Saunders Comprehensive Review for the NCLEX-PN®
Examination
9th Edition
• Author(s)Linda Anne Silvestri; Angela Silvestri
ANATOMY AND PHYSIOLOGY TEST BANK
Cardiovascular (Questions 1–4)
1. A client has an area of myocardial ischemia due to
atherosclerotic narrowing of a coronary artery. Which change at
the cellular level most directly explains impaired contractile
function in the ischemic myocardium?
A. Reduced ATP production by mitochondria in cardiomyocytes
B. Increased synthesis of cardiac troponin I
C. Decreased intracellular sodium concentration
D. Increased resting membrane potential (more negative)
Correct: A
Rationale — correct (A): Myocardial ischemia reduces oxygen
delivery, limiting oxidative phosphorylation in mitochondria and
rapidly decreasing ATP production. ATP is required for cross-
bridge cycling and for the sarco/endoplasmic reticulum Ca²⁺-
ATPase (SERCA) pumps that resequester Ca²⁺; without ATP,
contractility falls.
,Why B is wrong: Troponin I is released into the bloodstream
from damaged myocytes (marker of injury), not synthesized to
improve function. Increased troponin indicates necrosis.
Why C is wrong: Ischemia tends to impair Na⁺/K⁺-ATPase (ATP-
dependent), causing intracellular Na⁺ to rise, not fall.
Why D is wrong: Ischemia causes membrane depolarization
(less negative), not a more negative resting potential, due to ion
pump failure and ion shifts.
2. A patient with chronic hypertension develops concentric left
ventricular hypertrophy (LVH). Which physiological change
explains the decreased left-ventricular compliance seen with
concentric LVH?
A. Cardiomyocyte hyperplasia leading to chamber dilation
B. Increased collagen deposition in the ventricular interstitium
C. Loss of myocardial nuclei and decreased protein synthesis
D. Reduced afterload causing myocardial remodeling
Correct: B
Rationale — correct (B): Concentric LVH from long-standing
pressure overload leads to increased myocyte size and often
interstitial fibrosis (↑ collagen). Excess collagen stiffens the
ventricle and reduces compliance, impairing diastolic filling.
Why A is wrong: Hypertrophy is due to cardiomyocyte
hypertrophy (increased cell size), not hyperplasia; concentric
LVH often decreases chamber compliance without dilation.
Why C is wrong: Loss of nuclei/protein synthesis is not the
,mechanism of adaptive hypertrophy.
Why D is wrong: Reduced afterload would not cause concentric
hypertrophy; increased afterload (e.g., hypertension) does.
3. A client with severe aortic stenosis has syncope on exertion.
Which mechanism best explains exertional syncope in aortic
stenosis?
A. Sudden loss of atrial contraction leading to decreased cardiac
output
B. Inability to sufficiently increase stroke volume because of
fixed outflow obstruction
C. Reflex vasodilation due to high left ventricular end-diastolic
pressure
D. Exercise-induced ventricular fibrillation from ischemia
Correct: B
Rationale — correct (B): In severe aortic stenosis, the aortic
valve area is fixed and limits forward stroke volume. During
exertion the heart cannot augment stroke volume to meet
increased metabolic demand; cardiac output fails to rise,
causing hypotension and syncope.
Why A is wrong: Loss of atrial contraction (e.g., AF) can reduce
preload modestly but is not the primary cause of exertional
syncope in aortic stenosis.
Why C is wrong: Elevated LVEDP typically increases sympathetic
tone; reflex vasodilation is not the predominant mechanism for
exertional syncope here.
, Why D is wrong: Ventricular fibrillation is possible but less likely
as the direct cause of exertional syncope in stable aortic
stenosis; the typical mechanism is inadequate cardiac output.
4. A client’s focus of infection has produced a systemic
inflammatory response; serum albumin falls while capillary
permeability rises. Which capillary starling change explains
increased interstitial edema?
A. Increased capillary hydrostatic pressure only
B. Decreased interstitial oncotic pressure only
C. Decreased plasma oncotic pressure and increased capillary
permeability
D. Increased lymphatic drainage
Correct: C
Rationale — correct (C): Systemic inflammation increases
capillary permeability (allowing plasma proteins to escape) and
decreases plasma oncotic pressure (e.g., hypoalbuminemia).
The net result is less plasma oncotic pull and more protein in
interstitium—both favor fluid movement into interstitial space
and edema.
Why A is wrong: Hydrostatic pressure may contribute but the
question emphasizes hypoalbuminemia and permeability;
hydrostatic pressure alone doesn’t explain the protein shift.
Why B is wrong: Interstitial oncotic pressure often increases
(not decreases) when proteins leak out; decreased interstitial
oncotic pressure would oppose edema.
