Chapter 32: Alterations of Cardiovascular Function

MULTIPLE CHOICE
1. What is the initiating event that leads to the development of atherosclerosis?
a. Release of the inflammatory cytokines
b. Macrophages adhere to vessel walls.
c. Injury to the endothelial cells that line the artery walls
d. Release of the platelet-deprived growth factor
ANS: C

Atherosclerosis begins with an injury to the endothelial cells that line the arterial walls.
Possible causes of endothelial injury include the common risk factors for atherosclerosis, such
as smoking, hypertension, diabetes, increased levels of low-density lipoprotein (LDL),
decreased levels of high-density lipoprotein (HDL), and autoimmunity. The remaining options
occur only after the endothelial cells are injured.
PTS: 1

REF: Page 1145

2. What is the effect of oxidized low-density lipoproteins (LDLs) in atherosclerosis?

a. LDLs cause smooth muscle proliferation.
b. LDLs cause regression of atherosclerotic plaques.
c. LDLs increase levels of inflammatory cytokines.
d. LDLs direct macrophages to the site in the endothelium.
ANS: A

Oxidized LDLs are toxic to endothelial cells, cause smooth muscle proliferation, and activate
further immune and inflammatory responses. This selection is the only option that accurately
identifies the effects of LDLs.
PTS: 1

REF: Page 1145

3. Which inflammatory cytokines are released when endothelial cells are injured?
a. Granulocyte-macrophage colony-stimulating factor (GM-CSF)
b. Interferon-beta (IFN-), interleukin 6 (IL-6), and granulocyte colony-stimulating

factor (G-CSF)
c. Tumor necrosis factoralpha (TNF-), interferon-gamma (IFN-), and interleukin 1
(IL-1)
d. Interferon-alpha (IFN-), interleukin-12 (IL-12), and macrophage colonystimulating factor (M-CSF)
ANS: C

Numerous inflammatory cytokines are released, including TNF-, IFN-, IL-1, toxic oxygen
radicals, and heat shock proteins. This selection is the only option that accurately identifies
which inflammatory cytokines are associated with endothelial cell injury.
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REF: Page 1145

4. When endothelia cells are injured, what alteration contributes to atherosclerosis?

a. The release of toxic oxygen radicals that oxidize low-density lipoproteins (LDLs).

b. Cells are unable to make the normal amount of vasodilating cytokines.

c. Cells produce an increased amount of antithrombotic cytokines.
d. Cells develop a hypersensitivity to homocysteine and lipids.
ANS: B

Injured endothelial cells become inflamed and cannot make normal amounts of antithrombotic
and vasodilating cytokines. This selection is the only option that accurately identifies the
factor that contributes to atherosclerosis.
PTS: 1

REF: Page 1145

5. Which factor is responsible for the hypertrophy of the myocardium associated with

hypertension?
a. Increased norepinephrine
b. Adducin

c. Angiotensin II
d. Insulin resistance

ANS: C

Of the available options, only angiotensin II is responsible for the hypertrophy of the
myocardium and much of the renal damage associated with hypertension.
PTS: 1

REF: Pages 1132-1138

6. What pathologic change occurs to the kidneys glomeruli as a result of hypertension?

a. Compression of the renal tubules
b. Ischemia of the tubule
c. Increased pressure from within the tubule
d. Obstruction of the renal tubule
ANS: B

In the kidney, vasoconstriction and resultant decreased renal perfusion cause tubular ischemia
and preglomerular arteriopathy. This selection is the only option that accurately identifies the
pathologic change to the kidney that occurs as a result of hypertension.
PTS: 1

REF: Pages 1134-1136

7. What effect does atherosclerosis have on the development of an aneurysm?

a. Atherosclerosis causes ischemia of the intima.
b. It increases nitric oxide.
c. Atherosclerosis erodes the vessel wall.
d. It obstructs the vessel.
ANS: C

Atherosclerosis is a common cause of aneurysms because plaque formation erodes the vessel
wall. This selection is the only option that accurately identifies the effect that atherosclerosis
has on aneurysm development.
PTS: 1

