" occlusion. I'm not sure if he fell short of being 100%, but I suspect the lesion was near the bifurcation of the circ. The patient was treated in a full-service cardiac center, but we do not have a record of the outcome. 

Dave Richley's picture

I’ve been reading a Spanish study (authors include Bayes de Luna) that was published in J Electrocardiol in 2012. This was of a series of 7 patients who had acute LMCA occlusion that presented with an ECG showing ST elevation typical of anterior MI.  4/7 patients died, and the authors hypothesised that this pattern indicated a lack of collateral circulation and conferred a grave prognosis. Most of their patients presented in shock; 4/7 had RBBB and all had left anterior fascicular block. It was stated that the ‘typical’ LMCA occlusion ECG pattern of widespread ST depression + ST elevation in aVR and V1 is due to widespread ischaemia when there is a well-developed (but still inadequate) collateral circulation.

If, therefore, acute LMCA occlusion with ST elevation indicates poor collateralisation and consequently a very poor early prognosis, this may be why it is seen infrequently. Perhaps the ‘typical’ pattern with ST elevation only in aVR and V1 is only seen much more frequently because the patients, having a good collateral circulation, tend to have a better survival rate.

Ken -minor point, but should we say that the left poster hemifascicle is perfused rather than innervated by the coronary arteries? (sorry, I know that everyone hates a pedant).

Dave R

Submitted by Dawn on

I do not believe I have cath images from this patient - it was from a huge file of ECGs with only small, hand-written notes on them.  (sigh...)  Your comment has made me REALLY want to see the cath images, and I will be scurrying back to my voluminous files to see if I can find a cath that goes with this ECG.  That will require that I find the original ECG without the patient info redacted.  I sure do wish I had kept better records all those years - but I was busy working, and didn't have the luxury of time, taking care of multiple high-risk patients undergoing procedures. Because most of my ECGs come from donations from friends, my 30+ years in the ED, and several years in the Cardiac Center Admit and Recovery Unit (Cath lab, EP lab, Procedures,), I was usually too busy to do more than take a quick copy and scribble a note.  

 

Would welcome comments from cath lab people on what you have seen regarding left main and proximal LCA occlusions.  

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