Nursing (NURS 5315) Exam Cardiac and
Pulmonary 3 – University of Texas at Arlington |
Questions and Answers.
SECTION 1: Heart Failure (HFrEF & HFpEF) – Questions 1–8
Q1: A 68-year-old Black male with long-standing hypertension presents with exertional dyspnea,
fatigue, and lower extremity edema. Echocardiogram shows LVEF of 55% but evidence of
diastolic dysfunction with elevated E/e' ratio and left atrial enlargement. BNP is 450 pg/mL.
Which pathophysiological mechanism BEST explains this presentation?
A. Reduced myocardial contractility with compensatory RAAS activation leading to volume
expansion
B. Impaired ventricular relaxation and increased passive stiffness with elevated filling pressures
despite preserved contractility [CORRECT]
C. Primary valvular regurgitation causing chronic volume overload with eccentric hypertrophy
D. Afterload reduction from systemic vasodilation leading to high-output failure
Correct Answer: B
Rationale: This patient presents with HFpEF (preserved EF ≥50% with diastolic dysfunction),
which is more prevalent in older Black adults with hypertension. The pathophysiology involves
impaired active relaxation (early diastole) and increased passive ventricular stiffness (late
diastole), leading to elevated left ventricular end-diastolic pressure and pulmonary venous
congestion despite normal systolic contractility. Option A describes HFrEF pathophysiology
(reduced contractility). Option C describes volume overload from regurgitant lesions, which
typically causes eccentric hypertrophy and elevated EF initially. Option D is physiologically
incoherent—afterload reduction does not cause heart failure. Advanced practice relevance:
HFpEF now accounts for >50% of heart failure hospitalizations in older adults and requires
different therapeutic approaches than HFrEF; the E/e' ratio >14 confirms elevated filling
pressures.
Q2: A 62-year-old female with HFrEF (LVEF 30%) develops progressive dyspnea and weight gain
over 2 weeks. Laboratory studies show elevated BUN, hyponatremia (Na+ 128), and NT-proBNP
>5000 pg/mL. Which neurohormonal mechanism MOST directly contributes to her
hyponatremia?
,A. Excessive renal sodium retention from aldosterone escape
B. Non-osmotic vasopressin (ADH) release due to decreased effective arterial blood volume
[CORRECT]
C. Primary polydipsia from hypothalamic osmoreceptor dysfunction
D. Diuretic-induced renal tubular sodium wasting
Correct Answer: B
Rationale: In advanced HFrEF, decreased effective arterial blood volume (despite total body
water overload) triggers non-osmotic vasopressin release from the posterior pituitary.
Vasopressin activates V2 receptors in renal collecting ducts, causing free water retention and
dilutional hyponatremia—a marker of advanced disease and poor prognosis. Option A is
incorrect because aldosterone promotes sodium retention, not hyponatremia. Option C
describes psychogenic polydipsia, unrelated to HF pathophysiology. Option D describes thiazide
diuretic effects, but the question asks about the underlying neurohormonal mechanism, not
iatrogenic causes. Advanced practice relevance: Hyponatremia in HFrEF predicts mortality;
vasopressin antagonists (tolvaptan) may be used in hospitalized patients.
Q3: A 58-year-old male with dilated cardiomyopathy (LVEF 25%) is being evaluated for
guideline-directed medical therapy. His cardiologist explains that the failing heart relies on the
Frank-Starling mechanism to maintain cardiac output. Which statement BEST describes why this
compensatory mechanism ultimately fails in HFrEF?
A. The Frank-Starling curve shifts upward, allowing unlimited preload augmentation
B. Increased preload moves the operating point to the descending limb of the Frank-Starling
curve, worsening contractility [CORRECT]
C. Beta-adrenergic receptor upregulation prevents adequate catecholamine response
D. Decreased afterload from systemic vasodilation exhausts preload reserve
Correct Answer: B
Rationale: The Frank-Starling mechanism states that increased ventricular preload (end-diastolic
volume) augments stroke volume up to an optimal point. In HFrEF, progressive volume overload
and ventricular dilation shift the operating point to the descending limb of the flattened Frank-
Starling curve, where further preload increases actually decrease stroke volume and worsen
wall stress (Laplace's law: wall stress = pressure × radius / 2 × thickness). Option A is incorrect—
the curve shifts downward, not upward. Option C is incorrect; beta-receptors are
downregulated, not upregulated, in chronic HF. Option D is incorrect because afterload is
increased, not decreased, in HF due to neurohormonal activation. Advanced practice relevance:
,Diuretics and vasodilators aim to move the patient back to the ascending limb of the curve by
reducing preload and afterload.
