Myocardial Infarction Nursing Care Plan & Management


  • 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.
Risk Factors
  • Infarctions may occur for a variety of reasons, but coronary thrombosis of a coronary artery narrowed with plaque is the most common cause.
  • Other causes include spasms of the coronary arteries; blockage of the coronary arteries by embolism of thrombi, fatty plaques, air, or calcium; and disparity between myocardial oxygen demand and coronary arterial supply.
  • Multiple risk factors have been identified for coronary artery disease and MI.
  • Modifiable risk factors include cigarette smoking, which causes arterial vasoconstriction and increases plaque formation. A diet high in saturated fats, cholesterol, sugar, salt, and total calories increases the risk for MIs. Elevated serum cholesterol and low-density lipoprotein levels increase the chance for atherosclerosis. Hypertension and obesity increase the workload of the heart, and diabetes mellitus decreases the circulation to the heart muscle.
  • Hostility and stress may also increase sympathetic nervous system activity and pose risk.
  • A sedentary lifestyle diminishes collateral circulation and decreases the strength of the cardiac muscle.
  • Medications can also prevent risks.
  • Oral contraceptives may enhance thrombus formation, cocaine use can cause coronary artery spasm, and anabolic steroid use can accelerate atherosclerosis.
  • Some factors—such as age, family history, and gender—cannot be modified.
  • Aging increases the atherosclerotic process, family history may increase the risk by both genetic and environmental influences, and males are more prone to MIs than are premenopausal women.
  • Premenopausal women have the benefit of protective estrogens and a lower hematocrit, although heart disease is on the rise in this population, possibly because of an increased rate of smoking in women. Once women become postmenopausal, their risk for MI increases, as it also does for men over age 50.
  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.
Difference of the pain of Angina and Myocardial Infarction
 Angina PectorisMyocardial Infarction
Predisposing/ Precipitating FactorsExertion, especially in colds; emotional stress; heavy mealsMay transpire during rest
QualityPressing, tight, squeezing, viselike heavy occasionally burningPressing, tight, squeezing, viselike heavy occasionally burning
Region/ RadiationSubsternal or retrosternal, which may radiate to shoulder, arms, neck, lower jaw, or upper abdomen slight to the left side.Substernal or retrosternal, which may radiate to shoulder, arms, neck, lower jaw, or upper abdomen slight to the left side.
SeverityMild to moderate, rarely to be described as severeMore severe
TimingPain usually is 1 to 3 minutes up to 10 minutes long, or may even last up to 15 to 20 minutes. This pain can be relieved by rest or Nitroglycerin (vasodilator)Pain usually last for 20 minutes or even hours. This type of pain is not relieved by rest or Nitroglycerin, but could be addressed by Morphine Sulfate (narcotic analgesic).
Associated SymptomsDyspnea, nausea and vomiting, sweating, and weakness.Dyspnea, nausea and vomiting, sweating, and weakness.
PathophysiologyA temporary myocardial ischemia which is usually secondary coronary atherosclerosis.A prolonged myocardial ischemia which leads to an irreversible myocardial damage or necrosis.

Source: Balita, C. (2008). Ultimate learning guide to nursing review. Manila, Philippines: Tri-Mega Printing

Primary Nursing Diagnosis
  • Altered tissue perfusion (myocardial) related to narrowing of the coronary artery(ies) associated with atherosclerosis, spasm, or thrombosis
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.
Medical Management

The goals of medical management are to minimize myocardial damage, preserve myocardial function, and prevent complications such as lethal dysrrhythmias and cardiogenic shock.

  • Oxygen administration is initiated at the onset of chest pain.
  • Reperfusion via emergency use of thrombolytic medications or percutaneous coronary interventions (PCI).
  • Coronary artery bypass or minimally invasive direct coronary bypass (MIDCAB).
  • Analgesic
    1. For relief of pain. This is a priority. Pain may cause shock.
    2. Morphine Sulfate. Lidocaine or Nitroglycerine administered intravenously.
  • Thrombolytic Therapy:
    1. To disitegrate blood clot by activating the fibrinolytic processes.
    2. Streptokinase, urokinase and tissue plasminogen activator (TPA) are currently used.
    3. Adminstration is most crucial between 3 to 6 hours after the initial infarction has occurred.
    4. Detect for occult bleeding during and after thrombolytic therapy
    5. Assess neurologic status changes which may indicate G.I. bleeding or cardiac tamponade.
  • Anticoagulant and antiplatelet medications are administered after thrombolytic therapy to maintain arterial patency.
  • Other medications: Beta-adrenergic blockings agents; diazepam (Valium)