NURS 261 Pathophysiology II
Cardiovascular Disorders Active Learning Guide
Instructions: These study guides are to enhance your learning. It is highly suggested you work with a
group to complete the study guides and spend some time in discussion about the topics. Terms and
definitions, you should always know. If there is content you do not understand, please provide questions
for the instructors. You will not be required to submit the study guides, only any questions you have.
Chapter 15
Terms
Know the terms on the following list:
1. Systole – cardiac contraction left ventricle contracts and blood is ejected from the chamber.
2. Diastole – cardiac relaxation left ventricle ends contraction.
3. Pulse pressure – difference between systolic and diastolic arterial.
4. Stroke volume – volume of blood ejected from left ventricle during systole, this is per
contraction.
1. How is blood pressure regulated? Brain in lower pons and medulla. sympathetic (constriction)
and parasympathetic (relaxation) responses. Baroreceptors are sensors that detect fluctuations
in BP. During a drop, they stimulate sympathetic nervous system, and rise parasympathetic.
The
RAAS responds to diminished circulation releasing renin, to stimulate the liver, to release
angiotensin, converting to angiotensin II causing vasoconstriction.
Posterior Pituitary- Antidiuretic Hormone Mechanism (ADH) is secreted which is vasopressin, to
increase water reabsorption.
Natriuresis – heart releases atrial natriuretic peptide (ANP) and brain releases brain natriuretic
peptide (BNP) during excess water in the blood stream.
2. How is cardiac output defined? The amount of blood the heart pumps through the circulatory
system in one minute. Amount put out by left ventricle. Stroke Volume x Heart Rate
3. How does peripheral vascular resistance affect CO? it can decrease or increase CO.
4. What is the difference between HDL and LDL?
HDL good – takes cholesterol to liver where it can be removed.
LDL bad – takes cholesterol directly to the arteries. (gross)
1
, NURS 261 Pathophysiology II
5. What causes HTN?
Cardiovascular damage. Or another disease process.
a. Fill out the table below
Negative effects on the vascular
Essential HTN Causes Secondary HTN Causes
system
None Cushing’s, pheochromocytoma, 2 major – effects
kidney disease, Shearing damaging force against
hyperaldosteronism, CAD, endothelial lining. Resistance
atherosclerosis. against heart’s left ventricle.
Other – effects
Excessive workload on heart, LV,
arteries, weakens endothelium,
retina, kidney, brain, & lower
extremity artery damage.
6. Know the stages of development of atherosclerosis. You do not need to write it out.
Areas of endothelial injury undergo inflammation
Inflammation of the artery lining attracts WBCs, platelets, and inflammatory mediators to the
site
WBCs take in LDLs, which are in the bloodstream and form foam cells
Endothelial cells secrete endothelin, which is a potent vasoconstrictor
Foam cells eventually form a fatty streak, which is early atherosclerotic plaque
Atherosclerotic plaque eventually matures into calcified plaque
Endothelial injury to inflammation… inflammation to WBC and platelets…. LDLs forming foam
cells… secretion of endothelin (vasoconstrictor)…. Foam cells create fatty streaks….
Atherosclerotic plaque turns into calcified plaque.
7. What is the difference between presentation of arterial ulcers and venous ulcers?
Arterial Ulcers- ischemic skin wounds that develop gradually due to lack of blood flow to
extremities. Obstructive atherosclerosis caused by lack of oxygen and blood delivered to lower
extremities. Pallor, pulse absent or low, thick toenails yellow and painful.
Venous Ulcers -
8. Peripheral Arterial Disease (PAD)
Arteriosclerosis of an extremity’s of peripheral artery. Caused by arteriosclerotic plaque that
obstructs blood flow.
a. Fill out the table describing the risk factors, clinical presentation, and how to diagnose
PAD.
2
Cardiovascular Disorders Active Learning Guide
Instructions: These study guides are to enhance your learning. It is highly suggested you work with a
group to complete the study guides and spend some time in discussion about the topics. Terms and
definitions, you should always know. If there is content you do not understand, please provide questions
for the instructors. You will not be required to submit the study guides, only any questions you have.
Chapter 15
Terms
Know the terms on the following list:
1. Systole – cardiac contraction left ventricle contracts and blood is ejected from the chamber.
2. Diastole – cardiac relaxation left ventricle ends contraction.
3. Pulse pressure – difference between systolic and diastolic arterial.
4. Stroke volume – volume of blood ejected from left ventricle during systole, this is per
contraction.
1. How is blood pressure regulated? Brain in lower pons and medulla. sympathetic (constriction)
and parasympathetic (relaxation) responses. Baroreceptors are sensors that detect fluctuations
in BP. During a drop, they stimulate sympathetic nervous system, and rise parasympathetic.
The
RAAS responds to diminished circulation releasing renin, to stimulate the liver, to release
angiotensin, converting to angiotensin II causing vasoconstriction.
Posterior Pituitary- Antidiuretic Hormone Mechanism (ADH) is secreted which is vasopressin, to
increase water reabsorption.
Natriuresis – heart releases atrial natriuretic peptide (ANP) and brain releases brain natriuretic
peptide (BNP) during excess water in the blood stream.
2. How is cardiac output defined? The amount of blood the heart pumps through the circulatory
system in one minute. Amount put out by left ventricle. Stroke Volume x Heart Rate
3. How does peripheral vascular resistance affect CO? it can decrease or increase CO.
4. What is the difference between HDL and LDL?
HDL good – takes cholesterol to liver where it can be removed.
LDL bad – takes cholesterol directly to the arteries. (gross)
1
, NURS 261 Pathophysiology II
5. What causes HTN?
Cardiovascular damage. Or another disease process.
a. Fill out the table below
Negative effects on the vascular
Essential HTN Causes Secondary HTN Causes
system
None Cushing’s, pheochromocytoma, 2 major – effects
kidney disease, Shearing damaging force against
hyperaldosteronism, CAD, endothelial lining. Resistance
atherosclerosis. against heart’s left ventricle.
Other – effects
Excessive workload on heart, LV,
arteries, weakens endothelium,
retina, kidney, brain, & lower
extremity artery damage.
6. Know the stages of development of atherosclerosis. You do not need to write it out.
Areas of endothelial injury undergo inflammation
Inflammation of the artery lining attracts WBCs, platelets, and inflammatory mediators to the
site
WBCs take in LDLs, which are in the bloodstream and form foam cells
Endothelial cells secrete endothelin, which is a potent vasoconstrictor
Foam cells eventually form a fatty streak, which is early atherosclerotic plaque
Atherosclerotic plaque eventually matures into calcified plaque
Endothelial injury to inflammation… inflammation to WBC and platelets…. LDLs forming foam
cells… secretion of endothelin (vasoconstrictor)…. Foam cells create fatty streaks….
Atherosclerotic plaque turns into calcified plaque.
7. What is the difference between presentation of arterial ulcers and venous ulcers?
Arterial Ulcers- ischemic skin wounds that develop gradually due to lack of blood flow to
extremities. Obstructive atherosclerosis caused by lack of oxygen and blood delivered to lower
extremities. Pallor, pulse absent or low, thick toenails yellow and painful.
Venous Ulcers -
8. Peripheral Arterial Disease (PAD)
Arteriosclerosis of an extremity’s of peripheral artery. Caused by arteriosclerotic plaque that
obstructs blood flow.
a. Fill out the table describing the risk factors, clinical presentation, and how to diagnose
PAD.
2
