33. MYOCARDIAL INFARCTION MI refers to the process by which areas of myocardial cells in the heart are permanently destroyed. An occlusion of a coronary artery, MI leads to oxygen deprivation, myocardial ischemia, and eventual necrosis. Its one component of acute coronary syndromeI. ASSESSMENTa. Subjective data:a.1 Important health information Past Health history Previous history of illness and family health history particularly of heart disease

History of present illness Description of events r/t current illness, including any self-treatments and response General The patient experiences severe, persistent chest pain thats unrelieved by rest or nitroglycerin. He may describe the pain as crushing or squeezing. Usually substernal, pain may radiate to the left arm, jaw, neck, or shoulder blades.b.1 Functional Health Patterns Health perception-health management Family History of heart disease Sedentary lifestyle Tobacco use Nutritional-Metabolic Indigestion Heartburn Nausea Belching Vomiting Elimination Sweating (diaphoresis) Straining at stool Activity exercise Palpitations Dyspnea Dizziness Weakness Cognitive-perceptual Chest pain or discomfort, palpitations.b. Objective data Neurologic Anxiety, restlessness, light-headedness may indicate sympathetic stimulation or a in contractility and cerebral oxygenation Integumentary Cool, clammy, diaphoretic, and pale appearance due to sympathetic stimulation from loss of contractility may indicate cardiogenic shock. Dependent edema may also be present due to poor contractility. Cardiovascular Heart sounds may include S3, S4, and a new set of a murmur jugular venous distention may be seen if the Mi has caused heart failure. Elevated BP because of symphatetic stimulation or because of contractility, impending cardiogenic shock or medications Pulse deficit may indicate atrial fibrillation In addition to ST segment and T-wave changes, ECG may show tachycardia, bradycardia, and dysrhythmia Gastrointestinal urinary output may indicate cardiogenic shock Respirations Shortness of breath Dyspnea, tachypnea Crackles if MI has caused pulmonary congestion Pulmonary edema may be present Psychological Fear with feeling of impending doom, or patient may deny that anything is wrong.

c. Possible Diagnostic findings Serial 12-lead ECG may show no abnormalities or may proveinconclusive during the first few hours after MI. When present,characteristic abnormalities on the ECG can help pinpoint thelocation of the MI. ST-segment monitoring tracks the hearts response to MI. Continuousmonitoring can immediately detect ischemic episodes.During an MI, monitoring can help differentiate between an STsegment elevated MI (STEMI) and a non ST-segment elevated MI (NSTEMI); differentiating between a STEMI and NSTEMI helps the practitioner better guide treatment. ST-segment monitoring can also identify patients at high risk for reocclusion after PTCA or MI and permits prompt intervention if reocclusion occurs. After MI, monitoring may reduce or eliminate the need for angiography in patients receiving thrombolytic drugs by gaugingthe efficacy of the drugs. Serial serum cardiac marker measurements show elevated CK, especially the CK-MB isoenzyme (the cardiac muscle fractionof CK), troponin I and T, and myoglobin. Echocardiography shows ventricular wall dyskinesia (with transmural MI).II. PSCHO/PATHOPHYSIOLOGY AbstractMI results from prolonged ischemia to the myocardium with irreversible cell damage and muscle death. Functionally, MI causes: reduced contractility with abnormal wall motion altered left ventricular compliance reduced stroke volume reduced ejection fraction elevated left ventricular end-diastolic pressureIn myocardial infarction (MI), blood supply to the myocardium is interrupted. Heres what happens:

Injury to the endothelial lining of the coronary arteries causes platelets, white blood cells, fibrin, and lipids to gather at the injured site. Foam cells, or residentmacrophages, gather beneath the damaged lining and absorb oxidized cholesterol, forming a fatty streak that narrows the arterial lumen.

As the arterial lumen narrows gradually, collateral circulation develops,which helps to maintain myocardial perfusion distal to the obstructed vessel lumen. The illustration above shows collateral circulation.

When myocardial demand for oxygen is more than the collateralcirculation can supply, myocardialmetabolism shifts from aerobic toanaerobic, producing lactic acid (A),which stimulates nerve endings.

Lacking oxygen, the myocardial cells die. This decreases contractility, stroke volume, and blood pressure.

