CONTOH JURNAL TERBARU TENTANG INFARK MIOKARD

JURNAL ABOUT INFARK MIOKARD

CHAPTER I

INTRODUCTION

A. Background

Diseases cardiovascular is a disease epidemic. In Indonesia, about 6 million people affected by a disease of the heart or blood vessels. Whereas in world mortality roughly 50 million / years from cardiovascular disease (PKV), 39 million of whom in developing countries. Diseases cardiovascular is a cause of of death the number one in the the world. According to the American Heart Association more and more deaths are caused by cardiovascular disease compared with the combined seventh leading cause of death next. This case shows the the occurrence of one deaths from cardiovascular disease each 33 seconds. (Ardyan pradana: 2011)  Myocardial infarction is the death of heart muscle tissue characterized by typical chest pain: a long illness more than 30 minutes, not relieved by rest or the provision of anti-angina (PKJPDN Harapan Kita, 2001). Meanwhile, according to Widiastuti (2003) Acute myocardial infarction (AMI) is a rapid occurrence of myocardial necrosis caused by an imbalance between blood flow and myocardial blood requirement. This situation is usually as a result of plaque rupture with thrombus formation resulting from coronary artery urgent reduction in the myocardial blood flow.

B. Purpose

1. General Purpose: adds to knowledge and insight about nursing care infarction myocardial

2. Specific Objectives:

a. To find out what it is myocardial infarction

b. To know the anatomy and physiology of myocardial infarction

c. To know classification of infarction myocardial

d. To determine the etiology of myocardial infarction

e. To determine the clinical manifestations of myocardial infarction

f. To determine the pathophysiology of myocardial infarction

g. Myocardial infarction to determine pathway

h. To determine the client with myocardial infarction complications

i. To find dianostik examination of myocardial infarction

j. To determine the management of myocardial infarction

CHAPTER II

THEORETICAL REVIEW

A.   Denifinisi Infarction miocard

Myocardial infarction (IM) is the death of myocardial cells caused by prolonged lack of oxygen. This is the last lethal response to myocardial ischemia is not resolved. Cell-cells myocardium begin to die after approximately 20 minutes experiencing shortage of of oxygen. After this period, the ability the cell to generate ATP basis aerobis vanished, and the cell does not can meet its energy needs. (Elizabeth Corwin J: 2000)

Myocardial infarction is also referred to as a heart attack, which refers to the section of myocardial tissue damage when the blood supply is suddenly interrupted either by chronic coronary artery narrowing or obstruction of aterossklerosis of embolus or thrombus. (Barbara engram: 1998) Infarction myocardial (IM) is decrease in blood flow through one or more artery coronary, resulting in ischemia myocardial and necrosis. (Marilyn Doenges E: 1999)
From the above definition it can be concluded that myocardial infarction is the death of cells due to myocardial ischemia.

B. Anatomy and Physiology

Cardiovascular system consists of three parts, namely the interplay of the heart, blood vessels, and blood.

1.  Heart

The heart is a muscular organ, berentuk cone, hollow, base peak above and below. Heart be inside thoracic, between the two pulmonary-lung and behind sternum and more overlooks leftward. Heart size approximately the size of a fist. Adult heart weighs between 220 to 260 grams. The heart is divided by a septum (partition) into two sides, the right left right. After was born does not is no relationship between the these two hemispheres this. Each hemisphere is further subdivided into two spaces, which is the so-called atria and the lower called the ventricles. Then there are the left atrium and ventricle while the right hand there are the atria and ventricles. The heart muscle is composed of a special nature. and wrapped in a membrane called the pericardium. Membrane is composed of two layers, namely the pericardium visceral is membrane are correlated in the heart and pericardium parietal is a layer of fibrous that folded out from the base of the heart and wrap around the heart as the bag loosely. Because of this arrangement, the heart is in two layers of the pericardium pockets, and between the two there is a liquid layer seris. Due to the nature of the fluid that lubricates, heart can move freely. Coated side of the heart endothelium. This layer is called the endocardium. Thick wall of the heart consists of three layers:
a. The pericardium: outer wrapper

b. Myocardium: muscle layer the middle

c. Endocardium: in the limit

Heart muscle wall is not as thick. Ventricular wall thickness and the wall to the left over tebah of the right ventricular wall, because the strength of left ventricular contraction is much greater than on the right. Atrial wall is composed of muscles that are thinner. Heart of the coronary arteries are functioning to supply blood to the heart in order to pump blood. Coronary artery is divided into right and left coronary arteries that leave the aorta and then branched out into smaller arteries. This small arteries heart and blood  all parts of the transplanted heart. Blood returning from the heart mainly collected in the coronary sinus and straight back into the right atrium. (Evelyn C. Pearce: 2009)
2. Blood vessel

