1. Left bundle branch block (LBBB) is a conduction abnormality caused by impaired conduction in the left bundle branch or its fascicles. 2. LBBB can be chronic or intermittent and is often caused by coronary artery disease or hypertension. 3. On ECG, LBBB is characterized by a QRS duration ≥120ms and other abnormalities including broad R waves and abnormal ST-T wave patterns. 4. LBBB can make ECG diagnosis of myocardial infarction difficult and criteria like Sgarbossa scores are used to help identify MI in the setting of LBBB.

1. LBBB
DR. ASWIN R. M.

2. ANATOMY

3. BLOOD SUPPLY
• HIS BUNDLE – LAD + AV NODAL ARTERY
• PROXIMAL RBBB – LAD + AV NODAL ARTERY
• DISTAL RBBB – LAD
• LAF – LAD
• LPF – DUAL SUPPLY IN MOST CASES RCA+LCX

4. BUNDLE BRANCH BLOCKS
• Intrinsic impairment of conduction in the left or
right bundle branches or its branches
• Can be chronic or intermittent
• Can be rate dependent
• Can be present without cardiac disease
• Most often due to CAD or HTN causing ischemic or
degenerative changes

5. LBBB
• Considered as Bifascicular block
• Complete LBBB
– Disease in main LBB (predivisional)
– Or in both of its fascicles (postdivisional).

6. LBBB EPIDEMIOLOGY
• ~ 1 % (0.2 to 1.1 % in different populations)
• Incidence Increases with age
• Etiology Structural and functional
• Structural
– CAD
– ACS
– Cardiomyopathy
– SHTN
– Aortic valve disease
– Post cardiac surgery esp aortic root surgeries
• Functional
– Rate dependent BBB

7. LBBB
1. QRS duration greater than or equal to 120 ms in adults, greater than 100 ms in
children 4 to 16 years of age, and greater than 90 ms in children less than 4
years of age.
2. Broad notched or slurred R wave in leads I, aVL, V5, and V6 and an occasional
RS pattern in V5 and V6
3. Absent q waves in leads I, V5, and V6, but in the lead aVL, a narrow q wave
may be present in the absence of myocardial pathology.
4. R peak time greater than 60 ms in leads V5 and V6 but normal in leads V1, V2,
and V3, when small initial r waves can be discerned in the above leads.
5. ST and T waves usually opposite in direction to QRS.
6. Positive T wave in leads with upright QRS may be normal (positive
concordance).
7. Depressed ST segment and/or negative T wave in leads with negative QRS
(negative concordance) are abnormal
8. The appearance of LBBB may change the mean QRS axis in the frontal plane to
the right, to the left, or to a superior, in some cases in a rate-dependent
manner.
AHA/ACCF/HRS Recommendations for the Standardization and Interpretation of the Electrocardiogram

8. STRICT CRITERIA
• QRS ≥ 140 ms for men and ≥130 ms for women
• QS or rS in V1-V2
• Mid-QRS notching or slurring in ≥2 contiguous leads

9. INCOMPLETE LBBB
1. QRS duration between 110 and 119 ms in adults, between 90 and 100 ms
in children 8 to 16 years of age, and between 80 and 90 ms in children
less than 8 years of age.
2. R peak time greater than 60 ms in leads V4, V5, and V6.
3. Absence of q wave in leads I, V5, and V6.
MECHANISM
1. Slowed conduction through the LBBB
2. Enlargement of the left ventricle – prolongation of the QRS complex
that mimics incomplete LBBB (
3. LBB has multiple fascicles, involvement of few major fascicles but not
all.
AHA/ACCF/HRS Recommendations for the Standardization and Interpretation of the Electrocardiogram

10. NONSPECIFIC OR UNSPECIFIED
INTRA VENTRICULAR
CONDUCTION DISTURBANCE
• QRS duration greater than
 110 ms in adults
 90 ms in children 8 to 16 years of age
 80 ms inchildren less than 8 years of age
 without criteria for RBBB or LBBB.
• RBBB criteria in the precordial leads and LBBB
criteria in the limb leads, and vice versa.

