Monday, April 22, 2013




1. Definition
Myocardial infarction is the death of heart muscle caused by lack of blood flow or oxygen. The cause is a narrowing or blockage of the coronary arteries.
2. Etiology
The cause may be due to narrowing of the coronary arteries due to atherosclerosis critical or complete arterial occlusion due to embolus or thrombus. Decrease in coronary blood flow can also be caused by shock and hemorrhage. In each case there is an imbalance between myocardial oxygen supply and demand.
3. Clinical Manifestations
a. Chest pain that occurs suddenly and continue not subside, usually above the lower sternal region and the upper abdomen, this is the main symptom.
b. Increased severity of pain can not be settled until the pain becomes unbearable.
c. This pain is very sick, such as tingling that can spread kebahu and continue down to the arm (usually the left arm).
d. Pain began spontaneously (not occur after activity or emotional disturbance), persist for several hours or days, and did not disappear with the help of rest or nitroglycerin (NTG).
e. Pain may spread to the jaw and neck.
f. Pain is often accompanied by shortness of breath, pale, cold, severe diaphoresis, dizziness
or head was floating, and nausea and vomiting.
g. Patients with diabetes mellitus will not experience severe pain because of neuropathy that accompanies diabetes can interfere neuroreseptor (dull pain experience).

4. Types of Myocardial Infarction
a. Subendocardial myocardial infarction.
            Subendocardial area is an area that is very sensitive to myocardial ischemia and infarction. Subendocardial myocardial infarction caused by subendocardial blood flow relative decline for a long time as a result of changes in the degree of narrowing of the coronary arteries or triggered by conditions such as hypotension, bleeding and hypoxia. The degree of necrosis can be increased if accompanied by increased myocardial oxygen demand, for example due to tachycardia or ventricular hypertrophy. Although at first it can be relatively mild clinical picture, a tendency further ischemia and infarction is a major threat after a patient is discharged from the Hospital.
b. Transmural myocardial infarction.
         At more than 90% of patients transmural myocardial infarction associated with coronary thrombosis. Seing thrombosis occurred in an area that is narrowed arteriosklerotik. Other causes are less common. Included here such as bleeding in the atherosclerotic plaque with intramural hematoma, spasms that usually occur in the atherosclerotic coronary embolism. Myocardial infarction can occur despite normal coronary vessels, but this is very rare.

