1. Review

2. What rhythms are present?

3. What is this rhythm and simple description of rhythm abnormality?

4. What is the rhythm?

5. What is the rhythm?

6. What is the rhythm?

7. Bonus: What serious / life threatening abnormality is present?

8. ECG 101 - Bundle Branch Blocks -
Scott E. Ewing DO
Lecture #5

9. Heart Physiology: Sequence of Excitation
Figure 17.14a

10. QRS Axis (Frontal Plane)
Hexaxial diagram
Lead axis designated by angular position relative to lead I (0°)
Mean QRS electrical axis measured with respect to this display

11. Normal Conduction
Conditions required normal intraventricular impulse conduction
Left and right ventricles are not in an enlarged state that would prolong the time required for their activation and recovery
No myocardial ischemia or infarction to disrupt the spread of the activation and recovery waves
Rapid impulse conduction through the right- and left-ventricular Purkinje networks so that the endocardial surfaces are activated almost simultaneously
No accessory pathways for conduction from the atria to the ventricles

12. Left Bundle Branch Block

13. LBBB

14. Successive Ventricular Activation
Comparison of patterns of QRS morphology in lead V1 when the two ventricles are activated successively rather than simultaneously
A ventricular beat
Bundle branch block
Ventricular tachycardia.
Artificially paced ventricular rhythm

15. LBBB – Definition QRS duration ≥120 ms
Broad, notched R waves in lateral precordial leads (V5 and V6) and usually leads I and aVl
Small or absent initial R waves in right precordial leads (V1 and V2) followed by deep S waves
Absent septal Q waves in left-sided leads
Prolonged intrinsicoid deflection (>60 ms) in V5 and V6

16. LBBB Comparison Normal leads V1 and V6
Typical QRS-T patterns in RBBB and LBBB
Note the secondary T wave inversions in leads with an rSR' complex with RBBB and in leads with a wide R wave with LBBB

17. Normal ECG

18. Typical LBBB

19. Interpretation: NSR with LBBB
QRS duration 0.16 second
Broad, notched R waves in lateral precordial leads
Small or absent initial R waves in right precordial leads followed by deep S waves
Absent septal Q waves in left-sided leads
Prolonged intrinsicoid deflection (>60 ms) in V5 and V6
Secondary T wave changes such that the ST-T wave vector points opposite in direction of the major vector of the QRS

20. Interpretation: NSR with LBBB
Complete LBBB may be associated with a normal, leftward, or rarely rightward axis
LBBB may mask or mimic the pattern of underlying myocardial infarction
LBBB is important as often a marker of underlying organic heart disease
Hypertensive heart disease
Severe coronary disease
Cardiomyopathy
Valvular disease

21. LBBB Mechanisms Almost completely reorganized pattern of LV activation
Initial septal activation right septal surface, absence of normal septal Q waves
Excitation wave spreads slowly by conduction from muscle cell to muscle cell
LV endocardial activation requires additional 40 – 180 ms
QRS complex is prolonged and can be very wide
Once LV activation begins, it proceeds in a relatively simple and direct manner around the free wall and then to the base of the heart

22. LBBB Mechanisms
Activation across the LV projects positive forces to left-sided leads and negative ones to right-sided leads
Spread through working muscle fibers results in notching and slurring from discontinuous propagation
ST-T wave changes are generated by abnormalities in conduction, called secondary T wave abnormalities
ST-T wave changes produced by direct abnormalities of the recovery process are called primary T wave abnormalities (often ischemic in origin)

23. LBBB Clinical Significance
Usually patients with underlying heart disease
With CAD, correlates with more extensive disease, more severe LV dysfunction, and reduced survival rates
Duration of the QRS complex often inversely related to LV EF
Abnormal ventricular activation pattern induces hemodynamic perturbations
abnormal systolic function with dysfunctional contraction
reduced ejection fraction and lower stroke volumes
reversed splitting of the second heart sound
functional mitral regurgitation

