Saunders Comprehensive Review for the NCLEX-PN®
Examination
9th Edition
• Author(s)Linda Anne Silvestri; Angela Silvestri
ANATOMY AND PHYSIOLOGY TEST BANK
Cardiovascular (3 items)
1.
A 68-year-old client reports sudden onset of crushing chest pain
radiating to the left arm, diaphoresis, and shortness of breath.
Which physiologic process explains the client’s chest pain?
A. Coronary artery vasospasm causing transient ischemia of
myocardial cells
B. Atherosclerotic plaque rupture with thrombus formation
causing myocardial ischemia
C. Mitral valve prolapse producing increased left ventricular
afterload
D. Pericardial effusion increasing intrapericardial pressure and
decreasing coronary perfusion
Correct: B
Rationale — correct (B): Acute coronary syndrome most
commonly results from rupture of an atherosclerotic plaque
,followed by thrombosis that occludes a coronary artery. This
causes abrupt cessation of oxygen delivery to myocardial tissue
→ ischemia and anaerobic metabolism → accumulation of lactic
acid and myocardial cell membrane injury, producing ischemic
chest pain and autonomic signs (diaphoresis).
Why others are incorrect:
A. Vasospasm (Prinzmetal) can cause ischemia but typically
presents in younger patients and with transient ST changes;
plaque rupture with thrombus is the most likely mechanism in
this older client with crushing pain.
C. Mitral valve prolapse causes mitral regurgitation or
palpitations rather than acute transmural ischemic pain; it does
not acutely block coronary blood flow.
D. Pericardial effusion/tamponade reduces ventricular filling
(preload) but does not typically produce localized crushing
chest pain radiating to the arm like myocardial ischemia does.
2.
A client with heart failure has an ejection fraction (EF) of 30%
and experiences nocturnal dyspnea. Which physiologic
mechanism best explains orthopnea and paroxysmal nocturnal
dyspnea in left-sided systolic heart failure?
A. Decreased left ventricular contractility causes pulmonary
venous congestion and interstitial edema.
B. Elevated right atrial pressure causes hepatic congestion and
fluid accumulation in lungs.
,C. Left ventricular hypertrophy increases stroke volume and
pulmonary circulation pressure.
D. Increased systemic vascular resistance (afterload) causes
peripheral edema that shifts to lungs at night.
Correct: A
Rationale — correct (A): Reduced left ventricular systolic
function → elevated left ventricular end-diastolic pressure →
elevated left atrial/pulmonary venous pressures → transudation
of fluid into pulmonary interstitium and alveoli, causing
orthopnea (worse when supine) and paroxysmal nocturnal
dyspnea.
Why others are incorrect:
B. Elevated right atrial pressure causes systemic venous
congestion (hepatomegaly, peripheral edema), not primary
pulmonary edema.
C. LV hypertrophy may be associated with diastolic dysfunction,
not increased stroke volume; hypertrophy raises filling
pressures, but the mechanism described is inaccurate for
nocturnal pulmonary symptoms.
D. Peripheral edema shifting to pulmonary edema overnight is
not a primary physiologic mechanism; pulmonary edema in left-
sided failure is due to elevated pulmonary venous pressures,
not redistribution of peripheral edema.
3.
, A nurse auscultates a crescendo-decrescendo systolic murmur
at the right sternal border that increases with Valsalva
maneuver. Which structural/functional correlate explains why
the murmur intensity increases with Valsalva?
A. Increased afterload increases aortic flow across the stenotic
valve.
B. Valsalva reduces venous return and left ventricular volume,
increasing dynamic obstruction.
C. Valsalva increases preload, stretching aortic valve leaflets and
increasing the gradient.
D. Valsalva increases heart rate, causing more turbulent flow
across a fixed lesion.
Correct: B
Rationale — correct (B): For hypertrophic obstructive
cardiomyopathy and dynamic outflow obstructions, Valsalva
(phase II) decreases venous return and left ventricular end-
diastolic volume → smaller LV cavity → septal-anterior leaflet
approximation increases obstruction → louder murmur.
Crescendo-decrescendo murmur at RSB that increases with
Valsalva suggests dynamic LVOT obstruction physiology.
Why others are incorrect:
A. Valsalva actually decreases venous return and often
decreases stroke volume and aortic flow; it does not increase
afterload.
C. Valsalva decreases preload (not increases), so valve leaflet
stretching is reduced rather than increased.
