Saunders Comprehensive Review for the NCLEX-PN®
Examination
9th Edition
• Author(s)Linda Anne Silvestri; Angela Silvestri
ANATOMY AND PHYSIOLOGY TEST BANK
1 — Cardiovascular: Heart sounds and valve pathology
A 68-year-old patient reports gradual shortness of breath on
exertion. On auscultation you hear a low-pitched, rumbling
diastolic murmur with an opening snap best heard at the apex.
Which valve is most likely affected and what is the primary
physiologic mechanism?
A. Aortic valve — incomplete closure causes regurgitant flow
into the left ventricle during diastole.
B. Mitral valve — leaflets stiffen and fuse causing impaired
opening and increased left atrial pressure.
C. Tricuspid valve — stenosis causing decreased right atrial
emptying.
D. Pulmonic valve — regurgitation causing increased right
ventricular preload.
Answer: B — Mitral valve; stiffening/fusion (mitral stenosis)
causing impaired opening and elevated left atrial pressure.
,Rationale:
• Correct (B): A low-pitched, rumbling diastolic murmur with
an opening snap at the apex is classic for mitral stenosis.
Pathophysiology: thickened/fused mitral leaflets reduce
mitral orifice area during diastole → impaired LV filling →
elevated left atrial pressure → pulmonary congestion and
exertional dyspnea.
• A: Aortic regurgitation produces a high-pitched diastolic
blowing murmur at the left sternal border and results from
incompetent closure of aortic cusps; not a rumbling
diastolic apex murmur.
• C: Tricuspid stenosis yields diastolic murmur at the lower
left sternal border and is rare; signs would be systemic
venous congestion rather than primary pulmonary
symptoms.
• D: Pulmonic valve regurgitation results in right-sided
diastolic findings and increased RV preload — not the apex
diastolic rumble with opening snap.
2 — Respiratory: V/Q mismatch and hypoxemia
A patient with a lobar pneumonia has hypoxemia (low PaO₂)
that does not fully correct with supplemental oxygen. Which
physiologic abnormality best explains this finding?
A. Increased physiologic dead space.
B. Shunt (perfusion without ventilation) in the affected lung
,region.
C. Decreased diffusion capacity due to thickened alveolar
membrane.
D. Alveolar hyperventilation causing respiratory alkalosis.
Answer: B — Shunt (perfusion without ventilation) in the
affected lung region.
Rationale:
• Correct (B): Lobar pneumonia fills alveoli with
inflammatory exudate → alveoli are perfused but not
ventilated → physiologic shunt. Blood passing through
nonventilated alveoli remains deoxygenated; supplemental
oxygen has limited effect because alveoli cannot take up
the oxygen.
• A: Increased dead space (ventilation without perfusion)
causes elevated PaCO₂ to decrease less efficiently and
reduces efficiency of ventilation; oxygenation often
improves with supplemental O₂.
• C: Diffusion impairment (e.g., pulmonary fibrosis) can limit
O₂ transfer, especially during exercise; however in lobar
consolidation the dominant problem is shunt.
• D: Hyperventilation affects CO₂ (PaCO₂) not primary cause
of refractory hypoxemia; it may raise pH but won’t correct
shunt physiology.
, 3 — Renal: Acid-base and renal compensation
A patient has chronic respiratory acidosis due to COPD and a
measured arterial HCO₃⁻ that is elevated. Which renal
mechanism explains the elevated bicarbonate?
A. Increased bicarbonate excretion in the collecting duct.
B. Enhanced ammoniagenesis and increased H⁺ excretion as
NH₄⁺.
C. Decreased proximal tubular reabsorption of bicarbonate.
D. Decreased activity of renal carbonic anhydrase.
Answer: B — Enhanced ammoniagenesis and increased H⁺
excretion as NH₄⁺.
Rationale:
• Correct (B): In chronic respiratory acidosis (elevated
PaCO₂), kidneys compensate by increasing H⁺ excretion
and generating new HCO₃⁻. Mechanisms include increased
ammoniagenesis (glutamine metabolism) in proximal
tubules producing NH₄⁺ for H⁺ excretion and adding new
bicarbonate to plasma.
• A: Increased bicarbonate excretion would lower HCO₃⁻ and
worsen acidosis — opposite of compensation.
• C: Decreased proximal reabsorption of HCO₃⁻ would
reduce plasma HCO₃⁻; not compensatory.
• D: Decreased renal carbonic anhydrase would impair
HCO₃⁻ regeneration; compensation requires the opposite
(functional carbonic anhydrase activity).
