Examination
9th Edition
• Author(s)Linda Anne Silvestri; Angela Silvestri
ANATOMY AND PHYSIOLOGY TEST BANK
1 — Cardiovascular (hemodynamics)
A 68-year-old male has progressive jugular venous distention,
hepatomegaly, and peripheral edema. Which physiologic
alteration best explains these findings?
A. Left ventricular systolic failure causing increased pulmonary
venous pressure
B. Right ventricular failure causing increased systemic venous
pressure
C. Decreased plasma oncotic pressure from hypoalbuminemia
D. Increased capillary hydrostatic pressure from arteriolar
vasodilation
Answer: B
Rationale (correct — B): Right ventricular failure reduces
forward flow into the pulmonary circulation, causing blood to
back up into the systemic venous system. Increased systemic
venous pressure produces jugular venous distention,
,hepatomegaly (congested liver), and peripheral (dependent)
edema.
Rationale (incorrect):
A. Left ventricular failure primarily causes pulmonary
congestion (dyspnea, crackles, pulmonary edema), not systemic
venous congestion.
C. Hypoalbuminemia causes generalized edema from decreased
oncotic pressure but would not cause JVD or hepatomegaly as a
primary finding.
D. Arteriolar vasodilation lowers arteriolar resistance and can
increase capillary hydrostatic pressure locally but does not
explain the constellation of JVD, hepatomegaly, and systemic
venous congestion.
2 — Cardiovascular (valve anatomy/function)
A patient has acute severe aortic regurgitation. Which
physiologic change produces the classic “water-hammer”
(bounding) pulse?
A. Increased end-diastolic volume and widened pulse pressure
B. Decreased stroke volume due to low preload
C. Increased systemic vascular resistance reducing pulse
pressure
D. Bradycardia causing greater systolic ejection force
Answer: A
,Rationale (correct — A): Aortic regurgitation allows blood to
flow back into the left ventricle during diastole, increasing end-
diastolic volume. The left ventricle accommodates by increasing
stroke volume during the next systole, producing a high systolic
pressure while diastolic pressure falls (regurgitant flow), leading
to a widened pulse pressure and bounding pulses.
Rationale (incorrect):
B. Stroke volume is usually increased (initially) rather than
decreased in acute regurgitation; low preload would not
produce bounding pulses.
C. Increased systemic vascular resistance tends to raise diastolic
pressure and narrow pulse pressure, opposite of the observed
finding.
D. Bradycardia may accentuate pulse pressure by increasing
diastolic filling time, but it is not the primary mechanism for a
water-hammer pulse in aortic regurgitation.
3 — Cardiovascular (coronary perfusion)
An older adult experiences ischemic chest pain when systolic
blood pressure is low (hypotension). Why does hypotension
worsen myocardial ischemia?
A. Coronary perfusion occurs primarily during systole and is
increased by low afterload
B. Coronary perfusion is pressure-dependent and mainly occurs
during diastole; low diastolic pressure reduces coronary flow
C. Hypotension directly increases myocardial oxygen demand
, through reflex tachycardia only
D. Myocardial perfusion relies entirely on venous pressure, so
arterial hypotension has no effect
Answer: B
Rationale (correct — B): Coronary blood flow occurs
predominantly during diastole because systolic myocardial
contraction compresses intramural coronary vessels. Coronary
perfusion pressure is roughly aortic diastolic pressure minus left
ventricular end-diastolic pressure; hypotension (low diastolic
pressure) reduces coronary perfusion leading to ischemia.
Rationale (incorrect):
A. Coronary perfusion is not primarily during systole; systole
impedes subendocardial flow.
C. Hypotension may increase demand (reflex tachycardia), but
the key mechanism for ischemia in hypotension is reduced
coronary perfusion pressure.
D. Coronary perfusion depends on arterial pressure; venous
pressure alone does not maintain myocardial perfusion.
4 — Cardiovascular (electrolytes & conduction)
A client with a serum potassium of 6.8 mEq/L complains of
lightheadedness and has peaked T waves on ECG. Which
physiologic effect of hyperkalemia explains slowed impulse
conduction and risk of cardiac arrest?
A. Increased resting membrane potential (less negative) leading