Acute Myocardial Infarction – Heart Attack

Myocardial infarction (MI) or Acute myocardial infarction (AMI), commonly known as a heart attack, results from the interruption of blood supply to a part of the heart, causing heart cells to die. This is most commonly due to occlusion (blockage) of a coronary artery.

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Understand Myocardial Infarction


  • Myocardial infarction occurs when myocardial tissue is abruptly and severely deprived of oxygen.
  • Ischemia can lead to necrosis of myocardial tissue if blood flow is not restored.
  • Infarction does not occur instantly but evolves over several hours.
  • Obvious physical changes do not occur in the heart until 6 hours after the infarction, when the infarcted area appears blue and swollen.
  • After 48 hours, the infarct turns gray, with yellow streaks developing as neutrophils invade the tissue.
  • By 8 to 10 days after infarction, granulation tissue forms.
  • Over 2 to 3 months, the necrotic area develops into a scar; scar tissue permanently changes the size and shape of the entire left ventricle.
  • Not all clients experience the classic symptoms of an MI.
  • Women may experience atypical discomfort, shortness of breath, or fatigue and often present with NSTEMI (non–ST elevation myocardial infarction) or T-wave inversion.
  • An older client may experience shortness of breath, pulmonary edema, dizziness, altered mental status, or a dysrhythmia.

Location of MI

  • Obstruction of the left anterior descending artery results in anterior wall or septal MI, or both.
  • Obstruction of the circumflex artery results in posterior wall MI or lateral wall MI.
  • Obstruction of the right coronary artery results in inferior wall MI.

Right-Sided Heart FailureLeft-Sided Heart Failure
• Dependent edema (legs and sacrum)
• Jugular venous distention
• Abdominal distention
• Hepatomegaly
• Splenomegaly
• Anorexia and nausea
• Weight gain
• Nocturnal diuresis
• Swelling of the fingers and hands
• Increased BP (from fluid volume excess) or
• decreased BP (from pump failure)
• Signs of pulmonary congestion
• Dyspnea
• Tachypnea
• Crackles in the lungs
• Dry, hacking cough
• Paroxysmal nocturnal dyspnea
• Increased blood pressure (from
• fluid volume excess)
• or decreased BP (from pump
• failure)

Risk factors

  • Atherosclerosis
  • Coronary artery disease
  • Elevated cholesterol levels
  • Smoking
  • Hypertension
  • Obesity
  • Physical inactivity
  • Impaired glucose tolerance
  • Stress

Diagnostic studies

  • Troponin level
    • Level rises within 3 hours.
    • Level remains elevated for up to 7 to 10 days.

Total creatine kinase level

  • Level rises within 6 hours after the onset of chest pain.
  • Level peaks within 18 hours after damage and death of cardiac tissue.

CK-MB isoenzyme

  • Peak elevation occurs 18 hours after the onset of chest pain.
  • Level returns to normal 48 to 72 hours later.
  • Myoglobin: Level rises within 2 hours after cell death, with a rapid decline in the level after 7 hours.

LDH level

  • Level rises 24 hours after MI.
  • Level peaks between 48 and 72 hours and falls to normal in 7 to 14 days.
  • Serum level of LDH1 isoenzyme rises higher than serum level of LDH2.

White blood cell count: An elevated white blood cell count of 10,000 to 20,000 /mm3 appears on the second day following the MI and lasts up to 1 week.


  • Electrocardiogram shows either ST elevation MI (STEMI), T wave inversion, or non-ST elevation MI (NSTEMI); an abnormal Q wave may also present.
  • Hours to days after the MI, ST and T wave changes will return to normal but the Q wave changes usually remain permanently.

Diagnostic tests following the acute stage

  • Exercise tolerance test or stress test may be prescribed to assess for electrocardiographic changes and ischemia and to evaluate for medical therapy or identify clients who may need invasive therapy.

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