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Barrier between the vessel wall and the lumen of the vessel Nonreactive to platelets and leukocytes Nonreactive to coagulation, fibrinolytic, and complement factors Endothelial wall alters as a result of inflammation and injury
Fatty Streak
Earliest lesions Characterized by lipid-filled smooth muscle cells Can begin as early as age 15 Potentially reversible with lowering LDL cholesterol
Fibrous Plaque
Beginning of progressive changes in the arterial wall Can appear by age 30 and increases with age Lipoproteins transport cholesterol and other lipids into the arterial intima Fatty streak is covered by collagen, forming a fibrous plaque Narrows the artery and a reduces blood flow to the distal tissues
Complicated Lesion
Continued inflammation resulting in plaque instability, ulceration, and rupture Platelets accumulate and thrombus forms Increase narrowing or total occlusion of lumen
Collateral Circulation
Factors contributing to the growth and extent of collateral circulation Inherited predisposition to develop new blood vessels Presence of chronic ischemia When occlusion occurs slowly there is an increased chance of adequate collateral circulation and adequate myocardial blood flow With rapid onset CAD or coronary spasm, there is not enough time to establish collateral vessels Diminished arterial flow results in more severe ischemia or infarction
Ethnicity White middle-aged men have highest incidence African American women have a higher incidence and death rate compared to white women Native Americans have mortality rates 2x high as other Americans Family history Familial hypercholesterolemia Genetic predisposition Autosomal dominant disorder
Elevated serum lipids Cholesterol >200 mg/dl Triglycerides >150 mg/dl Lipoproteins HDLs - high density high levels desirable low levels associated with risk for CAD LDLs - low density Elevated levels correlate most closely with increased incidence of CAD
Elevated blood pressure Hypertension: BP > 140/90 Increases risk of atherosclerosis Tobacco use Nicotine can cause catecholamine release HR, peripheral vasoconstriction, BP Platelet adhesion leading to emboli formation
Physical inactivity People who are active have higher HDLs Exercise increases collateral circulation & lowers BP Obesity BMI > 30 kg/m2 Leads to increased LDLs and triglycerides Associated with hypertension People who are apple-shaped (store fat in abdomen) have higher incidence of CAD
Diabetes & Metabolic syndrome Incidence of CAD 2-4x higher Obesity Hypertension Elevated triglycerides, abnormal serum lipids, elevated fasting blood glucose Insulin resistance
Psychological states Increase risk of CAD Include depression, hopelessness, anxiety, hostility, & anger Stress correlated with CAD Elevated homocysteine level Damage the inner lining of blood vessels Promote plaque build-up Alter the clotting mechanism to make clots more likely to occur
Health Promotion
Hypertension Have regular blood pressure checkups Take prescribed medications for blood pressure control Reduce salt intake Stop tobacco use; avoid exposure to environmental tobacco (secondhand) smoke Control or reduce weight Perform physical activity regularly
Health Promotion
Elevated serum lipids Reduce total fat intake Reduce animal (saturated) fat intake Take prescribed medications for lipid reduction Adjust total caloric intake to achieve and maintain ideal body weight Engage in regular physical activity Increase amount of complex carbohydrates and vegetable proteins in diet
Health Promotion
Tobacco use Enroll in a smoking cessation program Change daily routines associated with smoking to reduce desire to smoke Substitute other activities for smoking Ask caregivers to support efforts to stop smoking Avoid exposure to environmental tobacco smoke
Health Promotion
Physical Inactivity
Develop and maintain at least 30 minutes of moderate physical activity on most days of the week Increase activities to a fitness level
Health Promotion
Psychological State Increase awareness of behaviors that are detrimental to health Alter patterns that are conducive to stress Set realistic goals for self Reassess priorities in light of health needs Learn effective stress management strategies Seek professional help if feeling depressed, angry, or anxious Plan time for adequate rest and sleep
Health Promotion
Obesity
Change eating patterns and habits Reduce caloric intake to achieve BMI of <25 Increase physical activity to increase caloric expenditure Avoid fad and crash diets, which are not effective over time Avoid large, heavy meals
Health Promotion
Diabetes Follow the recommended diet Control or reduce weight Take prescribed anti-diabetic medications Monitor blood glucose levels regularly
