Authors: Mohd Farooq Parey, Kate Turnbull, Asim Aijaz / Editor: Frances Balmer / Codes: CC3, CP3, CP4, SLO1, SLO3Published: 26/10/2023

Context

Bifascicular block affects a substantial number of patients. It occurs in 1-2% of the adult population and the incidence increases with age. It is frequently associated with structural heart disease and fibrosis of the cardiac conduction system. Patients with underlying bifascicular block are at risk of progression to complete heart block. The rate of progression varies from 1 to 17%, and is more likely in symptomatic patients who present with syncope or pre-syncope1.

The European Society of Cardiology (ESC) and American College of Cardiology/Heart Rhythm Society (ACC/HRS) have both published guidelines on the evaluation and management of bifascicular block2,3.

Definition

Bifascicular block is defined as “a conduction defect of two of the three main fascicles of the His/Purkinje system located below the atrioventricular (AV) node”4.

Fig.1 Cardiac conduction system via Wikimedia Commons

It is widely accepted that bifascicular block is classified as a right bundle branch block (RBBB) combined with either a left anterior fascicular block (LAFB)or left posterior fascicular block (LPFB). However, some authors also consider bifascicular block to include a complete LBBB (i.e. affecting both the LAFB and LPFB).

Historically, the term trifascicular block has been used when bifascicular block is associated with 1st, 2nd or 3rd degree AV block. However, as 1st and 2nd degree blocks are due to AV node pathology rather than a fascicular conduction defect, this is a misnomer. A true trifascicular block requires a bifascicular pattern on ECG plus a complete (3rd degree) heart block, reflecting the fact that all three fascicles are disrupted.

N.B. Some authors refer to bifascicular block with 1st or 2nd degree block as “incomplete trifascicular block” and bifascicular block with 3rd degree block as “complete trifascicular block”5

Learning bite

Bifascicular block is a conduction defect of two of three main fascicles of the His/Purkinje system located below the AV node. 

Electrical impulses in the heart are generated in the right atrium by the sinoatrial (SA) node, stimulate the contraction of atrial myocardium, then propagate through the intranodal tracts to the AV node in the interatrial septum. From here, the impulses travel down the Bundle of His – a collection of specialised cardiac conduction cells that connect the AV node to the ventricles. The Bundle of His is divided into left and right bundles, and the left bundle is further divided into anterior and posterior fascicles (see figure below).  The left anterior fascicle (LAF) conducts the impulses towards the anterior and upper part of the left ventricle, while the left posterior fascicle (LPF) conducts impulses to the posterior and inferior areas. Electrical conduction continues through a network of filaments called Purkinje fibres resulting in the coordinated contraction of the ventricles.

Fig.1 Cardiac conduction system via Wikimedia Commons

Chronic bifascicular blocks are usually associated with structural heart disease (50-80%), ischaemic heart disease (40-60%) or congenital heart disease and fibrosis of the cardiac conduction system. blocks are usually associated with structural heart disease (50-80%), ischaemic heart disease (40-60%) or congenital heart disease and fibrosis of the cardiac conduction system1.

New onset bifascicular block with chest pain can be a manifestation of acute occlusion of the proximal left anterior descending artery (LAD), causing anterior wall myocardial infarction. In up to 30% of cases, the ECG will not show ST elevation and acute bifascicular block will be the only ECG change seen6.

Medications including digoxin, beta blockers and calcium channel blockers should always be considered as a cause. Electrolyte imbalance, particularly hyperkalemia, can also lead to bifascicular block.

Learning bite

Chest pain with a new bifascicular block on ECG suggests acute myocardial infarction due to proximal LAD occlusion. These patients need admission, cardiac monitoring and discussion with cardiology.

Bifascicular block by itself is usually asymptomatic and is an incidental finding on ECG.

In some patients, bifascicular block can progress to complete or intermittent heart block, as conduction through the single remaining fascicle fails. This can manifest as presyncope or syncope, dyspnoea or weakness on exertion. 

The rate of progression of bifascicular block to complete heart block is approximately 1% per year in asymptomatic patients, and as high as 17% per year in symptomatic individuals. The risk is higher if the bifascicular block is associated with 1st degree AV block.

Bifascicular block is diagnosed on ECG. Blood tests should also be considered to rule out specific causes of bifascicular block, such as electrolyte abnormalities or acute myocardial infarction.

ECG – Diagnostic criteria

Bifascicular block can present as one of the following two ECG patterns7:

1. RBBB + LAFB

This is the most common of the two patterns due to the fact that the anterior fascicle is supplied by a single coronary artery, the LAD. Other possible factors are its relationship to the LV outflow tract, resulting in mechanotrauma to the fascicle.