The arteries and arterioles that carry blood out of the heart, always bringing fresh blood contains oxygen, except the pulmonary artery that carries blood "dirty" which requires oxygenation. Venules and veins carry blood toward the heart and pulmonary veins except invariably carry oxygen-poor blood. Whereas capillaries is blood vessels which very small and there arterioles ends and venules began to. Capillary form the strands of blood vessels and branched-branch within the most of the networks the body's.
Arterial wall consists of three layers, namely the outer layer (tunica adventisia), the middle layer (tunica media), inner layer (tunica intima). Vein wall structure also consists of three layers, but the middle muscular layer is thinner, less powerful. While the capillary is composed of a single layer of endothelium layer. (Evelyn C. Pearce: 2009)
3. Blood

Blood is a liquid tissue consisting of two parts. Intercellular substance is a liquid called plasma and inside there are solid elements, namely blood cells. Blood cells consists from erythrocytes, leukocytes and platelets. Whereas plasma contains gas (oxygen and carbon dioxide), hormones, enzymes, and antigens. (Evelyn C. Pearce: 2009)

C. Classification of myocardial infarction

Affected by muscle layer of Acute Myocardial Infarction can be distinguished:
1. Acute myocardial infarction is transmural infarction involving the entire muscle layer of the heart (ventricular wall).

2. Acute Myocardial Infarction Non transmural / subendocardial myocardial infarction that are on the inside of the heart muscle (the myocardium-third).

Based oklusinya place on coronary arteries:

1. Acute Miokard Infarction Anterior.

2. Posterior Acute Myocardial Infarction.

3. Acute Myocardial Infarction Inferior. (Nn: 2012)

D. Etiology

The cause from infarction myocardial (MI) is rupture of the plaque atherosclerosis was on artery coronaria who caused spasme arterial or formation of thrombus. The point of acute myocardial infarction occurs when oxygen supply is not in accordance with the requirement is not handled properly so  death of the heart cells. Some things that cause interference oxygenation include:

1. Decreased supply of oxygen to myocardial.

Decrease in oxygen supply caused by three factors, among others:
a. Vascular factors

It is related to the blood vessels as a way  blood reaches the heart cells. Some things that could interfere with vascular  including: atherosclerosis, spasm, and arteritis. Spasm of the blood vessels can also occur in people with no history of previous heart disease, and is usually attributed to several things, among others:

1) Consuming certain drugs

2) emotional stress or pain

3) Exposure to cold temperatures who extreme

4) smoking.

b. Circulation Factor

Circulation associated with the smooth circulation of blood from the heart to the rest of the body to go back again to the heart. So the this case not will be separated from factor the pumping and blood volume who pumped. Condition which causing disruption on the circulation among others the condition of hypotension. Stenosis or insufficiency that occurs in heart valves (aortic, mitralis, and trikuspidalis) causes decreased cardiac output (COP). COP decrease followed by a decline in circulation causing some parts of the body are not well supplied with adequate blood, including in this case the heart muscle.

 
c. Blood factor

An oxygen-carrying blood to all parts of the body. If the carrying capacity of the blood is reduced, it is as good as any street (blood vessels) and heart pumping then it is not enough to help. Things-things that cause disruption of in haulage of blood among others: anemia, hypoxemia, and polycythemia.

2. Increasing the body's oxygen needs

In the normal person is able to offset the increased oxygen demand such as by increasing the heart rate to increase COP. However, if the person has heart disease, compensatory mechanisms eventually even more aggravate the condition due to increased oxygen demand, whereas the oxygen supply is not increased. Therefore, all activities that lead to increased oxygen demand will lead to infarction. For example: aktivtas excess, emotions, eating too much and others. Hypertrophy of myocardial infarction can be triggered because more oxygen is supplied to the cell, whereas intake of the pumping oksien decline due to ineffective.

