NURS 611 EXAM 2 PATHO ACTUAL EXAM
TEST BANK COMPLETE 200 QUESTIONS AND CORRECT DETAILED
ANSWERS WITH RATIONALES
ALREADY GRADED A+
Maryville University - NURS 611 Advanced Pathophysiology Examination Preparation
Aligned with current advanced practice nursing pathophysiology standards | 200 questions, 12 sections | Cognitive mix:
30% recall, 50% application, 20% analysis
Section 1
Section 1: Cardiovascular Pathophysiology - Structure and Function (Cardiac Anatomy, Conduction System, Cardiac
Cycle, & Hemodynamics)
Q1: A 54-year-old female presents with dyspnea on exertion. Echocardiography reveals a normal ejection
fraction but elevated left ventricular end-diastolic pressure (LVEDP) with preserved stroke volume. Which
hemodynamic principle best explains the elevated LVEDP despite normal stroke volume?
A. Increased afterload due to systemic vasoconstriction reducing forward output
B. Decreased contractility secondary to beta-adrenergic receptor downregulation
C. Increased preload stretching sarcomeres toward the optimal 2.2 micrometer length per the Frank-Starling
mechanism [CORRECT]
D. Reduced heart rate prolonging diastolic filling time and lowering cardiac output
Correct Answer: C
Rationale: Per the Frank-Starling law, increased venous return raises LVEDP, stretching sarcomeres toward their optimal
overlap (~2.2 micrometers) and increasing contractile force, which preserves stroke volume despite elevated filling pressure.
Afterload (A) affects ejection against resistance but does not primarily elevate LVEDP with preserved stroke volume.
Decreased contractility (B) would reduce EF, which is excluded by the stem. Reduced heart rate (D) prolongs filling and may
actually increase stroke volume, not elevate LVEDP pathologically.
NURS 611 Exam 2 - Cardiovascular & Hematologic Pathophysiology | Page 1
,NURS 611 EXAM 2 - TEST BANK - 200 QUESTIONS
Q2: A patient has a left ventricular afterload of 140 mmHg (severe hypertension) with a stroke volume of 50
mL (normal 70 mL). Which cellular mechanism most directly accounts for the reduced stroke volume at the
level of the cardiomyocyte?
A. Decreased sarcoplasmic reticulum calcium release due to downregulated ryanodine receptors
B. Shortened sarcomere shortening because myofilaments must generate greater tension before shortening can
occur against elevated aortic pressure [CORRECT]
C. Increased myosin ATPase activity accelerating cross-bridge cycling
D. Decreased preload due to venous capacitance constriction
Correct Answer: B
Rationale: Afterload represents the tension the ventricle must develop before ejection can begin. At high afterload,
myofilaments spend more time in isovolumetric tension generation and less in shortening, reducing stroke volume even though
contractility is unchanged. Option A describes impaired excitation-contraction coupling (true in chronic HF) but is not the
immediate hemodynamic mechanism. Option C would increase, not decrease, stroke volume. Option D is incorrect because
elevated afterload is independent of preload in this scenario.
Q3: The cardiac conduction system normally depolarizes in a specific sequence. Which structure initiates the
action potential, what is the approximate conduction velocity through the AV node, and why is this delay
physiologically important?
A. SA node; 0.05 m/s; allows complete ventricular filling before systole
B. AV node; 1 m/s; permits atrial kick contribution of 20-30% of ventricular filling
C. SA node; 0.05 m/s; allows complete atrial emptying and ventricular filling before ventricular contraction
begins [CORRECT]
D. Purkinje fibers; 4 m/s; synchronizes atrial and ventricular contraction
Correct Answer: C
Rationale: The sinoatrial (SA) node is the primary pacemaker (~60-100 bpm). The AV node conducts at ~0.05 m/s, the
slowest in the conduction system, creating a critical delay (~0.1s) that allows complete atrial emptying and optimal ventricular
filling before ventricular systole begins. Option A misattributes the pacemaker. Option B incorrectly assigns the pacemaker
role to the AV node. Option D incorrectly names Purkinje fibers as the initiator, and their fast conduction (2-4 m/s) actually
synchronizes ventricular contraction rather than initiating it.
Q4: A 67-year-old male has a heart rate of 75 bpm, stroke volume of 70 mL, and systemic vascular resistance
(SVR) of 1500 dynes-sec/cm5. Calculate cardiac output (CO) given central venous pressure (CVP) of 5 mmHg.
