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Left Anterior Fascicular Block (Hemiblock)

Sun, 09/13/2015 - 22:10 -- Dawn

This ECG provides an example of LEFT ANTERIOR FASCICULAR BLOCK (LAFB).  It is from a 71-year-old woman for whom we have no other history.  She also has first-degree AV block and right bundle branch block.  RBBB and LAFB together are called bifascicular block.  It is not uncommon to see this type of bifascicular block, as the right bundle branch and the  anterior fascicle of the left bundle share a blood supply. 

The conduction system below the AV node consists of the Bundle of His, the left bundle branch, and the right bundle branch.  While there is some variation among individuals, most of us have two main fascicles, or branches, of the left bundle.  The ANTERIOR-SUPERIOR fascicle carries the electrical impulse to the anterior wall of the left ventricle, and the POSTERIOR - INFERIOR fascicle carries the impulse to the inferior area of the left ventricle.

Blocks can occur at any level in the conduction system, including left bundle branch block, right bundle branch block, left anterior fascicular block, left posterior block, and bi-fascicular blocks. LAFB can have many causes, including myocardial infarction, cardiomyopathies, fibrosis of the cartilagenous ring, and aortic valve disease.  Left anterior fascicular block is much more common than left posterior fascicular block. Both are also called hemiblocks.

When LAFB is present, the initial septal depolarization forces are still left to right, providing a small initial q wave in Lead I and a small r wave in Lead III.  After septal depolarization is complete, the activation vector moves inferiorly and to the right as the electrical wavefront moves through the left posterior hemifascicle and right bundle branch. The impulse finally makes its way to the left and superiorly via slow conduction through myocardium normally depolarized by the left anterior hemifascicle, which is blocked.  It is because the terminal left ventricular activation moves upward and toward the left that the  inferior leads have negative deflections.

The diagnostic criteria for LAFB are:  LEFT AXIS DEVIATION (QRS axis between -45 degrees and -90 degrees); qR pattern in Lead I; rS pattern in Lead III; delayed activation time evident in Lead aVL - the time from onset of the QRS to the peak of the R wave is 45 ms or more. (This example barely makes that criteria, and it is difficult to measure due to the poor copy quality); QRS duration normal or slightly wide, but not 120 ms or more (unless there is also RBBB).  LAFB also causes poor R wave progression in the precordial leads, with late transition and S wave present in V6.

Before deciding on a diagnosis of LAFB, you must rule out previous or acute INFERIOR WALL M.I.  The pathological Q waves that can occur with necrosis can cause a left axis deviation in the frontal plane.  The presence of a small r wave in Lead III rules out pathological Q wave in that lead.  If any fascicular block (hemiblock or bundle branch block) occurs during the course of an M.I., the patient should be watched carefully for progression of the block.  Be prepared to pace if necessary in that situation. 

For more information on hemiblocks, check Dr. Ken Grauer's ECG Blog #90 - Basic Concepts-3, and also his video on hemiblocks and axis.

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Comments's picture
Nice example by Dawn of an ECG with multiple conduction defects. I’ll expand on several points mentioned in her discussion.
  • I found myself “on the fence” as to whether I would call this complete or incomplete RBBB. It is difficult to see the grid, which clearly is essential for optimal determination of QRS width. That said — I believe QRS duration IS slightly more than HALF a large box, which puts it at between 0.10-0.11 second. Although there are many who set 0.12 second as the necessary QRS prolongation criterion for RBBB to be complete — I have always accepted 0.11 second because the normal adult RV (right ventricle) is much thinner than the normal adult LV (left ventricle) — such that even when RBBB is complete, not as much time should be needed to get through the RV. In contrast — QRS duration needs to be at least 0.12 second for LBBB to be complete, since more time will be needed to traverse a blocked left ventricle. Diagnosis of “complete” RBBB despite QRS duration of only 0.11 second presumes QRS morphology is “typical” for RBBB (ie, with an rSR’ or equivalent pattern in V1 and with wide terminal S waves in left-sided leads I and V6). Given the narrowness of the S wave in lead I in this example (and the practically negligible s in lead aVL) in the setting of a barely borderline QRS duration and a somewhat less typical QRS morphology for the rSr’ we see in V1 — I would accept either “incomplete” or “complete” RBBB as valid interpretations. Keep in mind that part of the QRS prolongation we have in this case probably arises from the LAHB (Left Anterior HemiBlock) — which is another reason the RBBB is perhaps “incomplete” rather than “complete” …
  • Dawn states a series of criteria for making the diagnosis of LAHB (Left Anterior HemiBlockincluding: i) LAD (Left Axis Deviation) of at least -45 degrees); ii) specific QRS morphology (qR in lead I and rS in leads II,III); and iii) delayed activation time in lead aVL. While these are all cited criteria in the literature — I have always favored a far simpler approach that in my experience is equally accurate while allowing recognition of LAHB in less than 5 seconds. The rationale for my simpler approach is the lack of consensus among experts as to the true definition of LAHB — and that presence of competing conditions (ie, infarction, RBBB, chamber enlargement) complicates use of more specific criteria. For practical purposes — LAHB is present if there is “pathologic” LAD (where “pathologic” LAD is defined as a left axis more negative than -30 degrees). The “beauty” of this approach is that IF lead II is more negative than positive — then the mean QRS axis will be “pathologic” (ie, more negative than -30 degrees). This criterion works equally well in the presence of RBBB. So, all it takes a glance at lead II in this tracing to see that the net QRS deflection in lead II is definitely more negative than positive — so that there clearly is LAHB.
  • As per Dawn — diagnosis of inferior infarction may make diagnosis of LAHB more difficult, and vice versa. This is because these are “competing conditions”. That is, initial forces with inferior infarction are directed away from the inferior leads in the form of inferior Q waves — whereas initial forces with LAHB are directed toward the inferior leads in the form of a small r wave (because the intact left posterior hemifascicle directs the impulse initially inferiorly and to the right). So, what will be seen in the inferior leads when both LAHB and inferior infarction are present — will depend on whether initial negative forces from inferior infarction are greater than the initial positive forces from the LAHB. As a result, either condition may mask the other. PEARL — If in the presence of LAHB, there is a Q wave in lead II or notching in the descent of the QRS complex in one or more inferior leads — then it is likely that inferior infarction has also taken place. And when inferior infarction produces inferior QS complexes — there is presumably concomitant LAHB.
For those wanting more information on topics discussed above:

Ken Grauer, MD   [email protected] 

Submitted by josef on

Is it possible there is a  incompl. trifascilar block consisting of RSB+LAH+AVB1. Second , how is qR complex in aVR to explain (RIVA Stenose ? Tricyclische pharmarka ?) . Kind regards  Josef

Submitted by Dawn on

Josef, I somehow did not see your comment until now. I am not sure what "RSB" means - right bundle branch block, perhaps?  And by "AVB1", are you referring to first-degre AV block?  I'm afraid that sometimes abbreviations don't translate well between languages. 

Terminology in fascicular blocks varies somewhat among authors. A first-degree AV block may be considered part of a trifascicular block, but it is difficult to ascribe first-degree. AV block to the fascicles. It is more likely to occur in the AV node, as far as I am aware. 

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