NR283 Pathophysiology
Unit 4 – Chapter 12 Outline
Cardiovascular
1. How does blood flow through the heart? (p. 227-228)
1. The two atria are relax and are filled with blood (from the inferior and superior
venae cavae into the right atrium, and from the pulmonary veins into the left
atrium).
2. AV valves open as the pressure of the blood in the atria increases and the ventricle
are relaxed.
3. Blood flows into the ventricles, almost emptying the atria.
4. The conduction system stimulates the atrial muscle to contract, forcing any
remaining blood into the ventricles.
5. Atria relaxes
6. The two ventricles begin to contract, and pressure increase in the ventricles.
7. AV valves close
8. For a brief moment, all valves are closed, the ventricular myocardium continues to
contract, building up pressure in this isovolumetric phase (no change in blood
volume in the ventricles).
9. The increased pressure opens the semilunar valves; blood is forced into the
pulmonary artery and aorta.
10. At the end of the cycle, the atria have begun to fill again, the ventricles relax, and the
aortic and pulmonary valves close to prevent backflow or blood, and the cycle
repeats.
2. What determines cardiac output? (p. 228-230)
• Cardiac output is the volume of blood ejected by the ventricle in one minute and
depends on the heart rate and stroke volume, the volume pumped from one
ventricle in one contraction. This means that at rest, the heart pumps into the
system an amount equal to the total blood volume in the body every minute,
which is remarkable feat. When necessary, the normal heart can increase its
usual output by four or five times the minimum volume.
Cardiac output = Heart Rate x Stroke Volume
Amount of blood pumped Number of contractions Amount of blood ejected
by each ventricle in min. of the ventricles each from each ventricle with
minute each contraction.
, 3. Define preload, afterload, and contractility. (p. 228)
• Preload: refers to the mechanical state of the heart at the end of diastole with
the ventricles at their maximum volume.
• Afterload: Is the force required to eject blood from the ventricles and is
determines by the peripheral resistance to the opening of the semilunar valves.
o Example: Afterload is increased by a high diastolic pressure resulting from
excessive vasoconstriction.
• Contractility:
4. Describe the process of atherosclerosis? (Understand how a fatty streak and plaque
develops). (p. 235-237)
• Process begins with endothelial injury in the artery, often at a very young age.
• The endothelial injury causes inflammation in the area, which leads to elevated C-
reactive protein (CRP) levels.
• Monocytes, macrophages, and lipids accumulate in the intima or inner lining of
the artery and in the media or muscle layer.
• Smooth muscle cells proliferate or multiples; a plaque forms and inflammation
persists.
• Platelets adhere to the rough damage surface of the arterial wall, which forms a
thrombus and a partial obstruction of the artery.
• Lipids continue to build up at the arterial injury site, along with fibrous tissue.
• Platelets adhere and release prostaglandins, which precipitate inflammation and
vasospasm. This draws more platelets to aggregate at the site, enlarging the
thrombus.
• Arterial flow becomes more turbulent, promoting thrombus formation.
• The cycle persists, whereas the blood flow decreases as the lumen narrows.
• Plaque ulcerate and break open, which can precipitate more inflammation or a
thrombus may form at the site resulting in total obstruction in a very short time.
• Precipitating factor for myocardial infarction.
• Atheroma damages the arterial wall, weakening the structure and decreasing
elasticity.
• In time atheromas may calcify, causing rigidity of the wall.
• This can lead to aneurysm, a bulge in the arterial wall or a rupture and
hemorrhage of the vessel.
Unit 4 – Chapter 12 Outline
Cardiovascular
1. How does blood flow through the heart? (p. 227-228)
1. The two atria are relax and are filled with blood (from the inferior and superior
venae cavae into the right atrium, and from the pulmonary veins into the left
atrium).
2. AV valves open as the pressure of the blood in the atria increases and the ventricle
are relaxed.
3. Blood flows into the ventricles, almost emptying the atria.
4. The conduction system stimulates the atrial muscle to contract, forcing any
remaining blood into the ventricles.
5. Atria relaxes
6. The two ventricles begin to contract, and pressure increase in the ventricles.
7. AV valves close
8. For a brief moment, all valves are closed, the ventricular myocardium continues to
contract, building up pressure in this isovolumetric phase (no change in blood
volume in the ventricles).
9. The increased pressure opens the semilunar valves; blood is forced into the
pulmonary artery and aorta.
10. At the end of the cycle, the atria have begun to fill again, the ventricles relax, and the
aortic and pulmonary valves close to prevent backflow or blood, and the cycle
repeats.
2. What determines cardiac output? (p. 228-230)
• Cardiac output is the volume of blood ejected by the ventricle in one minute and
depends on the heart rate and stroke volume, the volume pumped from one
ventricle in one contraction. This means that at rest, the heart pumps into the
system an amount equal to the total blood volume in the body every minute,
which is remarkable feat. When necessary, the normal heart can increase its
usual output by four or five times the minimum volume.
Cardiac output = Heart Rate x Stroke Volume
Amount of blood pumped Number of contractions Amount of blood ejected
by each ventricle in min. of the ventricles each from each ventricle with
minute each contraction.
, 3. Define preload, afterload, and contractility. (p. 228)
• Preload: refers to the mechanical state of the heart at the end of diastole with
the ventricles at their maximum volume.
• Afterload: Is the force required to eject blood from the ventricles and is
determines by the peripheral resistance to the opening of the semilunar valves.
o Example: Afterload is increased by a high diastolic pressure resulting from
excessive vasoconstriction.
• Contractility:
4. Describe the process of atherosclerosis? (Understand how a fatty streak and plaque
develops). (p. 235-237)
• Process begins with endothelial injury in the artery, often at a very young age.
• The endothelial injury causes inflammation in the area, which leads to elevated C-
reactive protein (CRP) levels.
• Monocytes, macrophages, and lipids accumulate in the intima or inner lining of
the artery and in the media or muscle layer.
• Smooth muscle cells proliferate or multiples; a plaque forms and inflammation
persists.
• Platelets adhere to the rough damage surface of the arterial wall, which forms a
thrombus and a partial obstruction of the artery.
• Lipids continue to build up at the arterial injury site, along with fibrous tissue.
• Platelets adhere and release prostaglandins, which precipitate inflammation and
vasospasm. This draws more platelets to aggregate at the site, enlarging the
thrombus.
• Arterial flow becomes more turbulent, promoting thrombus formation.
• The cycle persists, whereas the blood flow decreases as the lumen narrows.
• Plaque ulcerate and break open, which can precipitate more inflammation or a
thrombus may form at the site resulting in total obstruction in a very short time.
• Precipitating factor for myocardial infarction.
• Atheroma damages the arterial wall, weakening the structure and decreasing
elasticity.
• In time atheromas may calcify, causing rigidity of the wall.
• This can lead to aneurysm, a bulge in the arterial wall or a rupture and
hemorrhage of the vessel.
