Bundle Branch Block, Left

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Left bundle branch block (LBBB) occurs when transmission of the cardiac electrical impulse is delayed or fails to conduct along the rapidly conducting fibers of the main left bundle branch or in both left anterior and posterior fascicles. Thus, the left ventricle depolarizes slowly via cell-to-cell conduction spreading from the right ventricle to the left ventricle. This results in the characteristic ECG pattern shown in

Embryology:

The cardiac conduction system develops from rings of specialized tissue found in the embryonic heart tube. One theory describes 4 different rings, each located between different segments of the heart tube. With looping and growth of the cardiac septi, the rings are brought together and develop into the sinus node, the AV node, and the penetrating bundle. Another theory describes a single ring of tissue located between the bulbus cordis and the primitive ventricle, which gives rise to the AV node, His bundle, right bundle branch, and left bundle branch.

Anatomy:

The specialized conduction system of the heart is composed of cells that conduct electrical impulses faster than the surrounding myocardium. The conduction system can be divided into distinct anatomic segments, and each segment is described in sequence beginning at the AV junction and ending with the Purkinje fibers.

The AV junction can be divided into 3 separate regions as follows: transitional cell zone, AV node, and penetrating portion of the AV bundle (His bundle, common bundle).

The transitional cell zone is where the right atrium merges with the compact AV node via discrete atrial pathways (termed the slow and fast pathways).

The next segment is the AV node, which lies anterior and superior to the ostium of the coronary sinus, directly above the insertion of the septal leaflet of the tricuspid valve. This area is located at the apex of the triangle of Koch, which is formed by the tricuspid annulus, the tendon of Todaro, and the ostium of the coronary sinus. The blood supply to the AV node is the AV nodal artery, which is a branch of the right coronary artery in 85-90% of individuals and a branch of the left circumflex coronary artery in 10-15% of individuals.

At the apex of the triangle of Koch the compact AV node becomes the penetrating bundle of His, which penetrates the central fibrous body at the attachment of the tendon of Todaro, runs between the membranous septum and the muscular septum, and bifurcates at the crest of the muscular ventricular septum. The His bundle is divided into 3 anatomic segments. The proximal or nonpenetrating segment lies distal to the AV node and proximal to the central fibrous body. The middle or penetrating segment penetrates the central fibrous body and runs posterior to the membranous septum. The distal or branching segment bifurcates at the crest of the muscular septum into the right and left bundle branches

The right bundle branch, a direct continuation of the penetrating bundle, originates distal to the attachment of the septal leaflet of the tricuspid valve with the membranous septum and surfaces on the right ventricular septum just below the papillary muscle of the conus. It is unbranched and proceeds toward the apex of the right ventricle along the posterior margin of the septal band, courses through the moderator band to the base of the anterior papillary muscle, and proceeds on to the right ventricular free wall.

The left bundle branch originates at the crest of the muscular ventricular septum just distal to the membranous septum. The left bundle branch arises in a fanlike fashion that descends inferiorly along the left ventricular septal surface beneath the noncoronary cusp of the aortic valve. The left bundle branch usually branches into 3 major fascicles. The anterior fascicle is directed to the base of the anterolateral papillary muscle, the posterior fascicle to the base of the posteromedial papillary muscle, and, in 60% of hearts, a central fascicle proceeds to the mid-septal region. When no central fascicle (40% of hearts) is present, the mid-septal region is supplied by radiations from the anterior fascicle or the anterior and posterior fascicles.

At the terminal aspect of each bundle branch, Purkinje fibers are interlaced on the endocardial surface of both ventricles and tend to be concentrated at the tips of the papillary muscles.

Electrophysiology of cardiac conduction

The heart is a 2-step mechanical pump that is coordinated by precisely timed electrical impulses. In order for optimal pump performance, sequential depolarizations of the atria and then the ventricles allow atrial contraction to provide complete diastolic filling of the ventricles (so-called "A-V synchrony"). Once filled, rapid activation of the ventricular myocardium provides for synchronized contraction to eject blood most effectively to the great vessels.

Normal cardiac conduction: Electrical excitation of the heart proceeds in a sequential manner from the atria to the ventricles and is demonstrated on the surface ECG The electrical impulse generated in the sinus node proceeds through the atria (reflected by the P wave on the ECG) to reach the AV node. As the impulse conducts through the AV node, conduction slows allowing time for atrial contraction to occur before ventricular activation (PR segment). Once through the compact AV node, the impulse conducts rapidly through the crux of the heart to the ventricles via the bundle of His (penetrating bundle) to the branching bundle, the bundle branches, the distal Purkinje fibers, and finally to the ventricular myocardial cells (narrow QRS complex). When depolarization is complete the ventricle repolarizes in preparation for conducting another impulse.