Examination
9th Edition
• Author(s)Linda Anne Silvestri; Angela Silvestri
ANATOMY AND PHYSIOLOGY TEST BANK
1 — Cardiovascular: Heart sounds and valve pathology
A 68-year-old patient reports gradual shortness of breath on
exertion. On auscultation you hear a low-pitched, rumbling
diastolic murmur with an opening snap best heard at the apex.
Which valve is most likely affected and what is the primary
physiologic mechanism?
A. Aortic valve — incomplete closure causes regurgitant flow
into the left ventricle during diastole.
B. Mitral valve — leaflets stiffen and fuse causing impaired
opening and increased left atrial pressure.
C. Tricuspid valve — stenosis causing decreased right atrial
emptying.
D. Pulmonic valve — regurgitation causing increased right
ventricular preload.
Answer: B — Mitral valve; stiffening/fusion (mitral stenosis)
causing impaired opening and elevated left atrial pressure.
,Rationale:
• Correct (B): A low-pitched, rumbling diastolic murmur with
an opening snap at the apex is classic for mitral stenosis.
Pathophysiology: thickened/fused mitral leaflets reduce
mitral orifice area during diastole → impaired LV filling →
elevated left atrial pressure → pulmonary congestion and
exertional dyspnea.
• A: Aortic regurgitation produces a high-pitched diastolic
blowing murmur at the left sternal border and results from
incompetent closure of aortic cusps; not a rumbling
diastolic apex murmur.
• C: Tricuspid stenosis yields diastolic murmur at the lower
left sternal border and is rare; signs would be systemic
venous congestion rather than primary pulmonary
symptoms.
• D: Pulmonic valve regurgitation results in right-sided
diastolic findings and increased RV preload — not the apex
diastolic rumble with opening snap.
2 — Respiratory: V/Q mismatch and hypoxemia
A patient with a lobar pneumonia has hypoxemia (low PaO₂)
that does not fully correct with supplemental oxygen. Which
physiologic abnormality best explains this finding?
A. Increased physiologic dead space.
B. Shunt (perfusion without ventilation) in the affected lung
,region.
C. Decreased diffusion capacity due to thickened alveolar
membrane.
D. Alveolar hyperventilation causing respiratory alkalosis.
Answer: B — Shunt (perfusion without ventilation) in the
affected lung region.
Rationale:
• Correct (B): Lobar pneumonia fills alveoli with
inflammatory exudate → alveoli are perfused but not
ventilated → physiologic shunt. Blood passing through
nonventilated alveoli remains deoxygenated; supplemental
oxygen has limited effect because alveoli cannot take up
the oxygen.
• A: Increased dead space (ventilation without perfusion)
causes elevated PaCO₂ to decrease less efficiently and
reduces efficiency of ventilation; oxygenation often
improves with supplemental O₂.
• C: Diffusion impairment (e.g., pulmonary fibrosis) can limit
O₂ transfer, especially during exercise; however in lobar
consolidation the dominant problem is shunt.
• D: Hyperventilation affects CO₂ (PaCO₂) not primary cause
of refractory hypoxemia; it may raise pH but won’t correct
shunt physiology.
, 3 — Renal: Acid-base and renal compensation
A patient has chronic respiratory acidosis due to COPD and a
measured arterial HCO₃⁻ that is elevated. Which renal
mechanism explains the elevated bicarbonate?
A. Increased bicarbonate excretion in the collecting duct.
B. Enhanced ammoniagenesis and increased H⁺ excretion as
NH₄⁺.
C. Decreased proximal tubular reabsorption of bicarbonate.
D. Decreased activity of renal carbonic anhydrase.
Answer: B — Enhanced ammoniagenesis and increased H⁺
excretion as NH₄⁺.
Rationale:
• Correct (B): In chronic respiratory acidosis (elevated
PaCO₂), kidneys compensate by increasing H⁺ excretion
and generating new HCO₃⁻. Mechanisms include increased
ammoniagenesis (glutamine metabolism) in proximal
tubules producing NH₄⁺ for H⁺ excretion and adding new
bicarbonate to plasma.
• A: Increased bicarbonate excretion would lower HCO₃⁻ and
worsen acidosis — opposite of compensation.
• C: Decreased proximal reabsorption of HCO₃⁻ would
reduce plasma HCO₃⁻; not compensatory.
• D: Decreased renal carbonic anhydrase would impair
HCO₃⁻ regeneration; compensation requires the opposite
(functional carbonic anhydrase activity).