REF: Pages 1141-1142

8. Regarding the endothelium, what is the difference between healthy vessel walls and those that

promote clot formation?

a. Inflammation and roughening of the endothelium of the artery are present.
b. Hypertrophy and vasoconstriction of the endothelium of the artery are present.

c. Excessive clot formation and lipid accumulation in the endothelium of the artery

are present.
d. Evidence of age-related changes that weaken the endothelium of the artery are

present.
ANS: A

Invasion of the tunica intima by an infectious agent also roughens the normally smooth lining
of the artery, causing platelets to adhere readily. This selection is the only option that
accurately describes the mechanism that supports abnormal clot formation.
PTS: 1

REF: Pages 1142-1143

9. What is the usual source of pulmonary emboli?

a. Deep venous thrombosis
c. Valvular disease
b. Endocarditis
d. Left heart failure
ANS: A

Pulmonary emboli originate in the venous circulation (mostly from the deep veins of the legs)
or in the right heart. This selection is the only option that accurately identifies the usual source
of pulmonary emboli.
PTS: 1

REF: Page 1143

10. Which factor can trigger an immune response in the bloodstream that may result in an

embolus?
a. Amniotic fluid
b. Fat

c. Bacteria
d. Air

ANS: A

Of the options available, only amniotic fluid displaces blood, thereby reducing oxygen,
nutrients, and waste exchange; however, it also introduces antigens, cells, and protein
aggregates that trigger inflammation, coagulation, and the immune response in the
bloodstream.
PTS: 1

REF: Pages 1143-1144

11. Which statement best describes thromboangiitis obliterans (Buerger disease)?

a. Inflammatory disorder of small- and medium-size arteries in the feet and

sometimes in the hands

b. Vasospastic disorder of the small arteries and arterioles of the fingers and, less

commonly, of the toes

c. Autoimmune disorder of the large arteries and veins of the upper and lower

extremities
d. Neoplastic disorder of the lining of the arteries and veins of the upper extremities
ANS: A

Buerger disease is an inflammatory disease of the peripheral arteries. Inflammation, thrombus

formation, and vasospasm can eventually occlude and obliterate portions of small- and
medium-size arteries. The digital, tibial, and plantar arteries of the feet and the digital, palmar,
and ulnar arteries of the hands are typically affected. This selection is the only option that
accurately describes Buerger disease.

PTS: 1

REF: Page 1144

12. Which statement best describes Raynaud disease?

a. Inflammatory disorder of small- and medium-size arteries in the feet and

sometimes in the hands

b. Neoplastic disorder of the lining of the arteries and veins of the upper extremities
c. Vasospastic disorder of the small arteries and arterioles of the fingers and, less

commonly, of the toes

d. Autoimmune disorder of the large arteries and veins of the upper and lower

extremities
ANS: C

Attacks of vasospasm in the small arteries and arterioles of the fingers and, less commonly, of
the toes characterize Raynaud phenomenon and Raynaud disease and is the only option that
accurately describes this disease.
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REF: Page 1144

13. What change in a vein supports the development of varicose veins?

a. Increase in osmotic pressure
c. Damage to the venous endothelium
b. Damage to the valves in veins
d. Increase in hydrostatic pressure
ANS: B

If a valve is damaged, permitting backflow, then a section of the vein is subjected to the
pressure exerted by a larger volume of blood under the influence of gravity. The vein swells as
it becomes engorged, and the surrounding tissue becomes edematous because increased
hydrostatic pressure pushes plasma through the stretched vessel wall. This selection is the
only option that accurately describes the development of varicose veins.
PTS: 1

REF: Pages 1129-1130

14. Superior vena cava syndrome is a result of a progressive increase of which process?
a. Inflammation
c. Distention
b. Occlusion
d. Sclerosis
ANS: B

Superior vena cava syndrome (SVCS) is a progressive occlusion of the superior vena cava
(SVC) that leads to venous distention in the upper extremities and head. The remaining
options are not associated with this disorder.
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REF: Page 1131

15. What term is used to identify when a cell is temporarily deprived of blood supply?
a. Infarction
c. Necrosis
b. Ischemia
d. Inflammation
ANS: B

Coronary artery disease (CAD) can diminish the myocardial blood supply until deprivation
impairs myocardial metabolism enough to cause ischemia, a local state in which the cells are
temporarily deprived of blood supply. This term is the only option that is used to identify a
temporarily deprived blood supply.

