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. Assessment: 1.

2.

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. 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. 4.

Atypical symptoms of MI include epigastric or abdominal distress, dull aching or tingling sensations, shortness of breath, and extreme fatigue (more frequent in women). 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, diabetesand obesity. Serial 12-lead electrocardiograms (ECGs) detect changes that usually occur within 2 to 12 hours, but may take 72

Diagnostic Evaluation: 1. 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. 3. 4.

Nonspecific enzymes including aspartate transaminase, lactate dehydrogenase, and myoglobulin may be elevated More specific creatinine phosphokinase isoenzyme CK-MB will be elevated. 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. 6.

White blood cell count and sedimentation rate may be elevated. Radionuclide imaging, positron emission tomography, and echocardiography may be done to evaluate heart

muscle. Pharmacologic Intervention: 1.

2. 3.

Pain control drugs to reduce catecholamine-induced oxygen demand to injured heart muscle. Opiate analgesics: Morphine Vasodilators: Nitroglycerin Anxiolytics: Benzodiazepines

Thrombolytic therapy by I.V. or intracoronary route, to dissolve thrombus formation and reduce the size of the infarction. Anticoagulants or other anti-platelet medications such as adjunct to thrombolytic therapy.

4. 5.

Reperfusion arrhythmias may follow successful therapy. 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 beatsthese may herald ventricular fibrillation or ventricular tachycardia. Monitor baseline vital signs before and 10 to 15 minutes after administering drugs. Alsomonitor blood pressure continuously when giving nitroglycerin I.V. Handle the patient carefully while providing care, starting I.V. infusion, obtaining baseline vital signs, and attaching electrodes for continuous ECG monitoring. Reassure the patient that pain relief is a priority, and administer analgesics promptly. Place the patient in supine position during administration to minimize hypotension. Emphasize the importance of reporting any chest pain, discomfort, or epigastric distress without delay. Explain equipment, procedures, and need for frequent assessment to the patient and significant others to reduce anxiety associated with facility environment. Promote rest with early gradual increase in mobilization to prevent deconditioning, which occurs during bed rest. Take measures to prevent bleeding if patient is thrombolitic therapy Be alert to signs and symptoms of sleep deprivation such as irritability, disorientation, hallucinations, diminished pain tolerance, and aggressiveness.

2. 3. 4. 5. 6. 7. 8. 9.

10. Tell the patient that sexual relations may be resumed on advise of health care provider, usually after exercise tolerance is assessed

Myocardial infarction (MI or AMI for acute myocardial infarction), commonly known as a heart attack, occurs when the blood supply to part of the heart is interrupted causing some heart cells to die. This is most commonly due to occlusion (blockage) of a coronary artery following the rupture of a vulnerable atherosclerotic plaque, which is an unstable collection of lipids (like cholesterol) and white blood cells (especially macrophages) in the wall of an artery. The resulting ischemia (restriction in blood supply) and oxygen shortage, if left untreated for a sufficient period of time, it can cause damage and/or death (infarction) of heart muscle tissue (myocardium).

POTENTIAL CONSIDERATIONS following discharge from care setting (dependent on clients age, physical condition/presence of complications, personal resources, and life responsibilities) Activity Intolerance imbalance between myocardial oxygen supply/demand. anticipatory Grievingperceived loss of general well-being, required changes in lifestyle, confronting mortality. decisional Conflict (treatment)multiple/divergent sources of information, perceived threat to value system, support system deficit. interrupted Family Processessituational transition and crisis. impaired Home Managementaltered ability to perform tasks, inadequate support systems, reluctance to request assistance. Diagnostic Studies ECG: ST elevation signifying ischemia; peaked upright or inverted T wave indicating injury; development of Q waves signifying prolonged ischemia or necrosis. Blood tests: Cardiac enzymes and isoenzymes: CPK-MB (isoenzyme in cardiac muscle): Elevates within 48 hours, peaks in 1220 hours, returns to normal in 4872 hours. Troponins: Troponin I (cTnI) and troponin T (cTnT): Levels are elevated at 46 hours, peak at 1418 hours, and return to baseline over 67 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 315 hours. Electrolytes: Imbalances of sodium and potassium can alter conduction and compromise contractility. WBC: Leukocytosis (10,00020,000) usually appears on the second day after MI due to the inflammatory process. 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, and phospholipids): Elevations may reflect arteriosclerosis as a cause for coronary narrowing or spasm. Coronary angiography: In hospitals with catheterization lab facilities, coronary angiography has become the gold standard for the assessment and treatment of myocardial infarction. 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 with/without stenting, or emergency heart surgery is imminent. 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). Digital subtraction angiography (DSA): Technique used to visualize status of arterial bypass grafts and to detect peripheral artery disease. 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). Diagnostic Studies ECG: ST elevation signifying ischemia; peaked upright or inverted T wave indicating injury; development of Q waves signifying prolonged ischemia or necrosis. Blood tests: Cardiac enzymes and isoenzymes: CPK-MB (isoenzyme in cardiac muscle): Elevates within 48 hours, peaks in 1220 hours, returns to normal in 4872 hours. Troponins: Troponin I (cTnI) and troponin T (cTnT): Levels are elevated at 46 hours, peak at 1418 hours, and return to baseline over 67 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 315 hours. Electrolytes: Imbalances of sodium and potassium can alter conduction and compromise contractility. WBC: Leukocytosis (10,00020,000) usually appears on the second day after MI due to the inflammatory process. 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, and phospholipids): Elevations may reflect arteriosclerosis as a cause for coronary narrowing or spasm. Coronary angiography: In hospitals with catheterization lab facilities, coronary angiography has become the gold standard for the assessment and treatment of myocardial infarction. 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 with/without stenting, or emergency heart surgery is imminent. 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). Digital subtraction angiography (DSA): Technique used to visualize status of arterial bypass grafts and to detect peripheral artery disease. 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).

Normal ecg tracing