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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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myocardial infarction
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
ecg on diagnosis of mi
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
ischemia
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
ischemia ecg changes
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
ischemia ecg changes1
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
injury
Injury
  • Acute, prolonged, reduction in blood supply to the myocardium
  • Reversible
injury ecg changes
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)
injury ecg changes1
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
injury ecg changes2
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
infarction ecg changes
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
infarction ecg changes1
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
infarction ecg changes3
Infarction: ECG Changes

R wave progression

anterior infarction

aVR aVL aVF

V1 V2 V3

V4 V5 V6

I II III

Anterior Infarction

Anterior infarction

Left

coronary

artery

inferior infarction

aVR aVL aVF

V1 V2 V3

V4 V5 V6

I II III

Inferior Infarction

Inferior infarction

Right

coronary

artery

lateral infarction

aVR aVL aVF

V1 V2 V3

V4 V5 V6

I II III

Lateral Infarction

Lateral infarction

Left

circumflex

coronary

artery

evolution of ecg changes in ami
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.
the hyper acute phase
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
the fully evolved phase
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)
the chronic stabilised phase
The Chronic Stabilised Phase
  • Isoelectric ST segments
  • T waves upright.
  • Pathological Q waves.
  • May take months or weeks.
reciprocal changes

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
reciprocal changes1
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

thrombolytic therapy
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).
thrombolytic therapy1
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
thrombolytic therapy2
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)