Q4: A 74-year-old female with HFpEF presents with acute pulmonary edema. Her blood
pressure is 180/110 mmHg. Echocardiogram shows concentric left ventricular hypertrophy,
normal LVEF, and grade III diastolic dysfunction. Which hemodynamic profile BEST characterizes
her acute decompensation?
A. Low output, low filling pressures with cardiogenic shock
B. High output, low systemic vascular resistance
C. Preserved output, markedly elevated left-sided filling pressures with pulmonary venous
congestion [CORRECT]
D. Right ventricular failure with low pulmonary artery pressures
Correct Answer: C
Rationale: HFpEF decompensation typically presents with preserved or hyperdynamic systolic
function but markedly elevated left ventricular filling pressures due to stiff, non-compliant
ventricles. The acute hypertensive episode increases afterload and worsens diastolic
dysfunction, causing abrupt pulmonary venous hypertension and flash pulmonary edema.
Option A describes cardiogenic shock (HFrEF or late-stage disease). Option B describes high-
output failure (thyrotoxicosis, anemia). Option D is contradictory—right ventricular failure
typically causes elevated, not low, pulmonary pressures. Advanced practice relevance: Acute
HFpEF decompensation with hypertension responds to afterload reduction (vasodilators) and
diuresis, unlike HFrEF where inotropes may be needed.
Q5: A 45-year-old male with non-ischemic cardiomyopathy (LVEF 35%) has NYHA Class III
symptoms despite optimal medical therapy. His cardiologist discusses the 2024 ACC/AHA
staging system. Which statement ACCURATELY describes his classification?
A. Stage A: At risk for HF without structural heart disease
B. Stage B: Structural heart disease without prior or current symptoms
C. Stage C: Structural heart disease with prior or current symptoms [CORRECT]
D. Stage D: Marked symptoms interfering with daily life despite optimized GDMT
Correct Answer: C
Rationale: According to the 2024 ACC/AHA/HFSA guidelines, Stage C is defined as structural
heart disease with prior or current symptoms of HF. This patient has reduced LVEF (structural
, disease) and Class III symptoms (current symptoms). Option A describes Stage A (risk factors
only). Option B describes Stage B (asymptomatic structural disease, e.g., post-MI with reduced
EF but no symptoms). Option D describes Stage D (refractory HF requiring specialized
interventions). Advanced practice relevance: Accurate staging guides prognosis and therapeutic
intensity; Stage C patients require comprehensive GDMT and monitoring for progression to
Stage D.
Q6: A 70-year-old female with HFrEF (LVEF 28%) has been stable on lisinopril, metoprolol
succinate, and spironolactone. She asks why she needs to continue medications despite feeling
better. Which pathophysiological rationale BEST explains the necessity of continued
neurohormonal blockade?
A. Medications temporarily suppress symptoms but do not modify disease progression
B. Continued RAAS and sympathetic blockade prevents adverse ventricular remodeling and
reduces mortality [CORRECT]
C. Discontinuation would cause acute rebound hypertension only, without cardiac
consequences
D. The medications are primarily for blood pressure control, not heart failure management
Correct Answer: B
Rationale: GDMT in HFrEF (ARNI/ACE-I, evidence-based beta-blockers, MRAs, SGLT2 inhibitors)
works through disease-modifying mechanisms that block maladaptive neurohormonal
activation. RAAS and sympathetic nervous system activation initially compensate for reduced
cardiac output but chronically cause progressive ventricular dilation, fibrosis, and apoptosis
(adverse remodeling). Continued blockade has been proven to reverse remodeling, reduce
hospitalization, and improve survival. Option A is incorrect—GDMT definitively modifies disease
progression. Option C is incorrect; discontinuation causes clinical decompensation and
remodeling progression. Option D is incorrect—while these drugs lower BP, their mortality
benefit in HF is independent of BP effects. Advanced practice relevance: Patient education must
emphasize that GDMT is lifelong and disease-modifying, not merely symptomatic.
Q7: A 65-year-old male with chronic HFrEF presents with worsening peripheral edema, elevated
JVD, and hepatomegaly, but clear lung fields. Which pathophysiological distinction BEST explains
this presentation?
