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ECG 101 - Ischemia and Infarction -

ECG 101 - Ischemia and Infarction -. Scott E. Ewing DO Lecture #7. Review. Heart Physiology Depolarization ECG Frontal Plane Rate Rhythm QRS Axis. Heart Physiology: Sequence of Excitation. Figure 17.14a. Einthoven’s Electrocardiograph. Rate. Rhythm. Atrial Junctional Ventricular

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ECG 101 - Ischemia and Infarction -

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  1. ECG 101- Ischemia and Infarction - Scott E. Ewing DO Lecture #7

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

  3. Heart Physiology: Sequence of Excitation Figure 17.14a

  4. Einthoven’sElectrocardiograph

  5. Rate

  6. Rhythm • Atrial • Junctional • Ventricular • Pacemaker • Last but not least

  7. 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

  8. Acute Ischemia and Infarction

  9. 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

  10. 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

  11. Ischemic T Wave Changes

  12. Ischemic T Wave Inversion

  13. Ischemic Biphasic T Wave Changes

  14. Acute Ischemia - T Wave Changes

  15. Ischemic ST Changes

  16. Acute Ischemia – ST Depression

  17. Acute Ischemia – ST Depression

  18. Acute Ischemia – ST Depression

  19. 60-year-old Male

  20. 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

  21. Elderly Male

  22. 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

  23. 84-year-old Female

  24. 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

  25. 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

  26. 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

  27. Evolution of ECG Changes • Normal ECG prior to MI • Hyperacute T wave changes - increased T wave amplitude and width • Marked ST elevation with hyperacute T wave changes (transmural injury) • Pathologic Q waves, less ST elevation, terminal T wave inversion (necrosis) • Pathologic Q waves 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)

  28. Evolution of ECG Changes

  29. Evolution of ECG Changes

  30. Infarct - ST Elevation

  31. Inferior Infarct – ST Elevation

  32. Old Infarct - Anterior Q Waves

  33. Old Infarct - Inferior Q Waves

  34. Persistent ST Changes

  35. Persistent T Wave Changes

  36. 34-year-old male with chest pain

  37. 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

  38. 68-year-old female with chest pain

  39. 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

  40. 53-year-old female with chest pain

  41. 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 LCX occlusion at LHC

  42. 36-year-old male with chest pain

  43. 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)

  44. 49-year-old male with chest pain

  45. 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

  46. Middle aged female with chest pain

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

  48. 52-year-old male with chest pain

  49. 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

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