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.
Understand Myocardial Infarction
Description
- 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 Failure Left-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
- 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.