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NUR 195 Ch 14 Nursing Management: Patients With Coronary Vascular Disorders with correct answers $17.99   Add to cart

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NUR 195 Ch 14 Nursing Management: Patients With Coronary Vascular Disorders with correct answers

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NUR 195 Ch 14 Nursing Management: Patients With Coronary Vascular Disorders with correct answers

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  • August 2, 2024
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  • 2024/2025
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NUR 195 Ch 14 Nursing Management:
Patients With Coronary Vascular
Disorders

Coronary Atherosclerosis - correct answer ✔✔- The most common cause of CVD in the US is
atherosclerosis, an abnormal accumulation of lipid, or fatty substances & fibrous tissue in the lining of
arterial blood vessel walls. These substances create blockages & narrow the coronary vessels in a way
that reduces blood flow to the myocardium.

- It is now known that atherosclerosis involves a repetitious inflammatory response to injury to the
artery wall & subsequent alteration in the structural & biochemical properties of the arterial walls.



Coronary Atherosclerosis: Pathophysiology (Figure 14-1) - correct answer ✔✔- Atherosclerosis begins as
fatty streaks of lipids that are deposited in the intima of the arterial wall. These lesions commonly begin
early in life, perhaps even in childhood. Genetics & environmental factors influence progression of these
lesions.

- Continued development of atherosclerosis involves an inflammatory response, which begins w/ injury
to the vascular endothelium. The injury may be initiated by smoking, HTN, & other factors.

- The presence of inflammation has multiple effects on the arterial wall, including the attraction of
inflammatory cells (macrophages or monocytes, WBCs). Macrophages infiltrate the injured vascular
endothelium & ingest lipids, which turns them into "foam cells." These foam cells are present in all
stages of atherosclerotic plaque formation. Activated macrophages also release biochemical substances
that can further damage the endothelium, attracting platelets & initiating clotting.

- Smooth muscle cells within the vessel wall subsequently proliferate & form a fibrous cap over a center
that is filled w/ lipid & inflammatory infiltrate. These deposits, called atheromas or plaques, protrude
into the lumen of the vessel, narrowing it and obstructing blood flow (Fig. 14-1).



Coronary Atherosclerosis: Pathophysiology (Figure 14-2) Cont'd - correct answer ✔✔- If the fibrous cap
of the plaque is thick & the lipid pool remains relatively stable, it can resist the stress from blood flow &
vessel movement. If the cap is thin & inflammation is ongoing, the lipid core may grow, causing it to
rupture, & this ruptured plaque is a focus for thrombus formation. The thrombus may then obstruct
blood flow, leading to sudden cardiac death or an acute MI (death of a portion of the heart muscle).

- Thus, atherosclerosis can produce narrowing of the lumen of a blood vessel, sudden obstruction of a
blood vessel due to plaque rupture, & weakening of a blood vessel, resulting in aneurysm formation or
emboli formation b/c of direct damage to the endothelium.

,- The anatomic structure of the coronary arteries makes them particularly susceptible to the
mechanisms of atherosclerosis. There are 3 major coronary arteries & they have multiple branches;
atherosclerotic lesions most often form where the vessels branch (Fig. 14-2).

- Although heart disease is most often caused by atherosclerosis of the coronary arteries, other
phenomena may also decrease blood flow to the heart. Ex: vasospasm (sudden constriction or
narrowing) of a coronary artery, myocardial trauma from internal or external forces, structural disease,
congenital anomalies, decreased oxygen supply (e.g., from acute blood loss, anemia, or low BP), &
increased oxygen demand (e.g., from rapid HR, thyrotoxicosis, or use of cocaine).



Coronary Atherosclerosis: Risk Factors

(Figure 14-3 & Box 14-1) - correct answer ✔✔- Epidemiologic studies point to several factors that
increase the probability that CAD will develop in a person. Some uncontrollable factors:

1) Age (men >45 yrs old, women >55 yrs old)

2) Gender (in persons less than 55 yrs of age, men are at a greater risk; after 55 yrs, men & women have
the same risk)

3) Race (African Am, Mexican Am, Native Am, & some Asian Am demonstrate increased risk)

4) Family hx of 1st-degree relative w/ premature dx of heart disease

- Modifiable risk factors: diabetes, htn, smoking, obesity, physical inactivity, & high blood cholesterol.