Broadly speaking there are two types of factors risk for every person for exposed to myocardial infarction acute, namely factors risk who could be modified and factors risk which not could be modified.

Risk Factors That Can be Modified

Is a risk factor which could be controlled so that with certain interventions then it could be eliminated. Are included in this group include:

a. Smoke

Role cigarette inside disease coronary heart this among others: raises atherosclerosis; an increase in thrombogenesis and vasoconstriction; an increase in blood pressure; trigger of arrhythmias cardiac, increase the oxygen demand cardiac, and a decrease capacity of transport of oxygen. Smoked 20 cigarettes or more a day can increase the risk of 2-3 times compared to non-smokers.

b. Consumption of alcohol

Although there are basic theories about the protective effects of low to moderate doses of alcohol, which he can increase endogenous thrombolysis, reduce platelet adhesion, and increased levels of HDL in circulation, but it is still controversial Not all literature supports this concept, even an increase in the dose of alcohol was associated with increased mortality cardiovascular because of arrhythmias, hypertension systemic and cardiomyopathy dilatation.
c. Infection

Chlamydia pneumoniae infection, intracellular gram-negative organisms and a common cause of respiratory tract disease, appear to be associated with atherosclerotic coronary disease.

d. Systemic hypertension

Hypertension Systemic led to increased afterload who basis not be directly will increase the workload cardiac. These conditions will lead to left ventricular hypertrophy as compensation for the increased afterload, which in turn increases the oxygen demand of the heart.
e. Obesity

There is a close relationship between body weight, increased blood pressure, increased blood cholesterol, insulin-dependent DM, and a low level of activity.
f. Lack of exercise

Regular aerobic activity lowers the risk of coronary heart disease, amounting to 20-40%.
g. Diabetes

Risk of coronary heart disease in patients with DM was 2-4 higher than the usual. This case relates with the existence of abnormalities metabolism lipid, obesity, hypertension systemic, an increase in thrombogenesis (an increase in adhesion levels platelet).
2. Risk Factors That Can not Be Modified

Is a risk factor that can not be changed or controlled, some of them:
a. Age

increased risk in men 45 years and women over 55 years (umumnnya after menopause).
b. Sex

Morbidity from coronary heart disease (CHD) in men two times greater than in women, this is related to estrogen is cardioprotective in women. This case proved to incidence of CHD increased with rapidly and finally equivalent with male in women after period menopause.

c. Family History

History of family members who experienced CHD blood sebelm 70 years of age is an independent risk factor for the occurrence of CHD. Aggregation of CHD families indicates a genetic predisposition to this condition. There is evidence that a positive family history of CHD patients at onset affects close family.

d. RAS

Incidence death of Akiat CHD in people Asia who staying in UK is higher compared with the peduduk local, whereas low figure contained on RAS apro-caribbean.

e. Geography

Level deaths due higher CHD in Ireland Northern, Scotland, and parts North of England and can reflect differences in diet, purity water, smoked, structure of socio-economic, and life of urban. (Nn: 2010)

E. Clinical Manifestations

Although most individuals do not show the real without myocardial infarction (a heart attack disguised), usually significant clinical manifestations (Elizabeth J Corwin, 2000):
1. Pain at the beginning of the (usually) abrupt, often described as having a crush and severe nature. Pain may spread to the upper body anywhere, but most of the spread to the left arm, neck or jaw. Nitrates can eliminate ischemia and break out the necrotic zone by lowering cardiac load.