24. LBBB Clinical Significance
Functional abnormalities in phasic coronary blood flow and reduced coronary flow reserve caused by delayed diastolic relaxation result in septal defects on exercise nuclear perfusion scans
Obscures or simulates other EKG patterns
Diagnosis of LVH is complicated by the increased QRS amplitude and axis shifts intrinsic to LBBB
Very high prevalence of LVH with LBBB makes defining criteria with high specificity difficult
Diagnosis of infarction may be obscured

26. Interpretation: Afib with LBBB
Coarse atrial fibrillatory waves (lead V1) may be mistaken for atrial flutter waves
With atrial fibrillation the atrial activity varies continuously and usually the ventricular response is completely variable
QRS complex here shows a typical LBBB morphology with secondary ST-T abnormalities

28. Interpretation: Atrial Flutter with 2:1 Conduction and LBBB
Wide-complex tachycardia
Classic LBBB pattern
If you look carefully, atrial activity in the limb leads, with negative polarity in lead II, at rate of 320 bpm
Thus, atrial flutter with 2:1 conduction and LBBB

30. Interpretation: SR with 2:1 AV Block and LBBB
Patient had a history of prior silent inferior MI, hypertension, and mitral regurgitation (the latter two factors accounting for the prominent LAA)
Underwent dual chamber pacemaker implantation for his 2:1 second-degree AV block with marked bradycardia
Location of the AV block was likely infranodal, given the presence of the LBBB and normal PR interval in the conducted beats

32. Interpretation: SR With LBBB
Sinus rhythm at 72 bpm with LBBB with QRS duration 0.16 second, normal AV conduction, QT interval at the upper limits of normal (0.42 s)
History of hypertension and idiopathic cardiomyopathy with an LV EF 35%
Acute MI cannot be ruled out by ECG alone in this context, the findings of tall right precordial T waves and J point elevations of this magnitude are consistent entirely with LBBB

33. Right Bundle Branch Block

34. RBBB

35. RBBB – Definition QRS duration ≥120 ms
Broad, notched R waves (rsr', rsR', or rSR' patterns) in right precordial leads (V1 and V2)
Wide and deep S waves in left precordial leads (V5 and V6)

36. RBBB Comparison Normal leads V1 and V6
Typical QRS-T patterns in RBBB and LBBB
Note the secondary T wave inversions in leads with an rSR' complex with RBBB and in leads with a wide R wave with LBBB

37. Normal ECG

38. Typical RBBB

39. Interpretation: NSR with RBBB
Sinus with RBBB
QRS duration > 0.12 second
rSR’ complex with a wide terminal R wave in V1
qRS complex with a wide S wave in V6
Secondary T wave changes
Usually associated with an underlying pathology causing RVH
COPD
Pulmonary hypertension
Atrial septal defect
Pulmonic stenosis
Also, age related degenerative changes
Finally, LAD occlusion in AMI since LAD typically supplies the proximal right bundle

40. RBBB Causes Age related degenerative disease of the conduction system
COPD
Pulmonary hypertension
Cor pulmonale / RVH
Pulmonic stenosis
Pulmonary embolus
Rheumatic heart disease
Myocarditis or cardiomyopathy
Ischemic heart disease (LAD typically supplies the proximal right bundle)
Congenital heart disease such as ASD

41. RBBB Mechanisms
Activation of the right side of the septum is initiated after slow transseptal spread of activation from the left septal surface
RV free wall then excited slowly, with variable participation of the specialized conduction system
Result is delayed and slowed activation of the RV with much or all of the RV undergoing activation after depolarization of the LV has been completed

42. RBBB Mechanisms
Because LV activation remains relatively intact, the early portions of the QRS complex are normal
Delayed activation of the RV causes prolongation of the QRS duration and a reduction in the cancellation of RV activation forces by the more powerful LV activation forces
Discordant ST-T wave patterns are generated by the same mechanisms as for LBBB; with RBBB, recovery forces are directed toward the earlier-activated LV and away from the RV

43. RBBB Clinical Significance
RBBB is common and often no evidence of structural heart disease
With new onset RBBB higher rate of CAD, CHF, mortality
With CAD, RBBB suggests advanced disease
RBBB interferes with other EKG diagnoses (lesser extent than LBBB)
RVH more difficult to make with RBBB because of the accentuated positive potentials in V1
Usual criteria for LVH can be applied but have lower sensitivities
Combination of LAA or LAD with RBBB suggests underlying LVH

