90
CARDIOVASCULAR PHYSIOLOGY CONCEPTS
therefore, preload is increased at
reduced heart rates. Choices “a,” “b,”
and “d” are incorrect because decreased
atrial contractility, blood volume, and
ventricular compliance lead to reduced
ventricular filling and therefore reduced
preload.
4.
The correct answer is “a” because
increased preload resulting from
increased venous return when lying
down causes length-dependent acti-
vation of actin and myosin, which
increases active tension development.
This is the basis for the Frank-Starling
mechanism. Being in heart failure,
increased output of the right ventricle
may not lead to a corresponding
increase in left ventricular stroke, there-
by causing pulmonary congestion and
difficulty breathing. Choices “b,” “c,”
and “d” are incorrect because decreased
muscle shortening, preload, and veloc-
ity of shortening all lead to a decrease in
stroke volume.
5.
The correct answer is “d” because ven-
tricular hypertrophy reduces ventricular
compliance, which results in elevated
end-diastolic pressures when the ventri-
cle fills. Choice “a” is incorrect because
decreased afterload leads to a reduction
in end-systolic volume, which results
in a secondary fall in end-diastolic vol-
ume and pressure. Choice “b” is incor-
rect because decreased venous return
decreases ventricular filling, which
decreases ventricular end-diastolic vol-
ume and pressure. Choice “c” is incor-
rect because increased inotropy reduces
end-systolic volume, which results in a
secondary fall in end-diastolic volume
and pressure.
6.
The correct answer is “a” because with
an ejection fraction (EF) of 25% and
a stroke volume (SV) of 50 mL, this
patient’s end-diastolic volume (EDV)
is 200 mL, which is much greater than
normal (usually <150 mL). The calcula-
tion is based on: EF = (SV/EDV) x 100,
and therefore EDV = (SV/EF) x 100
when EF is expressed as a percentage.
Choices “b,” “c,” and “d” are incorrect
because this low EF (normally >55%)
indicates ventricular failure (loss of inot-
ropy), which leads to a reduced SV and
an elevated end-systolic volume. Preload
(end-diastolic volume) is increased (as
calculated above) because the elevated
end-systolic volume leads to a secondary
increase in preload, and because of other
compensatory mechanisms discussed in
Chapter 9.
7.
The correct answer is “b” because an
increased arterial pressure increases left
ventricular afterload, which decreases
the velocity of fiber shortening as
shown by the force-velocity relation-
ship. Choices “a,” “c,” and “d” are
incorrect because increased afterload
decreases the velocity of fiber shorten-
ing, which decreases stroke volume.
This leads to an increase in left ventricu-
lar end-systolic volume and a second-
ary increase in preload (end-diastolic
volume).
8.
The correct answer is “b” because an
increase in inotropy increases stroke
volume, which is represented by the
width of the pressure-volume loop.
Choice “a,” “c,” and “d” are incorrect
because increased inotropy causes a par-
allel, upward shift in the force-velocity
relationship, which leads to an increase
in velocity of fiber shortening and there-
fore an increase in stroke volume at any
given afterload. Increased stroke volume
decreases end-systolic volume and leads
to a secondary decrease in left ventricu-
lar end-diastolic volume (preload).
9.
The correct answer is “b” because an
increase in end-diastolic volume will
increase stroke volume; however, stroke
volume changes are about one-fourth as
effective in changing myocardial oxygen
consumption as are changes in heart
rate, mean arterial pressure, or ventricu-
lar radius because of the relationships
between oxygen consumption, wall
stress, ventricular pressure, and ventric-
ular radius. For this reason, choices “a,”
“c,” and “d” are incorrect.
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