5. Pathophysiology
           The need for oxygen exceeds the capacity of oxygen supply by blood vessel disease which causes local myocardial ischemia. On temporary ischemia will cause reversible changes in cell and tissue levels, and suppress the function of the myocardium that would alter the aerobic metabolism to anaerobic metabolism. The formation of high-energy phosphate will decrease. The final result of anaerobic metabolism is lactic acid will accumulate so that the pH of the cell decreases.
Effects of hypoxia, acidosis and reduced energy quickly disrupt the function of the left ventricle, decreased force of contraction, fibers-fibers shorten, power and speed decreases. Wall motion segment ischemia to be abnormal, the parts will stand out whenever contractions. Power to decrease cardiac contraction and disruption would alter hemodynamic move. This varies according to the size Perunahan segment ischemia and the degree of response of the autonomic nervous system reflex compensation. Decline in left ventricular function can reduce cardiac output that will increase the volume of the left ventricle as a result jatung pressure will increase. Also the left ventricular end-diastolic pressure and the pressure in the lung capillaries will increase.  The hemodynamic manifestations of ischemia is often the case that an increase in bloodpressure and heart rate were light before the onset of pain that is sympathetic compensatory response to reduced myocardial function. Decrease in blood pressure is a sign that the affected myocardial ischemia is broad enough vagus response.
Myocardial ischemia is typically accompanied cardiogram changes due to changes in the cellular electrophysiological Tterbalik wave and ST segment depression. Attack ischemia usually subside within a few minutes when the imbalance between supply and demand of oxygen atara been fixed.
Changes in metabolic, functional, hemodynamic, and elektrokardiografik reversible.
Ischemia lasting more than 30-45 minutes will cause irreversible cellular damage and muscle death or necrosis. Infarcted myocardium section will cease to contract permanently. Infarcted tissue surrounded by areas of ischemia.
30 minutes after the occlusion, metabolic bleeding occurs as a result of ischemia. Glikosis anaerobic role in providing energy to produce lactase. Changes in electrical membrane potential, after 20 minutes of going on cellular changes include rupture sarkolema lisotum and structural defects which become irreversible in the central infarct zone. Zone ischemia is around infarct area may be composed of cells of normal or abnormal cells. Area ischemia can be flipped when circulation adequately met. The goal of therapy is to improve the ischemia area and prevent the expansion of the central zone of necrosis.
Myocardial infarction refers to the process of cardiac tissue damage caused by inadequate blood supply to the coronary blood flow is reduced. Possible cause of decreased blood supply due to narrowing of the coronary arteries due to atherosclerosis critical or total blockage of an artery by embolism or thrombus.
Decrease in coronary blood flow can also be caused by shock or hemorrhage. In each case it is always an imbalance between supply and oxygen demand of the heart.
Myocardial infarction usually affects the left ventricle, transmural myocardial infarction of the entire wall thickness, whereas subendocardial infarction nekrosisnya only occurs on the inside wall of the ventricle. Location of the infarct-related disease in certain areas in the coronary circulation, eg anterior wall infarction caused by lesions in the anterior descending ramus of the left anterior coronary artery, inferior wall infarction is usually disebsbkan by lesions in the right coronary artery.
Myocardial infarction reduces ventricular function due to muscle necrosis., Loss of contraction, while the surrounding muscle ischemia also impaired contraction.
Interfere with myocardial infarction and ventricular function predisposes to hemodynamic changes that include: Setbacks contraction, decreased stroke volume, abnormal wall motion, ejection fraction decreased, an increase in left ventricular volume at end systole and end diastole, and increased ventricular end-diastolic pressure. Compensation mechanism cardial output and perfusion which may include reflex sympathetic stimulation to increase the heart rate, vasoconstriction, ventricular hypertrophy, as well as water retention with myocardial demands. But planned to meet the needs and demands of the lowered oxygen.
Functional impairment is dependent on various factors, such as:
• Size infarction: 40% associated with cardiogenic shock.
• Location infarction: a larger anterior wall reduces the mechanical function compared to the
inferior wall.
• The function of the myocardium involved: old infarction myocardial function would endanger the rest.
• Collateral Circulation: may develop in response to chronic ischemia and regional
hypoperfusion to improve blood flow to the myocardium to threatened.
• Compensatory mechanisms of cardiovascular: working to maintain cardiac output and peripheral perfusion.
Myocardial infarction is most common in the left ventricle and can be expressed according to the area affected myocardium. If the three bulkhead wall transmural myocardial infarction and then called when only a part of the so-called infarct myocardium sebendokardial. Myocardial infarction can also be expressed in accordance with the location of the heart, which can generally occur in the posterior, anterior, septal anterior, anterolateral, and apical posteroinferior. The location and extent of the lesion determine the extent of deterioration function occurs, complications and healing.
With reduced ventricular function, required pressure and volume ventricular diastolic filling will stretch of myocardial fibers that increase the strength of contraction (Starling law suits). Circulatory filling pressure can be enhanced through the retention of sodium and water by the kidney that is usually accompanied by myocardial infarction left ventricular enlargement. While, due to dilatation of the heart may occur compensated cardiac hypertrophy cardiac compensation in an effort to enhance ventricular contraction and emptying.
Myocardial infarction healing process may take several weeks. Within 24 hours of going on cellular edema and leukocyte infiltration. Cardiac enzymes released to the cell. Tissue degradation and necrosis occurs in the second or third day. Scar tissue formation begins in the third week as fibrous connective tissue that replaces the necrotic tissue, scar tissue formed settled in 6 weeks to 3 months.
6. Factors Originator
Myocardial infarction trigger factor, namely:
a. Stress.
b. The weather is cold or hot.
c. Physical work.
d. Smoking.
e. Drinking coffee.
1. Complications Clinic
• heart failure kongesif
• Cardiogenic shock
• papillary muscle dysfunction
• ventricular septal defect
• cardiac rupture
• Ventricular Aneurysm
• thromboembolism
• Pericarditis
• Arrhythmia

