NSG 6020 Week 6 Knowledge Check V2.0 | NSG 6020 |
South University | 2026–2027 | Advanced Cardiovascular,
Peripheral Vascular & Lymphatic Assessment
Comprehensive Examination: Advanced Cardiovascular,
Peripheral Vascular, and Lymphatic System Assessment
Academic Level: Graduate Nursing (Advanced Practice)
Difficulty: Advanced/Complex
Total Questions: 150 Multiple-Choice
Primary References: Bates' Guide to Physical Examination & History Taking (13th Ed.), Bickley's
Physical Examination & Health Assessment, Current Nursing Practice Standards, ACC/AHA
Clinical Practice Guidelines
Table of Contents
Section Topic Area Questions
I Advanced Cardiovascular Anatomy & Physiology 1–20
Advanced Cardiac Assessment Techniques &
II 21–40
Hemodynamics
III Complex Heart Sounds, Gallops, and Murmurs 41–60
IV Peripheral Vascular System: Advanced Assessment 61–80
V Arterial & Venous Pathophysiology 81–100
VI Lymphatic System & Immunologic Assessment 101–120
VII Complex Clinical Scenarios & Differential Diagnosis 121–140
VIII Integration, Pharmacology, & Evidence-Based Practice 141–150
Section I: Advanced Cardiovascular Anatomy & Physiology
(Questions 1–20)
• 1. Which of the following correctly describes the relationship between the cardiac action
potential phases and the corresponding electrocardiographic (ECG) intervals, integrating both
cellular electrophysiology and surface recording?
A) Phase 0 (rapid depolarization) corresponds to the PR interval; Phase 3 (repolarization)
corresponds to the QT interval
B) Phase 0 (rapid depolarization) corresponds to the QRS complex; Phase 2 (plateau)
corresponds to the ST segment; Phase 3 (repolarization) corresponds to the T wave
C) Phase 4 (resting membrane potential) corresponds to the U wave; Phase 1 (early
repolarization) corresponds to the P wave
D) Phase 0 corresponds to the P wave; Phase 3 corresponds to the QRS complex
, 🔴🔴 B) Phase 0 (rapid depolarization) corresponds to the QRS complex; Phase 2
(plateau) corresponds to the ST segment; Phase 3 (repolarization) corresponds to the T
wave — The cardiac action potential's Phase 0 (rapid sodium influx) generates the QRS
complex; Phase 2 (calcium influx plateau) corresponds to the ST segment; Phase 3
(potassium efflux repolarization) produces the T wave. Phase 4 is the resting membrane
potential.
• 2. A 72-year-old patient with longstanding hypertension presents with a laterally displaced
PMI to the 6th intercostal space in the anterior axillary line. This finding is most consistent with
which of the following pathophysiological adaptations, and what is the underlying mechanism?
A) Concentric left ventricular hypertrophy secondary to chronic pressure overload, resulting
from increased afterload and sarcomere addition in parallel
B) Eccentric left ventricular hypertrophy secondary to chronic volume overload, resulting
from sarcomere addition in series
C) Dilated cardiomyopathy secondary to ischemic injury, resulting from myocyte apoptosis
and fibrosis
D) Right ventricular hypertrophy secondary to pulmonary hypertension, resulting from
increased right ventricular afterload
🔴🔴 A) Concentric left ventricular hypertrophy secondary to chronic pressure overload,
resulting from increased afterload and sarcomere addition in parallel — Chronic
hypertension increases afterload, causing the left ventricle to develop concentric
hypertrophy (sarcomeres added in parallel), which displaces the PMI laterally and inferiorly
as the ventricle enlarges.
• 3. The coronary arteries perfuse the myocardium primarily during diastole because:
A) The aortic valve is open during systole, preventing coronary artery filling
B) Myocardial compression during systole increases coronary vascular resistance, limiting
flow
C) The coronary arteries originate from the pulmonary artery during fetal development
D) Sympathetic stimulation during systole causes coronary vasoconstriction
🔴🔴 B) Myocardial compression during systole increases coronary vascular resistance,
limiting flow — During ventricular systole, the contracting myocardium compresses the
intramural coronary vessels, increasing vascular resistance and reducing flow. Coronary
perfusion is maximal during diastole when the myocardium relaxes.
• 4. Which of the following statements accurately describes the Frank-Starling mechanism at
the molecular level, and how does it relate to the clinical assessment of preload?