- New & emerging risk factors: proinflammatory conditions (such as periodontal disease), influenza,
sleep apnea, metabolic syndrome, & increased BMI



Coronary Atherosclerosis: Risk Factors

(Figure 14-3 & Box 14-1)

Cont'd - correct answer ✔✔- A cluster of metabolic abnormalities now known as metabolic syndrome
has emerged as a major risk factor for CAD. A dx of this syndrome includes 3 of the following conditions:

1) Insulin resistance (fasting glucose >100 mg/dL or abnormal glucose tolerance test)

2) Abdominal obesity (waist circumference >35 in. in women, >40 in. in men)

3) Dyslipidemia (triglycerides >150 mg/dL; HDL <50 mg/dL in women, <40 mg/dL in men)

4) Hypertension

5) Proinflammatory state (high lvls of C-reactive protein [CRP])

6) Prothrombotic state (high fibrinogen)

- Many ppl w/ type 2 DM fit this clinical picture. Measurement of lipoprotein, homocysteine (an amino
acid associated w/ cardiac disease), & CRP may also be appropriate in ppl that are identified as at risk

, - Additionally, a risk equivalent is a condition that places pts at high risk for experiencing a cardiac event,
such as a MI. Having 1 or more of these conditions may place pts at the same risk of having a cardiac
event as someone who has already experienced one. (Box 14-1)



Coronary Atherosclerosis: Clinical Manifestation and Assessment - correct answer ✔✔- Coronary
atherosclerosis produces symptoms & complications according to the location & degree of narrowing of
the arterial lumen, thrombus formation, & obstruction of blood flow to the myocardium.

- This obstruction to blood flow is usually progressive, causing an inadequate blood supply that deprives
the cardiac muscle cells of oxygen needed for their survival (known as ischemia). Angina pectoris refers
to chest pain that is brought about by myocardial ischemia.

- If the decrease in blood supply is significant enough, of long enough duration, or both, death of
myocardial cells, or MI, may result.

- Over time, irreversibly damaged myocardium undergoes degeneration & is replaced by scar tissue,
causing various degrees of myocardial dysfunction.

- Significant myocardial damage may result in persistently low CO, & if the heart cannot support the
body's needs for oxygenated blood, the result is heart failure. Myocardial hypoxia due to CAD may also
lead to lethal cardiac rhythm disturbances that may result in sudden cardiac death.

- In the elderly, sometimes there are no symptoms ("silent" CAD), making recognition & dx a clinical
challenge. Elderly pts should be encouraged to recognize their chest pain-like symptom as an indication
that they should rest or take prescribed meds. Pharmacologic stress testing may be used to dx CAD in
elderly pts b/c other conditions may limit the pt's ability to exercise.



Coronary Atherosclerosis: Prevention and Medical and Nursing Management - correct answer ✔✔-
Controlling cholesterol & treating hyperlipidemia, & managing htn & DM are discussed here; additional
medical & nursing management is discussed under angina.



Prevention and Medical and Nursing Management: Controlling Cholesterol Abnormalities (Table 14-1) -
correct answer ✔✔- The association of a high blood cholesterol lvl w/ CAD is well established. The
metabolism of fats is an important contributor to the development of CAD.

- Fats, which are insoluble in water, are encased in water-soluble lipoproteins that allow them to be
transported within the circulatory system. The various lipoproteins are categorized by their protein
content, which is measured in density. The density increases when more protein is present.

- 4 elements of fat metabolism—total cholesterol, LDL, HDL, & triglycerides—affect the development of
heart disease. Cholesterol is processed by the GI tract into lipoprotein globules called chylomicrons.
These are reprocessed by the liver as lipoproteins (Fig. 14-4).

- This is a physiologic process necessary for the formation of lipoprotein-based cell membranes & other
important metabolic processes.

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