2. Occurred nausea and vomiting that may be associated with severe pain

3. Limp feeling associated with decreased blood flow to skeletal muscle

4. Skin who cold a result of vasoconstriction simpatis

5. Urine output is reduced due to decreased renal blood flow and increased aldosterone / ADH.

F. Pathophysiology

Coronary artery atherosclerosis is the cause of coronary artery disease is most commonly found. Atherosclerosis causing  lipid and tissue fibrosa within the arteries coronary, so that been progressively narrow the  blood. When the lumen narrows the resistance to blood flow will increase and jeopardize myocardial blood flow. When the disease is more advanced, it will be followed by changes in luminal narrowing of the blood vessels which reduces the ability of vessels to dilate. With Thus a balance between provision of and needs of oxygen become not unstable so that the endanger myocardium who located adjacent to distal from regions lesion.
Oxygen demand exceeds the capacity of oxygen supply by blood vessel disorder causing myocardial ischemia workshops. Transient ischemia would cause reversible changes in cell and tissue levels, and suppress the function of the myocardium. Reduced oxygen levels encourage the myocardium to alter aerobic metabolism to anaerobic metabolism. Anaerobic metabolism through much glycolic efisienapabila not paired with aerobic metabolism through energy phosphate steeper decline big enough. The final result of anaerobic metabolism (ie lactic acid) will be buried so that the lower the Ph cells. the combined effects of hypoxia, reduced energy available, as well as acidosis quickly disrupt the function of the left ventricle. strength of regional myocardial contraction reduced the affected fibers and the fibers shorten and speed decreases. in addition, wall motion segment ischemia become abnormal; piece will stand out every time the left ventricle contracts.

Ischemia which lasted more dari30-45 minute will cause cell damage irreversible as well as necrosis or death muscle. Part myocardial infarction or necrosis contract will cease permanently. Infarcted tissue surrounded by an ischemic area that could potentially live. Infarct size end depends on the fate of the ischemic area is. When the edge of the necrotic area of ​​the infarct area will increase in size, whereas the improvement will reduce the area of ​​ischemic necrosis. Repair and restoration of regional ischemic coronary blood flow can be achieved by administration of thrombolytic drugs or primary perkutaneas transluminal coronary angioplasty (PTCA). If occurs repairs regions ischemia, then the necrosis of the ischemic area is increased size of infarction. (Sylvia A Prince and Lorraine M Wilson: 2005)

G. Pathway

(Download here) H. Clients with myocardial infarction complications
Complications arising in patients with myocardial infarction (Elizabeth J Corwin, 2000) is
1. Thromboembolism

Thromboembolic occur due to decreased myocardial contractility. An embolus these could hinder blood flow -sections cardiac who previously are not damaged by infarction its original. The embolus can also flow to other organs, blocking the flow of blood and cause the diorgan infarction.

2. Heart failure kongesif

Congestive heart failure occurs when the heart can not pump out all the blood it receives. Heart failure can occur soon after initial myocardial infarction when measuring very wide, or arising after the activation of baroreceptor reflexes. With the reactivation reflex-reflex baroreceptor happen increase in blood who back heart of the which damaged as well as kontriksi arteries and arterioles next to downstream. This causes the heart of collected blood and cause excessive stretching of the heart muscle cells. If stretching is great enough, it can decrease cardiac contractility due to lagging muscle cells in length-tension curve.
3. Dysrhythmias

Dysrhythmias may result from changes in electrolyte balance and pH decrease. Areas irritable heart of the action potential can begin to let go, causing dysrhythmias. SA node and AV, or transduction pathways (Purkinje fibers or bundle of His), can be a part of the zone of ischemic or necrotic affecting arcing or delivery of a signal. Fibrasi is the major cause death on infarction myocardial outside hospital.

4. Cardiogenic shock

Cardiogenic shock occurs when cardiac output is greatly reduced in a long time. Cardiogenic shock can be fatal at times infarction, or cause of death or the death or weakness of a few days or weeks later due to lung or kidney failed because these organs ischemia. Cardiogenic shock is usually associated with the damage as much as 40% of heart muscle mass.
5. Pericarditis

Occurs pericarditis, inflammation of lining of the heart (usually a few days after infarction). Pericarditis as part of a reaction inflammation after the injury and death of cell. Partially types of pericarditis can be arise a few weeks after infarction, and perhaps reflect an hypersensitivity reactions an immune against tissue necrosis.

6. Myocardial rupture

Once healed myocardial infarction, scar tissue is formed to replace cells that die miokadium. If the scar tissue is large enough, then the contractility of the heart can be permanently reduced. On partially of cases, scar tissue such weak so that then can occur ruptur myocardium or neurisma.