A. CO = 5.25 L/min [CORRECT]
B. CO = 5.0 L/min
C. CO = 4.5 L/min
D. CO = 6.0 L/min
Correct Answer: A
Rationale: CO = HR x SV = 75 beats/min x 70 mL/beat = 5250 mL/min = 5.25 L/min. The other options represent common
arithmetic errors: B uses HR=71 or SV=67; C subtracts 0.75; D adds extra. The SVR and CVP values would be needed to
compute MAP, but CO is determined purely by HR and SV. This question tests basic hemodynamic calculation relevant to
advanced practice interpretation of invasive monitoring.
NURS 611 Exam 2 - Cardiovascular & Hematologic Pathophysiology | Page 2
,NURS 611 EXAM 2 - TEST BANK - 200 QUESTIONS
Q5: Which layer of the heart wall contains the Purkinje fibers and is responsible for the heart's intrinsic
electrical conduction? This layer is embryologically derived from which germ layer?
A. Epicardium; mesoderm
B. Myocardium; mesoderm [CORRECT]
C. Endocardium; endoderm
D. Myocardium; neural crest
Correct Answer: B
Rationale: Purkinje fibers run in the subendocardial layer of the myocardium, which together with the endocardium is
mesodermally derived. The myocardium forms the bulk of the heart wall and contains the conduction system. The epicardium
(visceral pericardium) is also mesodermal but is the outer layer. The endocardium is mesodermal, not endodermal. Neural crest
contributes to the cardiac outflow tract septation but not the bulk myocardium.
Q6: The left anterior descending (LAD) artery supplies which regions of the heart? Understanding this
territory is essential because LAD occlusion is termed the 'widow-maker' lesion.
A. Inferior wall, right ventricle, and AV node
B. Anterior wall of left ventricle, interventricular septum, and bundle branches [CORRECT]
C. Lateral and posterior walls of left ventricle and SA node
D. Right atrium, right ventricle, and inferior interventricular septum
Correct Answer: B
Rationale: The LAD, a branch of the left main coronary artery, supplies the anterior LV wall, the anterior two-thirds of the
interventricular septum (where the bundle branches run), and the anterolateral papillary muscle. Occlusion causes large
anterior STEMI with high risk of cardiogenic shock and lethal arrhythmias. Option A describes the RCA dominant supply.
Option C describes the LCx supply. Option D is RCA territory (right system).
Q7: During the cardiac cycle, the isovolumetric contraction phase begins with closure of which valve(s) and
ends with opening of which valve(s)? What hemodynamic event defines this phase?
A. Mitral closes; aortic opens; ventricular pressure rises sharply without volume change [CORRECT]
B. Aortic closes; mitral opens; ventricular pressure falls rapidly
C. Tricuspid closes; pulmonary opens; right ventricular pressure exceeds PA pressure
D. Mitral closes; pulmonic opens; atrial pressure exceeds ventricular pressure
Correct Answer: A
Rationale: Isovolumetric contraction occurs after the mitral (and tricuspid) valves close when ventricular pressure exceeds
atrial pressure but is still below aortic (and pulmonic) pressure. Ventricular pressure rises sharply with all four valves closed,
so no volume changes occur. The phase ends when ventricular pressure exceeds aortic pressure, opening the aortic valve and
initiating ejection. Option B describes isovolumetric relaxation. Option C describes right-sided events but does not match the
classic phase definition. Option D mixes left and right sided valves incorrectly.
NURS 611 Exam 2 - Cardiovascular & Hematologic Pathophysiology | Page 3
, NURS 611 EXAM 2 - TEST BANK - 200 QUESTIONS
Q8: The dicrotic notch on the aortic pressure waveform represents which physiological event, and what is its
clinical significance during arterial line waveform analysis?
A. Opening of the aortic valve; marks onset of systole
B. Brief retrograde flow and aortic valve closure; marks end of systole and start of diastole [CORRECT]
C. Peak ventricular pressure; maximum stroke volume ejection
D. Atrial contraction; contributes 20-30% of ventricular filling
Correct Answer: B
Rationale: The dicrotic notch represents the brief retrograde flow and closure of the aortic valve, marking the transition from
systole to diastole. It is followed by the dicrotic wave as elastic recoil of the aorta pushes blood forward. Clinically, the dicrotic
notch on an arterial line trace confirms pulse contour and helps calibrate cardiac output monitoring devices. Option A
incorrectly identifies it as onset of systole. Option C describes peak systolic pressure. Option D describes atrial kick, which is
unrelated to the aortic waveform.
