Myocardial Infarction

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Presentation Transcript

Myocardial Infarction : 

Myocardial Infarction Reynel Dan Galicinao Angelia Galinato Fiona Samantha Ajoc

Myocardial Infarction : 

Myocardial Infarction Formation of localized necrotic areas within the myocardium Usually follows sudden coronary occlusion and abrupt cessation of blood and oxygen flow to the heart muscle Prolonged ischemia (>35-45min) produces irreversible damage and necrosis of the myocardium

Risk Factors : 

Risk Factors

Modifiable: : 

Modifiable: Atherosclerosis CAD, HPN Impaired glucose tolerance Obesity Elevated serum triglyceride, LDL, and cholesterol levels Decreased serum HDL levels Smoking Excessive intake of saturated fats, carbohydrates, salt Sedentary lifestyle Use of drugs (amphetamines [shabu], cocaine) Stress Type A personality (aggressive, competitive attitude, addiction to work, chronic impatience)

Non-modifiable : 

Non-modifiable Age: >45yo Genetic Predisposition: family hx of CAD, early coronary disease Race: American, African, Hispanic/Latino Sex: Men are more susceptible than premenopausal women, although incidence is rising among women who smoke and take hormonal contraceptive The incidence in postmenopausal women is equal in men Women have higher morbidity and mortality rates than men, (older and have more preexisting diseases when MI occurs, women delay seeking treatment longer than men do)

Causes : 


Slide 7: 

MI results from occlusion of one of the coronary arteries which can stem from: Atherosclerosis Coronary Thrombosis / Embolism Platelet aggregation Coronary artery stenosis/spasm Decreased blood flow with shock and/or hemorrhage Direct trauma

Pathophysiology : 


Slide 10: 

MI almost always occurs in the left ventricle due to occlusion of left anterior descending artery (LADA) & often significantly depresses left ventricular fcn (anterior wall infarction) Alterations in fcn depend on size and location of an infarct

Slide 11: 

Contractile fcn in the necrotic area cease permanently Healing requires formation of scar tissues that replace the necrotic myocardial muscle Scar tissue inhibits contractility

3 Areas which Develop in MI : 

3 Areas which Develop in MI Zone of Infarction – records pathologic Q wave in the ECG Zone of Injury – gives rise to elevated ST segment Zone of Ischemia – produces inversion of T wave

Classification of MI : 

Classification of MI Transmural infarct – extends from endocardium to epicardium Subendocardial infarct – affects the endocardial muscles Intramural infarction – seen in patchy areas of the myocardium; equally associated with angina pectoris

Complications of MI : 

Complications of MI Dysrhythmias Cardiogenic Shock Pericarditis Rapture of myocardium Ventricular aneurysm CHF Dressler’s Syndrome

Assessment Findings : 

Assessment Findings

Slide 16: 

Pain Cardinal symptom of MI: persistent, crushing substernal pain that may radiate to the left arm, jaw, neck, and shoulder blades Unrelieved by rest or nitroglycerine Anxiety and Apprehension Feeling of “doom”, restlessness Shock Systolic pressure <80mmHg, lethargy, cold clammy skin, diaphoresis, peripheral cyanosis, tachy/bradycardia, weak pulse

Slide 17: 

Oliguria Urine flow <30mL/hr Fever Slight temp elevation within 24h & extends 3-7days with leukocytosis, elevated ESR “Indigestion” “gas pains around the heart”, nausea & vomiting Acute Pulmonary Edema Sense of suffocation, dyspnea, orthopnea, gurggling, bubbling respiration

Diagnostic Studies : 

Diagnostic Studies

Slide 19: 

Total Creatine Kinase Level Rises within 3h after onset of chest pain Peaks within 24h after damage and death of cardiac tissue CK-MB isoenzyme Peak elevation: 18-24h after onset of chest pain Returns to N° 48-72h later Troponin level Rises within 3h Remains elevated up to 3wks

Slide 20: 

Myoglobin Rises within 1h after cell death Peaks in 6h Returns to N° within 24-36h or less LDH level Rises 24h after MI Peaks 48-72h Falls to N° in 7days WBC Elevated WBC (10,000-20,000 cells/mm3) on 2nd day following MI lasts up to 1wk

