Saunders Comprehensive Review for the NCLEX-PN®
Examination
9th Edition
• Author(s)Linda Anne Silvestri; Angela Silvestri
ANATOMY AND PHYSIOLOGY TEST BANK
Questions
1. (Cardiovascular) A client presents with progressive shortness
of breath, orthopnea, crackles auscultated bilaterally, and an S3
heart sound. These findings most directly reflect dysfunction of
which structure/function relationship?
A. Increased right atrial pressure → peripheral edema
B. Left ventricular systolic dysfunction → elevated pulmonary
capillary hydrostatic pressure
C. Tricuspid valve regurgitation → hepatic congestion
D. Decreased circulating albumin → pulmonary interstitial fluid
accumulation
Answer: B
Rationale — Correct (B): Left ventricular systolic dysfunction
(reduced ejection fraction) causes higher end-systolic and end-
diastolic pressures in the left ventricle. Those pressures
,transmit backward into the left atrium and pulmonary
capillaries, increasing hydrostatic pressure and promoting
transudation of fluid into the pulmonary interstitium and alveoli
— producing dyspnea, orthopnea, crackles, and an S3
(ventricular gallop) from rapid ventricular filling.
Rationale — Incorrect:
A. Right atrial pressure ↑ leads mainly to systemic venous
congestion (JVD, peripheral edema), not pulmonary crackles.
C. Tricuspid regurgitation causes right-sided congestion (hepatic
engorgement), not primary pulmonary edema.
D. Low albumin can cause edema generally, but isolated
hypoalbuminemia typically causes peripheral/third-space
edema and would not specifically explain an S3 or orthopnea
from pulmonary vascular pressure elevation.
2. (Cardiovascular — valves) A harsh, crescendo-decrescendo
systolic murmur heard best at the right upper sternal border
with radiation to the carotids most likely indicates:
A. Mitral regurgitation (insufficiency)
B. Aortic stenosis
C. Aortic regurgitation
D. Mitral stenosis
Answer: B
Rationale — Correct (B): Aortic stenosis is a systolic ejection
murmur (crescendo-decrescendo) heard at the right upper
,sternal border and often radiates to the carotids because the
turbulent jet from the stenotic aortic valve transmits into the
ascending aorta and carotid arteries. The murmur timing
(systolic ejection) and location reflect structure (aortic valve
leaflets narrowed) and hemodynamics (increased velocity
across a narrowed orifice).
Rationale — Incorrect:
A. Mitral regurgitation is holosystolic and best heard at the
apex, radiating to the axilla.
C. Aortic regurgitation is a diastolic decrescendo murmur best
heard along the left sternal border.
D. Mitral stenosis produces a diastolic rumbling murmur with an
opening snap, not a systolic crescendo-decrescendo murmur.
3. (Cardiovascular — conduction) A client with inferior wall
myocardial infarction develops bradycardia and hypotension.
Which anatomic explanation best accounts for these findings?
A. Ischemia of the sinoatrial node → loss of atrial automaticity
B. Ischemia of the atrioventricular (AV) node → impaired
conduction to ventricles
C. Ischemia of the left bundle branch → ventricular tachycardia
D. Ischemia of Purkinje fibers → increased heart rate
Answer: B
Rationale — Correct (B): The AV node is supplied most
commonly by the right coronary artery (which supplies the
, inferior wall in most people). An inferior MI can cause AV node
ischemia leading to AV block or slowed conduction →
bradycardia and hemodynamic compromise (hypotension). This
links location of ischemia (inferior wall/RCA distribution) to
conduction dysfunction.
Rationale — Incorrect:
A. SA node ischemia can produce bradycardia but SA nodal
ischemia is less commonly the mechanism in inferior MI; SA
node is usually supplied by the RCA in many people but the
scenario (inferior MI causing classic AV
block/bradycardia/hypotension) better fits AV nodal ischemia.
C. Left bundle branch ischemia typically causes bundle branch
block patterns, not primary bradycardia with hypotension as
described. Ventricular tachycardia is associated with different
infarct locations and arrhythmogenic substrate.
D. Purkinje fiber ischemia disrupts ventricular conduction and
can cause arrhythmias; it would not cause an increased heart
rate as the primary explanation.
4. (Cardiovascular — fluid balance) A patient with chronic heart
failure is prescribed an ACE inhibitor. Which mechanism
explains the expected therapeutic reduction in afterload?
