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Bundle Branch Blocks

Bundle branch blocks (BBBs) are important findings on electrocardiograms (EKGs) that signify disruptions in the heart’s electrical conduction pathways. Recognizing and interpreting these blocks are crucial for diagnosing and managing various cardiac conditions. This comprehensive guide delves into the types of bundle branch blocks, their mechanisms, EKG manifestations, and clinical significance.

The Normal Cardiac Conduction System

Before exploring bundle branch blocks, it’s essential to understand the normal conduction pathway:

  1. Sinoatrial (SA) Node: The heart’s natural pacemaker located in the right atrium initiates the electrical impulse.
  2. Atrioventricular (AV) Node: The impulse travels to the AV node, where there’s a brief delay to allow ventricular filling.
  3. Bundle of His: The impulse then moves into the bundle of His.
  4. Bundle Branches:
    • Right Bundle Branch (RBB): Conducts impulses to the right ventricle.
    • Left Bundle Branch (LBB): Splits into three fascicles:
      • Septal Fascicle: Arises from the LBB or the LAF or the LPF. Depolarizes the interventricular septum from left to right.
      • Left Anterior Fascicle (LAF): Supplies the anterior and superior portions of the left ventricle.
      • Left Posterior Fascicle (LPF): Supplies the posterior and inferior portions of the left ventricle.
  5. Purkinje Fibers: Distribute the impulse throughout the ventricles, leading to coordinated contraction.

Normal Ventricular Depolarization Sequence:

  • Septal Activation: Depolarization starts in the left side of the interventricular septum, moving from left to right. This is done by the septal fascicle.
  • Ventricular Activation: The impulse spreads down both the right and left bundle branches simultaneously, causing the ventricles to depolarize and contract together.
  • Free Wall Activation: Depolarization proceeds through the Purkinje fibers to the ventricular myocardium, from the endocardium to the epicardium.

Right Bundle Branch Block (RBBB)

In a complete bundle branch block (BBB), the QRS duration is typically greater than 120 milliseconds, while in an incomplete BBB, the QRS duration is between 100 and 120 milliseconds. This is true for both right and left bundle branches.

Mechanism of Conduction Alteration:

  • Site of Blockage: The RBB is impaired, slowing or preventing the conduction of electrical impulses to the right ventricle.
  • Altered Conduction Pathway:
    • The left ventricle depolarizes normally via the left bundle branch.
    • The right ventricle receives the impulse indirectly from the left ventricle through cell-to-cell transmission, which is slower.

Impact on Depolarization Sequence:

  • Initial Depolarization: The septum depolarizes normally from left to right, leading to a normal initial QRS vector.
  • Delayed Right Ventricular Depolarization: The right ventricle depolarizes after the left ventricle, causing secondary depolarization forces directed towards the right.

EKG Manifestations:

  • QRS Duration: Prolonged due to delayed right ventricular activation.
  • Leads V1 and V2 (Right Precordial Leads):
    • rsR′ or rSR′ Pattern: Characterized by an initial small r wave, an S wave, and a prominent secondary R′ wave due to delayed right ventricular depolarization.
    • Explanation: The initial r wave represents septal depolarization. The delayed R′ wave reflects the late activation of the right ventricle.
  • Leads V5, V6, I, and aVL (Left-Sided Leads):
    • Wide, Slurred S Waves: Result from the delayed right ventricular depolarization moving away from these leads.
  • ST-T Changes:
    • Secondary ST Depression and T Wave Inversion: May be seen in V1 and V2 due to the abnormal repolarization sequence.
  • The axis is generally normal. This is because the left ventricle is larger than the right ventricle and is the primary determinant of the QRS axis.

Clinical Significance:

  • Common Causes: Can be seen in normal individuals but also associated with conditions like pulmonary embolism, right ventricular hypertrophy, ischemic heart disease, or congenital heart defects.
  • Diagnostic Implications:
    • Difficulties in Diagnosing Right Ventricular Hypertrophy: RBBB obscures the typical EKG signs of RVH.
    • Ability to Diagnose Left-Sided Conditions: Left ventricular hypertrophy (LVH), left axis deviation (LAD), and Q-wave myocardial infarctions can still be diagnosed.

Left Bundle Branch Block (LBBB)

In a complete bundle branch block (BBB), the QRS duration is typically greater than 120 milliseconds, while in an incomplete BBB, the QRS duration is between 100 and 120 milliseconds. This is true for both right and left bundle branches.

