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Conduction abnormalities

Created: 28/8/2006
Updated: 10/8/2006
 

Sinus node block

This involves failure of the sinus node to depolarise or failure of impulse conduction from the sinus node to the atria.

It may be seen during anaesthesia (due to vagal reflexes); during drug therapy with digoxin, quinidine or phenylephrine; myocardial ischaemia or infarction; and due to ischaemia-induced fibrosis of the sinus node.

ECG changes: An absent P wave and often an absent QRS complex are seen.
Manifested by a gradual shortening of the P-P intervals until a pause occurs (i.e. the blocked sinus impulse fails to reach the atria).

Sino-atrial exit block

Sick sinus syndrome is a term used for a number of disorders that involve degenerative changes in the cardiac conduction system, resulting in sinus node dysfunction and, possibly, AV blocks too. Causes include myocardial ischaemia or infarction, hypertension, electrolyte and endocrine abnormalities, cardiomyopathies, inflammatory diseases and drug effects.

Atrioventricular (AV) blocks

Possible sites of AV block include:

  • AV node (most common).
  • His bundle (uncommon).
  • Bundle branch and fascicular divisions.

1st degree AV block: This may be seen in healthy individuals

Features include:

  • Prolonged PR interval - i.e. PR interval >0.20 s.
  • All P waves are conducted to the ventricles.

1st degree AV block

2nd degree AV block: All of the atrial impulses are not conducted to the ventricles. There may be, for example, a ventricular beat following every second or every third atrial beat (2:1 block, 3:1 block etc.).

2nd degree AV block is subdivided into two classes as follows:

(a) Mobitz Type I  (Wenckebach phenomenon)

The PR interval lengthens gradually until a P wave which fails to conduct to the ventricles occurs. The block in this case is almost always located in the AV node and may be caused by right coronary artery occlusion causing inferior wall infarctions.
 
Mobitz Type I or Wenckebach phenomenon)

(b) Mobitz Type II

This involves an intermittent block in conduction of the P wave into the ventricles, but the PR interval in surrounding beats is unaltered. Type II AV block is almost always located in the bundle branches.

Type II block may result from anterior wall infarctions. These blocks are generally permanent, with a greater risk of progressing to complete heart block.

Mobitz Type II

3rd degree /complete heart block: This involves total disruption of conduction between the atria and ventricles. In this situation, life is maintained by a spontaneous escape rhythm.

3rd degree block

In 'A', the ECG shows complete or 3rd degree AV block with a left ventricular escape rhythm, as evidenced by the upright QRS morphology. In 'B', the artificial right ventricular pacemaker rhythm is shown.

Narrow complex escape rhythm (<0.12s QRS complex): The escape rhythm originates in the His bundle and therefore the site of block lies more proximally in the AV node. The escape rhythm occurs at a rate of 50-60 bpm and is relatively reliable.
Treatment depends on aetiology. But chronic symptomatic blockade requires permanent pacing.

Broad complex escape rhythm (>0.12s QRS complex): The escape rhythm originates below the His bundle and therefore the site of blockade lies more distally in the His-Purkinje system. The resulting rhythm is slow (15-40 bpm) and unreliable. Dizziness and blackouts (Stoke-Adams attacks) often occur. Temporary followed by permanent pacing may be required.

Intraventricular blocks

Right bundle branch block (RBBB)

This involves: 

  • Total failure of conduction in the right bundle branch proximally. 
  • No change in the direction of depolarisation of the interventricular septum.
  • No change in the timing or direction of left ventricular depolarisation.

Right budle branch block

Diagnostic criteria for RBBB:

1) "Complete" RBBB has a QRS duration >0.12 s.
2) A secondary R wave is seen in V1. The secondary wave is usually broad and slurred (the complex in V1 may be rsr’, rSr’, RSr’, RSR’ or M-shaped).

Click for larger image

Additional features frequently seen in RBBB include:
1) Deep, slurred S waves in left precordial leads (typically V4,V5,V6).
2) Deep, slurred S waves usually seen in lead I and also aVL.
3) ST segment depression and T wave inversion are seen in the right precordial leads (typically in leads V1, V2, V3). This occurs due to secondary changes in ventricular repolarisation (ST segment and T waves).

The mean frontal plane QRS axis is usually within the normal range in uncomplicated complete RBBB. The axis may move 15-30° towards the right, but abnormal right axis deviation is not a routine feature of RBBB. If left axis deviation is present, think about left anterior fascicular block, and if right axis deviation is present, think about left posterior fascicular block in addition to the RBBB.

Clinical significance:
RBBB may occur congenitally in normal hearts. It can be seen in a variety of disorders, including ischaemic heart disease, hypertension, pulmonary embolism, cardiomyopathy, myocarditis, pericarditis, rheumatic heart disease, Chagas disease and congenitally in association with atrial septal defect and Fallot’s tetralogy.

Left bundle branch block (LBBB)

This involves:

  • Total failure of conduction in the left bundle branch system.
  • Complete reversal of the direction of depolarisation of the interventricular septum. 
  • Delay in the initiation and velocity of depolarisation of the free wall of the left ventricle.

Click for larger image

Diagnostic criteria for LBBB:

1) Total QRS duration >0.12 s.
2) No secondary R wave in V1 to indicate RBBB.
3) No septal q wave in V5, V6 or in leads further to the left (lead I and aVL in horizontal hearts).

Diagnostic criteria for LBBB

Additional features frequently seen in LBBB include:

1) The QRS complexes in some leads may be notched (leads I, aVL, V5 and V6).
2) The QRS complexes in V5, V6, I and aVL tend to have rsR’, "M" pattern or broad monophasic R waves.
3) Secondary ST depression and possibly T wave inversion may be seen in the left precordial leads (and in leads I and aVL).
4) ST segment elevation and abnormally tall T waves may be seen in the right precordial leads.
5) Abnormally deep S waves in the right precordial leads.
6) Initial r waves in the right precordial leads may be very small or absent.
7) In the precordial leads, the dominant direction of the ST segments and the T waves tends to be opposite to the dominant direction of the QRS complexes in any given lead.