PTS: 1

REF: Page 1148

16. The risk of developing coronary artery disease is increased up to threefold by which factor?
a. Diabetes mellitus
c. Obesity
b. Hypertension
d. High alcohol consumption
ANS: B

Hypertension is the only factor responsible for a twofold-to-threefold increased risk of

atherosclerotic cardiovascular disease.
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REF: Page 1151

17. Which risk factor is associated with coronary artery disease (CAD) because of its relationship

with the alteration of hepatic lipoprotein?

a. Diabetes mellitus
b. Hypertension

c. Obesity
d. High alcohol consumption

ANS: A

Of the available options, only diabetes mellitus is associated with CAD because of the
resulting alteration of hepatic lipoprotein synthesis; it increases triglyceride levels and is
involved in low-density lipoprotein oxidation.
PTS: 1

REF: Pages 1148-1151

18. Nicotine increases atherosclerosis by the release of which neurotransmitter?

a. Histamine
c. Angiotensin II
b. Nitric oxide
d. Epinephrine
ANS: D

Nicotine stimulates the release of catecholamines (e.g., epinephrine, norepinephrine), which

increases the heart rate and causes peripheral vascular constriction. As a result, blood pressure
increases, as do both cardiac workload and oxygen demand. None of the other options are
associated with this mechanism.
PTS: 1

REF: Page 1151

19. Which substance is manufactured by the liver and primarily contains cholesterol and protein?
a. Very lowdensity lipoproteins (VLDLs)
b. Low-density lipoproteins (LDLs)
c. High-density lipoproteins (HDLs)
d. Triglycerides
ANS: B

A series of chemical reactions in the liver results in the production of several lipoproteins that
vary in density and function. These include VLDLs, primarily triglycerides and protein;
LDLs, mostly cholesterol and protein; and HDLs, mainly phospholipids and protein. LDLs are
the only lipoproteins that are manufactured by the liver and primarily contain cholesterol and
protein.
PTS: 1

REF: Page 1149

20. Which elevated value may be protective of the development of atherosclerosis?

a.
b.
c.
d.

Very lowdensity lipoproteins (VLDLs)

Low-density lipoproteins (LDLs)
High-density lipoproteins (HDLs
Triglycerides

ANS: C

Low levels of HDL cholesterol are also a strong indicator of coronary risk, whereas high
levels of HDLs may be more protective for the development of atherosclerosis than low levels
of LDLs. Neither VLDLs nor elevated triglycerides are associated with a protective
mechanism.
PTS: 1

REF: Pages 1149-1151

21. Which laboratory test is an indirect measure of atherosclerotic plaque?

a. Homocysteine
b. Low-density lipoprotein (LDL)
c. Erythrocyte sedimentation rate (ESR)
d. C-reactive protein (CRP)
ANS: D

Highly sensitive CRP (hs-CRP) is an acute phase reactant or protein mostly synthesized in the
liver and, of the available options, is an indirect measure of atherosclerotic plaque-related
inflammation.
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REF: Page 1152

22. Cardiac cells can withstand ischemic conditions and still return to a viable state for how many

minutes?
a. 10
b. 15

c. 20
d. 25

ANS: C

Cardiac cells remain viable for approximately 20 minutes under ischemic conditions. If blood
flow is restored, then aerobic metabolism resumes, contractility is restored, and cellular repair
begins. If the coronary artery occlusion persists beyond 20 minutes, then myocardial
infarction (MI) occurs.
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REF: Page 1153

23. Which form of angina occurs most often during sleep as a result of vasospasms of one or more

coronary arteries?
a. Unstable
b. Stable

c. Silent
d. Prinzmetal

ANS: D

Of the options available, only Prinzmetal angina (also called variant angina) is chest pain
attributable to transient ischemia of the myocardium that occurs unpredictably and almost
exclusively at rest.
PTS: 1

