Category: Conduction Abnormalities

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

Feature	RBBB	LBBB
Site of Blockage	Right Bundle Branch	Left Bundle Branch
Affected Ventricle	Right Ventricle	Left Ventricle
Initial Depolarization	Normal septal depolarization	Altered septal depolarization (right to left)
QRS Duration	Prolonged	Prolonged
V1 and V2 Leads	rsR′ or rSR′ pattern (rabbit ears)	Deep, broad S waves
V5 and V6 Leads	Wide, slurred S waves	Broad, notched R waves (M-shaped)
ST-T Changes	T wave inversion in V1 and V2	ST depression and T wave inversion in V5 and V6
Cannot diagnose	Right 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 diagnose	pericarditis, left ventricular hypertrophy (LVH), left axis deviation (LAD), and Q-wave myocardial infarctions can still be diagnosed.	MI with Sgarbossa criteria.
Clinical Associations	Can be normal; pulmonary diseases	Often 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

Feature	LAFB	LPFB
Initial Depolarization	Posterior-Inferior Left Ventricle	Anterior-Superior Left Ventricle
Secondary Depolarization	Anterior-Superior Left Ventricle	Posterior-Inferior Left Ventricle
Mean QRS Axis	Left Axis Deviation	Right Axis Deviation (+90° to +180°)
Lead I and aVL	qR Pattern	rS Pattern
Leads II, III, and aVF	rS Pattern	qR Pattern
QRS Duration	Normal (< 0.12 sec)	Normal (< 0.12 sec)
Commonality	More Common (thin and long- so more prone to damage)	Less Common (thick and short)
Associated Conditions	Hypertension, CAD (supplied by LAD), Aortic Valve Disease	Significant 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 and Rate-Related Blocks

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.

The atrioventricular (AV) node acts as a critical gateway for electrical impulses traveling from the atria to the ventricles of the heart. When there’s a delay or blockage at this gateway, it can lead to various types of heart blocks, each with distinct patterns observable on an electrocardiogram (EKG). This article explores these heart block patterns in detail to aid in their recognition and understanding.

First-Degree Heart Block

A first-degree heart block represents a minor delay in the conduction of electrical impulses at the AV node, similar to a slight traffic slowdown on a highway. On an EKG, the hallmark of a first-degree heart block is a prolonged PR interval—the time it takes for the impulse to travel from the atria to the ventricles—that exceeds 0.2 seconds. Despite this delay, every atrial impulse still reaches the ventricles, so the heart rhythm remains regular.

Second-Degree Heart Block

Second-degree heart blocks are characterized by intermittent failures of electrical conduction from the atria to the ventricles. They are further classified into two types: Mobitz Type I (Wenckebach) and Mobitz Type II.

Mobitz Type I (Wenckebach)

In Mobitz Type I heart block, there is a progressive delay in AV node conduction until an impulse fails to conduct, resulting in a missed ventricular beat. This cycle then repeats.

On the EKG, this appears as progressively lengthening PR intervals with each beat until a QRS complex (which represents ventricular depolarization) is dropped. After the missed beat, the PR interval resets to a shorter duration, and the pattern starts over. Additionally, the R-R intervals (the time between ventricular contractions) typically shorten before the dropped beat.

A useful diagnostic tip is to compare the PR intervals just before and after the missing QRS complex; the PR interval following the dropped beat is shorter.

Mobitz Type II

Mobitz Type II heart block is more serious and can progress to a complete heart block. In this type, the AV node fails to conduct impulses intermittently without prior changes in the PR interval.

This means the PR intervals remain consistent, but some beats are suddenly dropped. On the EKG, there are more P waves (atrial depolarizations) than QRS complexes because some atrial impulses do not reach the ventricles. This irregularity can lead to bradycardia and symptoms such as dizziness or syncope.

2:1 Heart Block

A 2:1 heart block occurs when every alternate atrial impulse fails to conduct to the ventricles, resulting in one conducted beat followed by one blocked beat. This pattern makes it challenging to distinguish between Mobitz Type I and Mobitz Type II because only two beats are compared at a time. However, certain clues can aid differentiation:

• Examination of Other EKG Leads: Observing for patterns indicative of Mobitz Type I or II in different parts of the EKG may provide hints.
• Response to Physical Activity: If the heart rate does not increase appropriately with exercise—a condition known as chronotropic incompetence—it suggests Mobitz Type II.
• Presence of Symptoms: Symptoms like fatigue, lightheadedness, or fainting are more commonly associated with Mobitz Type II due to its potential to cause significant bradycardia.