2. Things That Can Lead Myocardium Infarction
a. Atherosclerosis
        Cholesterol gradually accumulate in large quantities under the intima layer of the artery. Then the area is infiltrated by fibrous tissue and often calcified. Furthermore there will be "atherosclerotic plaque" and will protrude into the blood vessels and block the blood flow in part or whole.
b. Acute coronary blockage
          Atherosclerotic plaque can cause a blood bekua local or thrombus and will clog arteries. Thrombus started in place ateroklerotik plaque that has grown so large that it was split intima layer, so that direct contact with the blood stream. Because these plaques cause smooth surfaces for blood, platelets begin to adhere, fibrin begin to pile up and netted blood cells and clog the vessels. Sometimes the clot irrespective of place attachment (the plaque ateroklerotik) and flows into the coronary artery branches were more peripheral in the same artery.
c. Collateral circulation in the heart
           When a coronary artery coronary meyempit slowly in a period of years, collateral vessels  may develop at the same time with the development arterosklerotik. But, in the end grown sclerotic process beyond the limits of the provision of collateral vessels to give the necessary blood flow. If this happens, then the work of the heart muscle becomes very limited, sometimes emikian limited so the heart can not pump a normal amount of blood flow that is needed.
3. Examination Support
a. Electrocardiographic (ECG): The pathological wave accompanied by ST segment elevation (ST elevation) is convex and followed by a negative T wave and symmetric. What really matters is that a wide Q abnormalities (more than 0.04 sec) and in (Q / R is more than 1/3).
Views differ between ST-segment elevation:
- STEMI (ST Elevation Myocardial Infarction)
- NSTEMI (Non ST Elevation Myocardial Infarction) - in the diagnosis when cardiac enzyme
Leads with ST elevation help health workers to see which areas of cardiac infarction. Also can predict the damaged artery.
Lead-influenced wall that show ST elevation leads that show ST segment depression Arteries suspected broken
b. Laboratory:
       Creatin fosfakinase (CPK). Iso increased CKMB enzyme. This occurs because of muscle damage, the intra-cell enzymes released into the blood stream. Normal 0-1 mU / ml. This enzyme levels have gone up on the first day (approximately 6 hours after the attack) and had returned to normal kenilai on day 3.
SGOT (Serum Glutamic Oxalotransaminase Test) Normal less than 12 mU / ml. Levels of these enzymes are usually just go up to 12-48 hours after the attack and will be back to normal kenilai on days 4 to 7.
LDH (Lactic De-hydroginase). Normal is less than 195 mU / ml. New enzyme levels rose normally after 48 hours, will be returned to normal values ​​between day 7 and 12.
c. Other tests are found elevated ESR, mild leukocytosis and sometimes mild hyperglycemia.
d. Catheterization: coronary angiography to determine the degree of obstruction.
e. Radiology. Radiology results do not indicate specifically myocardial infarction, only shows the enlargement of the heart.
4. Treatment of ischemia and infarction
Myocardial ischemia treatment aimed at improving the balance of oxygen (myocardial need for oxygen) and supplies oksigen.Untuk dilakukukan with recovery mechanisms:
1. Reduction in oxygen demand.
2. Increased oxygen supply
There are three major determinant for the reduction of oxygen demand, which can be
overcome with therapy are:
1. Pulse velocity
2. Contraction force
3. End load (artery pressure and ventricular size)
4. The burden of the heart's need for oxygen and the requirement can be reduced by lowering the heart rate, force of contraction, artery pressure and ventricular size.
Nitroglycerine Especially for dilated artery and vein peripheral to improve the distribution of coronary blood flow to the area of ​​ischemia include; kolateralis vasodilatation. Venous dilatation would increase the capacity of blood by venous diperifer addition, as a result of venous return to the heart decreases so as to minimize the volume and ventricular size. Thus peripheral vasodilation will consequently reduce the initial load would be reduced need for oxygen.
Propranol (Inderal)
           A beta adrenergic receptor inhibitor, inhibits the development of ischemia by selectively inhibits the sympathetic nervous system influence on the heart. This influence is channeled through the beta receptors. Beta stimulation increases the rate and cardiac kotraksi. Proprenol-pengarug inhibit this effect, thereby reducing myocardial oxygen requirements.
Digitalis can relieve angina that accompanies heart failure by increasing the contraction and consequently will increase bulk sekuncup. With the increase in ventricular emptying, reduced the size of the ventricles. Although the need for oxygen increases due to the increasing power of contraction, the end result of the influence of digitalis on heart failure myocardium is reducing the need for oxygen.
     Reduces blood volume and venous return to the heart, and thereby reducing the size and ventricular volume.
Vasodilator and antihypertensive drugs can reduce artery pressure and resistance to ventricular ejection, resulting in the ultimate burden decreased / reduced.
Sedatives and antidepressants can also reduce angina caused by stress or depression.