REF: Page 1154

24. When is the scar tissue that is formed after a myocardial infarction (MI) most vulnerable to

injury?
a. Between 5 and 9 days
b. Between 10 and 14 days

c. Between 15 and 20 days

d. Between 20 and 30 days

ANS: B

During the recovery period (10 to 14 days after infarction), individuals feel more capable of
increasing activities and thus may stress the newly formed scar tissue. After 6 weeks, the
necrotic area is completely replaced by scar tissue, which is strong but unable to contract and
relax like healthy myocardial tissue.
PTS: 1

REF: Page 1160

25. An individual who is demonstrating elevated levels of troponin, creatine kinaseisoenzyme

MB (CK-MB), and lactic dehydrogenase (LDH) is exhibiting indicators associated with which
condition?
a. Myocardial ischemia
c. Myocardial infarction (MI)
b. Hypertension
d. Coronary artery disease (CAD)
ANS: C

Cardiac troponins (troponin I and troponin T) are the most specific indicators of MI. Other
biomarkers released by myocardial cells include CK-MB and LDH, but they are not
associated with the other options.
PTS: 1

REF: Pages 1160-1161

26. What is the expected electrocardiogram (ECG) pattern when a thrombus in a coronary artery

permanently lodges in the vessel and the infarction extends through the myocardium from the
endocardium to the epicardium?
a. Prolonged QT interval
b. ST elevation myocardial infarction (STEMI)
c. ST depression myocardial infarction (STDMI)
d. Non-ST elevation myocardial infarction (non-STEMI)
ANS: B

Individuals with this pattern on an ECG usually have significant elevations in the ST segments
and are categorized as having STEMI. The other options are not associated with the described
pathologic condition.
PTS: 1

REF: Pages 1157-1158

27. How does angiotensin II increase the workload of the heart after a myocardial infarction (MI)?
a. By increasing the peripheral vasoconstriction
b. By causing dysrhythmias as a result of hyperkalemia
c. By reducing the contractility of the myocardium
d. By stimulating the sympathetic nervous system
ANS: A

Angiotensin II is released during myocardial ischemia and contributes to the pathogenesis of a

myocardial infarction (MI) in several ways. First, it results in the systemic effects of
peripheral vasoconstriction and fluid retention. These homeostatic responses are
counterproductive in that they increase myocardial work and thus exacerbate the effects of the
loss of myocyte contractility. Angiotensin II is also locally released, where it is a growth
factor for vascular smooth muscle cells, myocytes, and cardiac fibroblasts; promotes
catecholamine release; and causes coronary artery spasm. This selection is the only option that
accurately describes how angiotensin II increases workload after a MI.
PTS: 1

REF: Page 1159

28. The pulsus paradoxus that occurs as a result of pericardial effusion is caused by a dysfunction

in which mechanism?
a. Diastolic filling pressures of the right ventricle and reduction of blood volume in

both ventricles
b. Blood ejected from the right atrium and reduction of blood volume in the right

ventricle
c. Blood ejected from the left atrium and reduction of blood volume in the left

ventricle
d. Diastolic filling pressures of the left ventricle and reduction of blood volume in all

four heart chambers.

ANS: D

Pulsus paradoxus means that the arterial blood pressure during expiration exceeds arterial
pressure during inspiration by more than 10 mm Hg. This clinical finding reflects impairment
of diastolic filling of the left ventricle plus a reduction of blood volume within all four cardiac
chambers. This selection is the only option that accurately describes the mechanism.
PTS: 1

REF: Page 1164

29. A patient reports sudden onset of severe chest pain that radiates to the back and worsens with

respiratory movement and when lying down. These clinical manifestations describe:
c. Restrictive pericarditis
d. Acute pericarditis

a. Myocardial infarction (MI)

b. Pericardial effusion
ANS: D

Most individuals with acute pericarditis describe several days of fever, myalgias, and malaise,
followed by the sudden onset of severe chest pain that worsens with respiratory movements
and with lying down. Although the pain may radiate to the back, it is generally felt in the
anterior chest and may be initially confused with the pain of an acute MI. Individuals with
acute pericarditis also may report dysphagia, restlessness, irritability, anxiety, and weakness.
This selection is the only option with these symptoms.
PTS: 1

