1. Practical Electrocardiography – Bundle Branch Block
Scott Ewing, D.O.
Cardiology Fellow
October 5, 2006

2. Syllabus Introduction Axis Determination
Atrial Arrhythmias, Bradycardias, and AV Conduction Block
Junctional and Broad Complex Tachycardias
Myocardial Ischemia and Acute Myocardial Infarction
Conditions Affecting the Left Side of the Heart
Conditions Affecting the Right Side of the Heart
Conditions Not Primarily Affecting the Heart
Exercise Tolerance Testing

3. Left Bundle Branch Block

4. LBBB

5. 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

6. 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

8. 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

9. 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 also important since it is often a marker of underlying organic heart disease (hypertensive heart disease, severe coronary disease, cardiomyopathy or valvular disease)

10. 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

11. 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
RV is activated and recovers earlier than the LV, recovery vectors are directed toward the right and away from the left
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

12. LBBB Clinical Significance
Usually patients with underlying heart disease
Significantly reduced long-term survival reflecting severity of underlying cardiac 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

13. 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

15. 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 left bundle branch block morphology with secondary ST-T abnormalities

17. 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
Hence, atrial flutter with 2:1 conduction and LBBB.

19. Interpretation: SR with 2:1 AV Block and LBBB
Left atrial abnormality (LAA) also noted
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.

21. Interpretation: NSR With LBBB
Sinus rhythm at 72 bpm with LBBB with QRS duration 0.16 second, normal AV conduction (PR.0.17 second) and a QT interval at the upper limits of normal (0.42 second)
History of hypertension and idiopathic cardiomyopathy with an LV EF 35%
Ruled out for a myocardial infarction
Serum potassium was normal
Acute MI cannot be ruled out by EKG alone in this context, the findings of tall right precordial T waves and J point elevations of this magnitude are consistent entirely with LBBB

22. Right Bundle Branch Block

23. RBBB

24. 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)

25. 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

27. 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

28. Causes RBBB Rheumatic heart disease Cor pulmonale / RVH
Myocarditis or cardiomyopathy
Ischemic heart disease
Degenerative disease of the conduction system
Pulmonary embolus
Congenital heart disease such as ASD

29. 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
Because LV activation remains relatively intact, the early portions of the QRS complex are normal

30. RBBB Mechanisms
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
The late and unopposed emergence of RV forces produces increased anterior and rightward voltage
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

31. 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

33. 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
The AV Wenckebach sequences are "atypical" in that the RR intervals do not progressively shorten
Complete RBBB
LAA also noted along with non-specific repolarization abnormalities

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

37. 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 (only in those leads with a terminal R'). Upright T waves in such leads might indicate ischemia, etc. 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: Bundle branch block, especially RBBB does not render the EKG uninterpretable!!

39. Interpretation: NSR With Prior MI and RBBB
EKG shows sinus rhythm 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

40. Acute Ischemia and LBBB

41. Acute Ischemia and LBBB
Many different electrocardiographic criteria have been proposed for identifying acute infarction with LBBB (none sufficiently sensitive)
Features indicating possible acute ischemia
ST↑ in leads with positive QRS complex “inappropriate concordance”
ST↓ in leads V1, V2, or V3 which have predominantly negative QRS complexes “inappropriate concordance”
Extreme ST↑ (>5 mm) in leads V1 and V2
If doubt persists, serial electrocardiograms may show evolving changes.

43. Interpretation: Inferior AMI with LBBB
Sinus bradycardia and LBBB with primary ST-T wave changes
LBBB morphology with primary biphasic and inverted T waves in leads 2, 3 and aVF
Uncomplicated bundle branch blocks should have "secondary" T wave changes
Inverted T waves suggest that a "primary" or ischemic process is evolving in the inferior distribution
Pt had a myocardial infarction with a CK of 700 and 21% MB fraction
Ischemic EKG changes can sometimes be read despite the presence of a bundle branch block

45. Interpretation: Anterior AMI with LBBB
Evidence of prior and possibly evolving MI superimposed on LBBB
Prior MI is indicated by Q waves as part of a qR in I and V6
Notching of the ascending limb of the S wave in the mid-left chest leads consistent with prior MI (Cabrera's sign)
Biphasic T waves in the mid-left chest leads raise consideration of evolving ischemia/MI
Statement that "LBBB precludes diagnosing MI" is not correct
Yet, LBBB often does mask changes of prior or acute MI

46. Review

47. Bundle Branch Block Review
QRS duration ≥120 ms
LBBB
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

48. 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

50. Interpretation: NSR 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
Note: there is some baseline artifact here that at times simulates a pacemaker stimulus--however the patient did not have an electronic pacemaker and the P waves and wide QRS are due to native conduction entirely

52. Interpretation: SR with 2:1 block and RBBB
Slow AV nodal conduction (note long PR of conducted beats) 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 (may have neural basis)

54. 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

56. Interpretation: NSR With PAC’s and LBBB
Frequent PACs which appear in a bigeminal pattern, accounting for the “group beating” pattern, simulating sinus rhythm with AV Wenckebach with 3:2 conduction
However, the 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)