Nutritional Therapy
Calorie restrictions Decrease dietary fat/cholesterol Limit saturated fats and cholesterol and emphasize complex carbohydrates Fats only about 30% of calories
Reduce or omit red meats, eggs, whole milk Omega 3 fatty acids
Presence of cardiovascular symptoms Environmental patterns like diet and activity Values and beliefs about health and illness
ASA , Plavix
Low dose ASA (81mg) Studies show decrease in first MIs Can cause GI bleed
Use if benefit outweighs risk Plavix has decreased risk of bleed
Temporary myocardial ischemia = Angina (chest pain) Happens when oxygen supply is less than oxygen demand
Cardiac Non cardiac
Primary reason for insufficient blood flow is narrowing of coronary arteries by atherosclerosis
Physical exertion Temperature extremes Strong emotions Consumption of heavy meal Tobacco use or environmental tobacco smoke Sexual activity Stimulants Circadian rhythm patterns
Referred pain in left shoulder and arm is from transmission of the pain message to the cardiac nerve roots Pain usually lasts 3 to 5 minutes Pain subsides when precipitating factor relieved Pain at rest is unusual ECG reveals ST-segment depression and/or Twave inversion
Intermittent chest pain that occurs over a long period with the same pattern of onset, duration, and intensity of symptoms Constrictive Squeezing Heavy Choking Suffocating sensation
Silent Ischemia Ischemia that occurs in the absence of any subjective symptoms Associated with diabetic neuropathy Confirmed by ECG changes Up to 80% of patients with ischemia are asymptomatic Ischemia with or without pain has same prognosis
Nocturnal angina Occurs only at night but not necessarily during sleep or in recumbent position Angina decubitus Chest pain that occurs only while lying down Relieved by standing or sitting
Microvascular Angina
May occur in the absence of significant coronary atherosclerosis or coronary spasm Seen especially in women Pain is related to myocardial ischemia associated with abnormalities of the coronary microcirculation.
When ischemia is prolonged and is not immediately reversible, acute coronary syndrome (ACS) develops. ACS encompasses Unstable angina (UA) NonST-segment-elevation myocardial infarction (NSTEMI) ST-segment-elevation MI (STEMI)
Progression of CAD
Result
Partial occlusion of coronary artery: USA or NSTEMI Total occlusion of coronary artery: STEMI
Unstable Angina
Chest pain that is: New in onset Occurs at rest Has a worsening pattern Chronic stable angina can develop to unstable Significant change in the pattern of pain Increasing frequency Easily provoked by minimal or no exertion Unpredictable and represents a medical emergency
Myocardial Infarction
Result of sustained ischemia (>20 minutes), causing irreversible myocardial cell death (necrosis) Necrosis of entire thickness of myocardium takes 4 to 6 hours. Eighty percent to 90% of all acute MIs are secondary to thrombus formation
Myocardial Infarction
Infarctions are usually described according to the location of damage Anterior Inferior lateral posterior wall infarction
Myocardial Infarction
The degree of altered function depends on the area of the heart involved and the size of the infarct. Contractile function of the heart is disrupted in areas of myocardial necrosis. Most MIs involve the left ventricle (LV).
Pain
Total occlusion Anaerobic metabolism and lactic acid accumulation Severe, immobilizing chest pain not relieved by rest, position change, or nitrate administration Described as heaviness, constriction, tightness, burning, pressure, or crushing Common locations: Substernal, retrosternal, or epigastric areas; pain may radiate to neck, jaw, arms
Stimulation of sympathetic nervous system results in Release of glycogen Diaphoresis Vasoconstriction of peripheral blood vessels Skin: Ashen, clammy, and/or cool to touch
Cardiovascular Initially, HR and BP, then BP (secondary to in cardiac output) Crackles Jugular venous distention Abnormal heart sounds S3 or S4 New murmur
Nausea and vomiting Can result from reflex stimulation of the vomiting center by severe pain Fever Systemic manifestation of the inflammatory process caused by cell death
Diagnostic Studies
12-lead ECG Can rule out or confirm MI Changes in QRS complex, ST segment, & T wave Not always evident shortly after infarct Serum cardiac markers Released into blood from necrotic heart muscle after MI Troponin CK-MB Myoglobin Serial
ECG Changes
ECG Changes
Diagnostic Studies
Coronary angiography Cardiac catheterization Percutaneous coronary intervention (PCI) Stent Balloon angioplasty Stress testing Exercise Drug Persantine Adenocard Echocardiogram
