Concepts Of Cardiovascular And Respiratory Disorders

Concepts of Cardiovascular and Respiratory Disorders

Which cholesterol is considered the “good” cholesterol and what does it do?

The level of cholesterol plays an indispensable role in the cardiovascular disease process. For instance, hyperlipidemia increases the risk of the development of atherosclerotic cardiovascular disease. HDL (high-density lipoprotein) cholesterol is considered “good” cholesterol because it mops up cholesterol from the bloodstream and peripheral tissues to the liver where it is metabolized (Barter & Genest, 2019).

Cholesterol is ordinarily stored in foam cells of atherosclerotic plaques. Consequently, HDL cholesterol has anti-atherogenic and anti-inflammatory properties as it diminishes the size of the plaque and its bracketed inflammation. According to Barter and Genest (2019), HDL cholesterol is considered low when it is less than 40 mg/dl and high while it is desirable when it is 60 mg/dl or more.

How does inflammation contribute to the development of atherosclerosis?

Inflammation plays a central role in the development and progression of atherosclerosis (McCance & Huether, 2019). According to McCance and Huether (2019), atherosclerosis is a disease of chronic inflammation distinguished by a dysfunctional interplay between lipids and the immune system. Inflammation is present at all stages of atherosclerosis.

Endothelial injury leads to endothelial dysfunction. Endothelial cell dysfunction results in the expression of adhesion molecules such as vascular cell adhesion molecule-1 (VCAM-1), which result in monocyte adhesion and emigration into the intima. Subsequent macrophage and T-cell activation results in increased cytokine production that spearheads smooth muscle cell proliferation and matrix synthesis (Jebari-Benslaiman et al., 2022).

Additionally, macrophages oxidize LDL cholesterol. Oxidized LDL cholesterol is toxic to the intima and enhances endothelial cell injury causing a vicious cycle of endothelial cell injury and subsequent inflammation.

Given the history of the patient explain what contributed to the development of a deep venous thrombosis (DVT)

DVT originates from an interplay between venous stasis, endothelial damage, and hypercoagulability (McCance & Huether, 2019). Endothelial injury stimulates an inflammatory response as well as the activation of the coagulation system. On the other hand, venous stasis brings platelets into contact with the endothelium, prevents the dilution of activated clotting factors, and retards the inflow of clot-inhibiting factors.

This Virchow’s triad interrelates in various degrees to stimulate cytokine production and leucocyte adhesion that facilitate thrombus formation (Zhang et al., 2019). Consequently, factors predisposing to venous stasis, endothelial damage, and hypercoagulability increase the risk of developing DVT. The patient has risk factors for venous stasis, such as advanced age, immobility, and obesity.

Additionally, the patient had a hypercoagulable state significantly contributed by the surgery of the hip (Zhang et al., 2019). Finally, trauma due to surgery is the principal cause of endothelial injury. The ultimate result is the formation of a clot in the deep venous system whose propagation depends entirely on the balance between thrombolytic and coagulation pathways.

There is a clear relationship between emphysema and COPD, explain the pathophysiology of emphysema and the relationship to COPD

Emphysema is a condition characterized by permanent dilatation distal to the terminal bronchiole without fibrosis. It is ordinarily due to alveolar wall destruction. Irritants, particularly cigarette smoking, stimulate an inflammatory process that results in protease-antiprotease as well as oxidant-antioxidant imbalances. Proteases, particularly elastase, destroy elastic fibers leading to loss of elastic recoil and alveolar collapse (Brandsma et al., 2020).

Additionally, oxidants found in cigarette smoke and reactive oxygen species produced by activated neutrophils and macrophages leading to the depletion of local antioxidants such as glutathione and superoxide dismutase with subsequent oxidative damage. Ultimately, the destruction of the air sacs results leading to airflow obstruction. Since these changes are incompletely reversible, COPD results (Brandsma et al., 2020).

References

Barter, P., & Genest, J. (2019). HDL and ASCVD risk stratification – A debate. Atherosclerosis, 283, 7–12. https://doi.org/10.1016/j.atherosclerosis.2019.01.001

Brandsma, C.-A., Van den Berge, M., Hackett, T.-L., Brusselle, G., & Timens, W. (2020). Recent advances in chronic obstructive pulmonary disease pathogenesis: from disease mechanisms to precision medicine. The Journal of Pathology, 250(5), 624–635. https://doi.org/10.1002/path.5364

Jebari-Benslaiman, S., Galicia-García, U., Larrea-Sebal, A., Olaetxea, J. R., Alloza, I., Vandenbroeck, K., Benito-Vicente, A., & Martín, C. (2022). Pathophysiology of atherosclerosis. International Journal of Molecular Sciences, 23(6), 3346. https://doi.org/10.3390/ijms23063346

McCance, K. L., & Huether, S. E. (2019). Pathophysiology: The biologic basis for disease in adults and children (8th ed.). Mosby.