REF: Page 1163

30. Ventricular dilation and grossly impaired systolic function, leading to dilated heart failure,

characterize which form of cardiomyopathy?

a. Congestive
b. Hypertrophic
ANS: A

c. Septal
d. Dystrophic

Only dilated cardiomyopathy (congestive cardiomyopathy) is characterized by ventricular

dilation and grossly impaired systolic function, leading to dilated heart failure.
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REF: Page 1165

31. A disproportionate thickening of the interventricular septum is the hallmark of which form of

cardiomyopathy?
a. Dystrophic
b. Hypertrophic

c. Restrictive
d. Dilated

ANS: B

Only hypertrophic cardiomyopathy is characterized by a thickening of the septal wall, which

may cause outflow obstruction to the left ventricle outflow tract.
PTS: 1

REF: Page 1166

32. Amyloidosis, hemochromatosis, or glycogen storage disease usually causes which form of

cardiomyopathy?
a. Infiltrative
b. Restrictive

c. Septal
d. Hypertrophic

ANS: B

Restrictive cardiomyopathy may occur idiopathically or as a cardiac manifestation of systemic

diseases, such as scleroderma, amyloidosis, sarcoidosis, lymphoma, and hemochromatosis, or
a number of inherited storage diseases. This characterization is not true of the other forms of
cardiomyopathy.
PTS: 1

REF: Page 1167

33. Which condition is a cause of acquired aortic regurgitation?

a. Congenital malformation
c. Rheumatic fever
b. Cardiac failure
d. Coronary artery disease (CAD)
ANS: C

Rheumatic heart disease, bacterial endocarditis, syphilis, hypertension, connective tissue

disorders (e.g., Marfan syndrome, ankylosing spondylitis), appetite suppressing medications,
trauma, or atherosclerosis can cause acquired aortic regurgitation. This selection is the only
available option that is known to cause acquired aortic regurgitation.
PTS: 1

REF: Page 1169

34. Which predominantly female valvular disorder is thought to have an autosomal dominant

inheritance pattern, as well as being associated with connective tissue disease?

c. Tricuspid valve prolapse
d. Aortic insufficiency

a. Mitral valve prolapse

b. Tricuspid stenosis
ANS: A

Mitral valve prolapse tends to be most prevalent in young women. Studies suggest an
autosomal dominant and X-linked inheritance pattern. Because mitral valve prolapse often is
associated with other inherited connective tissue disorders (e.g., Marfan syndrome, EhlersDanlos syndrome, osteogenesis imperfecta), it is thought to result from a genetic or
environmental disruption of valvular development during the fifth or sixth week of gestation.
This provided history is not associated with any of the other options.
PTS: 1

REF: Page 1170

35. Which disorder causes a transitory truncal rash that is nonpruritic and pink with erythematous

macules that may fade in the center, making them appear as a ringworm?
Fat emboli
Rheumatic fever
Bacterial endocarditis
Myocarditis of acquired immunodeficiency syndrome

a.
b.
c.
d.

ANS: B

Erythema marginatum is a distinctive truncal rash that often accompanies acute rheumatic
fever. It consists of nonpruritic, pink erythematous macules that never occur on the face or
hands. This presentation is not associated with any of the other options.
PTS: 1

REF: Page 1172

36. What is the most common cause of infective endocarditis?

a. Virus
c. Bacterium
b. Fungus
d. Rickettsiae
ANS: C

Infective endocarditis is a general term used to describe infection and inflammation of the
endocardiumespecially the cardiac valves. Bacteria are the most common cause of infective
endocarditis, especially streptococci, staphylococci, or enterococci.
PTS: 1

REF: Page 1173

37. What is the most common cardiac disorder associated with acquired immunodeficiency

syndrome (AIDS)
a. Cardiomyopathy
b. Myocarditis

c. Left heart failure

d. Heart block

ANS: C

Pericardial effusion and left heart failure are the most common complications of human
immunodeficiency virus (HIV) infection. Other conditions include cardiomyopathy,
myocarditis, tuberculous pericarditis, infective and nonbacterial endocarditis, heart block,
pulmonary hypertension, and nonantiretroviral drug-related cardiotoxicity.
PTS: 1

