Factors Influencing Myocardial
Oxygen Consumption
Part of the difficulty in finding a suitable index
of oxygen consumption is that several factors
including frequency of contraction, inotropic
state, afterload, and preload (Table 4-1). For
example, doubling heart rate approximately
doubles oxygen consumption, because myo-
cytes are generating twice the number of ten-
sion cycles per minute. Increasing inotropy
increases oxygen consumption because both
the rate of tension development and the mag-
nitude of tension are increased, and they both
are associated with increased ATP hydroly-
sis and oxygen consumption. An increase in
afterload likewise increases oxygen consump-
tion because it increases the tension that must
be developed by myocytes. Increasing SV
by increasing preload (EDV) also increases
oxygen consumption.
Quantitatively, increased preload has less
impact on oxygen consumption than does an
increase in afterload (e.g., aortic pressure). To
understand why, we need to examine the rela-
tionship between wall stress, pressure, and
radius of the ventricle. As discussed earlier
(see Equation 4-2), ventricular wall stress (a)
is proportional to the intraventricular pressure
(P) multiplied by the ventricular internal radius
(r) and divided by the wall thickness (h).
P ■
Wall stress is related to the tension an individ-
ual myocyte must develop during contraction
to generate a given ventricular pressure. At a
given radius and wall thickness, a myocyte
T Heart rate
T Inotropy
T A fterload
T Preload1
'Changes in preload affect oxygen consum ption much less
than do changes in the other factors.
must generate increased contractile force (i.e.,
wall stress) to develop a higher pressure. The
contractile force must be increased even fur-
ther to generate the same elevated pressure if
the ventricular radius is increased. For exam-
ple, if the ventricle is required to generate
50% more pressure than normal to eject blood
because of elevated aortic pressure, the wall
stress that individual myocytes must generate
will be increased by approximately 50%. This
will increase the oxygen consumption of these
myocytes by about 50% because changes in
oxygen consumption are closely related to
changes in wall stress. As a second example,
if the radius of the ventricle is increased by
50%, the wall stress needed by the myocytes
to eject blood at a normal pressure will be
increased by about 50%. On the other hand,
if the ventricular EDV is increased by 50%
and the pressure and wall thickness remain
unchanged, the wall stress will be increased
by only about 14%. The reason for this is
that a large change in ventricular volume (V)
requires only a small change in radius (r). If
we assume that the shape of the ventricle is a
sphere, then
V = 4 n r 3
By rearranging this relationship, we find that
r —
Substituting this into the wall stress equation
results in
Eq. 4-4
a - P ' ^
Although no single acceptable model for the
shape of the ventricle exists because its shape
changes during contraction, a sphere serves
as a convenient model for illustrating why
changes in volume have a relatively small
affect on wall stress and oxygen consump-
tion. Using this model, Equation 4-4 shows
that increasing the EDV by 50% (by a factor of
1.5) represents only a 14% (cube root of 1.5)
increase in wall stress at a given ventricular
pressure, whereas a 50% increase in pressure
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