A) Increased end-diastolic volume stretches sarcomeres to optimal length, increasing actin-
myosin cross-bridge formation and stroke volume; preload is clinically estimated by central
venous pressure or pulmonary capillary wedge pressure
B) Increased end-diastolic volume decreases sarcomere length, reducing cross-bridge
formation and stroke volume; preload is estimated by heart rate
C) The Frank-Starling mechanism is independent of sarcomere length and is solely
determined by calcium availability; preload is estimated by blood pressure
D) The mechanism only operates in the right ventricle; preload is estimated by jugular
venous pressure alone
🔴🔴 A) Increased end-diastolic volume stretches sarcomeres to optimal length,
increasing actin-myosin cross-bridge formation and stroke volume; preload is clinically
estimated by central venous pressure or pulmonary capillary wedge pressure — The
, Frank-Starling law describes the relationship between end-diastolic volume (preload) and
stroke volume. Optimal sarcomere stretching (2.0–2.2 μm) maximizes cross-bridge
formation. Preload is clinically estimated by CVP (right heart) or PCWP (left heart).
• 5. A patient with severe aortic stenosis develops syncope during exertion. The
pathophysiological mechanism most directly responsible for this symptom is:
A) Fixed left ventricular outflow tract obstruction leading to inadequate cardiac output
augmentation during exercise, compounded by peripheral vasodilation and impaired
coronary perfusion
B) Right ventricular failure leading to decreased pulmonary blood flow
C) Mitral regurgitation developing secondary to left ventricular dilation
D) Complete heart block developing from calcification of the conduction system
🔴🔴 A) Fixed left ventricular outflow tract obstruction leading to inadequate cardiac
output augmentation during exercise, compounded by peripheral vasodilation and
impaired coronary perfusion — In aortic stenosis, the fixed obstruction prevents adequate
increase in cardiac output during exercise. Peripheral vasodilation from exertion further
reduces coronary perfusion pressure, leading to syncope.
• 6. Which of the following correctly describes the physiological splitting of S2 and its
relationship to respiratory variation in a patient with a normal heart?
A) During inspiration, increased negative intrathoracic pressure increases venous return to
the right ventricle, prolonging right ventricular ejection and delaying pulmonic valve closure,
resulting in audible splitting
B) During inspiration, decreased venous return to the right ventricle shortens right
ventricular ejection, causing earlier pulmonic valve closure
C) During expiration, increased venous return to the left ventricle delays aortic valve closure,
causing splitting
D) Splitting of S2 is a pathological finding that always indicates underlying cardiac disease
🔴🔴 A) During inspiration, increased negative intrathoracic pressure increases venous
return to the right ventricle, prolonging right ventricular ejection and delaying pulmonic
valve closure, resulting in audible splitting — Physiological splitting of S2 occurs during
inspiration due to increased venous return to the right heart, which prolongs right
ventricular systole and delays pulmonic valve closure relative to aortic valve closure.
• 7. The dicrotic notch on the arterial pressure waveform represents which of the following
hemodynamic events, and what is its clinical significance in assessing aortic valve function?
A) Opening of the aortic valve; signifies normal left ventricular ejection
B) Closure of the aortic valve; signifies the end of systole and the onset of diastole, and its
absence may indicate aortic regurgitation
C) Opening of the mitral valve; signifies the onset of ventricular filling
D) Closure of the mitral valve; signifies the onset of ventricular systole
🔴🔴 B) Closure of the aortic valve; signifies the end of systole and the onset of diastole,
and its absence may indicate aortic regurgitation — The dicrotic notch is a brief increase in
aortic pressure upon aortic valve closure, marking the end of systole. Its absence or
diminution may indicate aortic regurgitation.
• 8. A 55-year-old patient with a history of myocardial infarction presents with dyspnea on
exertion and orthopnea. On examination, you note an S3 gallop and jugular venous distention.
, Which of the following hemodynamic parameters would you expect to be elevated, and what is
the underlying pathophysiological mechanism?
A) Elevated pulmonary capillary wedge pressure (PCWP) due to left ventricular systolic
dysfunction and increased left ventricular end-diastolic pressure
B) Elevated central venous pressure (CVP) due to right ventricular systolic dysfunction
C) Elevated pulmonary artery systolic pressure due to pulmonary embolism
D) Elevated systemic vascular resistance due to compensatory vasoconstriction
🔴🔴 A) Elevated pulmonary capillary wedge pressure (PCWP) due to left ventricular
systolic dysfunction and increased left ventricular end-diastolic pressure — An S3 gallop in
a patient with a history of MI indicates left ventricular systolic dysfunction. Elevated LVEDP is
transmitted backward, increasing PCWP and causing pulmonary congestion (dyspnea,
orthopnea).
