Electrocardiography
Blocks


HOME Sinoatrial Exit Block Atrioventricular (AV) Block Fascicular Block Bundle Branch Block

 

Interference in the normal conduction of the electrical system of the heart can occur at many levels and is usually manifested on the surface ECG. These conduction abnormalities are represented by prolongation of the normal intervals or by complete termination of an electrical impulse. This section will go over the various areas where block can occur and the ECG criteria for each of them.


 

Sinoatrial Exit Block

In sinoatrial exit block, an impulse is generated within the SA node but does not exit the node. If sinoatrial exit block is complete, there is no way to tell if there is truly sinoatrial exit block or if there is asystole. Incomplete sinoatrial exit block follows a Wenckebach type pattern. The P to P interval continues to increase until a P wave is eventually dropped. If there is no evidence of prolongation of the P to P interval on the surface ECG, it is impossible to tell the difference between incomplete sinoatrial exit block and a sinus pause.

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Atrioventricular (AV) Block

First-degree AV Block

The normal PR interval is 120 to 200 milliseconds. A prolongation of this interval is considered first-degree AV block and is most commonly caused by a delay within the AV node but can also be caused by intra-atrial delay or subnodal delay in the His-Purkinje system. In a healthy normal population, approximately 1% will have a prolonged PR interval. PR prolongation in the ECG can best be seen in leads V1 and II.

Second-degree AV Block

Second-degree AV block involves atrial activity that intermittently does not result in ventricular activity and is caused by impaired conduction. Thus, non-conducted premature beats are not considered as AV block but instead are not conducted due to the refractory period. This type of block can occur in the AV node, the His-Purkinje system or the bundle branches. Type I was first described by Wenckebach in 1906 but was not formally distinguished from Type II until 1924 by Mobitz.

Type I second-degree AV block involves the progressive prolongation of the PR interval until a QRS complex does not follow or is dropped. Following the dropped beat, the PR interval returns to normal and, frequently, the cycle repeats. The prolongation of the PR interval is due to the atrial impulses arriving at a relatively refractory AV node. Each successive atrial beat takes longer and longer to propagate through the AV node until one is blocked. In addition, the R to R interval becomes progressively shorter until the dropped beat occurs. The pattern of Wenckebach is commonly referred to as group beating.

Type II second-degree AV block is less common and is clinically more serious. The level of block is below the AV node and there is usually a baseline bundle branch block. The dropped beat occurs when the other bundle branch blocks and there is bilateral bundle branch block which halts the propagation of the electrical impulse on the ECG. Unlike type I, there is no prolongation of the PR interval prior to the dropped beat. This type of block can be a precursor to third-degree AV block or complete heart block.

Second-degree AV block type indeterminate is a rhythm where there is 2:1 A:V conduction. Because every other beat is blocked, it is impossible to tell if there is PR prolongation from beat to beat. If there is type I or type II second-degree AV block elsewhere in the tracing, then that type of block is more likely the cause of the 2:1 block. If the QRS complex is narrow, it is more likely to be type I whereas if it is wide it is more likely to be type II. Unfortunately though, there are no hard and fast rules when 2:1 block is present and it should be labeled as second-degree AV block, type indeterminate.

Third-degree AV Block

Third-degree AV block or complete heart block is when no atrial impulses result in ventricular activation. The most common cause is bilateral bundle branch block not involving the AV node. There may also be trifascicular block involving the right bundle, left anterior fascicle and left posterior fascicle resulting in no ventricular activation despite normal conduction through the AV node.

At this point, two options exist: ventricular standstill or a subsidiary pacemaker takes over. The subsidiary pacemaker can be either junctional or ventricular although when bilateral bundle branch block exists, a junctional pacemaker would also be blocked. With the escape rhythm, the ventricles and atria beat independently of each other and there is AV dissociation.

On the ECG, AV dissociation refers to the atria and ventricles beating independently of each other while complete heart block refers only to this event occurring when the ventricular rate is less than the atrial rate. If the ventricular rate is higher than the atrial rate, such as in ventricular tachycardia, then there is AV dissociation but not complete heart block.

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Fascicular Block

The fascicular blocks are complex because the fascicles of the left bundle are not distinct. There is evidence that there are actually three fascicles and others believe that the fascicles are multiple fibers that fan out into the left ventricle. There are many variations to this anatomy. When there are three fascicles, the superioranterior fascicle is what is abnormal in anterior fascicular block; the posteriorinferior fascicle is abnormal in posterior fascicular block and the septal fascicle is small and not electrically apparent. If the fascicles fan out, the blocks are conceptual. Both fascicular blocks are frequently associated with right bundle branch block. Prognostically, neither of the fascicular blocks predict either morbidity or mortality but if present by themselves, there is an increased incidence of developing right bundle branch block.