45. Interpretation: SR with 2° Type I AV Block and RBBB
Sinus rhythm with 1° AV block and 2° Type I AV block
A 5:4 Wenckebach sequence is present in the middle of the recording
Complete RBBB
LAA also noted along with non-specific repolarization abnormalities

47. Interpretation: Atrial Flutter with 4:1 Conduction and RBBB
Flutter waves are well-seen in leads V1 and III
Rate of about 280 bpm, with a ventricular response at about 70 bpm
Classic RBBB pattern present
Patient had rheumatic mitral valve disease, moderate pulmonary hypertension, and tricuspid regurgitation

49. Interpretation: Anteroseptal MI with RBBB
Anterior precordial leads reveal a qR pattern marked ST elevation, and upright T waves
Three points are worth making with regard to a RBBB
Secondary T wave inversions are typically seen in the right precordial leads (leads with a terminal R'). Upright T waves in such leads might indicate ischemia. T wave inversions in leads with no terminal R' might also be ischemic
ST elevations are not normally seen in RBBB
Right precordial Q waves may be seen in RBBB without an infarct (especially in the setting of acute right ventricular overload), but if the Q waves extend past V2 or if they are slurred or wide, they suggest pathology
Bottom Line: RBBB does not render the ECG uninterpretable!!

51. Interpretation: SR With Prior MI and RBBB
SR with PAC’s
RBBB causing widely but physiologically split S2 on physical exam
Pathologic Q wave V1-V3 due to prior anteroseptal MI caused by left anterior descending occlusion

52. Fascicular Blocks

53. Conduction System
LAF and LPF indicate the left anterior and left posterior fascicles, respectively
(1), (2), and (3) indicate the locations at which intraventricular conduction abnormalities can produce alterations of the QRS complex and T wave

54. Conduction Anatomy LV opened to reveal the LBB and its fascicles
Anterior and posterior fascicles of the LBB are also designated superior and inferior, respectively, because these terms indicate their true anatomic positions

55. Conduction Anatomy LV viewed from apex upward towards base
Interventricular septum (S), LV free wall (FW), anterior (A) and inferior (I) regions of the LV
Typical appearances of the QRS complexes in leads I and aVF are presented for normal, LAFB, and LPFB LV activation

56. Left Anterior Fascicular Block
Left axis deviation (usually  -60 degrees)
Small Q in leads I and aVL, small R in II, III, aVF
Usually normal, sometimes slightly prolonged QRS duration
Late intrinsicoid deflection in aVL (> s)
Increased QRS voltage in limb leads

57. LAFB Mechanisms Initial activation of LV free wall via LPF
Activates inferior and rightward, thus Q wave leads I and aVL
Spreads superior and leftward, prominent R wave lead I and prominent S wave lead aVF
Left axis deviation to at least -45 degrees
QRS duration normal or prolonged s

58. Left Anterior Fascicular Block
53-year-old woman with no medical problems (A)
75-year-old man with a long history of poorly treated hypertension (B)
Arrows indicate the deep S waves in leads II, III, and aVF that reflect extreme left axis deviation

59. Left Posterior Fascicular Block
Right axis deviation (usually  120 degrees)
Small R in leads I and aVL, small Q in II, III, aVF
Usually normal, sometimes slightly prolonged QRS duration
Late intrinsicoid deflection in aVF (> s)
Increased QRS voltage in limb leads
No evidence of right ventricular hypertrophy

60. LAPB Mechanisms Initial activation of LV free wall via LAF
Activates superior and leftward, thus Q wave leads II, III, aVF
Spreads inferior and rightward, prominent R wave lead aVF and prominent S wave lead I
Right axis deviation to at least +90 degrees
QRS duration normal or prolonged s

61. Left Posterior Fascicular Block
Healthy 77-year-old woman
Arrows indicate the deep S waves in leads I and aVL typical of both LPFB and RVH