11. ECG CAHNGES
MECHANISM
• Block in conduction system myocardial spread of
electrical activity (cell to cell conduction)
• Ventricles depolarized successively rather than
simultaneously

13. SECONDARY ST T
WAVE CHANGES

14. RATE DEPENDENT
BUNDLE BRANCH BLOCK
• Tachycardia or Bradycardia dependent BBB
• HR at which BBB manifests-critical HR
• Reproducible each time
• Tachycardia dependent BBB
– Phase 3 aberrancy
– When impulses are transmitted at a faster rate than the
ability to repolarize from prior impulse in that part of
conducting system.
• Bradycardia dependent BBB
– Phase 4 aberrancy
– Due to gradual loss in transmemebrane resting potential
from prolonged diastole ( subsequent excitation from a
much negative potential)

15. ASHMAN PHENOMENON
• Gouaux and Ashman in 1947
• Aberrant ventricular conduction due to a change in
QRS cycle length
• More often affects RBB(longer RP)
• In AF, when a relatively long cycle is followed by a
relatively short cycle, the beat with a short cycle
often has bundle-branch block morphology.
• Refractory period proportionate to R-R interval
• Will be diagnosed as VPC

16. EXERCISE INDUCED
LBBB
• 0.4%-0.5% of patients undergoing exercise tests.
• May not specifically indiates underlying CAD
• But many studies observed higher rates of mortality
in such patients.

17. LBBB CLINICAL
EXAMINATION
• Narrow or paradoxical splitting of 2nd heart sound

18. LBBB ECHO
• ABNORMAL SEPTAL MOTION
– Early systolic movement of IVS towards the center of
LV followed by movement away from the center of LV
(paradoxical movement)
– Mimics RWMA
• BASAL & MID SEGMENTS
• APEX-ROCKING MOVEMENT
• PRESERVED THICKNESS USUALLY
• TEMPORAL DYSSYNCHRONY
• NORMAL LV GEOMETRY
• EARLY SYSTOLIC BEAKINIG OF IVS IN M MODE

19. LBBB ECHO

20. LBBB ECHO
 M-mode echo - early systolic downward motion of the ventricular septum
 Seen just after the peak R wave on ECG or just at the closing of mitral valve.

21. TISSUE DOPPLER
Septal flash

22. LBBB ECHO
ISCHEMIC RWMA LBBB RV PACED
MAXIMAL
LOCATION
DISTAL SEPTUM,
APEX ,
ANTERIOR WALL,
PROXIMAL /MID
ANTERIOR SEPTUM
DISTAL SEPTUM
OFTEN INFERIOR
THICKNESS THINNING PARTIALLY
PRESERVED
PARTILLY
PRESERVED
ABNORMAL
GEOMETRY
COMMON UNCOMMON UNCOMMON
TEMPORAL
DYSYNCHRONY
NO YES YES

23. LBBB & MI
Known LBBB patient
with ACS symptoms
Patient with ACS
symptoms on taking
ECG shows LBBB

24. LBBB & MI
• 2% of all patients who present with a suspected ACS
• Unique diagnostic and therapeutic challenge
• ECG changes of LBBB can mask & mimics acute MI
changes
• Not all new onset or presumed new onset LBBB is due
to coronary artery disease
• More likely to be older, female, and have a history of
pre-existing cardiovascular disease, hypertension, and
congestive heart failure than non-BBB patients with ACS
• These patients are at increased risk of adverse
outcomes – Not due to LBBB but by underlying ischemic
and structural heart disease that has contributed to
LBBB

25. HOW TO APPROACH
• 2004 ACC/AHA STEMI guidelines -New or presumed new onset
LBBB is considered STEMI equivalent
• LBB more diffuse structure than RBB – LBBB as part of MI
indicates extensive myocardial damage ( very rarely discrete
lesion in proximal conduction system).
• Newer studies has shown that Transmural MI as a cause of LBBB is
uncommon
• 2013 ACC/AHA STEMI guidelines –
– Has to be considered as STEMI equivalent.
– But not in isolation as new or presumed new onset STEMI are
infrequent
– Sgarbossa criteria should be also considered
• ESC 2017 –
– ECG diagnosis of STEMI difficult with LBBB.
– Concordant ST elevation best indicator of ongoing ischemia
– Clinical suspicion of ongoing Ischemia LBBB should be managed
similar to STEMI patients