Examination Diagnostic

Diagnostic examination (Barbara engram: 1998) is

1. ECG

Shows ST wave elevation, mean ischemia, decreased or flat T waves, presence of Q waves neklosis.
2. Cardiac enzymes and isoenzymes

CPK-MB (isoenzymes were found in the heart muscle) increased between 4-6 hours, peaking within 12-24 hours, returning to normal within 36-48 hours. LDH increased in 12-24 hours, peaking within 24-48 hours, and takes a long time to return to normal. AST (aspartate amonitransfererase) rise occurs within 6-12 hours, culminating in 24 hours, returning to normal within 3-4 days.

3. Electrolyte

Imbalances can affect conduction and may affect contractility, examples hipoklemia / hyperkalemia.
4. Leukocytes / white blood cells

Leukocytes (10000-20000) usually appears on the second day after the IM with respect to the inflammatory process.

5. GDA / pulse oximetry

Can indicate hypoxia or decreased disease process.

6. Cholesterol / serum tridlesirifa

Showed increased arterioskerosis IM

7. Photos chest

Normal or may show an enlarged heart or ventricular aneurysm is suspected GJK.
8. Echocardiogram

Possible done for determine dimensions of foyer, movement valves / walls ventricular, and configuration of / function valve.

9. Nuclear imaging tests

Thallium: evaluating flow blood mitochondria and cell status miokardia, sample location / extent of IM acute / previous.  Technetium: accumulation in ischemic cells around the necrotic area.

10. Imaging heart blood / MUGA

Evaluating ventricular penampilam special and general, regional wall motion, and ejection fraction (blood flow).

11. Coronary angiography

Illustrates the narrowing / blockage of coronary arteries and made in connection with the porch speed pressure measurements and assess left ventricular function.
12. Substraction digital angiography / DSA

Techniques which used for describe the status planting arteries and for detect the artery disease parifer.

J. Management

1. Medical

Medical management (Barbara engram: 1998) is

a. Pharmacology:

1) Anticoagulants (to prevent new clots)

2) Nitrate (for maintain vasodilation reduce afterload and preload)

3) Agents calcium channel blockers (to increase vasodilation and reduces myocardial contraction)

4) The dividers beta-adrenegrik (for reduce contractility miocard, up to needs of oxygen are met)
5) Agent trombolik as tissue plasminogen activator (tPA), urokinase or streptokinase (for blood clotting) can be given intravenously between 4-6 hours after an attack of chest pain.
b. Surgery

1) For persistent pain, chronic and severe chest pain that required tandur coronary artery bypass grafting (CABG), or trasluminal percutan coronary angioplasty (PTCA). Includes the placement and pumping PTCA balloon catheter tip occlusion on regional arterial lesions ateromasus to press and hold exceeds the vessel wall, to improve blood flow to the Myocardium. Patients tang single vessel disease and heart seizures occurring less than 1 (one) year should undergo PTCA. Patients must continue to constantly to experience therapeutic treatment of before procedure and the conversion of habits of / pattern of life, describe modification factor risk of since care discontinued. Procedure PTCA with anteriografi coronary unless the team CABG performed on cases with complications. Also laser angioplasty possible done. Although does not done treatment on angina, this case can help minimize intensity on chest pain.

2. Diet

For the recommended dietary guidelines lowers risk of coronary heart disease (from Smallcrab.com) is:
a. Fat consumption moderate, <30% of total caloric intake consisting of

1) Saturated fat <10%

2) polyunsaturated fat> 10%

3) The rest is monounsaturated by 10-15%

b. Carbohydrates 50-60% of total calorie intake

c. Protein as much as 10-20% (average) of total caloric intake.
Recommended foods:

a. Sources of folic acid: orange juice, beans, broccoli, and spinach.

b. Sources of vitamin B6: bananas, advokad, lean chicken, brown rice, and a type of wheat.

c. Sources of beta-carotene: carrots and green vegetables

d. Sources of Vitamin E: Vegetable oils and nuts.

e. Source of omega-3 fatty acids: tuna, mackerel, sardines, and lemusu.

f. Sources of lycopene: tomatoes, especially the cook

g. Sources of flavonoids: grapes, apples, onions, and tea.

h. High-fiber foods: vegetables and nuts.

CHAPTER III

ORPHANAGE NURSING

A. Nursing Assessment

Basics in the assessment of patients (Donges Marilyn E, et al: 1999) is
1. Activity

a. Symptoms: weakness, fatigue, can not sleep.

