Heart Failure: Med-Surg Nursing Exam | 2026/2027
HEART FAILURE
Questions and Answers for
Medical-Surgical Nursing
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2026/2027 Academic Year
75 Questions and Correct Answers
Already Graded A+ | 100% Verified
Exam-Ready Format | Expert-Aligned Structure
Evidence-Based GDMT Principles | ACC/AHA/HFSA Guideline-Aligned
NCSBN Clinical Judgment Framework Integration
Domain 1: Pathophysiology of Heart Failure (HFrEF vs. HFpEF)
Domain 2: Clinical Assessment & Diagnostic Findings
Domain 3: Pharmacologic Management (GDMT)
Domain 4: Fluid & Electrolyte Balance
Domain 5: Oxygenation & Perfusion Support
Domain 6: Patient Education & Self-Management
Domain 7: Complication Recognition
Domain 8: Discharge Planning & Transitional Care
Domain 9: Interprofessional Collaboration
Domain 10: NCLEX-RN Prioritization Strategies
, Heart Failure: Med-Surg Nursing Exam | 2026/2027
DOMAIN 1: Pathophysiology of Heart Failure (HFrEF vs. HFpEF)
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Question 1
A nurse is reviewing the pathophysiology of heart failure with a nursing student. Which statement by the
student indicates an accurate understanding of the difference between heart failure with reduced ejection
fraction (HFrEF) and heart failure with preserved ejection fraction (HFpEF)?
A) "HFrEF is characterized by impaired B) "HFpEF involves a dilated left ventricle with
ventricular filling due to a stiff, noncompliant left impaired contractility and an ejection fraction of
ventricle." 40% or less."
C) "HFrEF involves systolic dysfunction with D) "Both HFrEF and HFpEF share the same
reduced contractility and an ejection fraction of underlying mechanism of impaired ventricular
40% or less, while HFpEF involves diastolic contractility."
dysfunction with preserved EF of 50% or
greater."
Rationale: HFrEF (systolic heart failure) is defined by a left ventricular ejection fraction of 40% or less
with impaired contractility and ventricular dilation. HFpEF (diastolic heart failure) is characterized by a
preserved EF of 50% or greater with a stiff, noncompliant ventricle that impairs filling. Understanding
this distinction is essential for guiding pharmacologic therapy, as GDMT recommendations differ based
on HF classification per ACC/AHA/HFSA 2022 guidelines.
Question 2
A patient with chronic heart failure presents with fatigue, exercise intolerance, and bilateral ankle edema.
The nurse recognizes that activation of which neurohormonal system most significantly contributes to the
disease progression in heart failure?
A) Activation of the parasympathetic nervous B) Suppression of the renin-angiotensin-
system, which reduces heart rate and contractility aldosterone system (RAAS), leading to
vasodilation
C) Activation of the sympathetic nervous D) Increased release of atrial natriuretic peptide
system and renin-angiotensin-aldosterone (ANP), which promotes fluid retention
system (RAAS), causing vasoconstriction,
sodium retention, and ventricular remodeling
Rationale: In heart failure, decreased cardiac output triggers compensatory activation of the sympathetic
nervous system (SNS) and the renin-angiotensin-aldosterone system (RAAS). While initially
compensatory, chronic activation leads to vasoconstriction, sodium and water retention, increased
afterload, and adverse ventricular remodeling that worsens heart failure over time. This is why ACE
inhibitors, ARBs, ARNIs, beta-blockers, and MRAs are cornerstones of GDMT, as they counteract these
neurohormonal pathways.
Question 3
, Heart Failure: Med-Surg Nursing Exam | 2026/2027
A nurse is caring for a patient with HFrEF. Which pathophysiologic mechanism best explains why this
patient develops ventricular dilation and progressive systolic dysfunction over time?
A) Increased venous return causes volume B) Neurohormonal activation triggers
overload, leading to right ventricular hypertrophy maladaptive remodeling, including myocyte
without left ventricular involvement hypertrophy, apoptosis, and extracellular
matrix changes that progressively dilate and
weaken the ventricle
C) Diastolic stiffening prevents adequate filling, D) Peripheral vasodilation reduces afterload,
causing backward transmission of pressure to the causing reflex tachycardia and increased
pulmonary vasculature myocardial oxygen demand
Rationale: In HFrEF, sustained neurohormonal activation (SNS, RAAS, natriuretic peptides, endothelin,
vasopressin) drives maladaptive ventricular remodeling. Myocyte hypertrophy, apoptosis, and fibrosis
alter the extracellular matrix, resulting in progressive ventricular dilation, spherical chamber shape
change, and worsening systolic function. This remodeling process is a key therapeutic target of GDMT,
particularly ARNIs, beta-blockers, and MRAs, which can slow or partially reverse remodeling.
