NURS 3366 PATHOPHYSIOLOGY - TEST 2:
CARDIOVASCULAR, RESPIRATORY, RENAL,
FLUID/ELECTROLYTES, HEMATOLOGIC SYSTEMS -
Integrated Systems Assessment with Clinical
Rationales
SECTION 1: CARDIOVASCULAR PATHOPHYSIOLOGY (Questions 1-15)
1. A 68-year-old female with a 15-year history of hypertension presents with progressive
dyspnea on exertion and orthopnea. Echocardiogram reveals left ventricular
hypertrophy, normal left ventricular ejection fraction (65%), and abnormal diastolic filling
patterns. BNP is elevated at 450 pg/mL. Which pathophysiological mechanism BEST
explains her clinical presentation?
A) Systolic pump failure with reduced cardiac output
B) Myocardial fibrosis and impaired ventricular relaxation due to chronic pressure
overload
C) Acute volume overload from valvular regurgitation
D) Inflammatory cardiomyopathy with myocyte necrosis
[CORRECT ANSWER: B]
,System & Core Concept: Cardiovascular: Heart Failure with Preserved Ejection Fraction
(HFpEF) / Diastolic Heart Failure
Pathophysiological Mechanism: Chronic hypertension increases afterload, leading to
concentric left ventricular hypertrophy. Persistent pressure overload stimulates
fibroblast proliferation and collagen deposition (myocardial fibrosis) and alters titin
phosphorylation, resulting in a stiff, non-compliant ventricle. This impairs passive filling
during diastole, increasing left ventricular end-diastolic pressure (LVEDP) and causing
pulmonary congestion despite normal systolic contractility (preserved EF).
Clinical Cue Integration: The patient has long-standing hypertension (chronic pressure
overload), preserved EF (65%), LVH on echo, and elevated BNP with symptoms of
pulmonary congestion. This classic triad points to HFpEF, not systolic failure.
Why B is Right: It correctly identifies the primary mechanistic driver: chronic pressure
overload leading to diastolic dysfunction through fibrosis and impaired relaxation.
Why Other Choices Are Wrong:
[A]: Incorrect. Systolic pump failure would present with reduced EF (<50%). This
patient's EF is preserved (65%).
[C]: Incorrect. While valvular disease can cause heart failure, there is no mention of
regurgitation murmurs or valvular abnormalities on echo. The echocardiogram findings
specify LVH and diastolic dysfunction.
[D]: Incorrect. Inflammatory cardiomyopathy (myocarditis) typically presents with acute
onset, dilated cardiomyopathy, and reduced EF, not chronic hypertensive remodeling
with preserved EF.
,Key Takeaway: HFpEF = preserved EF + diastolic dysfunction from chronic pressure
overload/hypertrophy/fibrosis.
2. A 55-year-old male presents to the ED with substernal chest pain radiating to his left
arm, diaphoresis, and nausea. ECG shows ST-segment elevation in leads V1-V4. Cardiac
enzymes are pending. Which pathophysiological event is the PRIMARY cause of his
symptoms?
A) Acute thrombotic occlusion of the left anterior descending artery
B) Severe three-vessel coronary artery disease with collateral circulation
C) Transient coronary vasospasm without plaque rupture
D) Increased myocardial oxygen demand exceeding supply in stable CAD
[CORRECT ANSWER: A]
System & Core Concept: Cardiovascular: Acute Myocardial Infarction (STEMI)
Pathophysiological Mechanism: Atherosclerotic plaque rupture exposes subendothelial
collagen, triggering platelet activation, aggregation, and thrombus formation. Complete
occlusion of a coronary artery by thrombus leads to transmural ischemia, myocardial
necrosis, and ST-segment elevation on ECG.
Clinical Cue Integration: ST-segment elevation in contiguous anterior leads (V1-V4)
localizes to the left anterior descending (LAD) artery territory. The classic symptom
presentation (crushing substernal chest pain, radiation to left arm, diaphoresis, nausea)
is consistent with acute coronary occlusion.
Why A is Right: It identifies the acute, occlusive thrombotic event directly responsible for
transmural ischemia and ST-elevation.
, Why Other Choices Are Wrong:
[B]: Incorrect. While three-vessel disease indicates severe atherosclerosis, the acute
event is plaque rupture and thrombosis in a single culprit vessel. Collateral circulation
may actually protect against STEMI.
[C]: Incorrect. Vasospasm (Prinzmetal angina) presents with transient ST-elevation that
resolves with vasodilators, but this patient's presentation is consistent with thrombotic
occlusion, not spasm alone.
[D]: Incorrect. This describes stable angina or demand ischemia (Type 2 MI), which does
not cause ST-segment elevation or transmural infarction.
Key Takeaway: STEMI = acute plaque rupture + thrombotic occlusion + transmural
ischemia.
3. A 72-year-old male with acute anterior wall myocardial infarction develops sudden
onset of severe dyspnea, frothy pink sputum, and hypotension 48 hours post-infarction.
A new holosystolic murmur is heard at the apex radiating to the axilla. Which
pathophysiological complication has occurred?
