1. Scott Ewing, D.O. Cardiology Fellow Lecture #4
Practical Electrocardiography - Ischemia, Infarction, and Bundle Branch Blocks
Scott Ewing, D.O.
Cardiology Fellow
Lecture #4

2. Review Heart Physiology Depolarization ECG Frontal Plane Rate Rhythm
QRS Axis

3. Heart Physiology: Sequence of Excitation
Figure 17.14a

4. Depolarization

5. Einthoven’s Electrocardiograph

6. Rate

7. Rhythm
Atrial
Junctional
Ventricular
Pacemaker
Last but not least

8. 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

9. 8-Step Method ECG Interpretation
Rate
Rhythm
QRS Axis
P wave
PR interval
QRS complex
QT interval
ST segment and T wave

10. Rate

11. Rhythm
Atrial
Junctional
Ventricular
Pacemaker
Last but not least

12. Acute Ischemia and Infarction

14. Current-of-Injury Patterns With Acute Ischemia / Infarction
Resultant ST vector is directed toward the inner layer of the affected ventricle and the ventricular cavity. Overlying leads therefore record ST depression
ST vector is directed outward with overlying leads recording ST elevation

15. Acute Ischemia / NQWMI / NSTEMI
Evolving ST-T changes over time without the formation of pathologic Q waves
Evolving ST-T changes may include any of the following patterns:
Convex downward ST segment depression
T wave flattening or inversion
Biphasic T wave changes
Combinations of above changes

16. Ischemic T Wave Changes

17. Ischemic T Wave Inversion

18. Ischemic Biphasic T Wave Changes

19. Acute Ischemia - T Wave Changes

20. Ischemic ST Changes

21. Acute Ischemia – ST Depression

22. Acute Ischemia – ST Depression

23. Acute Ischemia – ST Depression

24. 60-year-old Male

25. Anterior Ischemia NSR with ventricular ectopy LAD consistent with LAFB
T wave inversions in V2-V5 with subtle upward bowing of the ST segments
Symmetric T wave inversions, especially with upward bowing of the ST segments is highly suggestive of LAD ischemia
LHC showed significant LAD (and OM) disease

26. Elderly Male

27. Severe Multivessel Ischemia
NSR with profound ST segment depression, consistent with severe subendocardial ischemia and probable NQWMI
Profound ST depressions of this type usually indicate severe multivessel disease and sometimes LM disease
Patient experienced severe CP and was transferred in cardiogenic shock
En route, developed refractory PEA, ventricular fibrillation, and died

28. 84-year-old Female

29. NQWMI NSR with leftward QRS axis (-7°)
LVH may be associated with ST-T abnormalities (i.e. "strain pattern"), like those in lead aVL
Prominent horizontal or downsloping ST depressions in other leads (I, II, aVF, V5, V6) strongly suggestive of ischemia superimposed on LVH
Patient had positive cardiac enzymes and underwent LHC showing LM and 3V CAD, followed by CABG

30. Current-of-Injury Patterns With Acute Ischemia / Infarction
Resultant ST vector is directed toward the inner layer of the affected ventricle and the ventricular cavity. Overlying leads therefore record ST depression
ST vector is directed outward with overlying leads recording ST elevation

31. AMI /STEMI / Q Wave MI Most acute MI's are located in the LV
With proximal RCA occlusion, up to 50% may also have RV infarction as well
More leads with MI changes (Q waves and ST elevation), the larger the infarct size and the worse the prognosis
LAD and it's branches usually supply the anterior and anterolateral walls of the LV and the anterior two-thirds of the septum
LCX and its branches usually supply the posterolateral wall of the LV
RCA supplies the RV, the inferior (diaphragmatic) and true posterior walls of the LV, and the posterior third of the septum
RCA also gives off the AV nodal coronary artery in 85-90% of individuals; in the remaining 10-15%, this artery is a branch of the LCX