Complete LBBB occurs when the electrical impulse is delayed or interrupted in either the main left bundle branch or in both the anterior and posterior fascicles. Conduction down the right bundle branch proceeds normally, and the right ventricle depolarizes in the normal fashion. In complete LBBB, conduction from the right ventricle passes first to the interventricular septum, then to the anterior and posterior portions of the left ventricle, and finally to the left lateral free wall. Delayed left ventricular depolarization accounts for the ECG findings in LBBB

Incomplete LBBB occurs in 2 forms, each called "hemiblock." In left anterior hemiblock, transmission of the electrical impulse proceeds normally along the main left bundle branch and the posterior fascicle, but is blocked or delayed in the anterior fascicle. This results in delayed activation of the anterior portion of the left ventricle. In left anterior hemiblock, the QRS complex may be of normal or only slightly prolonged duration due to normal rapid conduction down the right and left main bundle, and the left posterior fascicle. In addition, the QRS complex is directed superiorly in the frontal plane (left axis deviation).

With left posterior hemiblock, transmission of the electrical impulse proceeds normally along the main left bundle branch and the anterior fascicle but is blocked in the posterior fascicle. This results in delayed activation of the posterior left ventricle. The QRS complex is again of normal or only slightly prolonged duration, and inscribes a rightward axis in the frontal plane. Left posterior hemiblock is rarely observed in children, and diagnosis is difficult because of the common association of right axis deviation in children with congenital heart disease and right ventricular hypertrophy.

Frequency:

In the US: LBBB in children is associated with cardiovascular disease or surgery and is not observed in the general population. It may be present in as many as 20% of individuals following aortic valve replacement.

Mortality/Morbidity: LBBB alone may rarely progress to complete heart block and sudden death, but morbidity/mortality rates are more importantly determined by associated systemic or cardiovascular disease than by the LBBB itself. Patients with LBBB, left axis deviation, and first-degree heart block or LBBB associated with near syncope or syncope require close follow-up and/or electrophysiologic study.

History: The important points to cover when obtaining a history from a child with LBBB include known congenital heart disease and/or prior cardiac surgery. Questions regarding fatigue, exercise intolerance, presyncope, and syncope may further indicate the clinical significance of the finding of LBBB.

Physical: On physical examination ausculatory findings in patients with LBBB include an absent or diminished first heart sound and reversed splitting of the second heart sound.

Causes:

LBBB in children is not a benign entity and is associated with both anatomic malformations and abnormalities of the conduction system. LBBB has been observed following surgery in the left ventricular outflow tract, septal myomectomy, and replacement of the aortic valve. It also is observed in patients with left ventricular hypertrophy, progressive conduction system disease, myocarditis, cardiomyopathy, hemochromatosis, sclerodegenerative diseases, myocardial infarction, aortic valve endocarditis, and rheumatic fever with aortic valve involvement.

Left anterior hemiblock has been associated with coronary artery disease, left ventricular hypertrophy, cardiomyopathy, tetralogy of Fallot repair, ventricular septal defect repair, septal myomectomy, subvalvar aortic resection, and anomalous origin of the left coronary artery from the pulmonary artery. Left anterior hemiblock may be present in patients with autosomal dominant bundle branch disease and has been associated with lentiginosis. It has been observed in patients with an AV canal and Down syndrome, tricuspid atresia, double outlet right ventricle, single ventricle, and transposition of the great vessels with a ventricular septal defect. In these cases, LAH may reflect an abnormal course of left bundle fascicles rather than anterior hemiblock per se.

Left posterior hemiblock is observed in patients with congenital aortic stenosis, endocarditis, diphtheritic myocarditis, and following congenital heart surgery.

Problems to be Considered:

Intraventricular conduction delay
Left ventricular hypertrophy
Wolff-Parkinson-White syndrome
Premature ventricular complexes
Isorhythmic idioventricular rhythm
Supraventricular tachycardia with bundle branch aberrancy
Ventricular paced rhythm

Lab Studies:

Blood work is rarely necessary, but cardiac enzymes (troponins, CPK) and ESR may be useful if myocarditis is suspected. When cardiomyopathy is considered, specific blood work to evaluate underlying causes may be helpful.