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Left Anterior Fascicular Block (LAFB)

When anterior fascicular block is present, the activation in the left ventricle propagates in a posterior to lateral to anterior-superior fashion. Although the conduction is abnormal, in the pure form, there is no or little delay in conduction on the surface ECG. The change in conduction of the left ventricle explains the characteristic findings of LAFB on the surface ECG. The figure below demonstrates the activation of the left ventricle and the ECG appearance of aVF, aVL and aVR. Leads II and III are similar to aVF while lead I is similar to aVL. Typical criteria for LAFB include an axis between -45 degrees and -90 degrees (some accept -30 to -90 degrees), small R waves (r waves) in leads II, III and aVF and small Q waves (q waves) in leads I and aVL. Another criteria is the observation that the final R wave in aVR is after the final R wave in aVL. This criteria is explained conceptually in the figure where the wave of propagation is directed toward aVL before it is directed at aVR.

Although the overall duration of the QRS complex is normal, the intinsicoid deflection in lead aVL may be delayed and if it is over 45 milliseconds, this provides additional evidence of LAFB. Finally, because the left ventricle is activated from one side to the other, there may be increased amplitude in the limb leads, especially aVL, which can mimic left ventricular hypertrophy. Criteria for LAFB are also in list form.
Some things to be wary of with LAFB are that it can mask left ventricular hypertrophy, right bundle branch block and anterior and inferior infarcts. In addition, it can imitate left ventricular hypertrophy and anterior and lateral infarcts. If LAFB is present, the precordial lead criteria should be used for left ventricular hypertrophy.

Criteria for Left Anterior Fascicular Block

 
  1. Left Axis Deviation (-30 or -45 to -90 degrees)
  2. Small R waves in leads II, III and aVF
  3. Small Q waves in leads I and aVL
  4. Normal QRS duration
  5. Delayed intrinsicoid deflection in aVL
  6. Terminal R wave in aVR after the terminal R wave in aVL
  7. Increased QRS voltage in the limb leads, especially aVL
 
   
   
   
   
   
   

 

   

 

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Left Posterior Fascicular Block (LPFB)

Posterior fascicular block can be thought of as the mirror image of anterior fascicular block in the limb leads. The propagation wave proceeds from an anterior-superior position to the lateral wall to the posterior-inferior wall. Similarly to LAFB, the QRS duration is not prolonged. The figure below shows the wave of propagation in LPFB and the ECG appearance of aVF, aVL and aVR. Lead I is similar to aVL while leads II and III are similar to aVF. The criteria for LPFB include right axis deviation usually greater than +120 degrees, small Q waves (q waves) in leads I and aVL and small R waves (r waves) in leads II, III and aVF.

Similar to LAFB, there may be a delayed intrinsicoid deflection of over 45 milliseconds in lead aVF and there can be increased voltage in the limb leads imitating left ventricular hypertrophy. An additional factor in diagnosing LPFB is the absence of ECG criteria for right ventricular hypertrophy. Right ventricular hypertrophy can have the exact ECG appearance as LPFB with normal conduction through the fascicle. Of note, anterior infarction can be both obscured and imitated by LPFB. The criteria for LPFB is listed.

Criteria for Left Posterior Fascicular Block
 
  1. Right Axis Deviation(greater than +120 degrees)
  2. Small Q waves in leads II, III and aVF
  3. Small R waves in leads I and aVL
  4. Normal QRS duration
  5. Delayed intrinsicoid deflection in aVF
  6. Increased QRS voltage in the limb leads
  7. No ECG evidence of right ventricular hypertrophy
 
   
   
   
   
   
   

 

 

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Bundle Branch Block

Left Bundle Branch Block (LBBB)

The LBBB occurs either when the main left bundle is blocked or when each of the left fascicles are blocked. The QRS is prolonged and has characteristic ECG changes with associated ST-T wave changes. The criteria for LBBB is listed below. When LBBB is present, the wave of propagation goes down the right bundle branch and activates the right ventricle. The septum is activated in a right to left direction providing a negative deflection in V1 and initial positive deflection in V6. Normally, there are small non-diagnostic Q waves in the left precordial leads and sometimes leads I and aVL, which are absent in uncomplicated LBBB. There is also a monophasic R wave in the left precordial leads and leads I and aVL. The left ventricle is then activated by electrical propagation through the muscle.

A normal axis or left axis deviation can be present in LBBB. Patients with LBBB and left axis deviation have a higher incidence of cardiomyopathy. Patients with LBBB have a ten-fold increase risk of sudden death than patients without LBBB.

The ST-T wave changes in LBBB are due to changes in conduction and are referred to as secondary ST-T wave changes. The T wave is directed in the opposite direction of the direction of the QRS complex. Because the T wave changes are part of the LBBB, there is no clinical significance. On the other hand, if the T waves are directed in the same direction as the QRS complex, they are considered primary T wave changes and are due to a reason other than the LBBB.