Zhang, W., Huai, Y., Wang, W., Xue, K., Chen, L., Chen, C., & Qian, A. (2019). A Retrospective cohort study on the risk factors of deep vein thrombosis (DVT) for patients with a traumatic fracture at Honghui Hospital. BMJ Open, 9(3), e024247. https://doi.org/10.1136/bmjopen-2018-024247

Concepts of Cardiovascular and Respiratory Disorders Assignment Instructions

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Learning Resources
Required Readings (click to expand/reduce)

McCance, K. L. & Huether, S. E. (2019). Pathophysiology: The biologic basis for disease in adults and children (8th ed.). St. Louis, MO: Mosby/Elsevier.

Chapter 32: Structure and Function of the Cardiovascular and Lymphatic Systems; Summary Review
Chapter 33: Alterations of Cardiovascular Function (stop at Dysrhythmias); Summary Review
Chapter 35: Structure and Function of the Pulmonary System; Summary Review 
Chapter 36: Alterations of Pulmonary Function (stop at Disorders of the chest wall and pleura); (obstructive pulmonary diseases) (stop at Pulmonary artery  hypertension); Summary Review
Inamdar, A. A. & Inamdar, A. C. (2016). Heart failure: Diagnosis, management, and utilization, 5(7). doi:10.3390/jcm5070062

QUESTION 1

Scenario 1: Myocardial Infarction

CC: “I woke up this morning at 6 a.m. with numbness in my left arm and pain in my chest. It feels tight right here (mid-sternal).” “My dad had a heart attack when he was 56-years-old and I am scared because I am 56-years-old.”

HPI: Patient is a 56-year-old Caucasian male who presents to Express Hospital Emergency Department with a chief complaint of chest pain that radiates down his left arm. He states this started this morning and has been getting worse, pointing to the mid-sternal area, “it feels like an elephant is sitting on my chest and having a hard time breathing”. He rates the pain as 9/10. Nothing has made the pain better or worse. He denies any previous episode of chest pain. Denies nausea, or lightheadedness. Nitroglycerin 0.4 mg tablet sublingual x 1 which decreased pain to 7/10.

Lipid panel reveals Total Cholesterol 424 mg/dl, high density lipoprotein (HDL) 26 mg/dl, Low Density Lipoprotein (LDL) 166 mg/dl, Triglycerides 702 mg/dl, Very Low-Density Lipoprotein (VLDL) 64 mg/dl

His diagnosis is an acute inferior wall myocardial infarction.

Question:

Which cholesterol is considered the “good” cholesterol and what does it do?

QUESTION 2

Scenario 1: Myocardial Infarction

His diagnosis is an acute inferior wall myocardial infarction.

Question:

How does inflammation contribute to the development of atherosclerosis

QUESTION 3

Scenario 2: Pleural Friction Rub

A 35-year-old female with a positive history of systemic lupus erythematosus (SLE) presents to the Emergency Room (ER) with complaints of sharp retrosternal chest pain that worsens with deep breathing or lying down. She reports a 5-day history of low-grade fever, listlessness and says she feels like she had the flu. Physical exam reveals tachycardia and a pleural friction rub. She was diagnosed with acute pericarditis.

Question:

Because of the result of a pleural friction rub, what does the APRN recognize?

QUESTION 4

Scenario 4: Deep Venous Thrombosis (DVT)

A 81-year-old obese female patient who 48 hours post-op left total hip replacement. The patient has had severe nausea and vomiting and has been unable to go to physical therapy. Her mucus membranes are dry. The patient says the skin on her left leg is too tight. Exam reveals a swollen, tense, and red colored calf. The patient has a duplex ultrasound which reveals the presence of a deep venous thrombosis (DVT).

Question:

Given the history of the patient explain what contributed to the development of a deep venous thrombosis (DVT)

QUESTION 5

Scenario 5: COPD

A 66-year-old female with a 50 pack/year history of cigarette smoking had a CT scan and was diagnosed with emphysema. He asks if this means he has chronic obstructive pulmonary disease (COPD).

Question:

There is a clear relationship between emphysema and COPD, explain the pathophysiology of emphysema and the relationship to COPD.