Mechanism of Conduction Alteration:

  • Site of Blockage: The LBB is impaired, affecting the conduction to the left ventricle.
  • Altered Conduction Pathway:
    • The right ventricle depolarizes normally via the RBB.
    • The left ventricle receives the impulse indirectly from the right ventricle through slow cell-to-cell conduction.

Impact on Depolarization Sequence:

  • Altered Septal Activation: The normal left-to-right septal depolarization is reversed, occurring from right to left due to the impulse traveling from the right ventricle to the left.
  • Delayed Left Ventricular Depolarization: The left ventricle depolarizes after the right ventricle.

EKG Manifestations:

  • QRS Duration: prolonged due to delayed left ventricular activation.
  • Leads V5 and V6, I, and aVL (Left-Sided Leads):
    • Broad, sometimes Notched (‘M’-Shaped) R Waves: Reflect delayed left ventricular depolarization.
    • Absence of q Waves: Due to altered septal depolarization.
  • Leads V1 and V2 (Right Precordial Leads):
    • Deep, Broad S Waves: Result from the depolarization moving away from these leads.
  • ST-T Changes: These are usually discordant. They move in the opposite direction as the QRS complex vector.
    • ST Depression and T Wave Inversion: Common in leads with positive QRS complexes (e.g., V5 and V6) due to abnormal repolarization.
    • ST Elevation and Upright T Waves: May be seen in V1 and V2.
  • May cause Left Axis Deviation

Clinical Significance:

  • Common Causes: Often associated with underlying heart disease such as hypertension, coronary artery disease, cardiomyopathies, or valvular heart diseases.
  • Diagnostic Challenges:
    • Myocardial Infarction (MI): LBBB can mask or mimic the EKG signs of MI, making diagnosis challenging. Modified Sgarbossa Criteria help in diagnosing MI in the presence of LBBB by evaluating concordant and discordant ST-segment changes. The presence of any of these criteria in the appropriate clinical setting is concerning:
      • At least one lead with ≥1 mm of concordant ST elevation.
      • At least one lead of V1-V3 with ≥1 mm of concordant ST depression.
      • At least one lead anywhere with ≥1 mm of ST elevation and proportionally excessive discordant ST elevation (≥25% of the depth of the preceding S-wave).
    • Cannot diagnose LVH but most people with LBBB have LVH.

RBBB vs. LBBB

FeatureRBBBLBBB
Site of BlockageRight Bundle BranchLeft Bundle Branch
Affected VentricleRight VentricleLeft Ventricle
Initial DepolarizationNormal septal depolarizationAltered septal depolarization (right to left)
QRS DurationProlongedProlonged
V1 and V2 LeadsrsR′ or rSR′ pattern (rabbit ears)Deep, broad S waves
V5 and V6 LeadsWide, slurred S wavesBroad, notched R waves (M-shaped)
ST-T ChangesT wave inversion in V1 and V2ST depression and T wave inversion in V5 and V6
Cannot diagnoseRight ventricular hypertrophy (RVH)may be missed (though presence of RAD can suggest RVH), ischemia based on ST-T changes based on V1, V2 and V3.LVH (but most people with LBBB have LVH), RVH, Q-wave MI (modified Sgarbossa criteria help), ST-T changes are harder to diagnose, axis deviation, WPW.
Can diagnosepericarditis, left ventricular hypertrophy (LVH), left axis deviation (LAD), and Q-wave myocardial infarctions can still be diagnosed.MI with Sgarbossa criteria.
Clinical AssociationsCan be normal; pulmonary diseasesOften indicates underlying heart disease

Left Anterior Fascicular Block (LAFB)

Mechanism of Conduction Alteration

Blockage Site: LAFB occurs due to a conduction block in the left anterior fascicle of the left bundle branch.

Altered Conduction Pathway:

Primary Pathway Blocked: The anterior and superior regions of the left ventricle are no longer depolarized via the usual pathway.

Alternative Conduction: The impulse travels down the intact left posterior fascicle to the inferior and posterior regions first.

Delayed Depolarization: Depolarization of the anterior and superior regions occurs later via cell-to-cell conduction from the posterior regions.

Impact on Depolarization Vectors

Initial Vector: The initial depolarization vector is directed inferiorly and rightward due to the unopposed activation of the posterior-inferior left ventricle.

Secondary Vector: The delayed activation of the anterior-superior left ventricle creates a vector that is superior and leftward.

Resultant Mean QRS Axis: The overall QRS axis shifts markedly to the left, typically between -45° and -90°, resulting in left axis deviation (LAD).

