The bifascicular block is due to a coronary blood supply occlusion or mechanotrauma to the fascicle. Because of a single coronary artery blood supply to the anterior fascicle or it's relationship with left ventricular outflow tract, the involvement of the left anterior fascicle is more common than left posterior fascicle. The block of two fascicles, the heart's electrical impulse is conducted through one fascicle.
Differentiating bifascicular block from other Diseases
Bifascicular block must be differentiated from other diseases that cause similar ECG findings, such as:
Ventricular tachycardia: Ventricular tachycardia is associated with atrioventricular dissociation which makes it different from the supraventricular rhythm with bifascicular block.
Accelerated idioventricular rhythm: Accelerated idioventricular rhythm is associated with atrioventricular dissociation which makes it different from the supraventricular rhythm with bifascicular block.
Wolff-Parkinson-White syndrome: The short PR interval which is not typically seen in bifascicular block can help in differentiating between bifascicular block and ventricular pacing.
Right ventricular and biventricular pacing: The presence of pacemaker spikes in ventricular pacing can help in differentiating between bifascicular block and ventricular pacing.
Epidemiology and Demographics
The bifascicular block occurs in approximately 1 to 2 % of adult population.
Patients of all age groups may develop bifascicular block.
Bifascicular block is more commonly observed among elderly patients. The highest incidence of bifascicular block was observed in males aged 70-74 years and females older than 80 years.
Causes:
Common causes of bifascicular block development include :
Ischemic hear disease
Hypertension
Anterior MI
Hyperkalemia
Degeneration of conduction system in Lev's disease
Congenital heart disease
Structural heart disease
Aortic valve disease (especially aortic stenosis)
Natural History, Complications and Prognosis
The majority of patients remain asymptomatic until the progression of bradycardia due to atrioventricular block.
The bifascicular block may progress to atrioventricular block in 1 to 4% of individuals and in 17% of symptomatic individuals annually. The risk of complete atrioventricular block is increased in patients with a first-degree atriventricular block.
Common complications of bifascicular block include ventricular tachycardia and complete heart block.
The long-term prognosis in patients with symptomatic bifascicular block is poor. The mortality of patients with bifascicular block is ranged between 2% to 15% with a 9% risk of sudden death. A higher mortality rate (29-38%) was reported in patients with syncope in the setting of structural heart disease and low left ventricular ejection fraction. However, the progression of bifascicular block to complete heart block is infrequent in asymptomatic patients.[2]
Diagnosis
Diagnostic Criteria
Bifascicular block is diagnosed on ECG.
Findings on ECG include: 1) right bundle branch block and left anterior fascicular block, or 2) right bundle branch block and left posteror fascicular block, or 3) left anterior fascicular block and left posterior fascicular block.
The ECG findings in right bundle branch block include: 1) supraventricular rhythm, 2) QRS complex ≥ 120 ms, 3) slurred S-wave in lead I, 4) Terminal R-wave in lead V1.
The ECG findings in left anterior fascicular block include: 1) left axis deviation, 2) presence of rS complexes in inferior leads, 3) qR complexes in high lateral leads, 4) widening of QRS complexes
The ECG findings in left posterior fascicular block include: 1) right axis deviation, 2) qR complexes in inferior leads, 3) rS complexes in high lateral leads, 4) widening of QRS complexes Surawicz, Borys (2008). Chou's electrocardiography in clinical practice : adult and pediatric. Philadelphia, PA: Saunders/Elsevier. ISBN9781437711028.
Symptoms
Most of the patients with bifascicular block are aysmptomatic.
Symptoms of bifascicular block may include the following:
Pre-syncope
Syncope
Sudden death
Physical Examination
Patients with bifascicular block do not have any specific signs in the physical examination.
Bradycardia may be present.
Laboratory Findings
Hyperkalemia may cause development of bifascicular block. Potassium level should be checked in patients with bifascicular block.
Imaging Findings
There are no imaging findings associated with bifascicular block.
Treatment
Patients with asymptomatic bifascicular block do not need any treatment [3].