Slide 21: 

ECG ST segment elevation, T wave inversion, pathologic Q wave Hours to days after MI, ST and T wave changes will return to N° Q wave usually remains permanently

Dx Test following Acute Stage : 

Dx Test following Acute Stage Exercise Tolerance Test / Stress Test Assess for electrocardiographic changes and ischemia Evaluate for medical therapy Identify pts who may need invasive therapy

Slide 23: 

Thallium scan – assess ischemia or necrotic muscle tissue Multigated cardiac pool imaging scans – evaluate left ventricular fcn Cardiac catheterization – determine the extent and location of obstructions of the coronary arteries

Collaborative Management : 

Collaborative Management

Medications : 

Medications Analgesic Relief of pain This is a priority; pain may cause shock Administer IV Morphine sulfate, Lidocaine, or Nitroglycerine

Slide 26: 

Thrombolytic Therapy Disintegrate dlood clot by activating fibrinolytic processes Streptokinase, Urokinase, Tissue Plasminogen Activator (TPA) Administration is most crucial between 3-6h after initial infarction has occurred Detect for occult bleeding during and after thromolytic therapy Assess neurologic status changes (may indicate GI bleeeding or cardiac tamponade)

Slide 27: 

Anticoagulant and antiplatelet medications - administered after thrombolytic therapy to maintain arterial patency. Other meds: Beta-adrenergic blocking agents; Diazepam (Valium)

Treatment : 


Goals : 

Goals Prevention of further tissue injury and limitation of infarct size Maximize myocardial tissue perfusion and reduce myocardial tissue demands

Slide 30: 

Supplemental O2 by nasal cannula – increase myocardial oxygen supply; relieves pain Cardiac monitoring – detect occurrence of dysrhythmias Percutaneous transluminal coronary angioplasty – reopen occluded artery

Nursing Diagnoses : 

Nursing Diagnoses Acute pain Decreased cardiac output Ineffective tissue perfusion: Cardiopulmonary Excess fluid volume Imbalanced nutrition: Less than body requirements

Slide 32: 

Fatigue Activity intolerance Ineffective sexuality patterns Anxiety Ineffective coping Ineffective denial

Nursing Management : 

Nursing Management

Slide 34: 

Promoting Oxygenation and Tissue Perfusion Instruct pt to avoid over fatigue; stop activity immediately in the presence of chest pain, dyspnea, light-headedness, faintness O2 therapy for first 24-48h or longer if pain, hypotension, dyspnea, dysrhythmia persist Monitor VS changes Position pt to Semi-Fowler’s

Slide 35: 

Promoting Adequate CO Monitor: Dysrhythmias, ECG tracings VS Effects of ADLs on cardiac status Rate and rhythm of pulse Administer pharmacotherapy as prescribed Promote rest, minimize unnecessary disturbances

Slide 36: 

Promoting Comfort Relieve pain Admin morphine sulfate as ordered To decrease sympathetic stimulation, which increases myocardial oxygen demand Prevent shock from severe pain

Slide 37: 

Providing Rest CBR with TP for 34-48h Admin diazepam (Valium) as ordered Explain purpose of CCU For continuous monitoring and safety during early recovery period Provide psychosocial to pt and SO Calmness and competency are extremely reassuring

Slide 38: 

Promoting Activity Gradual increase in activity after first 24-48h May be allowed to sit on a chair for increasing periods of time May begin ambulation on 4th or 5th day Monitor for signs of dysrhythmia, chest pain, changes in VS during activity

Slide 39: 

Promoting Nutrition and Elimination Small frequent feedings Low-calorie, low-cholesterol, low-sodium diet Avoid stimulants Avoid very hot or very cold beverages and gas-forming foods Avoid use of Valsalva Maneuver Use bedside commode Administer stool softener as ordered

Slide 40: 

Promoting Relief of Anxiety and Feeling of Well-Being Provide opportunity for pt and SO to explore concerns and identify alternative coping methods Facilitate Learning Start teaching when pt is free of pain and excessive anxiety Promote positive attitude and active participation of pt and SO

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