Sedentary lifestyles, irregular exercise schedule.

b. Signs: tachycardia, dispenia at rest / activity.

2. Circulation:

a. Symptoms: a history of IM previous, artery disease coronary, GJK, the problem TD, diabetes mellitus.

b. Mark:

TD: can be normal or up / down, postural changes recorded from the bed to sit / stand
Nadi: can the normal, full /, or weak / strong quality with slow capillary refill, irregular (dysrhythmias) may occur.

Heart sounds: extra heart sounds: S3/S4 may indicate heart failure / decreased contractility or ventricular complain.

Murmurs: when there is indicates fails valve or muscle dysfunction papillary.
Friction: disurigai pericarditis.

Heart rhythm: can regular or irregular.

Edema: juguler venous distention, edema dependent / peripheral, generalized edema, there

may krekels with heart failure / ventricular.

Color: pale or cyanosis / bark ash-ash, nails flat, on the membrane mucosa and lip.
3. Intregitas Ego:

a. Symptom

1) Denying symptoms of oenting / the existence of condition.

2) Fear of death, feelings of doom is imminent.

3) Angry at the disease / treatment that is "not necessary".

4) Worried about family, work, finances.

b. Sign

1) Refuse, denial, anxiety, lack of eye contact.

2) Restlessness, angry, behavior attacking.

3) Focus on yourself / pain.

4. Elimination

a. Signs: normal / decreased bowel sounds

5. Food / fluid

a. Symptoms: nausea, loss of appetite, burping, solar flexus painful liver or burning

b. Signs: decreased skin turgor, dry skin / burning, weight loss.

6. Hygiene

a. Symptoms / signs: difficulty perform the task nursing.

7. Neurosensori

a. Symptoms: dizziness, pulsed during sleep / moment wake up

b. Sign of: changes mental, weakness.

8. Pain / discomfort

a. Symptoms: Chest pain that arises suddenly

b. Sign

1) The face grimacing posture changes

2) Crying, moaning

3) changes in the frequency of the automatic response / heart rhythm, blood pressure, breathing, consciousness.

9. Breathing

a. Symptom

1) Disnea with / without work, disnea noktural

2) Cough with / without sputum production

3) history of smoking, chronic respiratory disease
b. Sign

1) Increased respiratory rate, shortness of breath / strong

2) Pallor / sianosis

3) The sound of the breath: clean or krekels / wheezing

4) Sputum: clean, thick pink

10. Social interaction

a. Symptoms: stress, difficulty köping with stressor the existing.

b. Signs: difficulty resting in peace, too emotional responses.

B. Nursing Diagnosis

1. Acute pain associated with the buildup of lactic acid

2. Ineffective breathing pattern related to hyperventilation

3. Disorders gas exchange relate with changes membrane-capillary alveolar

4. Excess fluid volume related to kidney dysfunction, urinary retention

5. Decrease in cardiac output associated with the frequency and heart rhythm disturbances

6. Activity intolerance related to imbalance between supply and demand of oxygen. (Judith M Wilkinson and Nancy R Ahern: 2011)

C. Nursing plans and Rational Measures

Plans nursing and rational action (Judith M Wilkinson and Nancy R Ahern: 2011) is
1. Acute pain associated with the buildup of lactic acid

Expected results:

a. Patients reported physical wellbeing and psychological

b. The patient will demonstrate effective individual relaxation techniques to achieve comfort

c. Patients will melaorkan better sleep patterns

d. Patients will report reduced pain

Nursing interventions

Rational
         Perform Comprehensive assessment of pain include the location, characteristics, onset and duration, frequency, quality, intensity / severity of pain and the precipitation factor
subjective experience which must depicted patient for know the pain scale.  Ask the patient to assess pain or discomfort on a scale of 0-10  Pain as a subjective experience and should be described by .Bantu patients to assess pain by comparing it with other experiences.

Perform change of position, message backs and relaxation  Assist in reducing the perception or response . to give control situation, increase positive behavior.
Perform transfer of pain through television, radio, tape and supporting interaction

Helps patient in order that can divert concentration of against pain, to the something which create a relaxing.

Ensure provision of analgesia therapy or non-pharmacological strategies before performing procedures that cause pain.

