,NUR 265 EXAM 2 - Original Practice Study Guide
NUR 265 Exam 2 | Medical-Surgical Nursing | Galen College | Q & A |
2026/2027 100%Pass (PDF)
1. Following sudden dyspnea and pleuritic chest discomfort in a postoperative adult, which
pathophysiologic change most directly produces hypoxemia in pulmonary embolism?
A) Increased diffusion distance from chronic alveolar fibrosis
B) Ventilated alveoli receiving little or no perfusion
C) Global suppression of medullary respiratory drive
D) Excess surfactant causing alveolar overdistention
Correct Answer: Ventilated alveoli receiving little or no perfusion
Rationale: A pulmonary embolus blocks pulmonary arterial flow, creating regions that are ventilated but poorly perfused.
This ventilation-perfusion mismatch increases physiologic dead space and impairs oxygenation. Fibrosis causes
diffusion limitation rather than the abrupt perfusion defect of PE, and neither medullary suppression nor excess
surfactant explains the typical acute mechanism. The alternative choices represent different mechanisms or lower-
priority interpretations and should be separated from the defining pathophysiologic relationship in the stem.
2. A hospitalized adult with a confirmed lower-extremity DVT suddenly becomes tachycardic and
hypoxemic. Which change should be interpreted as most concerning for embolization?
A) A mild increase in appetite
B) Gradual bilateral ankle edema after prolonged standing
C) New pleuritic chest pain with unexplained dyspnea
D) Localized bruising at a venipuncture site
Correct Answer: New pleuritic chest pain with unexplained dyspnea
Rationale: New unexplained dyspnea, tachycardia, hypoxemia, and pleuritic chest pain in a person with DVT strongly
suggest pulmonary embolization. Dependent edema can occur for many reasons and is not specific for acute PE.
Appetite and minor venipuncture bruising do not indicate pulmonary vascular obstruction. The alternative choices
represent different mechanisms or lower-priority interpretations and should be separated from the defining
pathophysiologic relationship in the stem.
3. Why can a large pulmonary embolus cause hypotension?
A) It causes immediate left ventricular hypertrophy
B) It abruptly raises pulmonary vascular resistance and strains the right ventricle
C) It lowers systemic vascular resistance through chronic anemia
D) It increases left ventricular preload by diverting blood through the lungs
Correct Answer: It abruptly raises pulmonary vascular resistance and strains the right ventricle
Rationale: A large embolus sharply increases pulmonary vascular resistance. The right ventricle may dilate and fail
against the sudden afterload, reducing blood flow through the lungs and therefore left-sided preload and cardiac output.
The process is acute, so left ventricular hypertrophy is not the mechanism.
4. Which finding best reflects impaired gas exchange rather than the source of a pulmonary embolus?
A) Unilateral calf swelling
B) Sudden reduction in oxygen saturation
C) Recent prolonged immobility
Page 2
, NUR 265 EXAM 2 - Original Practice Study Guide
D) Tenderness along a deep leg vein
Correct Answer: Sudden reduction in oxygen saturation
Rationale: A falling oxygen saturation reflects the pulmonary consequence of embolic obstruction and ventilation-
perfusion mismatch. Calf swelling, immobility, and deep venous tenderness relate to venous thrombosis risk or source
rather than the gas-exchange impairment produced after embolization. The alternative choices represent different
mechanisms or lower-priority interpretations and should be separated from the defining pathophysiologic relationship in
the stem.
5. A priority concept for this presentation is that following sudden dyspnea and pleuritic chest discomfort
in a postoperative adult, which pathophysiologic change most directly produces hypoxemia in pulmonary
embolism?
A) Increased diffusion distance from chronic alveolar fibrosis
B) Excess surfactant causing alveolar overdistention
C) Global suppression of medullary respiratory drive
D) Ventilated alveoli receiving little or no perfusion
Correct Answer: Ventilated alveoli receiving little or no perfusion
Rationale: A pulmonary embolus blocks pulmonary arterial flow, creating regions that are ventilated but poorly perfused.
