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

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Presentation on theme: "+ ECG Changes in Myocardial Infarction Clerk Karen G. Amoloza."— Presentation transcript:

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: transmural vs subendocardial Localization: anterior vs inferoposterior 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

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12 + 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

13 + 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

14 + Infarction: ECG Changes

15 + R wave progression

16 + Localizing Ischemia, Injury and Infarction Leads Site of occulusion AnteriorV1 – V4LAD SeptalV1 – V2LAD LateralI, aVL, V5, V6Circumflex, RCA High LateralI, aVLCircumflex, RCA InferiorII, III, aVFRCA, circumflex PosteriorV1 – V2RCA

17 + Anterior Infarction Anterior infarction I II III aVR aVL aVFV1 V2 V3V4 V5 V6 Left coronary artery

18 + Inferior Infarction Inferior infarction I II III aVR aVL aVFV1 V2 V3V4 V5 V6 Right coronary artery

19 + Lateral Infarction Lateral infarction I II III aVR aVL aVFV1 V2 V3V4 V5 V6 Left circumflex coronary artery

20 + 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.

21 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

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23 + The Fully Evolved Phase 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)

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

25 + Reciprocal Changes II, III, aVF I, aVL, V leads 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

26 + 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

27 + 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).

28 + 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

29 + Thrombolytic Therapy Relative Contraindications Current use of any anti-coagulant (INR ≥ 2) Recent ( 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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