Patients with acute bifascicular block may need a temporary pacemaker due to the possibility of complete heart block development.
In patients with chronic bifascicular block, pacemaker implantation is needed in symptomatic patients, particularly syncope. It is also indicated in asymptomatic patients with intermittent third-degree, type II second-degree AV block, or alternating bundle branch block. Asymptomatic patients who undergo electrophysiologic study and have an incidental finding of prolonged HV interval (> 100 ms) or block below the His at long cycle length may need permanent pacing. Another indication for pacemaker therapy is the presence of neuromuscular disease (myotonic muscular dystrophy, Kearns-Sayre syndrome, peroneal muscular dystrophy, Erb's dystrophy) regardless of the presence of symptoms. [4]
Prevention
There are no primary preventive measures available for [disease name].
Effective measures for the primary prevention of [disease name] include [measure1], [measure2], and [measure3].
Once diagnosed and successfully treated, patients with [disease name] are followed-up every [duration]. Follow-up testing includes [test 1], [test 2], and [test 3].
2012 ACC/AHA/HRS Guidelines for Device-Based Therapy of Cardiac Rhythm Abnormalities (DO NOT EDIT)[5][6]
Permanent Pacing in Chronic Bifascicular Block (DO NOT EDIT)[6]
"2. Permanent pacemaker implantation is reasonable for an incidental finding at electrophysiological study of a markedly prolonged HV interval (greater than or equal to 100 milliseconds) in asymptomatic patients. (Level of Evidence: B)[21]"
"3. Permanent pacemaker implantation is reasonable for an incidental finding at electrophysiological study of pacing-induced infra-His block that is not physiological. (Level of Evidence: B)[33]"
↑Olshansky, Brian; Chung, Mina K.; Pogwizd, Steven M.; Goldschlager, Nora (2017). "Bradyarrhythmias—Conduction System Abnormalities": 28–86. doi:10.1016/B978-0-323-39968-5.00002-0.
↑Vijayaraman, Pugazhendhi; Ellenbogen, Kenneth A. (2017). "Atrioventricular Conduction System Disease": 399–453. doi:10.1016/B978-0-323-37804-8.00014-6.
↑Schurmann, Paul; Valderrábano, Miguel (2018). "Cardiac Pacing for Bradycardia, Heart Block, and Heart Failure": 344–351. doi:10.1016/B978-0-323-47870-0.00038-6.
↑Epstein AE, DiMarco JP, Ellenbogen KA, Estes NA, Freedman RA, Gettes LS, Gillinov AM, Gregoratos G, Hammill SC, Hayes DL, Hlatky MA, Newby LK, Page RL, Schoenfeld MH, Silka MJ, Stevenson LW, Sweeney MO, Tracy CM, Epstein AE, Darbar D, DiMarco JP, Dunbar SB, Estes NA, Ferguson TB, Hammill SC, Karasik PE, Link MS, Marine JE, Schoenfeld MH, Shanker AJ, Silka MJ, Stevenson LW, Stevenson WG, Varosy PD (2013). "2012 ACCF/AHA/HRS focused update incorporated into the ACCF/AHA/HRS 2008 guidelines for device-based therapy of cardiac rhythm abnormalities: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines and the Heart Rhythm Society". J. Am. Coll. Cardiol. 61 (3): e6–75. doi:10.1016/j.jacc.2012.11.007. PMID23265327.
↑ 6.06.16.2 Epstein AE, DiMarco JP, Ellenbogen KA, Estes NAM III, Freedman RA, Gettes LS, Gillinov AM, Gregoratos G, Hammill SC, Hayes DL, Hlatky MA, Newby LK, Page RL, Schoenfeld MH, Silka MJ, Stevenson LW, Sweeney MO. 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 (Writing Committee to Revise the ACC/AHA/NASPE 2002 Guideline Update for Implantation of Cardiac Pacemakers and Antiarrhythmia Devices). Circulation. 2008; 117: 2820–2840. PMID 18483207