Hypotension stimulates baroreceptors, which in turn stimulate theadrenal glands to release epinephrine and norepinephrine. This cycle is shown above. These catecholamines increase heart rate and cause peripheralvasoconstriction, further increasing myocardial oxygen demand.

Damaged cell membrane in the infarcted area allow intracellular contents into the vascular circulation,asshownabove.. Ventricular arrhythmias then develop with elevated serum levels of potassium, creatine kinase (CK), CK-MB, aspartateaminotransferase, and lactate dehydrogenase.

INJURY SITEAll myocardial cells are capable of spontaneous depolarization and repolarization, so the electrical conduction system may be affected by infarct, injury, or ischemia.The illustration above shows an injury site.

Extensive damage to the left ventricle may impair its ability to pump, allowing blood to back up into the left atrium and, eventually, into the pulmonary veins and capillaries, as shown in the illustration above. Crackles may be heard in the lungs on auscultation. Pulmonary artery wedge pressure is increased.

As back pressure rises, fluid crosses the alveolar-capillary membrane, impeding diffusion of oxygen (O2) and carbon dioxide (CO2). Arterial blood gas measurements may show decreased partial pressureof arterial oxygen and arterial pH and increased partial pressure of arterial carbon dioxide.

Thrombolytic therapy Glycoprotein IIB/IIIA receptor antagonistsDiagram (Pathophysiology with treatment &clinical manifestations

Change in the condition of plaque in the coronary artery

Aspirin antiplatelet aggregatesElevated ST segment Q waveappearsActivations of platelets

Formation of thrombus

NitratesAltered repolarization of the myocardiumElevated CPK-MB Elevated myoglobin Troponin T & Troponin ISchemia of tissue in the region supplied by the artery

Release of lysosomal enzymes

Coronary blood supply less than demand

Beta-blockersLactic acid productionAnaerobic glycolysis

OxygenMyocardial cell death

Myocardial irritabilityNitro-glycerin

Angina

Stimulation of the sympathetic nervous sysytem

Decreased contractilityDys-rhytmiasAnti-dysrhythmics

Increased Heart needs

Angiotensin-Converting EnzymeinhibitorsDecreased left ventricular function

Increased O2 needsIncreased afterload

Increased preloadNItratesDecreased cardiac output

CVP PCWPDecreased LV ejection fractionVaso-contrictionFluid restriction

III. A. FORMULATION OF NURSING DIAGNOSIS # 1 Priority Nursing diagnosis # 1 Ineffective Cardiopulmonary tissue perfusion r/t reduced coronary blood flowIV. A. FORMULATION OF NURSING PLAN #1After 8 hours of Nursing Intervention, client will be relief of chest pain or any discomfortV. A. NURSING INTERVENTIONS #1 DependentNursing interventionsRationale

1. Initially assess, document and report to the physician the ff;

a.) The patients description, including location, intensity, radiation, duration, and factors that affect it. Other symptoms such as nausea, diaphoresis, or complaints of unusual fatigueb.) The effect of chest discomfort on cardiovascular perfusion to the heart (e.g. change in blood pressure, heart sounds) to the brain (e.g changes in LOC), to the kidneys (e.g. in urine output) and to the skin (e.g. color, temperature)

1. These data assist in determining the cause and affect of the discomfort and provide a baseline data with which post-theraphy symptoms can be compared.a.) There are many conditions associated with discomfort. There are characteristic clinical findings of ischemic pain and symptoms.

b.) MI decreases myocardial contractility and ventricular compliance and may produce dysrhythmias. Cardiac output is reduced, resulting in reduced blood pressure and decreased oragn perfusion. The heart rate may increase as compensatory mechanism to maintain cardiac output.

Ensure physical rest ; use of the bedside commode with assistance ; backrest elevated to promote comfort ; diet as tolerated ; arms supported during upper extremity activity ; use of stool softener to prevent straining at stool. Provide a restful environment, and allay fears and anxiety by being supportive, calm and competent. Individualized visitation based on patients response.2. Physical rest reduces myocardial oxygen consumption. Fear and anxiety precipitate the stress response ; this results in increased levels of endogenous catecholamines, which increases myocardial oxygen consumption. Also with increased epinephrine, the pain threshold id decreased, and pain increases myocardial oxygen consumption.