Examination
9th Edition
• Author(s)Linda Anne Silvestri; Angela Silvestri
ANATOMY AND PHYSIOLOGY TEST BANK
Cardiovascular (3 items)
1.
A 68-year-old client reports sudden onset of crushing chest pain
radiating to the left arm, diaphoresis, and shortness of breath.
Which physiologic process explains the client’s chest pain?
A. Coronary artery vasospasm causing transient ischemia of
myocardial cells
B. Atherosclerotic plaque rupture with thrombus formation
causing myocardial ischemia
C. Mitral valve prolapse producing increased left ventricular
afterload
D. Pericardial effusion increasing intrapericardial pressure and
decreasing coronary perfusion
Correct: B
Rationale — correct (B): Acute coronary syndrome most
commonly results from rupture of an atherosclerotic plaque
,followed by thrombosis that occludes a coronary artery. This
causes abrupt cessation of oxygen delivery to myocardial tissue
→ ischemia and anaerobic metabolism → accumulation of lactic
acid and myocardial cell membrane injury, producing ischemic
chest pain and autonomic signs (diaphoresis).
Why others are incorrect:
A. Vasospasm (Prinzmetal) can cause ischemia but typically
presents in younger patients and with transient ST changes;
plaque rupture with thrombus is the most likely mechanism in
this older client with crushing pain.
C. Mitral valve prolapse causes mitral regurgitation or
palpitations rather than acute transmural ischemic pain; it does
not acutely block coronary blood flow.
D. Pericardial effusion/tamponade reduces ventricular filling
(preload) but does not typically produce localized crushing
chest pain radiating to the arm like myocardial ischemia does.
2.
A client with heart failure has an ejection fraction (EF) of 30%
and experiences nocturnal dyspnea. Which physiologic
mechanism best explains orthopnea and paroxysmal nocturnal
dyspnea in left-sided systolic heart failure?
A. Decreased left ventricular contractility causes pulmonary
venous congestion and interstitial edema.
B. Elevated right atrial pressure causes hepatic congestion and
fluid accumulation in lungs.
,C. Left ventricular hypertrophy increases stroke volume and
pulmonary circulation pressure.
D. Increased systemic vascular resistance (afterload) causes
peripheral edema that shifts to lungs at night.
Correct: A
Rationale — correct (A): Reduced left ventricular systolic
function → elevated left ventricular end-diastolic pressure →
elevated left atrial/pulmonary venous pressures → transudation
of fluid into pulmonary interstitium and alveoli, causing
orthopnea (worse when supine) and paroxysmal nocturnal
dyspnea.
Why others are incorrect:
B. Elevated right atrial pressure causes systemic venous
congestion (hepatomegaly, peripheral edema), not primary
pulmonary edema.
C. LV hypertrophy may be associated with diastolic dysfunction,
not increased stroke volume; hypertrophy raises filling
pressures, but the mechanism described is inaccurate for
nocturnal pulmonary symptoms.
D. Peripheral edema shifting to pulmonary edema overnight is
not a primary physiologic mechanism; pulmonary edema in left-
sided failure is due to elevated pulmonary venous pressures,
not redistribution of peripheral edema.
3.
, A nurse auscultates a crescendo-decrescendo systolic murmur
at the right sternal border that increases with Valsalva
maneuver. Which structural/functional correlate explains why
the murmur intensity increases with Valsalva?
A. Increased afterload increases aortic flow across the stenotic
valve.
B. Valsalva reduces venous return and left ventricular volume,
increasing dynamic obstruction.
C. Valsalva increases preload, stretching aortic valve leaflets and
increasing the gradient.
D. Valsalva increases heart rate, causing more turbulent flow
across a fixed lesion.
Correct: B
Rationale — correct (B): For hypertrophic obstructive
cardiomyopathy and dynamic outflow obstructions, Valsalva
(phase II) decreases venous return and left ventricular end-
diastolic volume → smaller LV cavity → septal-anterior leaflet
approximation increases obstruction → louder murmur.
Crescendo-decrescendo murmur at RSB that increases with
Valsalva suggests dynamic LVOT obstruction physiology.
Why others are incorrect:
A. Valsalva actually decreases venous return and often
decreases stroke volume and aortic flow; it does not increase
afterload.
C. Valsalva decreases preload (not increases), so valve leaflet
stretching is reduced rather than increased.