Imaging Studies:

Cardiac evaluation requires a thorough physical examination, repeat ECG, and an echocardiogram. A chest x-ray (CXR) may be helpful depending on clinical circumstances. A 24-hour ambulatory ECG recording would reveal if other arrhythmias are present (eg, second- or third-degree heart block, atrial or ventricular extrasystoles or tachycardia). Other investigational studies may be selected to diagnose or exclude suspected associated abnormalities that may be the cause of the LBBB.

Other Tests:

Left bundle branch block - The ECG criteria necessary to diagnose LBBB in children include the following:
- The duration of the QRS complex is prolonged for age (> 0.09 sec in a child less than 4 years of age and > 0.10 seconds in children 4 - 16 years of age).
- No Q wave is seen in leads I, aVL, and V₆.
- Prominent QS pattern is observed in lead V₁ with or without a small initial R wave.
- Tall, wide, and often notched R wave is seen in leads I, aVL, and V₆.
- Tall R wave is seen in lead V₆.

Left anterior hemiblock - The ECG criteria necessary to diagnose left anterior hemiblock in children include the following:

Duration of the QRS complex is normal or prolonged by <0.02 seconds for age.

The frontal plane QRS axis is from -30 to -90 degrees.

A Q wave is present in leads I and aVL.

Major QRS forces in lead aVF are negative.

Slurred S waves are present in the left precordial leads.

A late R wave (>0.045 seconds) is observed in lead aVR.

The terminal R wave in lead aVL is slurred.

The diagnosis of left anterior hemiblock in children is difficult. A superior frontal plane QRS axis is present in some forms of congenital heart disease (AV canal, double outlet right ventricle, tricuspid atresia, single ventricle) with a normal anterior fascicle. In these patients, the diagnosis of left anterior hemiblock cannot be made by ECG. When the frontal plane QRS axis in a child is between 0 and -90 degrees, the patient should be considered to have left axis deviation. The diagnosis of left anterior hemiblock should be reserved for patients who have a previously normal ECG and develop left axis deviation following congenital heart surgery or other injury to the left anterior fascicle.

Left posterior hemiblock - The ECG criteria necessary to diagnose left posterior hemiblock in children include the following:

Duration of the QRS axis is normal or only slightly prolonged for age.

Q wave is present in leads II, III, and aVF.

Frontal plane QRS axis is +120 to +180 degrees.

S wave is present at the end of the QRS complex in leads I and aVF.

Medical Care:

Patients with LBBB require complete cardiac evaluation, and those with LBBB and near syncope or syncope may require pacemaker insertion.

Progression from left anterior hemiblock to higher degrees of block is unusual, and patients require only observation.

Surgical Care: Some patients with LBBB, markedly prolonged QRS duration, and congestive heart failure may benefit from biventricular pacing techniques that provide more rapid synchronized left ventricular contractions.

Consultations: Children with LBBB should be referred to a pediatric cardiologist for a careful and complete evaluation.

Activity: Activity restrictions will depend primarily on underlying cardiac cause of LBBB pattern, and if patient develops important arrhythmias (bradycardia, tachycardia) during prolonged exertion.

Further Inpatient Care:

Continuous telemetry may be considered if there is concern that LBBB is associated with other arrhythmias (see above).

Further Outpatient Care:

LBBB may rarely progress to complete heart block and sudden death. In these patients, prognosis is more dependent upon the associated cardiac disease than LBBB itself. A yearly evaluation, including an ECG, is recommended, with more frequent follow-up as indicated by underlying cardiac disease and changes in clinical course and symptoms.

Patients with LBBB, left axis deviation, and first-degree heart block or LBBB and near or complete syncope require close follow-up, and should be referred for electrophysiology consultation and possibly pacemaker insertion.

Complications:

If LBBB progresses to complete heart block the patient may experience syncope or sudden death.

Prognosis:

Progression to complete heart block is rare, and prognosis is more dependent upon the associated cardiac disease than the LBBB itself. Significant and progressive morbidity associated with concomitant congestive heart failure may be improved with biventricular pacing.

Medical/Legal Pitfalls:

LBBB in children is not a benign entity and is associated with both anatomic malformations and abnormalities of the conduction system and may progresses to complete heart block and sudden death.

Children with LBBB require a complete workup and consultation with a pediatric cardiologist.

Failure to have a child with newly diagnosed LBBB properly evaluated could result in poor outcome (bodily injury from abrupt syncope, permanent neurological damage, or death).

BIBLIOGRAPHY

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