EKG Manifestations

QRS Duration: Usually normal (< 0.12 seconds) because the total ventricular depolarization time isn’t significantly prolonged.

Axis Deviation: Pronounced LAD without other identifiable causes.

Lead-Specific Changes:

Leads I and aVL (High-Lateral Leads):

qR Pattern: Small initial q waves followed by tall R waves.

Explanation: The initial inferior-rightward vector produces small q waves.The delayed anterior-superior depolarization produces a strong leftward and superior vector, resulting in prominent R waves.

Leads II, III, and aVF (Inferior Leads):

rS Pattern: Small initial r waves followed by deep S waves.

Explanation: The initial inferior-rightward vector produces small r waves, but the dominant leftward vector results in deep S waves.

Other Features:

Normal or Slightly Prolonged QRS: Due to asynchronous ventricular activation.

No ST-T Changes: ST segments and T waves are generally normal unless other pathologies are present.

Clinical Significance

Isolated LAFB: Can occur without apparent heart disease but often associated with conditions affecting the left side of the conduction system, such as hypertension, aortic valve disease, or coronary artery disease.

Importance of LAD: Significant LAD in the absence of other causes (e.g., inferior myocardial infarction) strongly suggests LAFB.

Left Posterior Fascicular Block (LPFB)

Mechanism of Conduction Alteration

Blockage Site: LPFB occurs due to a conduction block in the left posterior fascicle of the left bundle branch.

Altered Conduction Pathway:

Primary Pathway Blocked: The posterior and inferior regions of the left ventricle are no longer depolarized via the normal route.

Alternative Conduction: The impulse travels down the intact left anterior fascicle to the anterior-superior regions first.

Delayed Depolarization: Depolarization of the posterior-inferior regions occurs later via cell-to-cell conduction from the anterior regions.

Impact on Depolarization Vectors

Initial Vector: The initial depolarization vector is directed superiorly and leftward due to the unopposed activation of the anterior-superior left ventricle.

Secondary Vector: The delayed activation of the posterior-inferior left ventricle creates a vector that is inferior and rightward.

Resultant Mean QRS Axis: The overall QRS axis shifts markedly to the right, typically between +90° and +180°, resulting in right axis deviation (RAD).

EKG Manifestations

QRS Duration: Usually normal (< 0.12 seconds), similar to LAFB.

Axis Deviation: Pronounced RAD without other identifiable causes.

Lead-Specific Changes:

Leads II, III, and aVF (Inferior Leads):

qR Pattern: Small initial q waves followed by tall R waves.

Explanation: The initial superior-leftward vector produces small q waves.The delayed posterior-inferior depolarization produces a strong inferior and rightward vector, resulting in prominent R waves.

Leads I and aVL (High-Lateral Leads):

rS Pattern: Small initial r waves followed by deep S waves.

Explanation: The initial superior-leftward vector produces small r waves, but the dominant inferior-rightward vector results in deep S waves.

Other Features:

Normal or Slightly Prolonged QRS: Due to the altered sequence of ventricular activation.

No ST-T Changes: ST segments and T waves are generally unaffected unless concomitant pathologies exist.

Clinical Significance

Isolated LPFB: Less common than LAFB because the left posterior fascicle is shorter, thicker, and has a dual blood supply, making it more resistant to injury.

Association with Heart Disease: Often associated with significant underlying heart disease, such as ischemic heart disease or cardiomyopathies.

Importance of RAD: Significant RAD without other causes (e.g., right ventricular hypertrophy) suggests LPFB.

Comparative Summary of LAFB and LPFB

FeatureLAFBLPFB
Initial DepolarizationPosterior-Inferior Left VentricleAnterior-Superior Left Ventricle
Secondary DepolarizationAnterior-Superior Left VentriclePosterior-Inferior Left Ventricle
Mean QRS AxisLeft Axis DeviationRight Axis Deviation (+90° to +180°)
Lead I and aVLqR PatternrS Pattern
Leads II, III, and aVFrS PatternqR Pattern
QRS DurationNormal (< 0.12 sec)Normal (< 0.12 sec)
CommonalityMore Common (thin and long- so more prone to damage)Less Common (thick and short)
Associated ConditionsHypertension, CAD (supplied by LAD), Aortic Valve DiseaseSignificant Heart Disease (supplied by LAD and Posterior Descending Artery (PDA))

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Left Anterior Fascicular Block (LAFB)

LAFB involves blockage in the left anterior fascicle of the left bundle branch.