A. Isolated left heart failure with preserved right ventricular function
B. Right heart failure with systemic venous congestion and preserved pulmonary circulation
Pulmonary 3 – University of Texas at Arlington |
Questions and Answers.
SECTION 1: Heart Failure (HFrEF & HFpEF) – Questions 1–8
Q1: A 68-year-old Black male with long-standing hypertension presents with exertional dyspnea,
fatigue, and lower extremity edema. Echocardiogram shows LVEF of 55% but evidence of
diastolic dysfunction with elevated E/e' ratio and left atrial enlargement. BNP is 450 pg/mL.
Which pathophysiological mechanism BEST explains this presentation?
A. Reduced myocardial contractility with compensatory RAAS activation leading to volume
expansion
B. Impaired ventricular relaxation and increased passive stiffness with elevated filling pressures
despite preserved contractility [CORRECT]
C. Primary valvular regurgitation causing chronic volume overload with eccentric hypertrophy
D. Afterload reduction from systemic vasodilation leading to high-output failure
Correct Answer: B
Rationale: This patient presents with HFpEF (preserved EF ≥50% with diastolic dysfunction),
which is more prevalent in older Black adults with hypertension. The pathophysiology involves
impaired active relaxation (early diastole) and increased passive ventricular stiffness (late
diastole), leading to elevated left ventricular end-diastolic pressure and pulmonary venous
congestion despite normal systolic contractility. Option A describes HFrEF pathophysiology
(reduced contractility). Option C describes volume overload from regurgitant lesions, which
typically causes eccentric hypertrophy and elevated EF initially. Option D is physiologically
incoherent—afterload reduction does not cause heart failure. Advanced practice relevance:
HFpEF now accounts for >50% of heart failure hospitalizations in older adults and requires
different therapeutic approaches than HFrEF; the E/e' ratio >14 confirms elevated filling
pressures.
Q2: A 62-year-old female with HFrEF (LVEF 30%) develops progressive dyspnea and weight gain
over 2 weeks. Laboratory studies show elevated BUN, hyponatremia (Na+ 128), and NT-proBNP
>5000 pg/mL. Which neurohormonal mechanism MOST directly contributes to her
hyponatremia?
,A. Excessive renal sodium retention from aldosterone escape
B. Non-osmotic vasopressin (ADH) release due to decreased effective arterial blood volume
[CORRECT]
C. Primary polydipsia from hypothalamic osmoreceptor dysfunction
D. Diuretic-induced renal tubular sodium wasting
Correct Answer: B
Rationale: In advanced HFrEF, decreased effective arterial blood volume (despite total body
water overload) triggers non-osmotic vasopressin release from the posterior pituitary.
Vasopressin activates V2 receptors in renal collecting ducts, causing free water retention and
dilutional hyponatremia—a marker of advanced disease and poor prognosis. Option A is
incorrect because aldosterone promotes sodium retention, not hyponatremia. Option C
describes psychogenic polydipsia, unrelated to HF pathophysiology. Option D describes thiazide
diuretic effects, but the question asks about the underlying neurohormonal mechanism, not
iatrogenic causes. Advanced practice relevance: Hyponatremia in HFrEF predicts mortality;
vasopressin antagonists (tolvaptan) may be used in hospitalized patients.
Q3: A 58-year-old male with dilated cardiomyopathy (LVEF 25%) is being evaluated for
guideline-directed medical therapy. His cardiologist explains that the failing heart relies on the
Frank-Starling mechanism to maintain cardiac output. Which statement BEST describes why this
compensatory mechanism ultimately fails in HFrEF?
A. The Frank-Starling curve shifts upward, allowing unlimited preload augmentation
B. Increased preload moves the operating point to the descending limb of the Frank-Starling
curve, worsening contractility [CORRECT]
C. Beta-adrenergic receptor upregulation prevents adequate catecholamine response
D. Decreased afterload from systemic vasodilation exhausts preload reserve
Correct Answer: B
Rationale: The Frank-Starling mechanism states that increased ventricular preload (end-diastolic
volume) augments stroke volume up to an optimal point. In HFrEF, progressive volume overload
and ventricular dilation shift the operating point to the descending limb of the flattened Frank-
Starling curve, where further preload increases actually decrease stroke volume and worsen
wall stress (Laplace's law: wall stress = pressure × radius / 2 × thickness). Option A is incorrect—
the curve shifts downward, not upward. Option C is incorrect; beta-receptors are
downregulated, not upregulated, in chronic HF. Option D is incorrect because afterload is
increased, not decreased, in HF due to neurohormonal activation. Advanced practice relevance:
,Diuretics and vasodilators aim to move the patient back to the ascending limb of the curve by
reducing preload and afterload.