Q9: Preload is clinically estimated using which hemodynamic parameter, and how does it relate to the
Frank-Starling mechanism? In a patient with volume overload, what change in this parameter would you
expect?
A. Right atrial pressure; increased preload leads to decreased stroke volume
B. Pulmonary artery occlusion pressure (wedge pressure); increased preload stretches sarcomeres toward
optimal length, increasing stroke volume up to a physiologic maximum [CORRECT]
C. Systemic vascular resistance; increased preload decreases contractility
D. Ejection fraction; increased preload increases afterload
Correct Answer: B
Rationale: Preload is best estimated clinically by the pulmonary artery occlusion pressure (PAOP/PCWP), which reflects left
atrial and LV end-diastolic pressure. Per the Frank-Starling mechanism, increased preload stretches sarcomeres toward optimal
overlap (~2.2 micrometers), increasing stroke volume up to a point beyond which overstretch reduces force generation
(descending limb). RA pressure (A) estimates right-sided preload only. SVR is afterload, not preload. Ejection fraction reflects
contractility, not preload.
Q10: Coronary blood flow to the left ventricle occurs predominantly during which phase of the cardiac cycle,
and what is the underlying mechanism?
A. Systole; high aortic pressure drives blood into coronary arteries
B. Diastole; relaxation of the myocardium relieves intramyocardial compressive forces on subendocardial
vessels [CORRECT]
C. Both equally; coronary flow is independent of cardiac phase
D. Atrial systole; atrial kick augments coronary perfusion
Correct Answer: B
Rationale: Left coronary blood flow occurs predominantly during diastole because during systole, intramyocardial pressure
(especially in the subendocardium) exceeds coronary perfusion pressure, compressing intramural vessels. In diastole, the
myocardium relaxes and perfusion occurs down the gradient from aortic diastolic pressure to LV end-diastolic pressure. This is
why tachycardia (which shortens diastole) is poorly tolerated in coronary disease. The right coronary system, with lower
intramyocardial pressures, does perfuse during both phases.
NURS 611 Exam 2 - Cardiovascular & Hematologic Pathophysiology | Page 4
TEST BANK COMPLETE 200 QUESTIONS AND CORRECT DETAILED
ANSWERS WITH RATIONALES
ALREADY GRADED A+
Maryville University - NURS 611 Advanced Pathophysiology Examination Preparation
Aligned with current advanced practice nursing pathophysiology standards | 200 questions, 12 sections | Cognitive mix:
30% recall, 50% application, 20% analysis
Section 1
Section 1: Cardiovascular Pathophysiology - Structure and Function (Cardiac Anatomy, Conduction System, Cardiac
Cycle, & Hemodynamics)
Q1: A 54-year-old female presents with dyspnea on exertion. Echocardiography reveals a normal ejection
fraction but elevated left ventricular end-diastolic pressure (LVEDP) with preserved stroke volume. Which
hemodynamic principle best explains the elevated LVEDP despite normal stroke volume?
A. Increased afterload due to systemic vasoconstriction reducing forward output
B. Decreased contractility secondary to beta-adrenergic receptor downregulation
C. Increased preload stretching sarcomeres toward the optimal 2.2 micrometer length per the Frank-Starling
mechanism [CORRECT]
D. Reduced heart rate prolonging diastolic filling time and lowering cardiac output
Correct Answer: C
Rationale: Per the Frank-Starling law, increased venous return raises LVEDP, stretching sarcomeres toward their optimal
overlap (~2.2 micrometers) and increasing contractile force, which preserves stroke volume despite elevated filling pressure.
Afterload (A) affects ejection against resistance but does not primarily elevate LVEDP with preserved stroke volume.
Decreased contractility (B) would reduce EF, which is excluded by the stem. Reduced heart rate (D) prolongs filling and may
actually increase stroke volume, not elevate LVEDP pathologically.
NURS 611 Exam 2 - Cardiovascular & Hematologic Pathophysiology | Page 1
,NURS 611 EXAM 2 - TEST BANK - 200 QUESTIONS
Q2: A patient has a left ventricular afterload of 140 mmHg (severe hypertension) with a stroke volume of 50
mL (normal 70 mL). Which cellular mechanism most directly accounts for the reduced stroke volume at the
level of the cardiomyocyte?