26. SGARBOSSA CRITERIA
•ST-elevation of ≥1 mm and concordant with the
QRS complex5 points
•ST-segment depression ≥1 mm in lead V1, V2, or V33 points
•ST elevation ≥5 mm and discordant with the QRS
complex2 points
 Proposed in 1996
 To diagnose AMI in the setting of a known chronic LBBB.
 Current data shows usefulness in new or indeterminate-age LBBB also
• Score of ≥ 3 has specificity for AMI greater than 95% and is associated with higher
30-day mortality compared with LBBB patients with discordant ST-segment
elevation alone
• Sensitivity of a Sgarbossa score of ≥ 3 is only approximately 20%

27. SGARBOSSA POSITIVE

28. MODIFIED SGARBOSSA
CRITERIA
A. ≥ 1 lead with ≥1 mm of concordant STelevation
B. ≥ 1 lead of V1-V3 with ≥ 1 mm of concordant ST
depression
C. ≥ 1 lead anywhere with ≥ 1 mm STE and proportionally
excessive discordant STE, as defined by ≥ 25% of the
depth of the preceding S-wave.
Any of above three is STEMI equivalent
Improved sensitivity but with reduced specificity compared
with the original Sgarbossa criteria (90 vs. 98%)

29. OTHER SIGNS OF MI IN
LBBB
• The presence of QR complexes in leads I, V5, or V6 or
in II, III, and avf with LBBB strongly suggests
underlying infarction
• Prominent notching of the ascending part of a wide S
wave in the midprecordial leads (V3 V4) -Cabrera's
sign
• Prominent notching in ascending limb of a wide R
wave in lead I, aVL, V5, or V6 - Chapman's sign

30. CABRERA'S SIGN
prominent (0.05 sec) notching in the
ascending limb of the S wave in leads
V3 and V4;

31. CHAPMAN'S SIGN
Prominent notching in ascending limb of a wide R wave
in lead I, aVL, V5, or V6

32. PROPOSED NEW
CRITERIA
• Cai et al

33. RADIONUCLEOTIDE
MYOCARDIAL PERFUSION
IMAGING
• Stress ECG not usefull in LBBB
• For evaluation of underlying CAD
• Both Excersise & Pharmacologic
• Excersise testing
– High incidence of false positive results in septal &
anteroseptal
– More apparent with tachycardia associated with
excersise
– Perfusion defects in the inferior and lateral zones are
not LBBB-related – signifies LCX or RCA disease

34. PHARMACOLOGIC
STRESS TESTING
• Preferred over exercise testing
• Dobutamine testing has same disadvantage as
exercise testing
• Should preferentially undergo Vasodilator
(dipyridamole or adenosine) radionuclide imaging
ACC/AHA/ASNC Guidelines for the Clinical Use of Cardiac Radionuclide Imaging

35. IMPACT ON LV FUNCTION
Normal heart, closely tuned electrical function – results
in a cordinated sequence of mechanical function results
in efficient
Biventricular filling,
contraction
Relaxation
& pump function
LBBB – Dysynchronous mechanical activity of different
part of heart

36. AV DYSYNCHRONY
• There is a delay between atrial and ventricular
contraction
• Reduced LV filling
– shortened ventricular filling time
– superimposition of atrial contraction on early passive
filling,
• The ratio between LV diastolic filling time and duration of
a complete cardiac cycle (A LV filling time of < 40%
cardiac cycle is indicative of A-V dys.)
• It can also be associated with late diastolic (presystolic)
mitral regurgitation (MR).

