Cardiovascular Disorders
Cardiovascular Disorders
Study online at https://quizlet.com/_a8jfp
1. Preload pressure right when the ventricles have filled (before they pump)
2. Afterload pressure behind the aortic valve that the left ventricle has to surpass to pump
through. Pressure against the aortic valve right before the left ventricle pumps.
In people with high blood pressure, the ventricle needs to overcome a greater
pressure to pump through the aortic valve; bigger workload for the heart.
3. Cardiac Output Amount of blood pumped by each ventricle in 1 minute
4. Stroke volume Amount of blood ejected from each ventricle with each contraction
5. Cardiac Output ?? = heart rate (HR) x stroke volume (SV)
6. Coronary Artery a condition affecting arteries of the heart that reduces the flow of blood and
Disease (CAD) the delivery of oxygen and nutrients to the myocardium; most often caused by
atherosclerosis
7. Coronary Artery Complications are:
Disease (CAD) - Angina
- Ischemia
- MI
- Arrhythmias
- CHF
8. Arteriosclerosis Degenerative changes in the small arteries and arterioles. Elasticity is lost, the
walls become thick and hard, and the lumen gradually narrows and may become
obstructed.
9. Arteriosclerosis Non-modifiable risk factors:
- Age: more common after age 40
- Gender: women are protected by hormones which produce higher HDL levels
and help regulate cholesterol until menopause
- Genetic or familial factors appear to have a strong influence on serum lipid levels,
1
, Cardiovascular Disorders
Cardiovascular Disorders
Study online at https://quizlet.com/_a8jfp
metabolism, and cell receptors for lipids; some conditions are inherited, such as
familial hypercholesterolemia.
10. Arteriosclerosis Modifiable risk factors:
- Diet
- Cigarettes
- Sedentary lifestyle
- DM
- Poorly controlled hypertension
- Oral contraceptives + smoking
- high cholesterol + high BP
11. Arteriosclerosis Diagnostic tests:
o Serum lipid levels
o Serum levels of high-sensitivity C-reactive protein (CRP) indicate the presence
of inflammation
o Exercise stress testing
o Nuclear medicine studies can be used to determine the degree of tissue
perfusion, the presence of collateral circulation (alternate routes your body has),
and the degree of local metabolism.
12. Atherosclerosis A type of arteriosclerosis differentiated by the presence of atheromas.
13. Atheroma Plaques consisting of lipids, cells, fibrin, and cell debris, often with attached
thrombi, which form inside the walls of large arteries, particularly at points of
bifurcation.
14. Low-density Have a high lipid content and transport cholesterol from the liver to the cells. Binds
lipoproteins to receptors on cells and enters them; it is the "bad" lipoprotein that promotes
(LDL) atheromas formation
15. Have a low lipid content and transport cholesterol away from peripheral cells to
the liver, where it undergoes catabolism and excretion. It is the "good" lipoprotein
2
, Cardiovascular Disorders
Cardiovascular Disorders
Study online at https://quizlet.com/_a8jfp
High-density
lipoproteins
(HDL)
16. Atheroma Formation:
1. Endothelial (inner layer) injury in an artery causes inflammation in the area,
leading to elevated C-reactive protein levels.
2. White blood cells and lipids accumulate and smooth muscle cells multiply
(proliferate).
3. A plaque forms and inflammation persists.
4. Platelets adhere to the rough damaged surface of the arterial wall forming a
thrombus and partial obstruction of the artery.
5. Lipids and fibrin continue to build up at the site of arterial injury
6. Platelets adhere and release prostaglandins, which precipitate inflammation
and vasospasm. This draws more platelets to the site, enlarging the thrombus.
7. Blood flow progressively decreases as the lumen narrows
8. If plaque breaks, it may precipitate more inflammation or a thrombus may form
at the site, resulting in total obstruction in a very short amount of time.
17. Atorvastatin (Lip- Class: HMG-CoA Reductase Inhibitor (Statin)
itor)
18. Atorvastatin (Lip- Used for hypercholesterolemia
itor)
19. Atorvastatin (Lip- The statins act by inhibiting HMG-CoA reductase. As the liver makes less choles-
itor) terol, it responds by making more LDL receptors on the surface of liver cells. The
greater number of LDL receptors in liver cells results in increased removal of LDL
from blood. Blood levels of both LDL and cholesterol are reduced, although at
least 2 weeks of therapy are required before these effects are realized.