Question 4
A patient with HFpEF asks the nurse, "Why do I have shortness of breath if my doctor said my heart
pumping function is normal?" What is the nurse's best response?
A) "Your heart muscle is too weak to pump B) "Even though the pumping function is
effectively, which causes fluid to back up into preserved, your heart muscle has become stiff
your lungs." and cannot relax properly during filling,
causing pressure to build up in your lungs and
create shortness of breath."
C) "Shortness of breath in HFpEF is caused by D) "Your symptoms are likely due to a lung
increased pulmonary artery pressure unrelated to condition rather than a heart problem, since your
heart function." ejection fraction is normal."
Rationale: HFpEF is characterized by diastolic dysfunction in which the left ventricle has impaired
relaxation and increased stiffness. This leads to elevated left ventricular end-diastolic pressure (LVEDP),
which is transmitted backward to the left atrium and pulmonary vasculature, causing pulmonary
congestion and dyspnea. Despite a preserved ejection fraction (50% or greater), patients experience
symptoms identical to HFrEF. This distinction is important for patient education and for guiding
treatment, as HFpEF has fewer evidence-based pharmacologic options compared to HFrEF.
Question 5
A nurse is assessing a patient with advanced heart failure. The patient's cardiac output is decreased, and
the nurse understands that cardiac output is determined by which two primary factors?
A) Heart rate and systemic vascular resistance B) Stroke volume and systemic vascular resistance
C) Heart rate and stroke volume D) Preload and afterload only
, Heart Failure: Med-Surg Nursing Exam | 2026/2027
Rationale: Cardiac output (CO) equals heart rate (HR) multiplied by stroke volume (SV). Stroke volume
is determined by preload, afterload, and contractility. In heart failure, reduced contractility (HFrEF) or
impaired filling (HFpEF) decreases stroke volume. Compensatory tachycardia initially maintains cardiac
output but increases myocardial oxygen demand. Understanding the determinants of cardiac output is
foundational for nursing management of heart failure patients, as interventions target one or more of
these components (e.g., diuretics reduce preload, ACE inhibitors reduce afterload).
Question 6
A patient with long-standing hypertension is diagnosed with HFpEF. The nurse understands that which
structural change in the left ventricle most commonly underlies this patient's condition?
A) Left ventricular dilation with eccentric B) Left ventricular concentric hypertrophy
hypertrophy and thinned walls with increased wall thickness and decreased
chamber size
C) Right ventricular dilation secondary to chronic D) Aneurysmal dilation of the left ventricular apex
pulmonary hypertension following myocardial infarction
Rationale: Chronic hypertension increases afterload, leading to left ventricular concentric hypertrophy
(increased wall thickness with a relatively normal or reduced chamber size). Over time, this hypertrophy
causes diastolic dysfunction as the thickened, stiff ventricle impairs relaxation and filling. Concentric
hypertrophy is the most common structural substrate in HFpEF, distinguishing it from the eccentric
hypertrophy and chamber dilation seen in HFrEF. Management focuses on blood pressure control,
diuretics for congestion, and management of comorbidities.
Question 7
The nurse is explaining the Frank-Starling mechanism to a patient newly diagnosed with heart failure.
Which statement accurately describes this principle as it relates to heart failure?
A) "The Frank-Starling mechanism allows your B) "When your heart muscle is stretched by
heart to continue increasing its pumping efficiency increased blood volume, it initially contracts
indefinitely when more blood returns to it." more forcefully, but in heart failure, this
mechanism becomes overwhelmed and the
heart can no longer keep up with the increased
volume."
C) "The Frank-Starling mechanism only applies to D) "This mechanism refers to the ability of the
the right side of the heart and has no relevance to heart to increase rate without affecting stroke
left-sided heart failure." volume."
Rationale: The Frank-Starling law states that, within physiological limits, increased sarcomere stretch
(preload) leads to increased force of contraction and stroke volume. In early heart failure, this mechanism
compensates for reduced ejection fraction by increasing preload to maintain cardiac output. However, as
heart failure progresses, the ventricle operates on the flattened portion of the Starling curve, where
further increases in preload no longer improve stroke volume and instead lead to pulmonary and systemic
congestion. This is the pathophysiologic rationale for diuretic therapy in heart failure.