37. INTERVENTRICULAR
DYSSYNCHRONY
• Delay between RV and LV activation.
• RV contraction will precede LV contraction
• abnormal septal motion
• and a decreased LV Function

38. INTERVENTRICULAR
DYSSYNCHRONY
• Normal ventricular activation sequence is disrupted,
resulting in
• Dis cordinated contraction of the LV segments.
• Those LV wall segments, which contract early (ex septum),
do not contribute to the LV output,
• Late contracting segments do so at a higher wall stress – are
hypercontractile stretches the early contracting segments
• Asymmetric hypertrophy and assymetric LV dilatation
• MR worsens
– LV remodeling
– Presystolic regurgitation
– delayed contraction of papillary muscle rootattachments.

39. LV FUNCTION AND LBBB

40. INTRAVENTRICULAR
DYSYNCHRONY
• Inter-ventricular mechanical delay(IVMD) &LV PEF

41. • Inter-ventricular mechanical delay(IVMD) values of
> 40 ms
• LV PEP of > 140 ms are considered pathological
Pulse tissue Doppler for IVMD
• The time from QRS onset to the peak myocardial
systolic velocities (Sm) of the RV free wall (tricuspid
annulus) versus the same time of LV lateral mitral
annulus (apical 4-chamber view)

42. INTRAVENTRICULAR
DYSYNCHRONY
Septal-to-posterior wall motion delay SPWMD
• Difference in timing of septal and posterior wall
contraction
• M-mode in PLAX
• SPWMD is the difference between the time from
the onset of ECGderived Q wave to the initial peak
posterior displacement of the septum, and the time
from the onset of QRS to the peak systolic
displacement of posterior wall

43. • SPWMD> 130 ms was considered pathological

44. • Lateral wall post-systolic displacement LWPSD
• Difference of
• QRS onset to maximal systolic displacement of the
basal LV lateral wall(assessed by M-mode in the
apical 4-chamberview)
• QRS onset to the beginning of transmitral E velocity
(assessed by pulsed Doppler of mitral inflow)
• Positive LWPSD, i.e. a longer interval -severe post
systolic contraction
• Independent predictor of CRT response

45. Pulsed Tissue Doppler – used to measure
• time interval between the onset of ECG derived QRS
and the Sm peak (= time to Sm peak)
• time interval between the onset of QRS and the
onset of Sm (= time to Sm onset), which correspond
to LV PEP
• Intra-ventricular mechanical delay has been defined
for differences of > 65 ms of time to Sm Peak
between LV segments

47. 3-D Echocardiography
• allows intraventricular dyssynchrony to be
evaluated by analyzing LV wall motion in multiple
apical planes during the same cardiac cycle.
• It also offers better spatial resolution thana single
plane.

48. CRT IN LBBB
CRT or biventricular pacing aims at eliminating the
electrical dysynchrony

49. CRT INDICATIONS IN WIDE QRS
LVEF NYHA
LBBB
or Not
ECG ACC/AHA ESC
<35 II III IV(ambulatory) LBBB SR QRS >150 Class I Class I
<35
II III IV(ambulatory)
LBBB
SR QRS 120-149
ms
Class IIa
Class I
III IV(ambulatory
Non
LBBB
SR QRS >150
Class IIa (NYHA
II also)
<35
II
Non
LBBB
SR QRS >150
Class IIb
Class IIa
III IV(ambulatory)
SR QRS 120-149
ms
Class IIb (NYHA
II also)
<30
I – Ischemic cause
of heart failure
LBBB
SR QRS >150

50. PACING IN LBBB
• Patient with syncope
2013 ESCGuidelines on cardiac pacing and cardiac resynchronization therapy

51. PACING
Class I
• LBBB + unexplained syncope and abnormal EPS
– HV interval ≥70 ms.
– Second- or third-degree His-Purkinje block
demonstrated during incremental atrial pacing or with
pharmacological challenge.
• Alternating BBB
Class IIb
• BBB + unexplained syncope & non diagnostic
investigations.
– Pacing may be considered in selected patients
Class III
• Asymptomatic BBB

52. THANK YOU