REF: Page 1175

38. A patient is diagnosed with pulmonary disease and elevated pulmonary vascular resistance.

Which form of heart failure may result from pulmonary disease and elevated pulmonary
vascular resistance?
a. Right heart failure
c. Low-output failure
b. Left heart failure
d. High-output failure

ANS: A

Right heart failure is defined as the inability of the right ventricle to provide adequate blood
flow into the pulmonary circulation at a normal central venous pressure. This condition is
often a result of pulmonary disease and the resulting elevated pulmonary vascular resistance.
PTS: 1

REF: Page 1181

39. What cardiac pathologic condition contributes to ventricular remodeling?

a. Left ventricular hypertrophy
c. Myocardial ischemia
b. Right ventricular failure
d. Contractile dysfunction
ANS: C

Of the options available, myocardial ischemia contributes to inflammatory, immune, and

neurohumoral changes that mediate a process called ventricular remodeling.
PTS: 1

REF: Page 1175

40. In systolic heart failure, what effect does the renin-angiotensin-aldosterone system (RAAS)

have on stroke volume?

Increases preload and decreases afterload.
Increases preload and increases afterload.
Decreases preload and increases afterload.
Decreases preload and decreases afterload.

a.
b.
c.
d.

ANS: B

Activation of the RAAS not only causes an increase in preload and afterload, but it also
causes direct toxicity to the myocardium. This selection is the only option that accurately
identifies the effect that the RAAS has on stroke volume in this situation.
PTS: 1

REF: Page 1175 | Page 1177

41. What is the cause of the dyspnea resulting from a thoracic aneurysm?
a. Pressure on surrounding organs
c. Formation of atherosclerotic lesions
b. Poor oxygenation
d. Impaired blood flow
ANS: A

Clinical manifestations depend on the location of the aneurysm. Pressure of a thoracic

aneurysm on surrounding organs cause symptoms of dysphagia (difficulty in swallowing) and
dyspnea (breathlessness). This selection is the only option that accurately describes the cause
of dyspnea resulting from a thoracic aneurysm.
PTS: 1

REF: Page 1142

42. Which statement is true concerning the cells ability to synthesize cholesterol?
a. Cell production of cholesterol is affected by the aging process.
b. Cells produce cholesterol only when dietary fat intake is low.
c. Most body cells are capable of producing cholesterol.
d. Most cholesterol produced by the cells is converted to the low-density form.
ANS: C

Although cholesterol can easily be obtained from dietary fat intake, most body cells can also
manufacture cholesterol. This selection is the only option that accurately describes the cellular
role in cholesterol synthesis.
PTS: 1

REF: Page 1149

43. What is the trigger for angina pectoris?

a. Atherosclerotic lesions
b. Hyperlipidemia

c. Myocardial necrosis
d. Myocardial ischemia

ANS: D

Angina pectoris is chest pain caused by myocardial ischemia. None of the other options are
considered triggers for angina pectoris.
PTS: 1

REF: Page 1154

44. Individuals being effectively managed for type 2 diabetes mellitus often experience a healthy

decline in blood pressure as a result of what intervention?

Managed carbohydrate intake
Appropriate exercise
Insulin-sensitivity medication therapy
Introduction of minimal doses of insulin

a.
b.
c.
d.

ANS: C

Many people with type 2 diabetes mellitus, who are treated with drugs that increase insulin
sensitivity, experience a decline in their blood pressure without taking antihypertensive drugs.
Although the other medications may be included in the management plan, the other options
are not associated with a decrease in hypertension.
PTS: 1

REF: Page 1136

MULTIPLE RESPONSE
45. Which statements are true regarding fatty streaks? (Select all that apply.)
a. Fatty streaks progressively damage vessel walls.
b. Fatty streaks are capable of producing toxic oxygen radials.
c. When present, inflammatory changes occur to the vessel walls.
d. Oxidized low-density lipoproteins (LDLs) are involved in their formation.
e. Fatty streaks are formed by killer T cells filled with oxidized LDLs.
ANS: A, B, C, D