HEART FAILURE
Questions and Answers for
Medical-Surgical Nursing
━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━
2026/2027 Academic Year
75 Questions and Correct Answers
Already Graded A+ | 100% Verified
Exam-Ready Format | Expert-Aligned Structure
Evidence-Based GDMT Principles | ACC/AHA/HFSA Guideline-Aligned
NCSBN Clinical Judgment Framework Integration
Domain 1: Pathophysiology of Heart Failure (HFrEF vs. HFpEF)
Domain 2: Clinical Assessment & Diagnostic Findings
Domain 3: Pharmacologic Management (GDMT)
Domain 4: Fluid & Electrolyte Balance
Domain 5: Oxygenation & Perfusion Support
Domain 6: Patient Education & Self-Management
Domain 7: Complication Recognition
Domain 8: Discharge Planning & Transitional Care
Domain 9: Interprofessional Collaboration
Domain 10: NCLEX-RN Prioritization Strategies
, Heart Failure: Med-Surg Nursing Exam | 2026/2027
DOMAIN 1: Pathophysiology of Heart Failure (HFrEF vs. HFpEF)
───────────────────────────────────────────────────────────────────────────
Question 1
A nurse is reviewing the pathophysiology of heart failure with a nursing student. Which statement by the
student indicates an accurate understanding of the difference between heart failure with reduced ejection
fraction (HFrEF) and heart failure with preserved ejection fraction (HFpEF)?
A) "HFrEF is characterized by impaired B) "HFpEF involves a dilated left ventricle with
ventricular filling due to a stiff, noncompliant left impaired contractility and an ejection fraction of
ventricle." 40% or less."
C) "HFrEF involves systolic dysfunction with D) "Both HFrEF and HFpEF share the same
reduced contractility and an ejection fraction of underlying mechanism of impaired ventricular
40% or less, while HFpEF involves diastolic contractility."
dysfunction with preserved EF of 50% or
greater."
Rationale: HFrEF (systolic heart failure) is defined by a left ventricular ejection fraction of 40% or less
with impaired contractility and ventricular dilation. HFpEF (diastolic heart failure) is characterized by a
preserved EF of 50% or greater with a stiff, noncompliant ventricle that impairs filling. Understanding
this distinction is essential for guiding pharmacologic therapy, as GDMT recommendations differ based
on HF classification per ACC/AHA/HFSA 2022 guidelines.
Question 2
A patient with chronic heart failure presents with fatigue, exercise intolerance, and bilateral ankle edema.
The nurse recognizes that activation of which neurohormonal system most significantly contributes to the
disease progression in heart failure?
A) Activation of the parasympathetic nervous B) Suppression of the renin-angiotensin-
system, which reduces heart rate and contractility aldosterone system (RAAS), leading to
vasodilation
C) Activation of the sympathetic nervous D) Increased release of atrial natriuretic peptide
system and renin-angiotensin-aldosterone (ANP), which promotes fluid retention
system (RAAS), causing vasoconstriction,
sodium retention, and ventricular remodeling
Rationale: In heart failure, decreased cardiac output triggers compensatory activation of the sympathetic
nervous system (SNS) and the renin-angiotensin-aldosterone system (RAAS). While initially
compensatory, chronic activation leads to vasoconstriction, sodium and water retention, increased
afterload, and adverse ventricular remodeling that worsens heart failure over time. This is why ACE
inhibitors, ARBs, ARNIs, beta-blockers, and MRAs are cornerstones of GDMT, as they counteract these
neurohormonal pathways.
Question 3
, Heart Failure: Med-Surg Nursing Exam | 2026/2027
A nurse is caring for a patient with HFrEF. Which pathophysiologic mechanism best explains why this
patient develops ventricular dilation and progressive systolic dysfunction over time?
A) Increased venous return causes volume B) Neurohormonal activation triggers
overload, leading to right ventricular hypertrophy maladaptive remodeling, including myocyte
without left ventricular involvement hypertrophy, apoptosis, and extracellular
matrix changes that progressively dilate and
weaken the ventricle
C) Diastolic stiffening prevents adequate filling, D) Peripheral vasodilation reduces afterload,
causing backward transmission of pressure to the causing reflex tachycardia and increased
pulmonary vasculature myocardial oxygen demand
Rationale: In HFrEF, sustained neurohormonal activation (SNS, RAAS, natriuretic peptides, endothelin,
vasopressin) drives maladaptive ventricular remodeling. Myocyte hypertrophy, apoptosis, and fibrosis
alter the extracellular matrix, resulting in progressive ventricular dilation, spherical chamber shape
change, and worsening systolic function. This remodeling process is a key therapeutic target of GDMT,
particularly ARNIs, beta-blockers, and MRAs, which can slow or partially reverse remodeling.
