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NR 507 Week 2 Edapt Notes – Cardiovascular Disorders (Advanced Pathophysiology)

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INSTANT PDF DOWNLOAD – NR 507 Week 2 Edapt: Cardiovascular Disorders. Includes key concepts on cardiac physiology, hypertension, heart failure, and coronary artery disease. Organized notes from Chamberlain University’s Advanced Pathophysiology course, designed for efficient review and clinical exam preparation. Includes highlighted terms, tables, and pathophysiologic summaries. NR507 Week 2, NR507 cardiovascular, NR507 Edapt, NR507 cardiac disorders, NR507 heart failure, NR507 hypertension, NR507 Chamberlain, NR507 pathophysiology, NR507 cardiac notes, NR507 module 2, NR507 heart disease, NR507 study guide, NR507 review notes, NR507 midterm prep, NR507 PDF download, NR507 coronary artery disease, NR507 advanced pathophysiology, NR507 heart exam, NR507 study bundle, NR507 cardiac function, NR507 clinical review, NR507 cardiology, NR507 2025

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WEEK 2 Edapt:
Cardiovascular Disorders
Key Concepts

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NR 507 week 2 edapt Cardiovascular Disorders

Coronary Artery Disease




Coronary Artery Disease: is caused by atherosclerosis and affects the heart
by obstructing the supply of oxygenated blood, altering myocardial cell
metabolism and nutrient uptake. The progression of plaque build-up in the
arteries causes resistance, lessening the ability for oxygenated blood and
nutrients to flow through, and can lead to myocardial ischemia or infarction.




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Coronary arteries are blood vessels that supply the heart with blood to pump
through the circulatory system. Blood flows through the coronary arteries,
where deoxygenated blood arrives on the right side of the heart and travels
to the pulmonary arteries to release carbon dioxide (CO2) and obtain
oxygen.

Oxygenated blood is then carried from the lungs through the pulmonary
veins to the left side of the heart, flowing through the aorta to the body’s
organs.


Pathophysiology of Coronary
Artery Disease
Coronary artery disease (CAD) is a complex chain of events where
atherosclerotic changes (e.g., plaque accumulation) invade the arteries and
damage the endothelial (inner) layer. Under normal functioning, the
endothelium maintains a balance between vasoconstriction and vasodilation,
preventing platelets from aggregating and controlling fibrin production.

When the endothelium layer becomes damaged, inflammatory processes will
occur. Macrophages attach, setting up phagocytosis; plaque formation and
vasoconstriction occur, marking the beginning of atherosclerosis. As plaque
accumulates, a thrombus, or clot, can form, which disrupts normal blood
flow. With disease progression, myeloid cells can destabilize the plaque in
the arterial wall and cause its rupture, triggering a myocardial infarction (MI)
or stroke.




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Coronary Artery Disease and Pathway to Acute Coronary
Syndromes




Coronary artery disease (CAD) is the most common type of heart disease and the
leading cause of mortality in the United States. When atherosclerosis reaches a
clinically significant level, chronic stable angina or acute coronary syndrome (ACS)
may occur.

ACS may lead to unstable angina or myocardial infarction (MI), which are medical
emergencies. ACS forms a pathophysiologic continuum, depriving the heart muscle
of oxygen and essential nutrients for cellular uptake and metabolism and interfering
with the heart’s pumping ability.


Atherosclerosis progression: Is a condition in which arteries harden and
become stiff due to buildup of cholesterol within the tunica intima.




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