DependentNursing interventionRationale

1. administer oxygen as prescribed1. oxygen therapy may increase the oxygen supply to the myocardium if actual oxygen saturation is less than normal

2. administer medication therapy as prescribed and evaluate the patients response continuously.

3. Check the patients blood pressure after giving nitroglycerin, especially the first dose.

2. Medication therapy is the first line of defense in preserving myocardial tissue. The side effcts of these medications can be hazardous and the patients status must be assessed.

CollaborativeNursing interventionRationale

Obtain a 12-lead ECG recording during the sympatomatic event as prescribed, to determine extension of infarction.An ECG during symptoms may be useful in the diagnosis of an extension of MI

VI. A. FORMULATION OF EVALUATION #1After 8 hours of nursing intervention patient is able to report of beginning relief of chest discomfort and symptoms at once as seen by appears comfortable and pain or symptom free, are rested; respiratory rate, cardiac rate, and blood pressure return to prediscomfort level, has an adequate cardiac output as evidenced by normal heart rate and rhythm, blood pressure of within normal level, has adequate urine output.III. B. FORMULATION OF NURSING DIAGNOSIS # 2 Nursing Diagnosis # 2 Potential Ineffective air exchange r/t fluid overload IV. B. FORMULATION OF NURSING PLANAfter 8 hours of nursing intervention, client will not experience any respiratory difficulties. V. B. NURSING INTERVENTIONS # 2 IndependentNursing interventionRationale

1. Initially, every 4 hours, and with chest discomfort, or symptoms, assess, document, and report to the physician abnormal heart sounds (particularly S3 and S4 gallops and the holosystolic murmur of left ventricular papillary muscle dysfunction), abnormal breath sounds (particularly crackles) , and patient intolerance to specific activities.1.These data are useful in diagnosing left ventricular failure. Diastolic filling sounds (S3 and S4) results form the decreased left ventricular compliance associated with MI. Papillary muscle dysfunctiona(from infarction of the papillary muscle) can result in mitral regurgitation and a reduction in storke volume, leading to ventricular failure. The presence of crackles(usually at the lung bases) may indicate pulmonary congestion from increased left heart pressure. The association of symptoms and activity can be used as the guide for activity prescription and a basis for patient teaching.

2. Teach patient :a.) to adhere to the diet prescribed(for example, explain low sodium, low calorie diet)

b.) To adhere to activity prescription a.) Low sodium diet may reduce extracellular volume thus reducing preload and afterload, and thus myocardial oxygen oxygen consumption.b.) The activity prescription is determined individually to maintain the heart rate and blood pressure within safe limits.

3. Watch for signs and symptoms of fluid retention(crackles, cough, tachypnea, and edema. Carefully monitordaily weight, intake and output, respirations, serumenzyme levels, and blood pressure. Auscultate foradventitious breath sounds periodically (patients onbed rest commonly have atelectaticcrackles) and forS3 or S4 gallops.

3. Fluid retention mayindicate impending heart failure.

DependentNursing interventionsRationale

To promote compliance with the prescribed medication regimen and othertreatment measures, thoroughly explain dosages and therapy. Warn about drug adverse effects, and advise the patient to watch for and report signs of toxicityTo anticipate possible effects of the drugs.

CollaborativeNursing interventionRationale

1. Ask the dietary department to provide a clear liquid diet until nausea subsides1. A low-cholesterol, low-sodium diet may be ordered.

2.Counsel the patient about lifestylechanges. Review dietary restrictions. Ifthe patient must follow a low-sodium orlow-fat and low-cholesterol diet, provide a list of undesirable foods. Ask the dietician to speak to the patient and his family2. to learn more on appropriate diet.

3. Recommend his participation in a cardiac rehabilitation program for exercise, education, symptom management, and support with risk modification.

3. that will help manage the disease

VI. B. FORMULATION OF NURSING EVALUATION #2After 8 hours of nursing intervention, patient experiences no shortness of breath, dyspnea on exertion, orthopnea, or paroxysmal nocturnal dyspnea and a total relief of chest discomfort, appears comfortable and rested as evidenced by respiratory rate of less than 20 breaths/min with physical activity and 16 breaths/min with rest, skin color is normal, PaO2 and PaCO2 within normal range,heart rate is less than 100 beats/min and greater than 60 beats/min, with blood pressure within patients normal limits.

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