32. Evolution of ECG Changes
Normal ECG prior to MI
Hyperacute T wave changes - increased T wave amplitude and width; may also see ST elevation
Marked ST elevation with hyperacute T wave changes (transmural injury)
Pathologic Q waves, less ST elevation, terminal T wave inversion (necrosis)
Pathologic Q waves are usually defined as duration >0.04 s or >25% of R-wave amplitude
Pathologic Q waves, T wave inversion (necrosis and fibrosis)
Pathologic Q waves, upright T waves (fibrosis)

33. Evolution of ECG Changes

34. Evolution of ECG Changes

35. Infarct - ST Elevation

36. Inferior Infarct – ST Elevation

37. Posterior Infarct – ST Elevation!!!

38. Old Infarct - Anterior Q Waves

39. Old Infarct - Inferior Q Waves

40. Persistent ST Changes

41. Persistent T Wave Changes

42. 34 Year Old Male With Chest Pain

43. 34-year-old male with chest pain

44. Acute Anterior MI Acute anterior wall Q wave myocardial infarction
Reciprocal inferior ST depressions
Hyperacute T waves
Distribution of changes is consistent with a proximal LAD occlusion
Confirmed at LHC and treated with PTCA and stenting

45. 68-year-old female with chest pain

46. Acute Anterior MI Note Q waves and loss of R waves V1 - V4
ST elevation in V2 - V6
LAFB is also present, but does not account for the loss of R wave progression
LHC revealed 3-vessel disease with a 90% mid-LAD "culprit" lesion

47. 53-year-old female with chest pain

48. Acute Lateral MI ST elevations in I and aVL
Reciprocal ST depressions inferiorly consistent with acute lateral MI
Remember: ST elevations like this are never reciprocal but indicate the primary region of ischemia (diagonal or circumflex lesion)
Confirmed left circumflex occlusion at LHC

49. 36-year-old male with chest pain

50. Acute Pericarditis
Always consider myocardial infarction first when you see ST elevations
But don't forget the differential diagnosis of ST elevations
Ischemic heart disease
Pericarditis
Left bundle branch block (LBBB)
Normal ("early repolarization") variant
Two features here point to pericarditis
First, diffuseness of the ST elevations (I, II, III, aVF, V3-V6)
Second, PR depression in II, aVF, V4-V6 and PR elevation seen in aVR (attributed to subepicardial atrial injury)

51. 49-year-old male with chest pain

52. Acute Pericarditis Diffuse ST segment elevations (I, II, aVF, V2-V6)
Subtle PR segment deviations (elevated in aVR and depressed in the inferolateral leads)
ST elevations are due to a ventricular current of injury from the pericardial inflammation
PR changes are due to an associated atrial current of injury
Note that the PR and ST segment vectors point in opposite directions, i.e., PR up and ST down in aVR and PR down and ST up in inferolateral leads

53. Middle aged female with chest pain

54. Acute Myocardial Infarction
Marked inferior and lateral ST segment elevation
ST segment depression in anterior leads V1-V4
ST elevations (“current of injury” pattern) indicate transmural ischemia of the infero-lateral wall
ST depression most consistent with reciprocal change from the ST elevation generated by the acute posterior and lateral ischemia
Remember, acute pericarditis causes diffuse ST segment elevation (e.g., leads I, II, III, aVL, aVF, and the precordial leads)
Reciprocal ST depressions of the type seen here (V1-V4), are never a feature of pericarditis alone

55. 52-year-old male with chest pain

56. ST Elevation Myocardial Infarction
Slight inferior ST elevation with T wave inversion
Minimal reciprocal ST depression in aVL
Relatively low limb lead voltage makes these findings more subtle

57. Left Bundle Branch Block

58. LBBB

59. 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

60. 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

62. 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

63. 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

64. 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

65. 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

67. 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

69. 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

71. 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

73. Interpretation: NSR 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

74. Right Bundle Branch Block

75. RBBB

76. 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)

77. 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

79. 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

80. Causes RBBB 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)
Age related degenerative disease of the conduction system
Congenital heart disease such as ASD

81. 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

82. 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 ECG 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

84. 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

86. 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

88. 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 ECG uninterpretable!!

90. Interpretation: NSR 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

91. Acute Ischemia and LBBB

92. 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.

94. 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

96. 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

97. Review

98. 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

99. 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

101. 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

103. 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)

105. 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

107. 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)