That patients are able to control through the barrier effect of sympathetic stimulation.
2. Ineffective breathing pattern related to hyperventilation

Expected results:
a. Patients will show optimum breathing during mechanical ventilator attached
b. Patients will have the speed and rhythm of respiration within normal limits
c. Patients will have pulmonary function within normal limits
Nursing interventions

Rational
        Monitor respiratory pattern Knowing patterns of respiratory patient's Auskultasi sound of breath, note the area the decline  May indicate pulmonary edema due to cardiac decompensation secondary.  Collect and analyze patient data to regulate electrolyte balance

         To determine the level of the electrolyte balance of patients  Elevate extremities to improve venous blood flow So that the blood can return heart of the
Inform about relaxation techniques to improve breathing patterns  Help reduce the perception of pain responses by manipulating the body's physiological adaptation to pain
Consult with a nutritionist to provide a diet with adequate protein and sodium restriction Sodium causes fluid retention and should be limited

3. Disorders gas exchange relate with changes membrane-capillary alveolar
Expected results:

a. Patients will have pulmonary function within normal limits

b. Patients will have a symmetrical lung expansion

c. Patients did not experience shallow breathing / orthopnea

d. Patients will not use the muscles to breathe accessories

Nursing interventions

Rational
Assess lung sounds, breathing frequency, and business  breath and sputum production as an indicator of the use of supporting tools  Cardiac pump failure can cause respiratory stress dis  Teach the patient breathing and relaxation techniques
Help reduce the perception of pain responses by manipulating the body's physiological adaptation to pain  Teach patient effective coughing  Take action to reduce oxygen consumption (eg, reduce anxiety, pain)  In order to save the body needs oxygen
Adjust the position to reduce dyspnea  Patients are not expected to experience shortness of breath  Consult with your doctor about the importance of checking artery (GDA) and the use of assistive devices are recommended in accordance with the patient's condition changes  To determine the acid-base balance disorders  Give prescribed drugs (eg sodium bicarbonate)  To maintain acid-base balance  

4. Excess fluid volume related to kidney dysfunction, urinary retention
Expected results:
a. Patients will declare verbally understanding of fluid and dietary restrictions
b. Patients will be verbally expressed understanding of the drugs prescribed
c. Patients will maintain vital signs within normal limits for patient
d. Hemotokrit within normal limits

Nursing interventions

Rational
Determine the location and derjat parifer edema, sacral and periorbital on a scale of 1 + to 4 +
To determine the location and severity of edema edema that can be done immediately
Assess the limb or body part to poor circulation and edema of skin integrity
Knowing the severity of edema  Weigh weight every day and monitor trends  Sudden changes in body weight showed fluid balance.

Maintain accurate intake and output Meet the needs of adult body fluids but requires restrictions on the heart decompensation.  Maintain patient and allocate fluid restriction

So that the patient does not have excess fluid  Consult with a nutritionist to provide a diet with adequate protein and sodium restriction  Sodium increases fluid retention and should be limited.  Collaboration sesuia indication diuretics (furosemide / Lasix, Hydralazine / Apresoline, Spironlakton / Hidronolak-ton/Aldactone)  Diuretics may be necessary to correct the excess fluid volume.  

5. Decrease in cardiac output associated with the frequency and heart rhythm disturbances
Expected results:

a. Patients will have a cardiac index and ejection fraction within normal limits

b. Paien will have normal skin color

c. Patients will show increased tolerance to physical activity (for example: not experience dyspnea, chest pain)

d. Patients will identify the signs and symptoms of the condition can reported.
Nursing interventions

Rational
Change the position of the patient to a flat or Trendelenburg position when the patient's blood pressure is at a position lower than the usual range  . Elevating the head of the bed can ↓ labor effort to breathe and reduce venous return and preload

For sudden hypotension, weight / long pairs of intravenous access for the administration of intravenous fluids / medications to increase blood pressure  To facilitate the administration of drugs to increase blood pressure

Reposition the patient every 2 hours / maintain other activities appropriate / needed to reduce static parifer circulation. Bedrest in the supine position causes plasma volume → postural hypotension and syncope  Give or titrate the anti-arrhythmia drugs, inotropic, and vasodilator nitroglycerin to maintain contractility, preload and afterload in accordance with a medical program and protocol  Drug delivery can maintain cardiac contractility to do cardiac rehab center if necessary About providing support or additional pengawasasn belanjut and participation in the process of healing and well-being.