A) Papillary muscle rupture causing acute mitral regurgitation
B) Ventricular septal defect from septal wall rupture
C) Free wall rupture with cardiac tamponade
D) Dressler's syndrome with pericardial effusion
[CORRECT ANSWER: A]
CARDIOVASCULAR, RESPIRATORY, RENAL,
FLUID/ELECTROLYTES, HEMATOLOGIC SYSTEMS -
Integrated Systems Assessment with Clinical
Rationales
SECTION 1: CARDIOVASCULAR PATHOPHYSIOLOGY (Questions 1-15)
1. A 68-year-old female with a 15-year history of hypertension presents with progressive
dyspnea on exertion and orthopnea. Echocardiogram reveals left ventricular
hypertrophy, normal left ventricular ejection fraction (65%), and abnormal diastolic filling
patterns. BNP is elevated at 450 pg/mL. Which pathophysiological mechanism BEST
explains her clinical presentation?
A) Systolic pump failure with reduced cardiac output
B) Myocardial fibrosis and impaired ventricular relaxation due to chronic pressure
overload
C) Acute volume overload from valvular regurgitation
D) Inflammatory cardiomyopathy with myocyte necrosis
[CORRECT ANSWER: B]
,System & Core Concept: Cardiovascular: Heart Failure with Preserved Ejection Fraction
(HFpEF) / Diastolic Heart Failure
Pathophysiological Mechanism: Chronic hypertension increases afterload, leading to
concentric left ventricular hypertrophy. Persistent pressure overload stimulates
fibroblast proliferation and collagen deposition (myocardial fibrosis) and alters titin
phosphorylation, resulting in a stiff, non-compliant ventricle. This impairs passive filling
during diastole, increasing left ventricular end-diastolic pressure (LVEDP) and causing
pulmonary congestion despite normal systolic contractility (preserved EF).
Clinical Cue Integration: The patient has long-standing hypertension (chronic pressure
overload), preserved EF (65%), LVH on echo, and elevated BNP with symptoms of
pulmonary congestion. This classic triad points to HFpEF, not systolic failure.
Why B is Right: It correctly identifies the primary mechanistic driver: chronic pressure
overload leading to diastolic dysfunction through fibrosis and impaired relaxation.
Why Other Choices Are Wrong:
[A]: Incorrect. Systolic pump failure would present with reduced EF (<50%). This
patient's EF is preserved (65%).
[C]: Incorrect. While valvular disease can cause heart failure, there is no mention of
regurgitation murmurs or valvular abnormalities on echo. The echocardiogram findings
specify LVH and diastolic dysfunction.
[D]: Incorrect. Inflammatory cardiomyopathy (myocarditis) typically presents with acute
onset, dilated cardiomyopathy, and reduced EF, not chronic hypertensive remodeling
with preserved EF.
,Key Takeaway: HFpEF = preserved EF + diastolic dysfunction from chronic pressure
overload/hypertrophy/fibrosis.
2. A 55-year-old male presents to the ED with substernal chest pain radiating to his left
arm, diaphoresis, and nausea. ECG shows ST-segment elevation in leads V1-V4. Cardiac
enzymes are pending. Which pathophysiological event is the PRIMARY cause of his
symptoms?
A) Acute thrombotic occlusion of the left anterior descending artery
B) Severe three-vessel coronary artery disease with collateral circulation
C) Transient coronary vasospasm without plaque rupture
D) Increased myocardial oxygen demand exceeding supply in stable CAD
[CORRECT ANSWER: A]
System & Core Concept: Cardiovascular: Acute Myocardial Infarction (STEMI)
Pathophysiological Mechanism: Atherosclerotic plaque rupture exposes subendothelial
collagen, triggering platelet activation, aggregation, and thrombus formation. Complete
occlusion of a coronary artery by thrombus leads to transmural ischemia, myocardial
necrosis, and ST-segment elevation on ECG.
Clinical Cue Integration: ST-segment elevation in contiguous anterior leads (V1-V4)
localizes to the left anterior descending (LAD) artery territory. The classic symptom
presentation (crushing substernal chest pain, radiation to left arm, diaphoresis, nausea)
is consistent with acute coronary occlusion.
Why A is Right: It identifies the acute, occlusive thrombotic event directly responsible for
transmural ischemia and ST-elevation.
, Why Other Choices Are Wrong:
[B]: Incorrect. While three-vessel disease indicates severe atherosclerosis, the acute
event is plaque rupture and thrombosis in a single culprit vessel. Collateral circulation
may actually protect against STEMI.
[C]: Incorrect. Vasospasm (Prinzmetal angina) presents with transient ST-elevation that
resolves with vasodilators, but this patient's presentation is consistent with thrombotic
occlusion, not spasm alone.
[D]: Incorrect. This describes stable angina or demand ischemia (Type 2 MI), which does
not cause ST-segment elevation or transmural infarction.
Key Takeaway: STEMI = acute plaque rupture + thrombotic occlusion + transmural
ischemia.
3. A 72-year-old male with acute anterior wall myocardial infarction develops sudden
onset of severe dyspnea, frothy pink sputum, and hypotension 48 hours post-infarction.
A new holosystolic murmur is heard at the apex radiating to the axilla. Which
pathophysiological complication has occurred?
A) Papillary muscle rupture causing acute mitral regurgitation
B) Ventricular septal defect from septal wall rupture
C) Free wall rupture with cardiac tamponade
D) Dressler's syndrome with pericardial effusion
[CORRECT ANSWER: A]