The mean frontal plane QRS axis is usually within the normal range in uncomplicated complete LBBB. The axis may move 15-30° towards the left when LBBB develops but abnormal left axis deviation is not a routine feature of LBBB. The axis may sometimes be indeterminate. When LBBB is combined with abnormal left axis deviation, extensive disease of the left ventricular conducting system is likely to be present.

Incomplete LBBB is diagnosed when:

1) There is no septal q wave in V5, V6 or in leads further to the left (leads I and aVL) and
2) The total QRS duration is 0.10-0.11 s.


Clinical significance:

LBBB always indicates significant cardiac disease. It is seen most commonly in ischaemic heart disease, hypertension, aortic stenosis and fibrous degeneration of the conducting tissue. It may also occur in congestive and hypertrophic cardiomyopathy, myocarditis, acute rheumatic fever, syphilis, cardiac tumours, post-cardiac surgery and in congenital heart disease.

Fascicular blocks

According to this concept, there are three fascicles of conduction:

1) Right bundle branch
2) Anterior division of the left bundle branch and
3) Posterior division of the left bundle branch.

We shall now consider unifascicular blocks of the divisions of the left bundle branch - i.e. left anterior hemiblock and left posterior hemiblock.

Normally, the left ventricle is depolarised simultaneously from two directions:

a) A depolarisation wave spreading from below upwards and to the left as a result of transmission through the posterior (inferior) division and
b) A depolarisation wave spreading from above downwards and to the left as a result of transmission through the anterior (superior) division.


Left anterior fascicular block (LAFB):

In this abnormality, the antero-superior division of the left bundle totally fails to conduct. Hence, the antero-superior part of the left ventricle (LV) is activated in the opposite direction by the depolarisation wave after it emerges from the postero-inferior part of the LV, which receives the wave in a normal manner through the posterior (inferior) division of the left bundle.

Diagnostic criteria for LAFB are:

1) Left axis deviation with QRS axis more negative than -30°.
2) Initial r waves in all inferior limb leads (leads II, III, aVF).
3) Other recognised causes of left axis deviation must be absent**.

Additional features frequently seen in LAFB include:

Total QRS duration is usually at the upper limit of normal (0.09-0.10 s)

Click here for larger image

Other causes of abnormal left axis deviation include:

  • Ventricular pre-excitations - e.g. Wolff-Parkinson-White syndrome. 
  • Inferior myocardial infarction. 
  • Tricuspid atresia and ostium primum atrial septal defect. 
  • Hyperkalaemia.

Clinical significance:

Chronic LAFB may be a normal finding in the elderly without evidence of heart disease. It may be present after acute myocardial ischaemia, hypertension, congestive and hypertrophic cardiomyopathy, myocarditis, calcific aortic stenosis and following aortic valve replacement.

Important differential diagnosis of LAFB

Abnormal left axis deviation is the most striking feature of LAFB. The second most common cause of an abnormal left axis deviation  is an inferior myocardial infarction.

The important difference in the ECG between the above two conditions is the presence of:

  • initial r waves in all inferior limb leads (II, III, aVF) in LAFB

BUT 

  • there are abnormal Q waves in the inferior leads in inferior myocardial infarction.


Left posterior fascicular block (LPFB):

This occurs less frequently than an LAFB. This is because the posterior division of the left bundle is thicker and shorter and has a much better blood supply than its counterpart.

In this abnormality, the postero-inferior division of the left bundle fails to conduct. Hence, the postero-inferior part of the LV is activated in the opposite direction by the depolarisation wave after it emerges from the antero-superior part of the LV, which receives the depolarisation wave in a normal manner through the antero-superior division of the left bundle.

In left posterior fascicular block, the only ECG features seen are:

1) A mild degree of right axis deviation (between +90° and +120°) and
2) Total QRS duration is at the upper end of normal (0.09-0.10 s).

Due to only subtle changes brought about by a left posterior fascicular block on the ECG, it is impossible to be sure about a LPFB from the ECG alone. Other possible causes of right axis deviation should be excluded (e.g. emphysema, right ventricular hypertrophy, atrial septal defect and an extensive antero-lateral myocardial infarction).

Bifascicular blocks:

When two fascicles are blocked simultaneously, a bifascicular block is said to exist. This includes the more common combination of right bundle branch block (RBBB) with left anterior fascicular block (manifest as LAD), and the less common RBBB with left posterior fascicular block.

Trifascicular block:

This is a combination of bifascicular block and 1st degree heart block.

Diagnostic criteria for RBBB with left anterior fascicular block are:

1) Total QRS duration = 0.12 s.
2) A secondary R wave in V1.
3) Mean QRS axis is more negative than -30°.
4) An initial r wave is seen in the inferior limb leads (II,III and aVF).

Click here for larger image

In RBBB with left posterior fascicular block, the ECG features are:

1) Total QRS duration = 0.12 s.
2) A secondary R wave in V1.
3) Mean QRS axis is more positive than +90°.

Clinical significance:

RBBB with LAFB is more common. But both of the above bifascicular blocks can occur in similar conditions. This includes conditions like atherosclerotic heart disease, calcific aortic stenosis, hypertrophic and congestive cardiomyopathy, and congenital endocardial cushion defects.

Although an RBBB with LPFB is less common, 60-70% of those that do occur progress to a complete heart block.


ArticleDate:20060828
SiteSection: Article
 
   
    
                                            
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