A. ACE inhibitors increase angiotensin II → systemic
vasoconstriction
B. ACE inhibitors cause bradykinin degradation → decreased
vasodilation
Examination
9th Edition
• Author(s)Linda Anne Silvestri; Angela Silvestri
ANATOMY AND PHYSIOLOGY TEST BANK
Questions
1. (Cardiovascular) A client presents with progressive shortness
of breath, orthopnea, crackles auscultated bilaterally, and an S3
heart sound. These findings most directly reflect dysfunction of
which structure/function relationship?
A. Increased right atrial pressure → peripheral edema
B. Left ventricular systolic dysfunction → elevated pulmonary
capillary hydrostatic pressure
C. Tricuspid valve regurgitation → hepatic congestion
D. Decreased circulating albumin → pulmonary interstitial fluid
accumulation
Answer: B
Rationale — Correct (B): Left ventricular systolic dysfunction
(reduced ejection fraction) causes higher end-systolic and end-
diastolic pressures in the left ventricle. Those pressures
,transmit backward into the left atrium and pulmonary
capillaries, increasing hydrostatic pressure and promoting
transudation of fluid into the pulmonary interstitium and alveoli
— producing dyspnea, orthopnea, crackles, and an S3
(ventricular gallop) from rapid ventricular filling.
Rationale — Incorrect:
A. Right atrial pressure ↑ leads mainly to systemic venous
congestion (JVD, peripheral edema), not pulmonary crackles.
C. Tricuspid regurgitation causes right-sided congestion (hepatic
engorgement), not primary pulmonary edema.
D. Low albumin can cause edema generally, but isolated
hypoalbuminemia typically causes peripheral/third-space
edema and would not specifically explain an S3 or orthopnea
from pulmonary vascular pressure elevation.
2. (Cardiovascular — valves) A harsh, crescendo-decrescendo
systolic murmur heard best at the right upper sternal border
with radiation to the carotids most likely indicates:
A. Mitral regurgitation (insufficiency)
B. Aortic stenosis
C. Aortic regurgitation
D. Mitral stenosis
Answer: B
Rationale — Correct (B): Aortic stenosis is a systolic ejection
murmur (crescendo-decrescendo) heard at the right upper
,sternal border and often radiates to the carotids because the
turbulent jet from the stenotic aortic valve transmits into the
ascending aorta and carotid arteries. The murmur timing
(systolic ejection) and location reflect structure (aortic valve
leaflets narrowed) and hemodynamics (increased velocity
across a narrowed orifice).
Rationale — Incorrect:
A. Mitral regurgitation is holosystolic and best heard at the
apex, radiating to the axilla.
C. Aortic regurgitation is a diastolic decrescendo murmur best
heard along the left sternal border.
D. Mitral stenosis produces a diastolic rumbling murmur with an
opening snap, not a systolic crescendo-decrescendo murmur.
3. (Cardiovascular — conduction) A client with inferior wall
myocardial infarction develops bradycardia and hypotension.
Which anatomic explanation best accounts for these findings?
A. Ischemia of the sinoatrial node → loss of atrial automaticity
B. Ischemia of the atrioventricular (AV) node → impaired
conduction to ventricles
C. Ischemia of the left bundle branch → ventricular tachycardia
D. Ischemia of Purkinje fibers → increased heart rate
Answer: B
Rationale — Correct (B): The AV node is supplied most
commonly by the right coronary artery (which supplies the
, inferior wall in most people). An inferior MI can cause AV node
ischemia leading to AV block or slowed conduction →
bradycardia and hemodynamic compromise (hypotension). This
links location of ischemia (inferior wall/RCA distribution) to
conduction dysfunction.
Rationale — Incorrect:
A. SA node ischemia can produce bradycardia but SA nodal
ischemia is less commonly the mechanism in inferior MI; SA
node is usually supplied by the RCA in many people but the
scenario (inferior MI causing classic AV
block/bradycardia/hypotension) better fits AV nodal ischemia.
C. Left bundle branch ischemia typically causes bundle branch
block patterns, not primary bradycardia with hypotension as
described. Ventricular tachycardia is associated with different
infarct locations and arrhythmogenic substrate.
D. Purkinje fiber ischemia disrupts ventricular conduction and
can cause arrhythmias; it would not cause an increased heart
rate as the primary explanation.
4. (Cardiovascular — fluid balance) A patient with chronic heart
failure is prescribed an ACE inhibitor. Which mechanism
explains the expected therapeutic reduction in afterload?
A. ACE inhibitors increase angiotensin II → systemic
vasoconstriction
B. ACE inhibitors cause bradykinin degradation → decreased
vasodilation