6. Activity intolerance related to imbalance between supply and demand of oxygen.
Expected results:

a. Patients will participate in physical activity is needed to increase normaldenyut cardiac, respiratory rate, and blood pressure monitoring pattern within normal limits
b. Patients will identify the activities / situations that cause anxiety that can lead to intolerance activity.

c. Patient will verbalize understanding of the needs of oxygenation, medications, and / or equipment that can increase tolerance for activity
Nursing interventions

Rational
Monitor response to activity kardiorespiratori To determine the level of tolerance for the activities undertaken by the patient  Regulate the use of energy to overcome / prevent fatigue and optimize function as aids patients to identify options activity

Lowering miokardiua work / oxygen consumption, lowering the risk of complications (eg expansion IM)

Monitor the oxygen response to the activities of self-care / nursing activity

To find out the needs of the patient response

Provide advice on and assistance in physical activity, cognitive, social and spiritual specifically to increase the range, frequency / duration of individual activities
Assist patients in performing activities Monitor vital signs before, during and after activity: stop the activity if the vital signs are not within the normal range for the patient or if there are signs that activity can not be tolerated. (Eg, chest pain, pallor, vertigo, dyspnea)

Tendency to determine a patient's response to activity and may indicate decreased oxygen miokardia that require decreased activity level / back bed rest, changes in the drug program, the use of supplemental oxygen. Limit visitors in accordance with the clinical state of the client.


Lowering myocardial work / oxygen consumption, lowering the risk of complications.

Klaborasikan with expert occupational physical (eg for security) So that patients can improve physical activity

CHAPTER IV

CLOSING

A. Knot

1. Myocardial infarction (IM) is the death of myocardial cells caused by prolonged lack of oxygen. This is the last lethal response to myocardial ischemia is not resolved. Cell-cells myocardium begin to die after approximately 20 minutes experiencing shortage of of oxygen. After this period, the ability the cell to generate ATP basis aerobis vanished, and the cell does not can meet its energy needs. (Elizabeth Corwin J: 2000)
2. Cardiovascular system consists of three parts, namely the interplay of the heart, blood vessels, and blood.

3. Affected by muscle layer of Acute Myocardial Infarction can be distinguished: acute myocardial infarction and acute transmural myocardial infarction non transmural.Sedangkan based oklusinya place in the coronary arteries: Acute Myocardial Infarction Anterior, Posterior Acute Myocardial Infarction, Inferior Acute Myocardial Infarction.
4. The cause tersering from infarction myocardial (MI) is rupture of the plaque atherosclerosis was on artery coronaria who caused spasme arterial or formation of thrombus.
5. The clinical manifestations of which are posed: Pain with sudden onset, nausea and vomiting occur, feeling weak, cold skin, decreased urine output.
6. Complications arising in patients with myocardial infarction (Elizabeth J Corwin, 2000) is thromboembolism, kongesif heart failure, dysrhythmias, cardiogenic shock, pericarditis, myocardial rupture.

7. Diagnostic examinations are ECG, electrolytes, cardiac enzymes and isoenzymes, leukocytes, etc.

8. Treatment for patients with myocardial infarction is

a. Medical  namely through pharmacology and surgery
b. Management of moderate-fat diet consumption is <30%, Carbohydrates 50-60% of total caloric intake, protein as much as 10-20% (average) of total caloric intake.
9. Nursing diagnosis for myocardial infarction

a. Acute pain associated with the buildup of lactic acid

b. Ineffective breathing pattern related to hyperventilation

c. Disorders gas exchange relate with changes membrane-capillary alveolar

d. Excess fluid volume related to kidney dysfunction, urinary retention

e. Decrease in cardiac output associated with the frequency and heart rhythm disturbances
i. Activity intolerance related to imbalance between supply and demand of oxygen.

B. Suggestion

Based on the above conclusions, the authors have some suggestions, such as:
a. In order to assist in the recovery efforts of myocardial infarction patients.
b. So that readers can apply the treatment regimen of patients of myocardial infarction