This ECG provides an example of LEFT ANTERIOR FASCICULAR BLOCK (LAFB).  It is from an elderly woman for whom we have no other history.

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); 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. 

Thanks to our Consulting Expert, Dr. Ken Grauer, for his editing assistance.

No instructor's collection should be without an atrial paced rhythm OR a right bundle branch block.  Here, you get both.  First, the atrial pacing.  This patient had a sinus node problem, but his AV conduction system was functional (if not perfect).  At this time, he is able to conduct impulses from the atria to the ventricles.  What he cannot do is reliably produce the impulse in his atria.   So, this pacemaker is currently pacing the right atrium, producing a paced "P" wave, which is then conducted to the ventricles.  The fifth beat on the strip shows a "native" beat - one produced by the patient.  No P wave is seen, so it is presumed to be a junctional beat.

As for conduction through the ventricles, there is a right bundle branch block.  The left bundle branch is ensuring that the ventricles receive the depolarization "message", and the ventricles are depolarizing and contracting.  However, the right ventricle gets the message a little late, since is arrives from the left ventricle, and not through a functioning right bundle branch.  This produces a terminal wave on each QRS that represents this delayed depolarization of the right ventricle.  In leads oriented to the left side of the heart, like I and V6, it is seen as a wide little S wave.  In V1, which is oriented to the patient's right, we see an R prime (R'), producing the easily-recognizable rSR' pattern of RBBB.

For your more advanced students, this patient has atypical T waves for RBBB.  Normally, the T waves axes should be OPPOSITE that of the terminal portion of the QRS.  So, Lead V1 correctly shows an inverted T wave, since the R' is a positive deflection.  There are inverted T waves in Leads III, aVF (II is biphasic), as well as in V4, V5, and V6.  We expected upright T waves here. Because we do not have clinical information for this patient, we will call them "non-specific" T wave changes, remembering that inverted T waves can be a sign of ischemia.

ALSO:  As noted in Dave Richley's comment below, there is a left axis deviation, with a negative Leads II, aVF and III, and a positive I and aVL.  This  indicates left anterior fascicular block, which is rather common with RBBB, since the right bundle branch and the left anterior fascicle share a blood supply. So, this person as a "bi-fascicular block". 

This is quite an interesting ECG, and the ECG Guru would love to hear what you think about it.  What we do know is that it is a wide-complex bradycardia in a patient for whom we have no clinical data, except that she is a 51 year old female.  The rhythm is probably junctional, as no P waves are seen and the rhythm is regular.  The rate of 63 per minute would be consistent with that. Interestingly, no disassociated sinus P waves are seen.  All slow wide-complex rhythms should be evaluated for idioventricular origin, or AIVR.  The QRS in V1 shows an atypical right bundle branch block pattern.  We usually look for rSR', or "bunny ears",  but  this ECG shows an upright R wave with a smaller, slurred r wave before it.  What makes this look like RBBB is the prominent wide little S wave in V6 and in Lead I.  We question the R wave progression, too.  Do you think it is possible that the electrodes for V2 and V3 are switched?  The axis is leftward, causing Lead II to be nearly biphasic - it represents a synthesis of what is seen in Leads I and III.  This is enough left axis shift to diagnose a left anterior fascicular block (with RBBB = bifascicular block). 

This is a great ECG, and we can't wait to hear from all you ECG Gurus out there. Maybe we will need to adjust our diagnosis after we hear from you.

This series of ECGs was obtained from a 60-year-old man who was involved in a one-car accident.  He sustained no injuries, but his blood alcohol level was far above the legal limit for intoxication at over 300 mmol/L.  ECG No. 1 shows the ECG obtained by paramedics in the field, which they incorrectly interpreted to be atrial fibrillation.  No medication was given.  The ER physician obtained ECG No. 2, and considered sinus tachycardia as the diagnosis, but also, because of the fast rate and the fact that the rate had not changed for at least 15 minutes, he considered SVT or atrial flutter with 2:1 conduction.  The ERP administered diltiazem (Cardizem) to the patient, which resulted in ECG No. 3.  The transition to the slower rate was not captured on rhythm strips, but the nurse's notes showed a gradual change over 15 minutes from a rate of 160 to 105/min.  

Usually, on the Instructors' Collection ECGs, we like to give the "answer".  In this case, however, there will undoubtedly be some discussion regarding what went on.  This discussion can be useful if you are teaching intermediate to advanced students.  Questions to consider:  1) Is the fast rhythm an SVT and, if so, which one?  2) Is it sinus tachycardia and, if so, what are the effects of the car accident and the alcohol?  3) Is the left anterior fascicular block relevant? (Criteria are left axis deviation, slightly widened QRS complex at 110 ms, no other obvious reason for the axis deviation). 4) Is the ST elevation in the inferior wall during the tachycardia a sign of acute M.I.?  The patient was lost to followup, so it is not known whether the ST changes were investigated.  Note the flat ST segment and inverted T waves in V1 during the tachycardia that resolve when the rate decreases. 

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