ECG criteria: 

  • RBBB – widened QRS with prominent R wave in V1, RSR pattern in V1-V3 and slurred S wave in V5-V6 
  • Left axis deviation (LAD) 
  • R waves with deep S waves in inferior leads 
  • Small Q waves with tall R waves in lead I and aVL
Fig.2 Bifascicular block8

2. RBBB + LPFB

The LPF is shorter and broader than the LAF and has a dual supply of blood from the right and left circumflex arteries. As such, block of the LPF is rare.

ECG criteria:

  • RBBB 
  • Right axis deviation (RAD) 
  • R waves with deep S waves in I and aVL 
  • Small Q waves with tall R waves in inferior leads
Fig.3 Bifascicular block1

Learning bite

As a rule, RBBB has a normal axis on ECG. Whenever RBBB occurs with axis deviation, LAFB or LPFB should be looked for to diagnose bifascicular block.

Blood tests

Bloods should be sent to exclude electrolyte imbalances, particularly hyperkalemia.

If a new bifascicular block is associated with chest pain, an occlusive myocardial infarction in the territory of the LAD should be considered. In absence of ST elevation, cardiac markers and bedside echocardiogram should be performed.

The aim of risk stratification in the ED is to identify those patients who are at high risk of developing complete heart block and who require admission for cardiology review and permanent pacemaker insertion (PPM).

Patients with isolated, asymptomatic bifascicular block are usually low risk.

Patients who present with bifascicular block and pre-syncope or syncope may be experiencing periods of complete heart block, so require admission. The ESC and ACC/HRS recognise bifascicular block as a high-risk ECG feature for cardiac syncope.

One study9 identified the following four independent risk factors for patients requiring PPM insertion:

  • Presence of syncope or pre-syncope       
  • QRS greater than 140 ms
  • Renal failure
  • HV interval greater than 64 ms

NB HV is a measurement derived from electrophysiological studies (EPS) and not relevant to risk assessment in the ED.

The management of bifascicular block depends on the clinical presentation.

Patients with asymptomatic bifascicular block do not usually require any intervention as the overall risk of progression to complete heart block is low. They can be discharged with safety netting, once electrolyte abnormalities have been ruled out.

Chest pain with acute bifascicular block can be a manifestation of proximal occlusion of the LAD. Patients should be thoroughly investigated with cardiac markers and echocardiography.

Syncope or pre-syncope is an indication for admission and monitoring as it suggests that there may be intermittent complete heart block and a permanent pacemaker (PPM) may be indicated.

  • The ESC recommends all symptomatic patients should undergo EPS10. A dual chamber permanent pacemaker (PPM) is indicated if there are positive findings on EPS, whereas an implantable loop recorder is recommended if EPS is negative or inconclusive.
  • The ESC also suggest that a PPM can be considered in selected patients with bifascicular block and unexplained syncope without EPS, for example in elderly, frail patients, high risk patients, or those with recurrent syncopal episodes.
  • The ACC/HRS also recommend a PPM is indicated in asymptomatic patients with chronic bifascicular block and
    • intermittent 3rd degree heart block
    • type II 2nd degree AV block
    • alternating bundle branch block11
  • The ACC/HRS also recommend considering a PPM in bifascicular block in the presence of neuromuscular disease (including myotonic muscular dystrophy, Kearns-Sayre syndrome, peroneal muscular dystrophy, and Erb’s dystrophy), irrespective of symptoms.

Learning bite

All symptomatic patients should be admitted under Cardiology for consideration of a PPM.

  • Failing to recognise bifascicular block – make sure to look for LAFB or LPFB in all cases of RBBB8.
  • Not recognising that new bifascicular block may be the only ECG change seen in patients with acute LAD occlusion.
  • Ventricular tachycardia (VT) can present with a bifascicular pattern. When VT originates in the left ventricle near the LPF it will present with a RBBB/LAFB pattern. When VT originates in the left ventricle near the LAF it will present with a RBBB/LPFB pattern. Make sure the ECG shows a supraventricular rhythm with bifascicular block rather than VT with a bifascicular pattern.
  • Atropine will not work for those patients who progress to episodes of trifascicular block (i.e. complete heart block) within the Emergency Department, as the block is below the AV node12. These patients will require pacing.
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  11. Epstein AE, DiMarco JP, Ellenbogen KA, et al. ACC/AHA/HRS 2008 guidelines for device-based therapy of cardiac rhythm abnormalities: executive summary: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines. Circulation.2008;117:2820–2840.
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