NCP Myocardial Infarction

 Myocardial infarction (MI) is caused by marked reduction/loss of blood flow through one or more of the coronary arteries, resulting in cardiac muscle ischemia and necrosis.


Inpatient acute hospital, step-down, or medical unit.




Heart failure: chronic

Psychosocial aspects of care

Thrombophlebitis: deep vein thrombosis

Patient Assessment Database


May report: Weakness, fatigue, loss of sleep

Sedentary lifestyle, sporadic exercise schedule

May exhibit: Tachycardia, dyspnea with rest/activity


May report: History of previous MI, CAD, HF, hypertension, diabetes mellitus

May exhibit: BP may be normal, increased, or decreased; postural changes may be noted from
lying to sitting/standing

Pulse may be normal, full/bounding, or have a weak/thready quality with delayed capillary
refill; irregularities (dysrhythmias) may be present

Heart sounds S3/S4 may reflect a pathological condition (e.g., cardiac failure, decreased
ventricular contractility or compliance)

Murmurs may reflect valvular insufficiency or papillary muscle dysfunction

Friction rub (suggests pericarditis)

Heart rate regular or irregular; tachycardia/bradycardia may be present

Edema: Jugular vein distention, peripheral/dependent edema, generalized edema

Color: Pallor or cyanosis/mottling of skin, nailbeds, mucous membranes, and lips may be


May report: Denial of significance of symptoms/presence of condition

Fear of dying, feelings of impending doom

Anger at inconvenience of illness/”unnecessary” hospitalization

Worry about family, job, finances

May exhibit: Denial, withdrawal, anxiety, lack of eye contact

Irritability, anger, combative behavior

Focus on self/pain


May exhibit: Normal or decreased bowel sounds


May report: Nausea, loss of appetite, belching, indigestion/heartburn

May exhibit: Poor skin turgor; dry or diaphoretic skin



May report/exhibit: Difficulty in performing self-care tasks


May report: Dizziness, fainting spells in or out of bed (upright or at rest)

May exhibit: Changes in mentation



May report: Sudden onset of chest pain unrelieved by rest or nitroglycerin (although most pain is deep and visceral, 20% of MIs are painless)

Location: Typically anterior chest (substernal, precordium); may radiate to arms, jaw, face;
may have atypical location such as epigastrium/abdomen; elbow, jaw, back, neck, between shoulder blades, severe sore throat; throat fullness (females)

Quality: Crushing, constricting, viselike, squeezing, heavy, steady

Intensity: Usually 10 on a scale of 0–10 or “worst pain ever experienced.” Note: Pain is sometimes absent in females, postoperative patients, those with prior stroke or heart failure, diabetes mellitus or hypertension, or the elderly. Studies indicate that up to one-third of persons experiencing MI do not have typical chest pain.

Precipitating factor: May/may not be associated with activity

May exhibit: Facial grimacing, changes in body posture, may place clenched fist on midsternum when describing pain

Crying, groaning, squirming, stretching

Withdrawal, lack of eye contact

Autonomic responses: Changes in heart rate/rhythm, BP, respirations, skin color/moisture, level of consciousness


May report: Dyspnea with/without exertion, nocturnal dyspnea

Cough with/without sputum production

History of smoking, chronic respiratory disease

May exhibit: Increased respiratory rate, shallow/labored breathing

Pallor or cyanosis

Breath sounds clear or crackles/wheezes

Sputum clear, pink-tinged


May report: Recent stress, e.g., work, family

Difficulty coping with recent/current stressors, e.g., money, work, family problems made worse by this illness/hospitalization

May exhibit: Difficulty resting quietly, overemotional responses (intense anger, fear)

Withdrawal from family


May report: Family history of heart disease/MI, diabetes, stroke, hypertension, peripheral vascular disease

Use of tobacco

Discharge plan

DRG projected length of inpatient stay: 4.9–7.0 days (2–4 days/critical care unit [CCU])

May require assistance with food preparation, shopping, transportation, homemaking/maintenance tasks; physical layout of home


ECG: ST elevation signifying ischemia; peaked upright or inverted T wave indicating injury; development of Q waves signifying prolonged ischemia or necrosis.

Cardiac enzymes and isoenzymes: CPK-MB (isoenzyme in cardiac muscle): Elevates within 4–8 hr, peaks in 12–20 hr, returns to normal in 48–72 hr.

LDH: Elevates within 8–24 hr, peaks within 72–144 hr, and may take as long as 14 days to return to normal. An LDH1 greater than LDH2 (flipped ratio) helps confirm/diagnose MI if not detected in acute phase.

Troponins: Troponin I (cTnI) and troponin T (cTnT): Levels are elevated at 4–6 hr, peak at 14–18 hr, and return to baseline over 6–7 days. These enzymes have increased specificity for necrosis and are therefore useful in diagnosing postoperative MI when MB-CPK may be elevated related to skeletal trauma.

Myoglobin: A heme protein of small molecular weight that is more rapidly released from damaged muscle tissue with elevation within 2 hr after an acute MI, and peak levels occurring in 3–15 hr.

Electrolytes: Imbalances of sodium and potassium can alter conduction and compromise contractility.

WBC: Leukocytosis (10,000–20,000) usually appears on the second day after MI because of the inflammatory process.

ESR: Rises on second or third day after MI, indicating inflammatory response.

Chemistry profiles: May be abnormal, depending on acute/chronic abnormal organ function/perfusion.

ABGs/pulse oximetry: May indicate hypoxia or acute/chronic lung disease processes.

Lipids (total lipids, HDL, LDL, VLDL, total cholesterol, triglycerides, phospholipids): Elevations may reflect arteriosclerosis as a cause for coronary narrowing or spasm.

Chest x-ray: May be normal or show an enlarged cardiac shadow suggestive of HF or ventricular aneurysm.

Two-dimensional echocardiogram: May be done to determine dimensions of chambers, septal/ventricular wall motion, ejection fraction (blood flow), and valve configuration/function.
Nuclear imaging studies: Persantine or Thallium: Evaluates myocardial blood flow and status of myocardial cells, e.g., location/extent of acute/previous MI.

Cardiac blood imaging/MUGA: Evaluates specific and general ventricular performance, regional wall motion, and ejection fraction.

Technetium: Accumulates in ischemic cells, outlining necrotic area(s).

Coronary angiography: Visualizes narrowing/occlusion of coronary arteries and is usually done in conjunction with measurements of chamber pressures and assessment of left ventricular function (ejection fraction). Procedure is not usually done in acute phase of MI unless angioplasty or emergency heart surgery is imminent.

Digital subtraction angiography (DSA): Technique used to visualize status of arterial bypass grafts and to detect peripheral artery disease.

Magnetic resonance imaging (MRI): Allows visualization of blood flow, cardiac chambers/intraventricular septum, valves, vascular lesions, plaque formations, areas of necrosis/infarction, and blood clots.

Exercise stress test: Determines cardiovascular response to activity (often done in conjunction with thallium imaging in the recovery phase).


1. Relieve pain, anxiety.
2. Reduce myocardial workload.
3. Prevent/detect and assist in treatment of life-threatening dysrhythmias or complications.
4. Promote cardiac health, self-care.


1. Chest pain absent/controlled.
2. Heart rate/rhythm sufficient to sustain adequate cardiac output/tissue perfusion.
3. Achievement of activity level sufficient for basic self-care.
4. Anxiety reduced/managed.
5. Disease process, treatment plan, and prognosis understood.
6. Plan in place to meet needs after discharge.