Q4: A 74-year-old female with HFpEF presents with acute pulmonary edema. Her blood
pressure is 180/110 mmHg. Echocardiogram shows concentric left ventricular hypertrophy,
normal LVEF, and grade III diastolic dysfunction. Which hemodynamic profile BEST characterizes
her acute decompensation?
A. Low output, low filling pressures with cardiogenic shock
B. High output, low systemic vascular resistance
C. Preserved output, markedly elevated left-sided filling pressures with pulmonary venous
congestion [CORRECT]
D. Right ventricular failure with low pulmonary artery pressures
Correct Answer: C
Rationale: HFpEF decompensation typically presents with preserved or hyperdynamic systolic
function but markedly elevated left ventricular filling pressures due to stiff, non-compliant
ventricles. The acute hypertensive episode increases afterload and worsens diastolic
dysfunction, causing abrupt pulmonary venous hypertension and flash pulmonary edema.
Option A describes cardiogenic shock (HFrEF or late-stage disease). Option B describes high-
output failure (thyrotoxicosis, anemia). Option D is contradictory—right ventricular failure
typically causes elevated, not low, pulmonary pressures. Advanced practice relevance: Acute
HFpEF decompensation with hypertension responds to afterload reduction (vasodilators) and
diuresis, unlike HFrEF where inotropes may be needed.
Q5: A 45-year-old male with non-ischemic cardiomyopathy (LVEF 35%) has NYHA Class III
symptoms despite optimal medical therapy. His cardiologist discusses the 2024 ACC/AHA
staging system. Which statement ACCURATELY describes his classification?
A. Stage A: At risk for HF without structural heart disease
B. Stage B: Structural heart disease without prior or current symptoms
C. Stage C: Structural heart disease with prior or current symptoms [CORRECT]
D. Stage D: Marked symptoms interfering with daily life despite optimized GDMT
Correct Answer: C
Rationale: According to the 2024 ACC/AHA/HFSA guidelines, Stage C is defined as structural
heart disease with prior or current symptoms of HF. This patient has reduced LVEF (structural
, disease) and Class III symptoms (current symptoms). Option A describes Stage A (risk factors
only). Option B describes Stage B (asymptomatic structural disease, e.g., post-MI with reduced
EF but no symptoms). Option D describes Stage D (refractory HF requiring specialized
interventions). Advanced practice relevance: Accurate staging guides prognosis and therapeutic
intensity; Stage C patients require comprehensive GDMT and monitoring for progression to
Stage D.
Q6: A 70-year-old female with HFrEF (LVEF 28%) has been stable on lisinopril, metoprolol
succinate, and spironolactone. She asks why she needs to continue medications despite feeling
better. Which pathophysiological rationale BEST explains the necessity of continued
neurohormonal blockade?
A. Medications temporarily suppress symptoms but do not modify disease progression
B. Continued RAAS and sympathetic blockade prevents adverse ventricular remodeling and
reduces mortality [CORRECT]
C. Discontinuation would cause acute rebound hypertension only, without cardiac
consequences
D. The medications are primarily for blood pressure control, not heart failure management
Correct Answer: B
Rationale: GDMT in HFrEF (ARNI/ACE-I, evidence-based beta-blockers, MRAs, SGLT2 inhibitors)
works through disease-modifying mechanisms that block maladaptive neurohormonal
activation. RAAS and sympathetic nervous system activation initially compensate for reduced
cardiac output but chronically cause progressive ventricular dilation, fibrosis, and apoptosis
(adverse remodeling). Continued blockade has been proven to reverse remodeling, reduce
hospitalization, and improve survival. Option A is incorrect—GDMT definitively modifies disease
progression. Option C is incorrect; discontinuation causes clinical decompensation and
remodeling progression. Option D is incorrect—while these drugs lower BP, their mortality
benefit in HF is independent of BP effects. Advanced practice relevance: Patient education must
emphasize that GDMT is lifelong and disease-modifying, not merely symptomatic.
Q7: A 65-year-old male with chronic HFrEF presents with worsening peripheral edema, elevated
JVD, and hepatomegaly, but clear lung fields. Which pathophysiological distinction BEST explains
this presentation?
A. Isolated left heart failure with preserved right ventricular function
B. Right heart failure with systemic venous congestion and preserved pulmonary circulation