  • EKG Characteristics:
    • QRS Duration: Less than 0.12 seconds.
    • Axis Deviation: Left axis deviation without other causes.
    • High-Lateral Leads (I and aVL): Show a qR pattern.
    • Inferior Leads: Display an rS pattern.

Mechanism Explained: The blockage redirects the depolarization pathway to the left posterior fascicle first, altering the axis and the EKG patterns accordingly.

• The initial depolarization of the posterior-inferior regions creates a vector pointing down and right.

• The delayed activation of the anterior-superior regions creates a stronger vector pointing up and left.

• The overall mean axis is dominated by the delayed, unopposed anterior-superior depolarization.

Left Posterior Fascicular Block (LPFB)

LPFB is less common and affects the left posterior fascicle.

  • EKG Characteristics:
    • QRS Duration: Less than 0.12 seconds.
    • Axis Deviation: Right axis deviation without other causes.
    • Inferior Leads: Show a qR pattern.
    • High-Lateral Leads (I and aVL): Display an rS pattern.

Mechanism Explained: With the posterior fascicle blocked, depolarization occurs via the left anterior fascicle, causing a shift in the heart’s electrical axis.

Bifascicular and Trifascicular Blocks

Bifascicular Block

Occurs when two fascicles are blocked, commonly RBBB combined with either LAFB or LPFB.

  • EKG Characteristics: Features of RBBB along with either left or right axis deviation, depending on the fascicle involved.

Mechanism Explained: Simultaneous blockage in two pathways significantly delays ventricular depolarization, increasing the risk of progression to complete heart block.

Trifascicular Block

Involves blockage in all three fascicles, leading to a high risk of complete heart block.

  • EKG Characteristics: Alternating right and left bundle branch block patterns, possibly with prolonged PR intervals.

Mechanism Explained: The conduction system is severely compromised, with intermittent or complete failure of impulse transmission from the atria to the ventricles.

Aberrant Conduction refers to temporary conduction abnormalities that often occur during tachycardia.

  • EKG Characteristics: Normal conduction at rest but showing RBBB patterns during increased heart rates.

Mechanism Explained: At higher rates, a specific conduction pathway (usually the right bundle branch as it has a longer refractory period) may not have sufficient time to repolarize, leading to transient blockages.

Wolff-Parkinson-White (WPW) Pattern

WPW is characterized by an accessory pathway (Bundle of Kent) that pre-excites the ventricles.

  • EKG Characteristics:
    • Short PR Interval: Due to early ventricular activation.
    • Delta Wave: Slurred upstroke in the QRS complex.
    • Wide QRS Complex: Resulting from the fusion of normal and accessory pathway conduction.

Mechanism Explained: The accessory pathway bypasses the AV node, allowing impulses to reach the ventricles prematurely, which alters the initial part of the EKG causing the delta wave. Eventually, the normal conduction pathway kicks in after delay at the AV node resulting in the rest of the QRS complex.

Diagnostic Limitations:

  • Ventricular Hypertrophy: Difficult to assess due to altered QRS morphology.
  • Myocardial Infarction: WPW can cause Q-waves and ST-T changes, mimicking infarction.
  • Axis Deviation and other conduction abnormalities: Hard to diagnose accurately in the presence of WPW.

Ventriculophasic Sinus Arrhythmia

Seen in second or third-degree atrioventricular block.

  • EKG Characteristics: Intermittent differences in PP intervals based on their relationship to the QRS complex. P waves surrounding a QRS complex have shorter intervals (i.e., they occur at a faster rate) compared to those without an intervening QRS.

Mechanism Explained: The variation in PP intervals is thought to be due to changes in autonomic tone or ventricular feedback affecting the sinus node timing.

Non-Specific Intraventricular Conduction Defect (NSIVCD)

Non-Specific Intraventricular Conduction Defect (NSIVCD) is a term used when there is abnormal ventricular conduction that does not fit the criteria for well-defined conduction blocks, such as Right Bundle Branch Block (RBBB), Left Bundle Branch Block (LBBB), or fascicular blocks like Left Anterior Fascicular Block (LAFB) and Left Posterior Fascicular Block (LPFB).

NSIVCD reflects a delay in the transmission of electrical impulses through the ventricles, leading to a prolonged and abnormal QRS complex.

This condition is not a diagnosis in itself but rather an EKG finding that reflects an underlying conduction abnormality that does not fit a known, well-defined pattern.

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