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 : 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 : 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 : 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