Question 4
A patient with HFpEF asks the nurse, "Why do I have shortness of breath if my doctor said my heart
pumping function is normal?" What is the nurse's best response?
A) "Your heart muscle is too weak to pump B) "Even though the pumping function is
effectively, which causes fluid to back up into preserved, your heart muscle has become stiff
your lungs." and cannot relax properly during filling,
causing pressure to build up in your lungs and
create shortness of breath."
C) "Shortness of breath in HFpEF is caused by D) "Your symptoms are likely due to a lung
increased pulmonary artery pressure unrelated to condition rather than a heart problem, since your
heart function." ejection fraction is normal."
Rationale: HFpEF is characterized by diastolic dysfunction in which the left ventricle has impaired
relaxation and increased stiffness. This leads to elevated left ventricular end-diastolic pressure (LVEDP),
which is transmitted backward to the left atrium and pulmonary vasculature, causing pulmonary
congestion and dyspnea. Despite a preserved ejection fraction (50% or greater), patients experience
symptoms identical to HFrEF. This distinction is important for patient education and for guiding
treatment, as HFpEF has fewer evidence-based pharmacologic options compared to HFrEF.
Question 5
A nurse is assessing a patient with advanced heart failure. The patient's cardiac output is decreased, and
the nurse understands that cardiac output is determined by which two primary factors?
A) Heart rate and systemic vascular resistance B) Stroke volume and systemic vascular resistance
C) Heart rate and stroke volume D) Preload and afterload only
, Heart Failure: Med-Surg Nursing Exam | 2026/2027
Rationale: Cardiac output (CO) equals heart rate (HR) multiplied by stroke volume (SV). Stroke volume
is determined by preload, afterload, and contractility. In heart failure, reduced contractility (HFrEF) or
impaired filling (HFpEF) decreases stroke volume. Compensatory tachycardia initially maintains cardiac
output but increases myocardial oxygen demand. Understanding the determinants of cardiac output is
foundational for nursing management of heart failure patients, as interventions target one or more of
these components (e.g., diuretics reduce preload, ACE inhibitors reduce afterload).
Question 6
A patient with long-standing hypertension is diagnosed with HFpEF. The nurse understands that which
structural change in the left ventricle most commonly underlies this patient's condition?
A) Left ventricular dilation with eccentric B) Left ventricular concentric hypertrophy
hypertrophy and thinned walls with increased wall thickness and decreased
chamber size
C) Right ventricular dilation secondary to chronic D) Aneurysmal dilation of the left ventricular apex
pulmonary hypertension following myocardial infarction
Rationale: Chronic hypertension increases afterload, leading to left ventricular concentric hypertrophy
(increased wall thickness with a relatively normal or reduced chamber size). Over time, this hypertrophy
causes diastolic dysfunction as the thickened, stiff ventricle impairs relaxation and filling. Concentric
hypertrophy is the most common structural substrate in HFpEF, distinguishing it from the eccentric
hypertrophy and chamber dilation seen in HFrEF. Management focuses on blood pressure control,
diuretics for congestion, and management of comorbidities.
Question 7
The nurse is explaining the Frank-Starling mechanism to a patient newly diagnosed with heart failure.
Which statement accurately describes this principle as it relates to heart failure?
A) "The Frank-Starling mechanism allows your B) "When your heart muscle is stretched by
heart to continue increasing its pumping efficiency increased blood volume, it initially contracts
indefinitely when more blood returns to it." more forcefully, but in heart failure, this
mechanism becomes overwhelmed and the
heart can no longer keep up with the increased
volume."
C) "The Frank-Starling mechanism only applies to D) "This mechanism refers to the ability of the
the right side of the heart and has no relevance to heart to increase rate without affecting stroke
left-sided heart failure." volume."
Rationale: The Frank-Starling law states that, within physiological limits, increased sarcomere stretch
(preload) leads to increased force of contraction and stroke volume. In early heart failure, this mechanism
compensates for reduced ejection fraction by increasing preload to maintain cardiac output. However, as
heart failure progresses, the ventricle operates on the flattened portion of the Starling curve, where
further increases in preload no longer improve stroke volume and instead lead to pulmonary and systemic
congestion. This is the pathophysiologic rationale for diuretic therapy in heart failure.