The presence of LBBB interferes with several other diagnoses that can be made with the ECG. The first of these is left ventricular hypertrophy (LVH). The ECG changes seen with LVH are similar to LBBB and, as the QRS widens with LVH, the difference between the two becomes less. The LBBB characteristically has a wider QRS and QT interval, a longer intrinsicoid deflection and the ST-T wave changes are more pronounced. The Q waves in the left precordial leads may be more pronounce in LVH and, as before, should be absent in LBBB. A large number of patients with LBBB on ECG have LVH on echocardiography making the discussion clinically insignificant. The diagnosis of infarction is also made difficult. The normal appearance of LBBB can seem to be a septal infarct and the ST-T wave changes can be consistent with either an ischemia or injury pattern. The diagnosis of left ventricular hypertrophy or Q wave infarction cannot be made in the presence of LBBB.

Clinically, in patients with coronary artery disease, the presence of LBBB provides a much lower survival rate than those patients without LBBB. Hemodynamically, there is dysfunctional ventricular contraction leading to decreased ejection fractions, decreased stroke volume and decreased cardiac output.

Criteria for Left Bundle Branch Block
 
  1. QRS duration greater than 120 milliseconds
  2. Notched R waves in V5 and V6 and usually leads I and aVL
  3. rS or QS pattern in V1 and V2
  4. Absent Q waves in V5, V6, I and aVL
  5. Delayed intrinsicoid deflection over 60 milliseconds in V5 and V6
 
   
   
   
 

Right Bundle Branch Block (RBBB)

The RBBB is more straightforward than the LBBB with a simpler etiology, less interference with the interpretation of the ECG, less hemodynamic implications and fewer clinical implications. The RBBB is caused by block in the right bundle and there are established diagnostic criteria on ECG. Although the right bundle is blocked, the left ventricle is activated normally. Septal depolarization is normal so the early portion of the QRS is normal including small R waves in the right precordial leads (V1 and V2) and small Q waves in the left precordial leads (V5 and V6). In the normal QRS pattern, right ventricular depolarization contributes little to the complex due to its small mass. When the right bundle is blocked, the time when the right ventricle is depolarized comes after the left ventricle and septum and shows up as a prominent R' in lead V1 and a prominent wide S wave in V5 and V6.

The axis in RBBB is normal unless LAFB or LPFB is also present.

The ST-T wave changes in RBBB are characteristic and considered secondary. As with LBBB, the T wave is directed in the opposite direction of the QRS complex. If the T waves are in the same directions as the QRS complex, they are considered primary T wave changes and represent ECG abnormalities. Unlike LBBB, there is a form of incomplete RBBB where the criteria for RBBB exist but the QRS duration is between 100 and 120 milliseconds.

There is no clinical implication of RBBB without overt cardiac disease. The presence of RBBB does interfere with the diagnosis of RVH due to the increased R wave voltage associated with RBBB. The diagnosis of RVH can be made with the initial R wave of greater than 1.5 mm and a right axis deviation. The diagnostic criteria for LVH remain the same but with decreased sensitivity and specificity. The diagnosis of LVH is also suggested with RBBB associated with left atrial enlargement and left axis deviation.

Criteria for Right Bundle Branch Block
 
  1. QRS duration greater than 120 milliseconds
  2. Broad notched R waves in V1 and V2 with an rSR', rsR' or rsr' pattern
  3. Wide and deep S waves in V5 and V6
 
   
   

Other causes of Prominent R waves in lead V1
 
  1. Right Ventricular Hypertrophy
  2. Posterior or Lateral Myocardial Infarction
  3. Wolff-Parkinson-White Syndrome
  4. Hypertrophic Cardiomyopathy (Septal)
  5. Duchenne’s Progressive Muscular Dystrophy
  6. Normal Variant
 
   
   
   
   
   

*Adapted from Practical Electrocardiography, Eighth Edition. Henry J.L. Marriott. Williams and Wilkins. 1988.

Non-specific Intraventricular Conduction Delay

A non-specific intraventricular conduction delay (IVCD) is a diagnosis used to describe a wide QRS complex that does not fit into the category of either a left bundle or right bundle branch block. The ECG may appear similar to either of bundle branch blocks in some leads but different from either bundles in other leads. The conduction abnormality is not due to an interruption in the bundles. It is caused by either an increase in ventricular mass or ventricular size.

Intermittent Bundle Branch Block

Intermittent bundle branch block is usually a rate dependent phenomenon. Both bundles have a refractory period. At lower heart rates, the bundle has time to recover prior to the next impulse. As the heart rate increases, the impulse arrives earlier and, if the bundle is still refractory, a bundle branch pattern is observed. There is usually a critical heart rate where the block develops. When the heart rate slows again, the rate at which the narrow QRS complex returns is lower than the critical rate. The lower the critical heart rate at which bundle branch block develops, the overall worse the prognosis.

There is also a bradycardia induced bundle branch block that is phase 4 dependent.

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