• 9. Which of the following best describes the role of the autonomic nervous system in
regulating cardiac output during acute hemorrhage?
A) Sympathetic activation increases heart rate and contractility via beta-1 adrenergic
receptors; parasympathetic withdrawal further increases heart rate; venous constriction
increases preload
B) Parasympathetic activation decreases heart rate to conserve oxygen; sympathetic
inhibition reduces afterload
C) Sympathetic activation causes coronary vasoconstriction, reducing myocardial oxygen
supply
D) The autonomic nervous system plays no role in acute hemorrhage compensation
🔴🔴 A) Sympathetic activation increases heart rate and contractility via beta-1
adrenergic receptors; parasympathetic withdrawal further increases heart rate; venous
constriction increases preload — Acute hemorrhage triggers baroreceptor-mediated
sympathetic activation (increased HR, contractility, vasoconstriction) and parasympathetic
withdrawal, maintaining cardiac output despite reduced circulating volume.
• 10. A patient with a chronic, large pericardial effusion presents with pulsus paradoxus. Which
of the following hemodynamic changes best explains this physical finding?
A) During inspiration, increased venous return to the right ventricle causes the
interventricular septum to bulge into the left ventricle, reducing left ventricular filling and
stroke volume, causing a fall in systolic blood pressure >10 mmHg
B) During expiration, increased left ventricular filling causes the septum to bulge into the
right ventricle
C) During inspiration, decreased venous return to the left ventricle causes a fall in stroke
volume
D) During expiration, decreased venous return to the right ventricle causes a fall in cardiac
output
🔴🔴 A) During inspiration, increased venous return to the right ventricle causes the
interventricular septum to bulge into the left ventricle, reducing left ventricular filling and
stroke volume, causing a fall in systolic blood pressure >10 mmHg — In cardiac
tamponade, the equalization of intracardiac pressures and the limited total cardiac volume
cause the septum to shift into the LV during inspiration, reducing LV filling and stroke
volume.
• 11. Which of the following correctly describes the relationship between myocardial oxygen
demand and supply in the context of coronary artery disease?
South University | 2026–2027 | Advanced Cardiovascular,
Peripheral Vascular & Lymphatic Assessment
Comprehensive Examination: Advanced Cardiovascular,
Peripheral Vascular, and Lymphatic System Assessment
Academic Level: Graduate Nursing (Advanced Practice)
Difficulty: Advanced/Complex
Total Questions: 150 Multiple-Choice
Primary References: Bates' Guide to Physical Examination & History Taking (13th Ed.), Bickley's
Physical Examination & Health Assessment, Current Nursing Practice Standards, ACC/AHA
Clinical Practice Guidelines
Table of Contents
Section Topic Area Questions
I Advanced Cardiovascular Anatomy & Physiology 1–20
Advanced Cardiac Assessment Techniques &
II 21–40
Hemodynamics
III Complex Heart Sounds, Gallops, and Murmurs 41–60
IV Peripheral Vascular System: Advanced Assessment 61–80
V Arterial & Venous Pathophysiology 81–100
VI Lymphatic System & Immunologic Assessment 101–120
VII Complex Clinical Scenarios & Differential Diagnosis 121–140
VIII Integration, Pharmacology, & Evidence-Based Practice 141–150
Section I: Advanced Cardiovascular Anatomy & Physiology
(Questions 1–20)
• 1. Which of the following correctly describes the relationship between the cardiac action
potential phases and the corresponding electrocardiographic (ECG) intervals, integrating both
cellular electrophysiology and surface recording?
A) Phase 0 (rapid depolarization) corresponds to the PR interval; Phase 3 (repolarization)
corresponds to the QT interval
B) Phase 0 (rapid depolarization) corresponds to the QRS complex; Phase 2 (plateau)
corresponds to the ST segment; Phase 3 (repolarization) corresponds to the T wave
C) Phase 4 (resting membrane potential) corresponds to the U wave; Phase 1 (early
repolarization) corresponds to the P wave
D) Phase 0 corresponds to the P wave; Phase 3 corresponds to the QRS complex
, 🔴🔴 B) Phase 0 (rapid depolarization) corresponds to the QRS complex; Phase 2
(plateau) corresponds to the ST segment; Phase 3 (repolarization) corresponds to the T
wave — The cardiac action potential's Phase 0 (rapid sodium influx) generates the QRS
complex; Phase 2 (calcium influx plateau) corresponds to the ST segment; Phase 3
(potassium efflux repolarization) produces the T wave. Phase 4 is the resting membrane
potential.