Examination
9th Edition
• Author(s)Linda Anne Silvestri; Angela Silvestri
ANATOMY AND PHYSIOLOGY TEST BANK
Cardiovascular (Questions 1–4)
1. A client has an area of myocardial ischemia due to
atherosclerotic narrowing of a coronary artery. Which change at
the cellular level most directly explains impaired contractile
function in the ischemic myocardium?
A. Reduced ATP production by mitochondria in cardiomyocytes
B. Increased synthesis of cardiac troponin I
C. Decreased intracellular sodium concentration
D. Increased resting membrane potential (more negative)
Correct: A
Rationale — correct (A): Myocardial ischemia reduces oxygen
delivery, limiting oxidative phosphorylation in mitochondria and
rapidly decreasing ATP production. ATP is required for cross-
bridge cycling and for the sarco/endoplasmic reticulum Ca²⁺-
ATPase (SERCA) pumps that resequester Ca²⁺; without ATP,
contractility falls.
,Why B is wrong: Troponin I is released into the bloodstream
from damaged myocytes (marker of injury), not synthesized to
improve function. Increased troponin indicates necrosis.
Why C is wrong: Ischemia tends to impair Na⁺/K⁺-ATPase (ATP-
dependent), causing intracellular Na⁺ to rise, not fall.
Why D is wrong: Ischemia causes membrane depolarization
(less negative), not a more negative resting potential, due to ion
pump failure and ion shifts.
2. A patient with chronic hypertension develops concentric left
ventricular hypertrophy (LVH). Which physiological change
explains the decreased left-ventricular compliance seen with
concentric LVH?
A. Cardiomyocyte hyperplasia leading to chamber dilation
B. Increased collagen deposition in the ventricular interstitium
C. Loss of myocardial nuclei and decreased protein synthesis
D. Reduced afterload causing myocardial remodeling
Correct: B
Rationale — correct (B): Concentric LVH from long-standing
pressure overload leads to increased myocyte size and often
interstitial fibrosis (↑ collagen). Excess collagen stiffens the
ventricle and reduces compliance, impairing diastolic filling.
Why A is wrong: Hypertrophy is due to cardiomyocyte
hypertrophy (increased cell size), not hyperplasia; concentric
LVH often decreases chamber compliance without dilation.
Why C is wrong: Loss of nuclei/protein synthesis is not the
,mechanism of adaptive hypertrophy.
Why D is wrong: Reduced afterload would not cause concentric
hypertrophy; increased afterload (e.g., hypertension) does.
3. A client with severe aortic stenosis has syncope on exertion.
Which mechanism best explains exertional syncope in aortic
stenosis?
A. Sudden loss of atrial contraction leading to decreased cardiac
output
B. Inability to sufficiently increase stroke volume because of
fixed outflow obstruction
C. Reflex vasodilation due to high left ventricular end-diastolic
pressure
D. Exercise-induced ventricular fibrillation from ischemia
Correct: B
Rationale — correct (B): In severe aortic stenosis, the aortic
valve area is fixed and limits forward stroke volume. During
exertion the heart cannot augment stroke volume to meet
increased metabolic demand; cardiac output fails to rise,
causing hypotension and syncope.
Why A is wrong: Loss of atrial contraction (e.g., AF) can reduce
preload modestly but is not the primary cause of exertional
syncope in aortic stenosis.
Why C is wrong: Elevated LVEDP typically increases sympathetic
tone; reflex vasodilation is not the predominant mechanism for
exertional syncope here.
, Why D is wrong: Ventricular fibrillation is possible but less likely
as the direct cause of exertional syncope in stable aortic
stenosis; the typical mechanism is inadequate cardiac output.
4. A client’s focus of infection has produced a systemic
inflammatory response; serum albumin falls while capillary
permeability rises. Which capillary starling change explains
increased interstitial edema?
A. Increased capillary hydrostatic pressure only
B. Decreased interstitial oncotic pressure only
C. Decreased plasma oncotic pressure and increased capillary
permeability
D. Increased lymphatic drainage
Correct: C
Rationale — correct (C): Systemic inflammation increases
capillary permeability (allowing plasma proteins to escape) and
decreases plasma oncotic pressure (e.g., hypoalbuminemia).
The net result is less plasma oncotic pull and more protein in
interstitium—both favor fluid movement into interstitial space
and edema.
Why A is wrong: Hydrostatic pressure may contribute but the
question emphasizes hypoalbuminemia and permeability;
hydrostatic pressure alone doesn’t explain the protein shift.
Why B is wrong: Interstitial oncotic pressure often increases
(not decreases) when proteins leak out; decreased interstitial
oncotic pressure would oppose edema.