62. Bifascicular Block
RBBB with a LAFB or LPFB

63. Review

64. Bundle Branch Block QRS duration ≥120 ms LBBB RBBB
Broad, notched R waves in leads V5 and V6 and usually leads I and aVl
Small or absent initial r waves in leads V1 and V2 followed by deep S waves
Absent septal q waves in left-sided leads
Prolonged intrinsicoid deflection (>60 ms) in V5 and V6
RBBB
Broad, notched R waves (rsr', rsR', or rSR' patterns) in leads V1 and V2
Wide and deep S waves in leads V5 and V6

65. Bundle Branch Block Review
Normal leads V1 and V6
Typical QRS-T patterns in RBBB and LBBB
Note the secondary T wave inversions in leads with an rSR' complex with RBBB and in leads with a wide R wave with LBBB

67. Interpretation: SR With LBBB
Patient had hypertrophic obstructive cardiomyopathy with chronic LBBB
Note evidence of LAA
Most patients with LBBB have LVH
Presence of LAA with LBBB is also strongly suggestive of underlying LVH

69. Interpretation: SR with 2:1 block and RBBB
Slow AV nodal conduction and infra-nodal block of His-Purkinje disease
RBBB, also LAA and LVH
Dual-chamber pacemaker was implanted
Marked T-wave inversions in the anterolateral leads with QT prolongation, which was not due to MI or CAD
Prominent T-wave inversions like these have been reported after episodes of profound bradycardia and syncope

71. PSVT with RBBB Classic RBBB morphology (rsR' in V1) making VT unlikely
No definite atrial activity is seen (P waves or flutter waves)
Regular rate 150 bpm excludes afib
Flutter waves? No.
Rhythm most consistent with PSVT
Most likely AVNRT

73. Interpretation: SR With PAC’s and LBBB
Frequent PACs which appear in a bigeminal pattern, accounting for the “group beating” pattern, simulating SR with AV Wenckebach with 3:2 conduction
Second P wave in each couplet is premature and has a different morphology, since it comes from an ectopic atrial site
Biphasic P waves with prominent negative component in V1 indicative of LAA
Subtle but important supportive finding is the distinct notching of the ascending part of the S wave in lead V5 with the LBBB
This finding in leads V3-V5 with LBBB is referred to a Cabrera’s sign and is a marker of myocardial scarring due to myocardial infarction or other causes
Biventricular heart failure was present with severe LV dysfunction with a LV EF 20-25% and both MR and TR (due to chemotherapy-induced cardiomyopathy)

75. Interpretation: SR with LAFB
Pure LAFB causes marked LAD (-45 degrees to -90 degrees)
Typically with rS complexes in II, III, and aVF, and qR complexes in I and aVL
QRS duration of <120 ms
RS or Rs complexes may be seen in the left chest leads with left anterior fascicular block

77. Interpretation: SR with RBBB and LAFB
Complete RBBB with LAFB
RBBB causes the classic RSR' morphology in V1
LAFB causes the left axis deviation
Note: the subtle variation in P wave morphology here is due to baseline artifact and not to wandering atrial pacemaker

79. Interpretation: SR with RBBB and RAD probably due to LPFB
76 year old man with idiopathic CM and a wide QRS, no clinical/echocardiographic evidence of RVH, no clinically significant CAD by cardiac catheterization
Borderline sinus bradycardia (59 bpm), prolonged PR interval (250 ms) and RBBB with marked RAD
Upright P wave in lead I precludes left arm/right arm lead reversal
Three major causes of RBBB with RAD in adults
Right ventricular overload/hypertrophy syndromes, acute or chronic
Lateral MI with RBBB
RBBB with LPFB, a diagnosis of exclusion, requiring ruling out RV overload or lateral MI, in particular as causes of the RAD
Non-diagnostic Q waves in the infero-lateral leads here without clinical evidence of prior MI
This patient was referred for EP study because of findings of RBBB with alternating right and left axis deviation on other ECGs, consistent with severe His-Purkinje (infranodal) conduction disease
Finding confirmed at EPS which revealed a markedly prolonged HV interval (91 ms, increasing to 110 ms after procainamide infusion) with only a minimally prolonged AH interval (123 ms) at a baseline sinus cycle length of 993 ms (about 60 bpm)
Pt underwent dual chamber PPM implantation because of the high risk of progression to complete heart block