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Coronary Artery Disease: comprised of chronic stable angina (CSA) &…

- - - - Fatty Streak Formation: the first visible lesion, LDL accumulates in the smooth muscle cells of the arterial intima. Monocytes, lymphocytes, mast cells, & neutrophils are drawn into the arterial wall as inflammation begins. As macrophages take up LDL particles they become foam cells that can accumulate in layers
        
        Fibrous Cap Formation: numerous foam cells and activates inflammatory cells accumulate within the intima of the artery. Increasing accumulation of extracellular lipid pools within the artery and causes cell necrosis progressively destorying the intima structure. Lipid rich necrotic tissue dominates the central area of the intima that can occupy 30-50% of arterial wall volume. Fibrous cap formation occurs from the fibrous tissue to cover the lipid rich necrotic cores to form a dominant lesion
        
        Complicated Lesion: continued inflammation can result in plaque instability, ulceration, and rupture. Platelets accumulate in large numbers, leading to a thrombus, and can adhere to the artery wall and cause total occlusion or partial, activation of exposed platelets causes expression of glycoprotein IIb/IIIa receptors that bind fibrinogen leading to further platelet aggregation and adhesion
        
        Collateral Circulation Formation: when atherosclerotic plaque occludes the normal flow of blood through a coronary artery a collateral circulation of specialized endogenous bypass vessels as a protective mechanism against ischemic injury can develop. Collateral circulation provides an alternative source of blood supply when the original vessel fails to provide sufficient blood. The growth and extent of collateral circulation depends on the inherited predisposition of angiogenesis and the presence of chronic ischemia.
        
        These lipid changes can be reversed with a diet low in LDL cholesterol.
- - - - Treatment/Management of High Risk Individuals
        
        Alteration of Lifestyle Factors: few people want to make lifestyle changes with no symptoms of disease, the nurse should assist these patients in clarifying their personal values, explain risk factors which may help them recognize their susceptibility to CAD.
        
        Smoking cessation causes CAD mortality to drop to those of non-smokers within 12 months.
        
        Modifiable risk factors: dyslipidemia, decreased HDL, elevated fasting blood glucose (> 5.8), hypertension (> 140/90 mmHg), physical inactivity, tobacco use, DM, obesity (WC > 102 cm in men; > 88 cm in women), diet, metabolic syndrome, psychological states
        
        May be harder to modify for some individuals based on social determinants of health.
        
        Income and social status
        
        Education and employment conditions
        
        Access to transportation & food
        
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        Personal health practices, coping skills, & social support networks
        
        Physical activity adults should accumulate at least 150 minutes of moderate to vigorous intensity aerobic PA per week, in bouts of 10 minutes or more to reduce CVD risk. PA increases HDL production, more efficient O2 extraction by the working muscles dereasing cardiac workload.
        
        Preventive programs should have an appropriate setting and a flexible approach that allows easy access, especially when that community includes vulnerable and deprived groups.
        
        Home-based exercise programs reduce the need for attending specialized, costly centers like gyms. Mail and telephone contact with patients rather than in office appointments
        
        Nutrition: B vitamins (B6 & B12, folic acid) have been shown to reduce serum levels of HC, reducing sodium intake can assist in lowering BP, major sources of CL should be eliminated (i.e. red meats), fat intake should account for 30% of all calories with majority of intake coming from mono and polyunsaturated sources (i.e. nuts, seeds, avocados, olive oil)
        
        CL Lowering Drug Therapy: complete lipid profile should be obtained every 5 years beginning at age 20, reassessed after 6 months of diet therapy, if still elevated additional dietary options or drug therapy may be started
- - - - Objective Cardiovascular Assessment: vital signs (HR, BP, respirations, temperature, SpO2 saturation), Inspection: general survey, skin ax (cyanosis, pallor, diaphoresis, clubbing, JVD), Palpation: capillary refill, presence of edema, presence of pulses, warmth, sensation, Percussion: cardiac dullness, Auscultation (heart sounds, apical HR, presence of carotid or renal bruits)
      - Identifying patient's attitudes and beliefs about health and illness can explain how disease and lifestyle changes may affect the patient and reveal possible misconceptions about heart disease. Knowing patient's educational background can determine teaching needs. It is important to know the names and dosages of the patient's medications and whether the they are compliant