Ignatius Yansen

RSU Kabupaten Tangerang

 Intrinsic impairment of conduction in the right
bundle branches
 Can be chronic or intermittent
 Can be rate dependant
 Can be present without cardiac disease
 Most often due to CAD or HTN causing ischemic or
degenerative changes
 Best recognized in precordial leads V1-V6
 Wide QRS complex > 0.12 s
 V1:
 Large terminal R’ waves with rR’ or rsR’ configuration
 Onset of intrinsicoid deflection (R peak time) > 0.05 s
 V6:
 Wide terminal S waves are present
 Septal q waves are preserved
 No Axis changing
 Physiologically On ECG

Unblocked R
ventricle R’
Blocked
ventricle

Two QRS’s out of ‘sync’ Single, wide QRS

• The initial QRS deflection
represents the septum
depolarizing from left to right.
This conduction is mediated by
the septal fascicle arising from
the left bundle branch
• The initial QRS is unchanged in
RBBB because conduction is
independent of the right bundle
branch
• Following the initial QRS, the left
ventricle rapidly depolarizes via
conduction from the LAF and LPF.
• The right ventricle is delayed.
• This produces a QRS vector oriented
to the left and posterior.
• The left ventricle is normally
dominant during the QRS and thus
the EKG still shows no abnormally
• Following left ventricular depolarization,
there continues to be delayed
depolarization of the right ventricle via
slow myocyte-to-myocyte spread.
• The right ventricle is now the dominate
electrical force and therefore the
terminal QRS vector is oriented to the
right and anterior. This shows on an ECG
as an additional tall upright R’ wave in V1
and a deep S wave in V6.
 Initial QRS remains
normal
 Middle portion of
QRS remains normal
 Terminal QRS is
sluggish and
dominated by right
ventricular forces
V1 = rSR’
V6 = qRS
 Uncomplicated: ST segment and T waves
normally discordant and opposite in direction
to the terminal portion of QRS complex.
 Myocardial abnormality: ST and T waves are
concordant with the terminal portion of QRS
complex  cardiomyopathy, myocardial
ischemia
 Incomplete RBBB has all the features of RBBB
except duration of QRS complex < 0.12 s
 RBBB often intermittent before it becomes
fixed. Usually rate related
 Incidence increases with age
 Can occur as a normal variant
 Most common cause is CAD (LAD)
 Other causes include both structural and functional causes
 Structural: anything causing RV dilatation or
hypertrophy, (acute PE, cor pulmonale, DCM, ect),
trauma (right heart cath, steering wheel, CABG,
ablation)
 Functional: rate-related bundle branch block
 Myocardial infarction
 Pulmonary embolism
 Chronic obstructive lung disease/cor pulmonale
 Pulmonary hypertension (primary or secondary)
 Hypertensive heart disease
 Degenerative disease of the conduction system
 Brugada syndrome
 Arrhythmogenic RV dysplasia
 Cardiomyopathy
 Chagas disease
 Congenital heart disease (eg, Ebstein anomaly)
 Prognosis depends on underlying etiology
 Worse prognosis for patients with type II second
degree atrioventricular (AV) block or
multifascicular block
 Generally good prognosis for patients without
underlying heart disease
 NO treatment necessary for isolated asymptomatic
RBBB
 Pacing may be necessary for symptomatic patients
or those with other AV or multifascicular block
 Ectopic Ventricular impulses
 Ventricular tachycardia
 Accelerated idioventricular rhythm
 True RBBB
 Sinus or supraventricular
 RBBB and stress testing still reliable
 RBBB and MI : RBBB does not concealed the
ECG changes associated in Q wave MI.
 RBBB and severe HF : CRT candidate
 Auscultatory findings: delayed closure of
pulmonary valves  wide splitting in second
heart sound