This ventilation-perfusion mismatch increases physiologic dead space and impairs oxygenation. Fibrosis causes
diffusion limitation rather than the abrupt perfusion defect of PE, and neither medullary suppression nor excess
surfactant explains the typical acute mechanism. The alternative choices represent different mechanisms or lower-
priority interpretations and should be separated from the defining pathophysiologic relationship in the stem.
6. When interpreting the underlying physiology, a hospitalized adult with a confirmed lower-extremity DVT
suddenly becomes tachycardic and hypoxemic. Which change should be interpreted as most concerning
for embolization?
A) Gradual bilateral ankle edema after prolonged standing
B) New pleuritic chest pain with unexplained dyspnea
C) A mild increase in appetite
D) Localized bruising at a venipuncture site
Correct Answer: New pleuritic chest pain with unexplained dyspnea
Rationale: New unexplained dyspnea, tachycardia, hypoxemia, and pleuritic chest pain in a person with DVT strongly
suggest pulmonary embolization. Dependent edema can occur for many reasons and is not specific for acute PE.
Appetite and minor venipuncture bruising do not indicate pulmonary vascular obstruction.
7. Clinical reasoning is most accurate when recognizing that why can a large pulmonary embolus cause
hypotension?
A) It causes immediate left ventricular hypertrophy
B) It abruptly raises pulmonary vascular resistance and strains the right ventricle
C) It lowers systemic vascular resistance through chronic anemia
D) It increases left ventricular preload by diverting blood through the lungs
Correct Answer: It abruptly raises pulmonary vascular resistance and strains the right ventricle
Rationale: A large embolus sharply increases pulmonary vascular resistance. The right ventricle may dilate and fail
against the sudden afterload, reducing blood flow through the lungs and therefore left-sided preload and cardiac output.
The process is acute, so left ventricular hypertrophy is not the mechanism. The alternative choices represent different
Page 3
NUR 265 Exam 2 | Medical-Surgical Nursing | Galen College | Q & A |
2026/2027 100%Pass (PDF)
1. Following sudden dyspnea and pleuritic chest discomfort in a postoperative adult, which
pathophysiologic change most directly produces hypoxemia in pulmonary embolism?
A) Increased diffusion distance from chronic alveolar fibrosis
B) Ventilated alveoli receiving little or no perfusion
C) Global suppression of medullary respiratory drive
D) Excess surfactant causing alveolar overdistention
Correct Answer: Ventilated alveoli receiving little or no perfusion
Rationale: A pulmonary embolus blocks pulmonary arterial flow, creating regions that are ventilated but poorly perfused.
This ventilation-perfusion mismatch increases physiologic dead space and impairs oxygenation. Fibrosis causes
diffusion limitation rather than the abrupt perfusion defect of PE, and neither medullary suppression nor excess
surfactant explains the typical acute mechanism. The alternative choices represent different mechanisms or lower-
priority interpretations and should be separated from the defining pathophysiologic relationship in the stem.
2. A hospitalized adult with a confirmed lower-extremity DVT suddenly becomes tachycardic and
hypoxemic. Which change should be interpreted as most concerning for embolization?
A) A mild increase in appetite
B) Gradual bilateral ankle edema after prolonged standing
C) New pleuritic chest pain with unexplained dyspnea
D) Localized bruising at a venipuncture site
Correct Answer: New pleuritic chest pain with unexplained dyspnea
Rationale: New unexplained dyspnea, tachycardia, hypoxemia, and pleuritic chest pain in a person with DVT strongly
suggest pulmonary embolization. Dependent edema can occur for many reasons and is not specific for acute PE.
Appetite and minor venipuncture bruising do not indicate pulmonary vascular obstruction. The alternative choices
represent different mechanisms or lower-priority interpretations and should be separated from the defining
pathophysiologic relationship in the stem.