Third-Degree Heart Block (Complete Heart Block)

In a third-degree heart block, there is a complete dissociation between atrial and ventricular activity. The electrical impulses from the atria do not conduct to the ventricles at all. As a result, the atria and ventricles beat independently.

On the EKG, both the P-P intervals (atrial rate) and R-R intervals (ventricular rate) are regular, but there is no relationship between them—they are not synchronized. The atrial rate is usually faster than the ventricular rate. The ventricles often rely on an escape rhythm originating from a secondary pacemaker within the heart’s conduction system, such as a junctional or idioventricular rhythm, to maintain a heartbeat.

The sinoatrial (SA) node functions as the heart’s natural pacemaker, generating electrical impulses that travel through the atria and ventricles, facilitating synchronized heartbeats. A sinoatrial exit block occurs when these impulses are produced by the SA node but experience delays or fail to reach the atrial tissue, resulting in disruptions to the heart’s rhythm. Since it is the atrial depolarization that generates the P wave (not the depolarization of the sinus node), a sinoatrial exit block is indicated by the absence of a P wave. This article offers a thorough examination of the various types of SA exit blocks, their electrocardiogram (EKG) manifestations, and methods to differentiate them from conditions such as sinus pause.

First-Degree Sinoatrial Exit Block

In a first-degree SA exit block, there is a delay between the generation of an impulse in the SA node and its transmission to the atria. This delay occurs before atrial depolarization, which is represented by the P-wave on an EKG. Since the delay precedes the initiation of the P-wave, it cannot be directly observed on an EKG tracing. The atrial and ventricular rhythms remain normal, and the condition is typically asymptomatic and undetectable without invasive electrophysiological studies.

Second-Degree Sinoatrial Exit Block

Second-degree SA exit blocks are characterized by intermittent failures of SA node impulses to reach the atria. There are two types: Type I (Wenckebach) and Type II. Each type has distinct patterns and implications for cardiac function.

Second-Degree SA Exit Block Type I (Wenckebach)

Characteristics

Type I SA exit block involves a gradual delay in the conduction of impulses from the SA node to the atria until an impulse is completely blocked. This results in a cyclic pattern where the intervals between P-waves (P-P intervals) progressively shorten until a P-wave is absent. After the missed beat, the cycle restarts.

EKG Interpretation

• Progressive Shortening of P-P Intervals: The time between successive P-waves decreases gradually.
• Dropped P-Wave: Eventually, a P-wave fails to appear, indicating that the impulse did not reach the atria.
• Pause Duration: The pause caused by the missing P-wave is less than twice the normal P-P interval, , signifying that one impulse has been blocked after a series of gradually shortening P-P intervals.

This forms a pattern similar to the “Wenckebach” pattern observed in some AV blocks. However, it is essential to note that, in this case of SA exit block, the PR interval stays consistent.

Analogy

Imagine a runner who becomes increasingly fatigued with each lap, causing them to slow down slightly each time. Eventually, they are too exhausted to complete a lap, rest briefly, and then resume running at their original pace.

Second-Degree SA Exit Block Type II

Characteristics

Type II SA exit block is marked by sudden, unexpected failures of SA node impulses to reach the atria without prior changes in conduction time. The P-P intervals are consistent until a P-wave is abruptly missing, resulting in a pause that is a multiple of the normal P-P interval.

EKG Interpretation

• Consistent P-P Intervals: The intervals between P-waves remain uniform.
• Sudden Dropped P-Wave: A P-wave is unexpectedly absent.
• Pause Duration: The pause equals two or more times the normal P-P interval, indicating that one or more impulses were blocked.

Distinguishing Factors

• The SA node continues to fire at regular intervals despite the block. So, the timing of subsequent P-waves aligns with the expected rhythm as if the block had not occurred.

Third-Degree Sinoatrial Exit Block

Characteristics

In a third-degree SA exit block, none of the SA node’s impulses reach the atria. The SA node continues to generate impulses, but a complete conduction block prevents atrial depolarization. This results in an absence of P-waves on the EKG.

EKG Interpretation

• Absent P-Waves: No atrial activity is detected because impulses fail to exit the SA node.
• Junctional or Ventricular Escape Rhythms: The heart may rely on subsidiary pacemakers, leading to slower heart rates and altered QRS complexes depending on the origin of the escape rhythm.
• This is virtually indistinguishable from sinus arrest on an EKG. This is because P-waves, which depict atrial activity, don’t show the activity of the SA node directly. However, if the conduction resumes in a short time, the P-waves reappear in sync with the expected timing as if no pause occurred since the SA node function itself is unaffected.