CHAPTER 4 ■
CARDIAC FUNCTION
91
PROBLEM 4-1
Stroke volume equals cardiac output divided
by heart rate. Because stroke volume uses
milliliters (mL) for units, cardiac output (8.8
U
min) must be expressed in mL/min (8800 mL/
min). This value, divided by a heart rate of
110 beats/min, gives a stroke volume of 80 mL/
beat.
PROBLEM 4-2
Because the right ventricular stroke volume
is 0.1% greater than the left ventricular stroke
volume of 60 mL/beat, the right ventricular
stroke volume can be calculated by multiply-
ing 60 times 1.001, which gives a stroke vol-
ume of 60.06 mL/beat. The difference in stroke
volume between the two ventricles therefore
is 0.06 mL/beat. To obtain the difference in
total stroke volume over 1 hour when the rate
is 75 beats/min, multiply the rate (75 beats/
min) x 60 min/h x stroke volume difference
(0.06 mL/beat). This calculation yields a value
of 270 mL, which represents the increase in
pulmonary blood volume that occurs after only
1 hour because of a small imbalance between
the outputs of the right and left ventricles.
PROBLEM 4-3
Myocardial oxygen consumption can be cal-
culated from Equation 4-3, such that
MV02 = CBF (CaOz - CvOz)
The control oxygen consumption is 50 mL/
min times the arterial-venous oxygen differ-
ence of 0.1 mL 0 2/mL blood, which equals
5 mL 0 2/min. Note that the arterial-venous
oxygen difference must be converted from mL
Oj/100 mL blood to mL Oz/mL blood. The
experimental oxygen consumption is 150 mL/
min times 0.14 mL 0 2/mL blood, which
equals 21 mL 0 2/min. This is a 320% increase
in oxygen consumption ([(21—5)/5] x 100).
CASE 4-1
A hypertrophied ventricle is less compli-
ant. This causes the end-diastolic pressure-
volume curve to shift up and to the left, as
shown in figure below. This shift reduces the
end-diastolic volume and increases the end-
diastolic pressure at the end of ventricular fill-
ing. The end-systolic volume will be normal
unless there is a significant change in inotropy
or aortic diastolic pressure (afterload). The
width of the pressure-volume loop is nar-
rower; therefore, the stroke volume is reduced.
200
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100
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0.
>
0
0
100
200
LV Volume (ml)
CASE 4-2
A systemic vasodilator reduces afterload on the
left ventricle. This causes the Starling curve
to shift up and to the left from its depressed
state (because of the loss of inotropy in fail-
ure) (Figure A in the next page). This shift
increases stroke volume and at the same time
point A to B. Systemic vasodilation reduces
aortic diastolic pressure, which enables the
ventricle to eject sooner, more rapidly, and
to a smaller end-systolic volume (Figure B in
the next page). The reduced end-systolic vol-
ume leads to a compensatory decrease in end-
diastolic volume; however, the reduction in
end-systolic volume is greater than the reduc-
tion in end-diastolic volume so that stroke
volume is increased. By increasing stroke vol-
ume and reducing the end-diastolic volume,
the ejection fraction (EF) is increased because
it is calculated as stroke volume (SV) divided
by end-diastolic volume (EDV) as follows:
EF = SV/EDV