• 2. A 72-year-old patient with longstanding hypertension presents with a laterally displaced
PMI to the 6th intercostal space in the anterior axillary line. This finding is most consistent with
which of the following pathophysiological adaptations, and what is the underlying mechanism?
A) Concentric left ventricular hypertrophy secondary to chronic pressure overload, resulting
from increased afterload and sarcomere addition in parallel
B) Eccentric left ventricular hypertrophy secondary to chronic volume overload, resulting
from sarcomere addition in series
C) Dilated cardiomyopathy secondary to ischemic injury, resulting from myocyte apoptosis
and fibrosis
D) Right ventricular hypertrophy secondary to pulmonary hypertension, resulting from
increased right ventricular afterload
🔴🔴 A) Concentric left ventricular hypertrophy secondary to chronic pressure overload,
resulting from increased afterload and sarcomere addition in parallel — Chronic
hypertension increases afterload, causing the left ventricle to develop concentric
hypertrophy (sarcomeres added in parallel), which displaces the PMI laterally and inferiorly
as the ventricle enlarges.
• 3. The coronary arteries perfuse the myocardium primarily during diastole because:
A) The aortic valve is open during systole, preventing coronary artery filling
B) Myocardial compression during systole increases coronary vascular resistance, limiting
flow
C) The coronary arteries originate from the pulmonary artery during fetal development
D) Sympathetic stimulation during systole causes coronary vasoconstriction
🔴🔴 B) Myocardial compression during systole increases coronary vascular resistance,
limiting flow — During ventricular systole, the contracting myocardium compresses the
intramural coronary vessels, increasing vascular resistance and reducing flow. Coronary
perfusion is maximal during diastole when the myocardium relaxes.
• 4. Which of the following statements accurately describes the Frank-Starling mechanism at
the molecular level, and how does it relate to the clinical assessment of preload?
A) Increased end-diastolic volume stretches sarcomeres to optimal length, increasing actin-
myosin cross-bridge formation and stroke volume; preload is clinically estimated by central
venous pressure or pulmonary capillary wedge pressure
B) Increased end-diastolic volume decreases sarcomere length, reducing cross-bridge
formation and stroke volume; preload is estimated by heart rate
C) The Frank-Starling mechanism is independent of sarcomere length and is solely
determined by calcium availability; preload is estimated by blood pressure
D) The mechanism only operates in the right ventricle; preload is estimated by jugular
venous pressure alone
🔴🔴 A) Increased end-diastolic volume stretches sarcomeres to optimal length,
increasing actin-myosin cross-bridge formation and stroke volume; preload is clinically
estimated by central venous pressure or pulmonary capillary wedge pressure — The
, Frank-Starling law describes the relationship between end-diastolic volume (preload) and
stroke volume. Optimal sarcomere stretching (2.0–2.2 μm) maximizes cross-bridge
formation. Preload is clinically estimated by CVP (right heart) or PCWP (left heart).
• 5. A patient with severe aortic stenosis develops syncope during exertion. The
pathophysiological mechanism most directly responsible for this symptom is:
A) Fixed left ventricular outflow tract obstruction leading to inadequate cardiac output
augmentation during exercise, compounded by peripheral vasodilation and impaired
coronary perfusion
B) Right ventricular failure leading to decreased pulmonary blood flow
C) Mitral regurgitation developing secondary to left ventricular dilation
D) Complete heart block developing from calcification of the conduction system
🔴🔴 A) Fixed left ventricular outflow tract obstruction leading to inadequate cardiac
output augmentation during exercise, compounded by peripheral vasodilation and
impaired coronary perfusion — In aortic stenosis, the fixed obstruction prevents adequate
increase in cardiac output during exercise. Peripheral vasodilation from exertion further
reduces coronary perfusion pressure, leading to syncope.
• 6. Which of the following correctly describes the physiological splitting of S2 and its
relationship to respiratory variation in a patient with a normal heart?
