that affects either the generation of force by
myocytes or their frequency of contraction
will alter oxygen consumption. In addition,
even in noncontracting cells, ATP utilized
by ion pumps and other transport functions
requires oxygen for the resynthesis of ATP.
How Myocardial Oxygen
Consumption is Determined
Oxygen consumption is defined as the vol-
ume of oxygen consumed per min (e.g., mL
O/min) and is sometimes expressed per 100
g of tissue weight (mL O/min per 100 g).
The myocardial oxygen consumption (MV02)
can be calculated by knowing the coronary
blood flow (CBF) and the arterial and venous
oxygen contents (Ca02 and Cv02) according
to the following equation that uses the Fick
Eq. 4-3
MV02 = CBF • (Ca02 - Cv02)
Myocardial oxygen consumption, therefore, is
equal to the CBF multiplied by the amount
of oxygen extracted from the blood (the arte-
rial-venous oxygen difference). The content
of oxygen in blood is usually expressed as mL
0/100 mL blood (or, vol % 0 2). The oxygen
content of arterial blood is normally about
20 mL 0/100 mL blood. To calculate the
myocardial oxygen consumption in the cor-
rect units, mL 0/100 mL blood is converted
to mL O/mL blood; with this conversion, the
arterial oxygen content is 0.2 mL O/mL blood.
For example, if CBF is 80 mL/min per 100 g,
the Ca02 is 0.2 mL O/mL blood and Cv02 is
0.1 mL O/mL blood, then MV02 = 8 mL O /
min per 100 g. This value of myocardial oxy-
gen consumption is typical for what is found
in a heart contracting at resting heart rates
against normal aortic pressures. During heavy
exercise, myocardial oxygen consumption can
increase to 70 mL O/min per 100 g, or more.
If contractions are arrested (e.g., by depolari-
zation of the heart with a high concentration
of potassium chloride), the myocardial oxy-
gen consumption decreases to about 2 mL
O/min per 100 g. This value represents the
energy costs of cellular functions not associ-
ated with contraction. Therefore, myocardial
depending on the state of mechanical activity.
Although myocardial oxygen consump-
tion can be calculated as described above,
generally it is not feasible to measure CBF and
coronary venous oxygen content except in
experimental studies. CBF can be measured
by placing flow probes on coronary arteries
or a thermodilution catheter within the coro-
nary sinus. Arterial oxygen content can be
taken from a peripheral artery, but the venous
oxygen content has to be obtained from the
coronary sinus by inserting a catheter into
the right atrium and then into the coronary
Indirect indices
of myocardial
consumption have been developed to esti-
mate myocardial oxygen consumption when
it is not feasible to measure it. Although no
index has proven to be satisfactory over a
wide range of physiologic conditions, one
simple index sometimes used in clinical stud-
ies is the pressure-rate product (also called
the double product). This index can be meas-
ured noninvasively by multiplying heart rate
and systolic arterial pressure (mean arterial
pressure sometimes is used instead of systolic
arterial pressure). The pressure-rate product
assumes that the pressure generated by the
ventricle is not significantly different than the
aortic pressure (i.e., there is no aortic valve
stenosis). Experiments have shown that a rea-
sonable correlation exists between changes
in the pressure-rate product and myocardial
oxygen consumption. For example, if arterial
pressure, heart rate, or both become elevated,
oxygen consumption will increase.
In an experimental study, administration
of an inotropic drug is found to increase
CBF from 50 to 150 mL/min and
increase the arterial-venous oxygen
difference (Ca02 - Cv02) from 10 to
14 mL O^IOO mL blood. Calculate the
percent increase in myocardial oxygen
consumption (MV02) caused by infusion
of this drug.
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