A. Decreased sarcoplasmic reticulum calcium release due to downregulated ryanodine receptors
B. Shortened sarcomere shortening because myofilaments must generate greater tension before shortening can
occur against elevated aortic pressure [CORRECT]
C. Increased myosin ATPase activity accelerating cross-bridge cycling
D. Decreased preload due to venous capacitance constriction
Correct Answer: B
Rationale: Afterload represents the tension the ventricle must develop before ejection can begin. At high afterload,
myofilaments spend more time in isovolumetric tension generation and less in shortening, reducing stroke volume even though
contractility is unchanged. Option A describes impaired excitation-contraction coupling (true in chronic HF) but is not the
immediate hemodynamic mechanism. Option C would increase, not decrease, stroke volume. Option D is incorrect because
elevated afterload is independent of preload in this scenario.
Q3: The cardiac conduction system normally depolarizes in a specific sequence. Which structure initiates the
action potential, what is the approximate conduction velocity through the AV node, and why is this delay
physiologically important?
A. SA node; 0.05 m/s; allows complete ventricular filling before systole
B. AV node; 1 m/s; permits atrial kick contribution of 20-30% of ventricular filling
C. SA node; 0.05 m/s; allows complete atrial emptying and ventricular filling before ventricular contraction
begins [CORRECT]
D. Purkinje fibers; 4 m/s; synchronizes atrial and ventricular contraction
Correct Answer: C
Rationale: The sinoatrial (SA) node is the primary pacemaker (~60-100 bpm). The AV node conducts at ~0.05 m/s, the
slowest in the conduction system, creating a critical delay (~0.1s) that allows complete atrial emptying and optimal ventricular
filling before ventricular systole begins. Option A misattributes the pacemaker. Option B incorrectly assigns the pacemaker
role to the AV node. Option D incorrectly names Purkinje fibers as the initiator, and their fast conduction (2-4 m/s) actually
synchronizes ventricular contraction rather than initiating it.
Q4: A 67-year-old male has a heart rate of 75 bpm, stroke volume of 70 mL, and systemic vascular resistance
(SVR) of 1500 dynes-sec/cm5. Calculate cardiac output (CO) given central venous pressure (CVP) of 5 mmHg.
A. CO = 5.25 L/min [CORRECT]
B. CO = 5.0 L/min
C. CO = 4.5 L/min
D. CO = 6.0 L/min
Correct Answer: A
Rationale: CO = HR x SV = 75 beats/min x 70 mL/beat = 5250 mL/min = 5.25 L/min. The other options represent common
arithmetic errors: B uses HR=71 or SV=67; C subtracts 0.75; D adds extra. The SVR and CVP values would be needed to
compute MAP, but CO is determined purely by HR and SV. This question tests basic hemodynamic calculation relevant to
advanced practice interpretation of invasive monitoring.
NURS 611 Exam 2 - Cardiovascular & Hematologic Pathophysiology | Page 2
,NURS 611 EXAM 2 - TEST BANK - 200 QUESTIONS
Q5: Which layer of the heart wall contains the Purkinje fibers and is responsible for the heart's intrinsic
electrical conduction? This layer is embryologically derived from which germ layer?
A. Epicardium; mesoderm
B. Myocardium; mesoderm [CORRECT]
C. Endocardium; endoderm
D. Myocardium; neural crest
Correct Answer: B
Rationale: Purkinje fibers run in the subendocardial layer of the myocardium, which together with the endocardium is
mesodermally derived. The myocardium forms the bulk of the heart wall and contains the conduction system. The epicardium
(visceral pericardium) is also mesodermal but is the outer layer. The endocardium is mesodermal, not endodermal. Neural crest
contributes to the cardiac outflow tract septation but not the bulk myocardium.
Q6: The left anterior descending (LAD) artery supplies which regions of the heart? Understanding this
territory is essential because LAD occlusion is termed the 'widow-maker' lesion.
A. Inferior wall, right ventricle, and AV node
B. Anterior wall of left ventricle, interventricular septum, and bundle branches [CORRECT]
C. Lateral and posterior walls of left ventricle and SA node
D. Right atrium, right ventricle, and inferior interventricular septum
Correct Answer: B
Rationale: The LAD, a branch of the left main coronary artery, supplies the anterior LV wall, the anterior two-thirds of the
interventricular septum (where the bundle branches run), and the anterolateral papillary muscle. Occlusion causes large
anterior STEMI with high risk of cardiogenic shock and lethal arrhythmias. Option A describes the RCA dominant supply.