A) During inspiration, increased negative intrathoracic pressure increases venous return to
the right ventricle, prolonging right ventricular ejection and delaying pulmonic valve closure,
resulting in audible splitting
B) During inspiration, decreased venous return to the right ventricle shortens right
ventricular ejection, causing earlier pulmonic valve closure
C) During expiration, increased venous return to the left ventricle delays aortic valve closure,
causing splitting
D) Splitting of S2 is a pathological finding that always indicates underlying cardiac disease
🔴🔴 A) During inspiration, increased negative intrathoracic pressure increases venous
return to the right ventricle, prolonging right ventricular ejection and delaying pulmonic
valve closure, resulting in audible splitting — Physiological splitting of S2 occurs during
inspiration due to increased venous return to the right heart, which prolongs right
ventricular systole and delays pulmonic valve closure relative to aortic valve closure.
• 7. The dicrotic notch on the arterial pressure waveform represents which of the following
hemodynamic events, and what is its clinical significance in assessing aortic valve function?
A) Opening of the aortic valve; signifies normal left ventricular ejection
B) Closure of the aortic valve; signifies the end of systole and the onset of diastole, and its
absence may indicate aortic regurgitation
C) Opening of the mitral valve; signifies the onset of ventricular filling
D) Closure of the mitral valve; signifies the onset of ventricular systole
🔴🔴 B) Closure of the aortic valve; signifies the end of systole and the onset of diastole,
and its absence may indicate aortic regurgitation — The dicrotic notch is a brief increase in
aortic pressure upon aortic valve closure, marking the end of systole. Its absence or
diminution may indicate aortic regurgitation.
• 8. A 55-year-old patient with a history of myocardial infarction presents with dyspnea on
exertion and orthopnea. On examination, you note an S3 gallop and jugular venous distention.
, Which of the following hemodynamic parameters would you expect to be elevated, and what is
the underlying pathophysiological mechanism?
A) Elevated pulmonary capillary wedge pressure (PCWP) due to left ventricular systolic
dysfunction and increased left ventricular end-diastolic pressure
B) Elevated central venous pressure (CVP) due to right ventricular systolic dysfunction
C) Elevated pulmonary artery systolic pressure due to pulmonary embolism
D) Elevated systemic vascular resistance due to compensatory vasoconstriction
🔴🔴 A) Elevated pulmonary capillary wedge pressure (PCWP) due to left ventricular
systolic dysfunction and increased left ventricular end-diastolic pressure — An S3 gallop in
a patient with a history of MI indicates left ventricular systolic dysfunction. Elevated LVEDP is
transmitted backward, increasing PCWP and causing pulmonary congestion (dyspnea,
orthopnea).
• 9. Which of the following best describes the role of the autonomic nervous system in
regulating cardiac output during acute hemorrhage?
A) Sympathetic activation increases heart rate and contractility via beta-1 adrenergic
receptors; parasympathetic withdrawal further increases heart rate; venous constriction
increases preload
B) Parasympathetic activation decreases heart rate to conserve oxygen; sympathetic
inhibition reduces afterload
C) Sympathetic activation causes coronary vasoconstriction, reducing myocardial oxygen
supply
D) The autonomic nervous system plays no role in acute hemorrhage compensation
🔴🔴 A) Sympathetic activation increases heart rate and contractility via beta-1
adrenergic receptors; parasympathetic withdrawal further increases heart rate; venous
constriction increases preload — Acute hemorrhage triggers baroreceptor-mediated
sympathetic activation (increased HR, contractility, vasoconstriction) and parasympathetic
withdrawal, maintaining cardiac output despite reduced circulating volume.
• 10. A patient with a chronic, large pericardial effusion presents with pulsus paradoxus. Which
of the following hemodynamic changes best explains this physical finding?
A) During inspiration, increased venous return to the right ventricle causes the
interventricular septum to bulge into the left ventricle, reducing left ventricular filling and
stroke volume, causing a fall in systolic blood pressure >10 mmHg
B) During expiration, increased left ventricular filling causes the septum to bulge into the
right ventricle
C) During inspiration, decreased venous return to the left ventricle causes a fall in stroke
volume
D) During expiration, decreased venous return to the right ventricle causes a fall in cardiac
output
🔴🔴 A) During inspiration, increased venous return to the right ventricle causes the
interventricular septum to bulge into the left ventricle, reducing left ventricular filling and
stroke volume, causing a fall in systolic blood pressure >10 mmHg — In cardiac
tamponade, the equalization of intracardiac pressures and the limited total cardiac volume
cause the septum to shift into the LV during inspiration, reducing LV filling and stroke
volume.
• 11. Which of the following correctly describes the relationship between myocardial oxygen
demand and supply in the context of coronary artery disease?
