Examination
9th Edition
• Author(s)Linda Anne Silvestri; Angela Silvestri
ANATOMY AND PHYSIOLOGY TEST BANK
Questions (1–20)
1 — Cardiovascular: Left ventricular function & pulse changes
A 68-year-old client with long-standing hypertension has a new
finding of a displaced apical impulse (shifted laterally) on
exam. Which physiological change best explains this finding?
A. Increased left ventricular end-systolic volume causing
concentric hypertrophy
B. Left ventricular dilation (eccentric hypertrophy) with
increased chamber size
C. Right ventricular hypertrophy causing mediastinal shift
D. Pericardial effusion lifting the apex anteriorly
Correct answer: B
Rationale
• B (correct): A laterally displaced apical impulse indicates
the heart’s apex has enlarged or shifted laterally — most
, commonly due to left ventricular dilation (eccentric
hypertrophy) that enlarges the chamber and moves the
point of maximal impulse (PMI) laterally. Hypertensive
heart disease over time can progress from concentric
hypertrophy to dilation if decompensation occurs.
• A (incorrect): Concentric hypertrophy thickens the
ventricular wall without markedly increasing chamber
radius; the PMI is usually not displaced laterally.
• C (incorrect): Right ventricular hypertrophy affects the
right side of the heart and can alter the precordial exam,
but it typically does not produce a laterally displaced apical
impulse.
• D (incorrect): Large pericardial effusion can obscure heart
sounds and produce muffled tones and a diffuse PMI, but
it usually does not cause a focal lateral displacement of the
apical impulse.
2 — Cardiovascular: Heart sounds & valve pathology
A 72-year-old complains of exertional dyspnea. On auscultation
you hear a low-pitched, rumbling diastolic murmur best heard
at the apex with an opening snap. Which structural
abnormality is most consistent with these findings?
A. Aortic stenosis causing turbulent systolic flow
B. Mitral stenosis due to thickened mitral leaflets and fused
commissures
,C. Tricuspid regurgitation with systolic flow back to the right
atrium
D. Ventricular septal defect creating a holosystolic murmur
Correct answer: B
Rationale
• B (correct): The classic murmur described (diastolic rumble
at the apex with an opening snap) is characteristic of
mitral stenosis, where leaflets are thickened and
commissures fused, producing obstructed flow from left
atrium to left ventricle during diastole and an opening
snap when the valve abruptly tenses. This increases left
atrial pressure and causes pulmonary congestion →
exertional dyspnea.
• A (incorrect): Aortic stenosis produces a systolic ejection
murmur best heard at the right upper sternal border (not a
diastolic rumble at the apex).
• C (incorrect): Tricuspid regurgitation is a systolic murmur
best heard along the left lower sternal border; it relates to
the right heart, not the apex diastolic sound described.
• D (incorrect): VSDs cause holosystolic murmurs and are
systolic in timing, not a diastolic rumble with an opening
snap.
3 — Cardiovascular: Preload, afterload & pulmonary edema
, A patient with acute left ventricular failure develops orthopnea
and bibasilar crackles. Which change in hemodynamics most
directly produces pulmonary edema in left heart failure?
A. Decreased pulmonary capillary hydrostatic pressure
B. Increased pulmonary capillary hydrostatic pressure from
elevated left atrial pressure
C. Increased plasma oncotic pressure pulling fluid into
capillaries
D. Decreased pulmonary capillary permeability
Correct answer: B
Rationale
• B (correct): In LV failure, the left ventricle cannot eject
forward flow, causing elevated LV end-diastolic pressure
and increased left atrial pressure. This transmits back to
pulmonary veins and raises pulmonary capillary hydrostatic
pressure, forcing fluid out into interstitium and alveoli →
pulmonary edema, crackles, orthopnea.
• A (incorrect): Decreased hydrostatic pressure would
reduce filtration, not cause edema.
• C (incorrect): Increased plasma oncotic pressure would
retain fluid in capillaries and oppose edema formation.
• D (incorrect): Pulmonary edema in LV failure is primarily
hydrostatic; capillary permeability is usually not decreased
(in fact, inflammation could increase permeability), so
decreased permeability would not cause edema.