Overview
- Lecture covers left anterior fascicular block (LAFB) from an EKG coding reference guide.
- Focus on recognition, mechanism, EKG features, causes, and clinical significance.
- Part of a multi-lecture series; prior parts cover normals, rhythms, AV conduction, and voltage/hypertrophy.
Anatomy And Mechanism
- Conduction path: sinus node → AV node → His bundle → right bundle + left bundle.
- Left bundle splits into anterior and posterior fascicles.
- LAFB = anatomical or functional block of left anterior fascicle.
- With LAFB, left ventricular depolarization relies on the left posterior fascicle.
- Anterior fascicle: thin, organized fibers supplying the anterolateral left ventricle.
- Anterior fascicle is more susceptible due to smaller arterial supply and thin fibers.
Key EKG Findings
- Main criterion: Left axis deviation between −45° and −90°.
- Lead patterns:
- Lead I and aVL: QR complexes (initial Q then prominent R).
- Inferior leads (II, III, aVF): RS complexes (initial R then deep S).
- R-wave peak time in aVL may be >45 ms (from QRS onset to R peak).
- QRS duration generally within normal limits; may be slightly prolonged.
- Axis example: machine-calculated axis often around −60° in LAFB.
- Probable LAFB: axis between −30° and −45° sometimes labeled probable LAFB.
- Criteria do not apply in congenital heart disease with infancy left axis deviation.
Why These EKG Changes Occur
- Block of the anterior fascicle causes initial depolarization vectors to be altered:
- Early vector toward inferior leads (small upward deflection).
- Dominant later vector (from posterior fascicle) directed superior-left, away from inferior leads producing S waves.
- In lateral leads (I, aVL) the initial vector is away (Q), later vector toward produces R.
- This shift produces characteristic QR in lateral leads and RS in inferior leads plus leftward axis.
Causes And Clinical Significance
- Can occur in healthy individuals; more significant with heart disease.
- Associated conditions:
- Hypertension and left ventricular hypertrophy
- Coronary artery disease and infarction affecting anterior fascicle
- Dilated or hypertrophic cardiomyopathy
- Degenerative conduction disease
- Myocarditis, amyloidosis, hyperkalemia
- LAFB is more common than left posterior fascicular block.
- Isolated LAFB often benign but can progress to bifascicular block (LAFB + RBBB) or complete heart block.
Diagnostic Notes And Pitfalls
- Primary diagnostic focus: left axis deviation (−45° to −90°).
- Look for QR in I and aVL; RS in II, III, aVF.
- R-wave peak time >45 ms in aVL supports diagnosis.
- Beware: LAFB can mimic an anterior septal myocardial infarction or mask an inferior MI.
- In congenital heart disease, neonatal left axis deviation invalidates criteria.
Key Terms And Definitions
- Left Anterior Fascicular Block (LAFB): Block of left anterior fascicle causing leftward shift of QRS axis.
- Left Axis Deviation: Frontal plane QRS axis shifted left; diagnostic range for LAFB is −45° to −90°.
- QR Complex: Q wave followed by R wave morphology in a lead.
- RS Complex: R wave followed by deep S wave morphology in a lead.
- R-wave Peak Time: Interval from QRS onset to peak of R wave; >45 ms in aVL may be noted.
Action Items / Next Steps For Learners
- Review prior lectures on axis determination and conduction system anatomy.
- Practice interpreting EKGs for axis and lead-specific QRS patterns (I, aVL, II, III, aVF).
- Consider differential causes when LAFB is present; correlate clinically for heart disease.
- Remember pitfalls: possible mimicry of anterior septal MI and masking of inferior MI.
- Use calipers to measure R-wave peak time and confirm >45 ms when suspected.
Summary Table: LAFB Diagnostic Features
| Feature | Typical Finding |
| Frontal QRS Axis | −45° to −90° (left axis deviation) |
| Lead I / aVL Morphology | QR complexes; initial Q then tall R |
| Leads II / III / aVF Morphology | RS complexes; prominent S in inferior leads |
| R-wave Peak Time (aVL) | May be >45 ms from QRS onset to R peak |
| QRS Duration | Usually normal or mildly prolonged |
| Common Causes | HTN, LVH, CAD, infarction, cardiomyopathy, myocarditis, amyloid, hyperkalemia |
| Clinical Significance | Often benign when isolated; may progress to bifascicular or complete heart block |