Option C describes the LCx supply. Option D is RCA territory (right system).
Q7: During the cardiac cycle, the isovolumetric contraction phase begins with closure of which valve(s) and
ends with opening of which valve(s)? What hemodynamic event defines this phase?
A. Mitral closes; aortic opens; ventricular pressure rises sharply without volume change [CORRECT]
B. Aortic closes; mitral opens; ventricular pressure falls rapidly
C. Tricuspid closes; pulmonary opens; right ventricular pressure exceeds PA pressure
D. Mitral closes; pulmonic opens; atrial pressure exceeds ventricular pressure
Correct Answer: A
Rationale: Isovolumetric contraction occurs after the mitral (and tricuspid) valves close when ventricular pressure exceeds
atrial pressure but is still below aortic (and pulmonic) pressure. Ventricular pressure rises sharply with all four valves closed,
so no volume changes occur. The phase ends when ventricular pressure exceeds aortic pressure, opening the aortic valve and
initiating ejection. Option B describes isovolumetric relaxation. Option C describes right-sided events but does not match the
classic phase definition. Option D mixes left and right sided valves incorrectly.
NURS 611 Exam 2 - Cardiovascular & Hematologic Pathophysiology | Page 3
, NURS 611 EXAM 2 - TEST BANK - 200 QUESTIONS
Q8: The dicrotic notch on the aortic pressure waveform represents which physiological event, and what is its
clinical significance during arterial line waveform analysis?
A. Opening of the aortic valve; marks onset of systole
B. Brief retrograde flow and aortic valve closure; marks end of systole and start of diastole [CORRECT]
C. Peak ventricular pressure; maximum stroke volume ejection
D. Atrial contraction; contributes 20-30% of ventricular filling
Correct Answer: B
Rationale: The dicrotic notch represents the brief retrograde flow and closure of the aortic valve, marking the transition from
systole to diastole. It is followed by the dicrotic wave as elastic recoil of the aorta pushes blood forward. Clinically, the dicrotic
notch on an arterial line trace confirms pulse contour and helps calibrate cardiac output monitoring devices. Option A
incorrectly identifies it as onset of systole. Option C describes peak systolic pressure. Option D describes atrial kick, which is
unrelated to the aortic waveform.
Q9: Preload is clinically estimated using which hemodynamic parameter, and how does it relate to the
Frank-Starling mechanism? In a patient with volume overload, what change in this parameter would you
expect?
A. Right atrial pressure; increased preload leads to decreased stroke volume
B. Pulmonary artery occlusion pressure (wedge pressure); increased preload stretches sarcomeres toward
optimal length, increasing stroke volume up to a physiologic maximum [CORRECT]
C. Systemic vascular resistance; increased preload decreases contractility
D. Ejection fraction; increased preload increases afterload
Correct Answer: B
Rationale: Preload is best estimated clinically by the pulmonary artery occlusion pressure (PAOP/PCWP), which reflects left
atrial and LV end-diastolic pressure. Per the Frank-Starling mechanism, increased preload stretches sarcomeres toward optimal
overlap (~2.2 micrometers), increasing stroke volume up to a point beyond which overstretch reduces force generation
(descending limb). RA pressure (A) estimates right-sided preload only. SVR is afterload, not preload. Ejection fraction reflects
contractility, not preload.
Q10: Coronary blood flow to the left ventricle occurs predominantly during which phase of the cardiac cycle,
and what is the underlying mechanism?
A. Systole; high aortic pressure drives blood into coronary arteries
B. Diastole; relaxation of the myocardium relieves intramyocardial compressive forces on subendocardial
vessels [CORRECT]
C. Both equally; coronary flow is independent of cardiac phase
D. Atrial systole; atrial kick augments coronary perfusion
Correct Answer: B
Rationale: Left coronary blood flow occurs predominantly during diastole because during systole, intramyocardial pressure
(especially in the subendocardium) exceeds coronary perfusion pressure, compressing intramural vessels. In diastole, the
myocardium relaxes and perfusion occurs down the gradient from aortic diastolic pressure to LV end-diastolic pressure. This is
why tachycardia (which shortens diastole) is poorly tolerated in coronary disease. The right coronary system, with lower
intramyocardial pressures, does perfuse during both phases.
NURS 611 Exam 2 - Cardiovascular & Hematologic Pathophysiology | Page 4