20. Atorvastatin (Lip- Interactions:
itor) - May increase digoxin levels by 20%
3
Cardiovascular Disorders
Study online at https://quizlet.com/_a8jfp
1. Preload pressure right when the ventricles have filled (before they pump)
2. Afterload pressure behind the aortic valve that the left ventricle has to surpass to pump
through. Pressure against the aortic valve right before the left ventricle pumps.
In people with high blood pressure, the ventricle needs to overcome a greater
pressure to pump through the aortic valve; bigger workload for the heart.
3. Cardiac Output Amount of blood pumped by each ventricle in 1 minute
4. Stroke volume Amount of blood ejected from each ventricle with each contraction
5. Cardiac Output ?? = heart rate (HR) x stroke volume (SV)
6. Coronary Artery a condition affecting arteries of the heart that reduces the flow of blood and
Disease (CAD) the delivery of oxygen and nutrients to the myocardium; most often caused by
atherosclerosis
7. Coronary Artery Complications are:
Disease (CAD) - Angina
- Ischemia
- MI
- Arrhythmias
- CHF
8. Arteriosclerosis Degenerative changes in the small arteries and arterioles. Elasticity is lost, the
walls become thick and hard, and the lumen gradually narrows and may become
obstructed.
9. Arteriosclerosis Non-modifiable risk factors:
- Age: more common after age 40
- Gender: women are protected by hormones which produce higher HDL levels
and help regulate cholesterol until menopause
- Genetic or familial factors appear to have a strong influence on serum lipid levels,
1
, Cardiovascular Disorders
Cardiovascular Disorders
Study online at https://quizlet.com/_a8jfp
metabolism, and cell receptors for lipids; some conditions are inherited, such as
familial hypercholesterolemia.
10. Arteriosclerosis Modifiable risk factors:
- Diet
- Cigarettes
- Sedentary lifestyle
- DM
- Poorly controlled hypertension
- Oral contraceptives + smoking
- high cholesterol + high BP
11. Arteriosclerosis Diagnostic tests:
o Serum lipid levels
o Serum levels of high-sensitivity C-reactive protein (CRP) indicate the presence
of inflammation
o Exercise stress testing
o Nuclear medicine studies can be used to determine the degree of tissue
perfusion, the presence of collateral circulation (alternate routes your body has),
and the degree of local metabolism.
12. Atherosclerosis A type of arteriosclerosis differentiated by the presence of atheromas.
13. Atheroma Plaques consisting of lipids, cells, fibrin, and cell debris, often with attached
thrombi, which form inside the walls of large arteries, particularly at points of
bifurcation.
14. Low-density Have a high lipid content and transport cholesterol from the liver to the cells. Binds
lipoproteins to receptors on cells and enters them; it is the "bad" lipoprotein that promotes
(LDL) atheromas formation
15. Have a low lipid content and transport cholesterol away from peripheral cells to
the liver, where it undergoes catabolism and excretion. It is the "good" lipoprotein
2
, Cardiovascular Disorders
Cardiovascular Disorders
Study online at https://quizlet.com/_a8jfp
High-density
lipoproteins
(HDL)
16. Atheroma Formation:
1. Endothelial (inner layer) injury in an artery causes inflammation in the area,
leading to elevated C-reactive protein levels.
2. White blood cells and lipids accumulate and smooth muscle cells multiply
(proliferate).
3. A plaque forms and inflammation persists.
4. Platelets adhere to the rough damaged surface of the arterial wall forming a
thrombus and partial obstruction of the artery.
5. Lipids and fibrin continue to build up at the site of arterial injury
6. Platelets adhere and release prostaglandins, which precipitate inflammation
and vasospasm. This draws more platelets to the site, enlarging the thrombus.
7. Blood flow progressively decreases as the lumen narrows
8. If plaque breaks, it may precipitate more inflammation or a thrombus may form
at the site, resulting in total obstruction in a very short amount of time.
17. Atorvastatin (Lip- Class: HMG-CoA Reductase Inhibitor (Statin)
itor)
18. Atorvastatin (Lip- Used for hypercholesterolemia
itor)
19. Atorvastatin (Lip- The statins act by inhibiting HMG-CoA reductase. As the liver makes less choles-
itor) terol, it responds by making more LDL receptors on the surface of liver cells. The
greater number of LDL receptors in liver cells results in increased removal of LDL
from blood. Blood levels of both LDL and cholesterol are reduced, although at
least 2 weeks of therapy are required before these effects are realized.
20. Atorvastatin (Lip- Interactions:
itor) - May increase digoxin levels by 20%
3