Complications
Dysrhythmias
Abnormal heart rhythms Most common complication Present in 80% of MI patients Most common cause of death in the pre-hospital period Life-threatening dysrhythmias seen most often with anterior MI, heart failure, or shock
Complications
Heart failure A complication that occurs when the pumping power of the heart has diminished Symptoms mild dyspnea restlessness agitation slight tachycardia. pulmonary congestion, crackles jugular vein distention
Complications
Cardiogenic shock Occurs when inadequate oxygen and nutrients are supplied to the tissues because of severe LV failure Mortality rate is high Signs and symptoms
Low BP Confusion pale, clammy skin Decreased urine output
Requires aggressive management control of dysrhythmias Intra-aortic balloon pump (IABP) therapy vasoactive drugs
Complications
Complications
Ventricular aneurysm Results when the infarcted myocardial wall becomes thinned and bulges out during contraction Signs and symptoms Chest pain Ventricular arrhythmias Heart failure Treatment Anticoagulation Surgery
Complications
Acute pericarditis An inflammation of visceral and/or parietal pericardium Occurs 2-3 days after MI May result in cardiac compression, LV filling and emptying, heart failure Signs and symptoms aggravated by inspiration, coughing, and movement of the upper body Pericardial friction rub may be heard on auscultation Chest pain different from MI pain Treatment includes pain relief with aspirin or corticosteroids
Complications
Dressler syndrome May also occur after cardiac surgery Characterized by pericarditis with effusion and fever that develop 4 to 6 weeks after MI Arthralgia Thought to be caused by an antigen-antibody reaction to the necrotic myocardium Treatment Short-term corticosteroids
Maintain cardiac output Treat pain Assess for complications Increase activity tolerance Relieve anxiety Ongoing and discharge teaching
Myocardial Revascularization Emergent PCI Treatment of choice for confirmed STEMI 90 minute door to table time Ambulatory 24 hours after the procedure Variety of procedures Percutaneous transluminal coronary angioplasty (PTCA) Intracoronary stenting Drug-eluting stents
Advantages of PCI Provide alternative to surgical intervention Performed under local anesthetic Patient ambulatory 24 hours after procedure Length of hospital stay decreased 1-3 days vs. 46 days after CABG Rapid return to work Return to work 57 days vs. 28 weeks after CABG
Nursing care post PCI Monitoring for signs of recurrent angina Monitor VS Evaluating groin site for signs of bleeding Monitor for infection Assess CMS of extremity used Assess for hematoma formation Bed rest
Thrombolytic therapy
Indications and contraindications
History of or current major bleeding problem (hemorrhagic stroke, GI bleed) prevents administration Administered at facilities that do not have PCI capabilities May still need PCI after thrombolytics if not fully effective
Time is muscle; 6-hour window Several thrombolytic agents available, such as:
Tissue plasminogen activator (t-PA) Streptokinase Reteplase
Coronary Artery Bypass Grafting Construction of new conduits Requires Sternotomy Cardiopulmonary bypass Common artery used: Internal mammary artery (IMA) Saphenous vein
Indications for CABG Unstable angina AMI Failure of percutaneous interventions Goals of CABG Increase blood flow to myocardium Relieve symptoms Prolong survival Improve quality of life
Drug Therapy
Antiplatelet aggregation therapy Chewable ASA 160 to 325 mg Nitroglycerin SL Given q 5 minutes 3 doses total IV nitroglycerin Goal: reduce anginal pain and improve coronary blood flow Immediate onset of action Titrated for pain relief Common side effects: HYPOTENSION HEADACHE
Drug Therapy
Morphine sulfate Given if chest pain not relieved with nitro SL Also acts as vasodilator and decreases myocardial oxygen consumption, reduces contractility, and decreased BP and HR Also reduces anxiety and fear -adrenergic blockers Decrease myocardial oxygen demand by reducing HR, BP, and contractility IV administration in acute phase i.e. metoprolol (Lopressor)
Drug Therapy
Angiotensin-converting enzyme (ACE) inhibitors Prevent ventricular remodeling and prevent or slow progression of HF i.e. captopril (Capoten), enalapril (Vasotec) Antidysrhythmia drugs Dysrhythmias are only treated in life threatening
Drug Therapy
Cholesterol-lowering drugs Must first obtain fasting lipid panel If LDL is elevated, cholesterol-lowering drugs are initiated Stool softeners Promote bowel movement Prevents straining and vagal stimulation from Valsalva maneuver
Nursing Diagnoses
Acute Pain Decreased Cardiac Output Anxiety Activity intolerance Risk for ineffective tissue perfusion