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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.
Assessment:
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.
Coronary Artery Diseases
• Is characterized by the accumulation of plaque within coronary arteries, which progressively enlarge, thicken and calcify. This causes
critical narrowing of the coronary artery lumen (75% occlusion), resulting in a decrease in coronary blood flow and an inadequate supply of
oxygen to the heart muscle.
• Ischemia may be silent (asymptomatic but evidenced by ST depression of 1 mm or more on electrocardiogram (ECG) or may be
manifested by angina pectoris (chest pain).
• Risk factor for Coronary Artery Disease include dyslipidemia, smoking, hypertension, male gender (women are protected until
menopause), aging, non-white race, family history, obesity, sedimentary lifestyle, diabetes mellitus, metabolic syndrome, elevated
homocysteine, and stress.
• Acute coronary syndrome is a complication of CAD due to lack of oxygen to the myocardium. Mnaifestations include unstable angina, non
ST-segment elevation infarction, and ST-segment elevation infarction.
• Other causes of angina include coronary artery spasm, aortic stenosis, cardiomyopathy, severe anemia, and thyrotoxicosis.
Assessment:
Chest pain is provoked by exertion or stress and is relieved by nitroglycerin and rest.
1. Character. Substernal chest pain, pressure, heaviness, or discomfort. Other
sensations include a squeezing, aching, burning, choking, strangling, or
cramping pain.
2. Severity. Pain maybe mild or severe and typically present with a gradual
buildup of discomfort and subsequent gradual fading away.
3. Location. Behind middle or upper third of sternum; the patient will generally
will make a fist over the site of pain (positive Levine sign; indicates diffuse
deep visceral pain), rather than point to it with fingers.
4. Radiation. Usually radiates to neck, jaw, shoulders, arms, hands, and
posterior intrascapular area. Pain occurs more commonly on the left side than
the right; may produce numbness or weakness in arms, wrist, or hands.
5. Duration. Usually last 2 to 10 minutes after stopping activity; nitroglycerin
relieves pain within 1 minute.
6. Precipitating factors. Physical activity, exposure to hot or cold weather, eating a heavy meal, and sexual intercourse increase the workload
of the heart and, therefore, increase oxygen demand.
7. Associated manifestation. Diaphoresis, nausea, indigestion, dyspnea, tachycardia, and increase in blood pressure.
8. Signs of unstable angina:
• A change in frequency, duration, and intensity of stable angina symptoms.
• Angina pain last longer than 10 minutes, is unrelieved by rest or sublingual nitroglycerin, and mimics signs and symptoms of
impending myocardial infarction.
Diagnostic Evaluation:
1. Resting ECG may show left ventricular hypertrophy, ST-T changes, arrhythmias, and possible Q waves.
2. Exercise stress testing with or without perfusion studies shows ischemia.
3. Cardiac catheterization shows blocked vessels.
4. Position emission tomography may show small perfusion defects.
5. Radionuclide ventriculography shows wall motion abnormalities and ejection fraction.
6. Fasting blood levels of cholesterol, low density lipoprotein, high density lipoprotein, lipoprotein A, homocysteine, and triglycerides may be
abnormal.
7. Coagulation studies, hemoglobin level, fasting blood sugar as baseline studies.
Pharmacologic Interventions:
1. Antianginal medications (nitrates, beta-adrenergic blockers, calcium channel blockers, and angiotensin converting enzyme inhibitors) to
promote a favorable balance of oxygen supply and demand.
2. Antilipid medications to decrease blood cholesterol and tricglyceride levels in patients with elevated levels.
3. Antiplatelet agents to inhibit thrombus formation.
4. Folic acid and B complex vitamins to reduce homocysteine levels.
Surgical Interventions:
1. Percutaneous transluminal coronary angioplasty or intracoronary atherectomy, or placement of intracoronarystent.
2. Coronary artery bypass grafting.
3. Transmyocardial revascularization.
Nursing Interventions:
1. Monitor blood pressure, apical heart rate, and respirations every 5 minutes during an anginal attack.
2. Maintain continuous ECG monitoring or obtain a 12-lead ECG, as directed, monitor for arrhythmias and ST elevation.
3. Place patient in comfortable position and administer oxygen, if prescribed, to enhance myocardial oxygen supply.
4. Identify specific activities patient may engage in that are below the level at which anginal pain occurs.
5. Reinforce the importance of notifying nursing staff whenever angina pain is experienced.
6. Encourage supine position for dizziness caused by antianginals.
7. Be alert to adverse reaction related to abrupt discontinuation of beta-adrenergic blocker and calcium channel blocker therapy. These drug
must be tapered to prevent a “rebound phenomenon”; tachycardia, increase in chest pain, and hypertension.
8. Explain to the patient the importance of anxiety reduction to assist to control angina.
9. Teach the patient relaxation techniques.
10. Review specific factors that affect CAD development and progression; highlight those risk factors that can be modified and controlled to
reduce the risk.