3. Why can a large pulmonary embolus cause hypotension?
A) It causes immediate left ventricular hypertrophy
B) It abruptly raises pulmonary vascular resistance and strains the right ventricle
C) It lowers systemic vascular resistance through chronic anemia
D) It increases left ventricular preload by diverting blood through the lungs
Correct Answer: It abruptly raises pulmonary vascular resistance and strains the right ventricle
Rationale: A large embolus sharply increases pulmonary vascular resistance. The right ventricle may dilate and fail
against the sudden afterload, reducing blood flow through the lungs and therefore left-sided preload and cardiac output.
The process is acute, so left ventricular hypertrophy is not the mechanism.
4. Which finding best reflects impaired gas exchange rather than the source of a pulmonary embolus?
A) Unilateral calf swelling
B) Sudden reduction in oxygen saturation
C) Recent prolonged immobility
Page 2
, NUR 265 EXAM 2 - Original Practice Study Guide
D) Tenderness along a deep leg vein
Correct Answer: Sudden reduction in oxygen saturation
Rationale: A falling oxygen saturation reflects the pulmonary consequence of embolic obstruction and ventilation-
perfusion mismatch. Calf swelling, immobility, and deep venous tenderness relate to venous thrombosis risk or source
rather than the gas-exchange impairment produced after embolization. The alternative choices represent different
mechanisms or lower-priority interpretations and should be separated from the defining pathophysiologic relationship in
the stem.
5. A priority concept for this presentation is that following sudden dyspnea and pleuritic chest discomfort
in a postoperative adult, which pathophysiologic change most directly produces hypoxemia in pulmonary
embolism?
A) Increased diffusion distance from chronic alveolar fibrosis
B) Excess surfactant causing alveolar overdistention
C) Global suppression of medullary respiratory drive
D) Ventilated alveoli receiving little or no perfusion
Correct Answer: Ventilated alveoli receiving little or no perfusion
Rationale: A pulmonary embolus blocks pulmonary arterial flow, creating regions that are ventilated but poorly perfused.
This ventilation-perfusion mismatch increases physiologic dead space and impairs oxygenation. Fibrosis causes
diffusion limitation rather than the abrupt perfusion defect of PE, and neither medullary suppression nor excess
surfactant explains the typical acute mechanism. The alternative choices represent different mechanisms or lower-
priority interpretations and should be separated from the defining pathophysiologic relationship in the stem.
6. When interpreting the underlying physiology, a hospitalized adult with a confirmed lower-extremity DVT
suddenly becomes tachycardic and hypoxemic. Which change should be interpreted as most concerning
for embolization?
A) Gradual bilateral ankle edema after prolonged standing
B) New pleuritic chest pain with unexplained dyspnea
C) A mild increase in appetite
D) Localized bruising at a venipuncture site
Correct Answer: New pleuritic chest pain with unexplained dyspnea
Rationale: New unexplained dyspnea, tachycardia, hypoxemia, and pleuritic chest pain in a person with DVT strongly
suggest pulmonary embolization. Dependent edema can occur for many reasons and is not specific for acute PE.
Appetite and minor venipuncture bruising do not indicate pulmonary vascular obstruction.
7. Clinical reasoning is most accurate when recognizing that why can a large pulmonary embolus cause
hypotension?
A) It causes immediate left ventricular hypertrophy
B) It abruptly raises pulmonary vascular resistance and strains the right ventricle
C) It lowers systemic vascular resistance through chronic anemia
D) It increases left ventricular preload by diverting blood through the lungs
Correct Answer: It abruptly raises pulmonary vascular resistance and strains the right ventricle
Rationale: A large embolus sharply increases pulmonary vascular resistance. The right ventricle may dilate and fail
against the sudden afterload, reducing blood flow through the lungs and therefore left-sided preload and cardiac output.
The process is acute, so left ventricular hypertrophy is not the mechanism. The alternative choices represent different
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