Practical Electrocardiography - Ischemia, Infarction, and Bundle Branch Blocks

1. 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’sElectrocardiograph

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)