a. Activity
o Weakness, fatigue, can not sleep
o sedentary lifestyles, irregular exercise schedule
o tachycardia, dyspnea at rest / activity
b. Circulation
o History of previous IM, coronary artery disease, GJK, TD problems, diabetes mellitus.
o TD: can be normal or up / down; postural changes recorded from bed to sitting / standing.
o Nadi: can be normal; filled / not strong, weak / strong quality with slow capillary refill;
irregular (dysrhythmias) may occur.
o The sound of the heart: S3/S3 extra heart sounds may indicate heart failure / complaints
decreased contractility or ventricular
o Murmur: when there is a demonstrated failure valve or papillary muscle dysfunction.
o Friction: dicuragai pericarditis
o cardiac rhythm: can regular or irregular
o Edema: jugular venous distention, edema dependent / peripheral, generalized edema, there
may krekels with heart failure / ventricular.
o Color: pale or cyanotic / gray leather, flat nails, the mucous membrane and lips.
c. Ego Integrity
o Denying important symptoms / conditions have been
o Fear of dying, feelings of doom is imminent
o Angry on disease / treatment that is "not necessary"
o Worry about family, work, finances.
o Refusal, denial, anxiety, lack of eye contact
o Restless, angry, attacking behavior
o Focus on yourself / pain.
d. Elimination:
o Normal or decreased bowel sounds
e. Food / fluid
Nausea, loss of appetite, belching, heartburn / burning.
o decrease in skin turgor; skin dry / berkringat
o Vomiting
o Changes in weight
f. Hygiene:
o Symptoms / signs: difficulty performing maintenance tasks
g. Neurosensori
o Dizziness, throbbing during sleep or when you wake up (sitting or resting)
o Changes in mental
o Weakness
h. Pain / discomfort
o sudden onset of chest pain (can not be associated with the activity), not relieved by rest or nitroglycerin.
o Location: typically on the anterior chest, substernal, prekordia; may spread to the arms, jaw and face.
o Quality: 'chursing' narrows, weight, sedentary depressed.
o Intensity: usually 10 on a scale of 1-10; may experience pain that has not been felt.
o Note: there may be no pain post-surgery patients, with diabetes mellitus or hypertension or elderly.
o face grimacing, changes in posture.
o Crying, moaning, stretch, stretch.
o Pulling away, loss of eye contact
o Automatic Response: changes in frequency / heart rhythm, blood pressure, skin color / moisture, breathing, consciousness.
i. Breathing
o Dyspnea with / without work, nocturnal dyspnea.
o Cough with / without sputum production.
o history of smoking, chronic respiratory disease.
o Increased respiratory rate, shortness of breath / strong.
o Pale or cyanotic.
o The sound of breath: clean or krekels / wheezing.
o Sputum: clean, thick pink
j. Social interaction
o Stress is now a working example, family
o Difficulty coping with a stressor that is, instances of disease, treatment in hospital
o Difficulty rest in peace, too emotional responses (constantly angry, scared)
o Pulling away from family
k. Counseling / learning
o Family history of heart disease / IM, DM, stroke, hypertension, peripheral vascular disease
o The use of tobacco.
o long treated DRG showed a mean: 7.3 days (2-4 days / ccu)
Repatriation plan
o Assistance with meal preparation, shopping, transportation, home care / maintain task, the
physical arrangement of the
2. Nursing priorities
a. Relief of pain, anxiety.
b. Lowering myocardial work
c. Prevent / detect and help treat life-threatening dysrhythmias or complications.
d. Improve heart health, self-care.

a. No chest pain / controlled
b. heart rate / rhythm to maintain adequate cardiac output / tissue perfusion.
c. Increase activity levels for basic self-care.
d. Anxiety is reduced / resolved
e. Disease process, treatment plan, and prognosis understood.