The oxidized LDLs penetrate the intima of the arterial wall and are engulfed by macrophages.
Macrophages filled with oxidized LDLs are called foam. Once these lipid-laden foam cells
accumulate in significant amounts, they form a lesion called a fatty streak. Once formed, fatty
streaks produce more toxic oxygen radicals and cause immunologic and inflammatory
changes, resulting in progressive damage to the vessel wall.
PTS: 1

REF: Page 1145 | Page 1147

46. What factors contribute to the development of orthostatic hypotension? (Select all that apply.)
a. Altered body chemistry

b.
c.
d.
e.

Drug action of certain antihypertensive agents

Prolonged immobility
Effects of aging on postural reflexes
Any condition that produces volume overload

ANS: A, B, C, D

Orthostatic hypotension may be acute or chronic. Acute orthostatic hypotension (temporary

type) may result from (1) altered body chemistry, (2) drug action (e.g., antihypertensives,
antidepressants), (3) prolonged immobility caused by illness, (4) starvation, (5) physical
exhaustion, (6) any condition that produces volume depletion (e.g., massive diuresis,
potassium or sodium depletion), and (7) venous pooling (e.g., pregnancy, extensive
varicosities of the lower extremities). Older adults are susceptible to this type of orthostatic
hypotension, in which postural reflexes are slowed as part of the aging process.
PTS: 1

REF: Page 1140

47. Which assessment findings are clinical manifestations of aortic stenosis? (Select all that

apply.)
a. Jugular vein distention
b. Bounding pulses
c. Hypotension
d. Angina
e. Syncope
ANS: D, E

The classic manifestations of aortic stenosis are angina, syncope, and heart failure. None of
the other options are associated with aortic stenosis.
PTS: 1

REF: Pages 1168-1169

48. Which risk factors are associated with infective endocarditis? (Select all that apply.)
a. Rheumatic fever
b. Intravenous drug use
c. Long-term indwelling catheterization
d. Aortic regurgitation
e. Heart valve disease
ANS: B, C, E

Risk factors for infective endocarditis include acquired valvular heart disease, intravenous
drug abuse, long-term indwelling catheterization (e.g., for pressure monitoring,
hyperalimentation, or hemodialysis), and recent cardiac surgery. Neither rheumatic fever nor
aortic regurgitation is considered a risk factor for infective endocarditis.
PTS: 1

REF: Page 1173 | Box 32-3

MATCHING

Match the descriptions with the corresponding terms.

______ A. Impairs flow from left atrium to left ventricle
______ B. Impairs flow from the left ventricle
______ C. Backflow into left atrium

______ D. Backflow into right atrium

______ E. Backflow into left ventricle
49.
50.
51.
52.
53.

Aortic stenosis
Aortic regurgitation
Mitral stenosis
Tricuspid regurgitation
Mitral regurgitation

49. ANS: B
PTS: 1
REF: Page 1168
MSC: Outflow obstruction increases pressure within the left ventricle as it tries to eject blood through
the narrowed opening. Left ventricular hypertrophy develops to compensate for the increased
workload.
50. ANS: E
PTS: 1
REF: Pages 1169-1170
MSC: During systole, blood is ejected from the left ventricle into the aorta. If the aortic semilunar
valve fails to close completely, then some of the ejected blood flows back into the left ventricle during
diastole.
51. ANS: A
PTS: 1
REF: Page 1169
MSC: Mitral stenosis impairs the flow of blood from the left atrium to the left ventricle.
52. ANS: D
PTS: 1
REF: Page 1170
MSC: Tricuspid regurgitation is more common than tricuspid stenosis and is usually associated with
cardiac failure and dilation of the right ventricle, secondary to pulmonary hypertension.
53. ANS: C
PTS: 1
REF: Page 1170
MSC: Mitral regurgitation permits the backflow of blood from the left ventricle into the left atrium
during ventricular systole, giving rise to a loud pansystolic (throughout systole) murmur heard best at
the apex that radiates into the back and axillae.