Myocardial Infarction

  • myocardial-infarction Refers to a dynamic process by which one or more regions of the heart muscle experience a severe and prolonged decrease in oxygen supply because of insufficient coronary blood flow. The affected muscle tissue subsequently becomes necrotic.
  • Onset of Myocardial Infarction may be sudden or gradual, and the process takes 3 to 6 hours to run its course.
  • It is the most serious manifestation of acute coronary syndrome, a complication of coronary artery disease (CAD).
  • Approximately 90% of Myocardial Infarction are precipitated by acute coronary thrombosis (partial or total) secondary to severe CAD (greater than 70% narrowing of the artery).
  • Other causative factors include coronary artery spasm, coronary artery embolism, infectious diseases causing arterial inflammation, hypoxia, anemia, and severe exertion or stress on the heart in the presence of significant coronary artery disease.


  1. Chest pain
    • Character: variable, but often diffuse, steady substernal chest pain. Other sensations include a crushing and squeezing feeling in the chest. Other sensations include a crushing and squeezing feeling in the chest.
    • Severity: pain may be severe; not relieved by rest or sublingual vasodilator therapy, requires opioids.
    • Location: variable, but often pain resides behind upper or middle third of sternum.
    • Radiation: pain may radiate to the arms (commonly the left), and to the shoulders, neck, back, or jaw.
    • Duration: pain continues for more than 15 minutes.
  2. Associated manifestations include anxiety, diaphoresis, cool clammy skin, facial pallor, hypertension or hypotension, bradycardia or tachycardia, premature ventricular or atrial beats, palpitations, dyspnea, disorientation, confusion, restlessness, fainting, marked weakness, nausea, vomiting, and hiccups.
  3. Atypical symptoms of MI include epigastric or abdominal distress, dull aching or tingling sensations, shortness of breath, and extreme fatigue (more frequent in women).
  4. Risk factors for MI include male gender, age over 45 for men, age over 55 for men, smoking; high blood cholesterol levels, hypertension, family history of premature CAD, diabetes and obesity.

Diagnostic Evaluation:

  1. Serial 12-lead electrocardiograms (ECGs) detect changes that usually occur within 2 to 12 hours, but may take 72 to 96 hours
    • ST-segment depression and T-wave inversion indicate a pattern of ischemia; ST elevation indicates an injury pattern.
    • Q waves indicate tissue necrosis and are permanent
  2. Nonspecific enzymes including aspartate transaminase, lactate dehydrogenase, and myoglobulin may be elevated
  3. More specific creatinine phosphokinase isoenzyme CK-MB will be elevated.
  4. Triponin T and I are myocardial proteins that increase in the serum about 3 to 4 hours after an MI, peak in 4 to 24 hours, and are detectable for upto 2 weeks; the test is easy to run, can help diagnose an MI up to 2 weeks earlier, and only unstable angina causes a false positive.
  5. White blood cell count and sedimentation rate may be elevated.
  6. Radionuclide imaging, positron emission tomography, and echocardiography may be done to evaluate heart muscle.

    Pharmacologic Intervention:

    1. Pain control drugs to reduce catecholamine-induced oxygen demand to injured heart muscle.
      • Opiate analgesics: Morphine
      • Vasodilators: Nitroglycerin
      • Anxiolytics: Benzodiazepines
    2. Thrombolytic therapy by I.V. or intracoronary route, to dissolve thrombus formation and reduce the size of the infarction.
    3. Anticoagulants or other anti-platelet medications such as adjunct to thrombolytic therapy.
    4. Reperfusion arrhythmias may follow successful therapy.
    5. Beta-adrenergic blockers, to improve oxygen supply and demand, decrease sympathetic stimulation to the heart, promote blood flow in the small vessels of the heart, and provide antiarrhythmic effects.
    6. Calcium channel blockers, to improve oxygen supply and demand.

    Nursing Interventions:

    1. Monitor continuous ECG to watch for life threatening arrhythmias (common within 24 hours after infarctions) and evolution of the MI (changes in ST segments and T waves). Be alert for any type of premature ventricular beats- these may herald ventricular fibrillation or ventricular tachycardia.
    2. Monitor baseline vital signs before and 10 to 15 minutes after administering drugs. Also monitor blood pressure continuously when giving nitroglycerin I.V.
    3. Handle the patient carefully while providing care, starting I.V. infusion, obtaining baseline vital signs, and attaching electrodes for continuous ECG monitoring.
    4. Reassure the patient that pain relief is a priority, and administer analgesics promptly. Place the patient in supine position during administration to minimize hypotension.
    5. Emphasize the importance of reporting any chest pain, discomfort, or epigastric distress without delay.
    6. Explain equipment, procedures, and need for frequent assessment to the patient and significant others to reduce anxiety associated with facility environment.
    7. Promote rest with early gradual increase in mobilization to prevent deconditioning, which occurs during bed rest.
    8. Take measures to prevent bleeding if patient is thrombolitic therapy
    9. Be alert to signs and symptoms of sleep deprivation such as irritability, disorientation, hallucinations, diminished pain tolerance, and aggressiveness.
    10. Tell the patient that sexual relations may be resumed on advise of health care provider, usually after exercise tolerance is assessed.

    Pathophysiology of Myocardial Infarction
    Nursing Care Plan – Myocardial Infarction

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