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ECG Changes in Myocardial Infarction

ECG Changes in Myocardial Infarction. Clerk Karen G. Amoloza. Myocardial Infarction. Death or necrosis of myocardial cells Diagnosis at the end of the spectrum of myocardial ischemia or acute coronary syndromes Ischemia  Injury  Infarction

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ECG Changes in Myocardial Infarction

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  1. ECG Changes in Myocardial Infarction Clerk Karen G. Amoloza

  2. Myocardial Infarction • Death or necrosis of myocardial cells • Diagnosis at the end of the spectrum of myocardial ischemia or acute coronary syndromes • Ischemia  Injury  Infarction • Occurs when myocardial ischemia exceeds a critical threshold and overwhelms myocardial cellular repair mechanisms that are designed to maintain normal operating function and hemostasis

  3. ECG on diagnosis of MI • cornerstone in diagnosis of acute and chronic IHD • Factors: • Nature of the process: reversibility (ischemia vs infarction) • Duration: acute vs chronic • Extent: transmuralvssubendocardial • Localization: anterior vsinferoposterior • Presence of other underlying abnormalities: chamber enlargement/hypertrophy, conduction defects

  4. Ischemia • Decrease in the perfusion of a certain area of the myocardium • Temporary, reversible reduction of blood supply • Earliest manifestation of reduced coronary blood flow

  5. Ischemia: ECG changes T wave • Normal T waves • ventricular repolarization • Same direction as and smaller than QRS complex • Upright, asymmetrical • T wave changes • Deeply inverted, symmetrical

  6. Ischemia: ECG changes Pseudonormalization of the T wave • Reversal to a normal upright T wave • Acute ischemia in patients with pre-existing T wave inversion from a past event

  7. Injury • Acute, prolonged, reduction in blood supply to the myocardium • Reversible

  8. Injury: ECG changes ST segment elevation • Subepicardial injury (outer ventricular wall) • Minutes to hours of an acute event • “Coved” or convex • upward displacement of the ST segment from the baseline • Factors: • Atherosclerosis with sudden clot formation • Coronary Artery Spasm (Prinzmetal’s Angina)

  9. Injury: ECG changes ST segment depression • Subendocardial injury (inner ventricular wall) • Small penetrating branches of the superficial epicardial coronary arteries • Poor perfusion • First area of the myocardium to sustain injury

  10. Injury: ECG changes ST segment depression • Clinical indicator of coronary artery disease during stress test • Assessment of Severity • Morphology (magnitude ands slope) during exercise • Duration of ST segment depression after exercise

  11. Infarction: ECG Changes Q waves • Indicate a loss of viable myocardium • May develop 1 to 2 hours after the onset of symptoms but can take anywhere from 12 to 24 hours to develop

  12. Infarction: ECG Changes Q waves • Insignificant Q waves • Small Q waves • <25% of the height of the adjacent R wave • Normal: Leads I, aVL, V5, V6 • Result from the normal process of septal depolarization • Significant Q waves • Deeper than 25% of the height of the adjacent R wave • >0.04s in duration

  13. Infarction: ECG Changes

  14. Infarction: ECG Changes R wave progression

  15. Localizing Ischemia, Injury and Infarction

  16. aVR aVL aVF V1 V2 V3 V4 V5 V6 I II III Anterior Infarction Anterior infarction Left coronary artery

  17. aVR aVL aVF V1 V2 V3 V4 V5 V6 I II III Inferior Infarction Inferior infarction Right coronary artery

  18. aVR aVL aVF V1 V2 V3 V4 V5 V6 I II III Lateral Infarction Lateral infarction Left circumflex coronary artery

  19. Evolution of ECG Changes in AMI • Development of acute ECG changes with gradual reversion of the ST segments and T waves to normal over time.

  20. The Hyper-acute Phase Less than 12 hours • “ST segment elevation is the hallmark ECG abnormality of acute myocardial infarction” (Quinn, 1996) • The ECG changes are evidence that the ischaemic myocardium cannot completely depolarize or repolarize as normal • Usually occurs within a few hours of infarction • May vary in severity from 1mm to ‘tombstone’ elevation

  21. The Fully Evolved Phase 24 - 48 hours from the onset of a myocardial infarction • ST segment elevation is less (coming back to baseline). • T waves are inverting. • Pathological Q waves are developing (>2mm)

  22. The Chronic Stabilised Phase • Isoelectric ST segments • T waves upright. • Pathological Q waves. • May take months or weeks.

  23. II, III, aVF I, aVL, V leads Reciprocal Changes • Are seen as ST depression in the opposite leads from where the ST elevation is seen • Leads II, III and aVF are opposite to Leads I, aVL, and all of the V leads • Therefore, if there is ST elevation in leads II, III and aVF any ST depression (if present) would be seen in leads I, aVL and any of the V leads

  24. Reciprocal Changes • ST segment depression seen in the opposite leads from ST segment elevation • Highly sensitive as an indicator of acute MI • Frequently seen in larger infarctions ST elevation Reciprocal ST depression

  25. Thrombolytic Therapy • Indications • ST segment elevation in two or more leads associated with acute chest pain • Time between onset of chest pain to initiation of therapy less than 24 hours (optimal time to initiate therapy is less than 6 hours, and the earlier the better).

  26. Thrombolytic Therapy • Absolute Contraindications • History of cerebrovascular hemorrhage at any time • History of non cerebrovascular hemorrhage, stroke or other CV event within 1 year • Marked hypertension (SBP > 180 or DBP > 110) at any time during acute presentation • Suspicion of aortic dissection • Active internal bleeding including menses

  27. Thrombolytic Therapy • Relative Contraindications • Current use of any anti-coagulant (INR ≥ 2) • Recent (< 2 weeks) invasive or surgical procedure or prolonged (> 10 min) CPR • Pregnancy • Hemorrhagic ophthalmic condition (ie. Hemorrhagic DM nephropathy) • Active PUD • History of severe hypertension that is adequately controlled • Streptokinase with preceding 5 days to 2 years (allergic reaction)

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