Frequent nursing diagnoses / major:
a. Chest pain associated with tissue ischemia secondary to coronary artery occlusion.
 Chest pain is gone / controlled§
 Demonstrate use of relaxation techniques§
 The client looked relaxed, easy to move§
1) Assess the patient's complaints of chest pain, including: location, radiation, duration, and factors that influence it.
R /: These data help determine the cause and effect of chest pain as well as a baseline to compare the symptoms of post-therapy.
2) Provide a physical break with the back elevated or in a cardiac chair.
R /: To reduce discomfort and dyspnea and physical rest also may reduce cardiac oxygen consumption.
3) Review the history of previous angina, pain resembling angina
R /: To compare the pain is there from the previous pattern, according to widespread identification of complications such as infarction, pulmonary embolism, or pericarditis
4) Instruct the patient to report pain immediately
R /: To provide appropriate interventions to reduce damage to the heart muscle tissue which further
5) Provide a quiet, slow activity, and comfortable action
R /: Lowering external stimuli
6) Helps relaxation techniques (breathing in / slowly, behavioral distraction, visualization,
imagination guidance.
R /: Helps in reducing perception / response to pain
7) Check the vital signs before and after the narcotic drug
R /: Hypotension / respiratory depression can occur as a result of drug administration. Where
these conditions can increase the damage miokardia ventricular failure
8) Collaboration with the medical team providing:
a) antianginal (NTG)
R /: To control the pain with coronary vasodilation, which increases coronary blood flow and
perfusion miokardia b) β blockers (atenolol)
R /: To control pain through the barrier effect of sympathetic stimulation, thus decreasing
cardiac function, systolic BP and myocardial oxygen demand
c) Mixture analgesics (Morphine Sulfate).
R /: To reduce severe pain, provide sedation and reduce myocardial work
d) Provision of oxygen along with analgesics
R /: To restore the heart muscle and to ensure maximum pain relief (sore lower oxygen
inhalation is associated with lower circulating levels of oxygen).
b. Activity intolerance bd imbalance between myocardial oxygen supply needs, ischemia / necrotic myocardial tissue, cardiac depressant drug effects
Criteria results:
Clients can increase tolerance activity can be measured by heart rate / rhythm of the heart
and a TD in the normal range§
skin felt warm, pink and dry§
1)      Monitor the heart rate, rhythm, and TD changes before, during, after the move as indicated
R /: To determine the level of client activity that does not burden the cardiac output
2) Increase the break, limit activity on the basis of pain / hemodynamic response, provide
2)      leisure activity that is not heavy
R /: Lowering myocardial work, thus lowering the risk of complications
3) Instruct the patient not to straining during defecation
R /: The Valsalva maneuver straining can result, causing bradycardia, decreased cardiac output, tachycardia and increased BP

4) Describe the pattern of a gradual increase in the level of akyivitas
R /: Activities that provide advanced control of the heart, increasing the strain and prevent excessive activity
5) Observation of symptoms that indicate intolerance to activity
R /: palpitations, irregular pulse, presence of chest pain or dyspnea may indicate a need for changes in exercise or diet program.
c. Bd risk of decreased cardiac output frequency changes, rhythm, conduction elektri, preload reduction / increase in systemic vascular resistance, muscle infarction, structural damage
Criteria results:
• TD, cardiac output within normal limits
• Urine output adequate
• No dysrhythmias
• Decreased dyspnea, angina
• Increased tolerance to activity
1) Monitor vital signs: heart rate, blood pressure, pulse
R /: To determine the changes in blood pressure, pulse so as to facilitate earlyintervention since TD may increase sympathetic stimulation, then fell when the cardiac output is affected.
2) Evaluation of the heart sounds S3, S4
R /: To megetahui complications in mitral GJK failed to S3, S4 because while miokardia ischemia, ventricular stiffness, and hypertension pulmonary / systemic
3) Auscultation of breath sounds
R /: To determine the presence of pulmonary congestion due to decreased myocardial function
4) Provide food portions small and easy to chew, limit your intake of caffeine, coffee, chocolate, cola
R /: To avoid miokardia work, bradycardia, increased heart rate
5) Collaboration
a) Give oxygen as indicated
R /: To meet the needs of myocardial ischemia and dysrhythmias further reduce
b) Maintain IV fluids
R /: Line a patent for emergency drug delivery dysrhythmias / chest pain
c) Review the EKG series
R /: Providing information in relation to the progress / improvement infarction, ventricular function, electrolyte balance, and the effects of drug therapy
d) Monitor the laboratory (cardiac enzymes, GDA, electrolytes)
R /: To determine the improvement / expansion of the myocardial hypoxia, hypokalemia / hypercalcemia
e) Give medication antidisritmia
d. Risk of changes in tissue perfusion bd decreased blood flow, for example vasikonstriksi, hypovolemia, and the formation of thromboembolism


Doenges, M.E, et all. 2000. Rencana asuhan keperawatan: pedoman untuk perencanaan dan pendokumentasian perawatan pasien, Edisi 3. EGC: Jakarta

Smeltzer, Suzanne C & Brenda G. Bare, 2001, Buku Ajar Keperawatan Medikal Bedah Brunner & Suddarth, Edisi 8, Volume 2. Penerbit Buku Kedokteran EGC : Jakarta.

Lynda Jual Carpenito R.N, M.S.N, 1995, Rencana Asuhan Dan Dokumentasi Keperawatan, Edisi 2. Penerbit Buku Kedokteran EGC : Jakarta

Persatuan Ahli Penyakit Dalam Indonesia, 1996, Buku Ajar Ilmu Penyakit Dalam, Jilid I, Edisi 3. Balai Penerbit FKUI : Jakarta.
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