Ganong's Review of Medical Physiology, 23rd Edition

CHAPTER 31The Heart as a Pump 519

result in both normal and transplanted hearts is thus a prompt
and marked increase in cardiac output.
One of the differences between untrained individuals and
trained athletes is that the athletes have lower heart rates,
greater end-systolic ventricular volumes, and greater stroke
volumes at rest. Therefore, they can potentially achieve a
given increase in cardiac output by further increases in stroke
volume without increasing their heart rate to as great a degree
as an untrained individual.

OXYGEN CONSUMPTION BY THE HEART

The basal O 2 consumption by the myocardium is about 2 mL/
100 g/min. This value is considerably higher than that of rest-
ing skeletal muscle. O 2 consumption by the beating heart is
about 9 mL/100 g/min at rest. Increases occur during exercise
and in a number of different states. Cardiac venous O 2 tension
is low, and little additional O 2 can be extracted from the blood

in the coronaries, so increases in O 2 consumption require in-

creases in coronary blood flow. The regulation of coronary

flow is discussed in Chapter 34.

O 2 consumption by the heart is determined primarily by

the intramyocardial tension, the contractile state of the myo-

cardium, and the heart rate. Ventricular work per beat corre-

lates with O 2 consumption. The work is the product of stroke

volume and mean arterial pressure in the pulmonary artery or

the aorta (for the right and left ventricle, respectively).

Because aortic pressure is 7 times greater than pulmonary

artery pressure, the stroke work of the left ventricle is approx-

imately 7 times the stroke work of the right. In theory, a 25%

increase in stroke volume without a change in arterial pres-

sure should produce the same increase in O 2 consumption as

a 25% increase in arterial pressure without a change in stroke

volume. However, for reasons that are incompletely under-

stood, pressure work produces a greater increase in O 2 con-

sumption than volume work. In other words, an increase in

afterload causes a greater increase in cardiac O 2 consumption

than does an increase in preload. This is why angina pectoris

due to deficient delivery of O 2 to the myocardium is more

common in aortic stenosis than in aortic insufficiency. In aor-

tic stenosis, intraventricular pressure must be increased to

force blood through the stenotic valve, whereas in aortic

insufficiency, regurgitation of blood produces an increase in

stroke volume with little change in aortic impedance.

It is worth noting that the increase in O 2 consumption pro-

duced by increased stroke volume when the myocardial fibers

are stretched is an example of the operation of the law of

Laplace. This law, which is discussed in detail in Chapter 32,

states that the tension developed in the wall of a hollow viscus

is proportionate to the radius of the viscus, and the radius of a

dilated heart is increased. O 2 consumption per unit time

increases when the heart rate is increased by sympathetic

stimulation because of the increased number of beats and the

increased velocity and strength of each contraction. However,

this is somewhat offset by the decrease in end-systolic volume

and hence in the radius of the heart.

TABLE 31–4 Changes in cardiac function with exercise. Note that stroke volume levels off, then
falls somewhat (as a result of the shortening of diastole) when the heart rate rises to high values.

Work (kg-m/min) O 2 Usage (mL/min) Pulse Rate (per min) Cardiac Output (L/min) Stroke Volume (mL) A-V O 2 Difference (mL/dL)

Rest 267 64 6.4 100 4.3

288 910 104 13.1 126 7.0

540 1430 122 15.2 125 9.4

900 2143 161 17.8 110 12.3

1260 3007 173 20.9 120 14.5

Reproduced with permission from Asmussen E, Nielsen M: The cardiac output in rest and work determined by the acetylene and the dye injection methods. Acta Physiol Scand
1952;27:217.

FIGURE 31–9 Cardiac responses to moderate supine
exercise in normal humans and patients with transplanted and
hence denervated hearts. (Reproduced with permission from Kent KM,
Cooper T: The denervated heart. N Engl J Med 1974;291:1017.)

Normal Transplant

O 2

consumption

Cardiac

output

Heart

rate

Stroke

volume Exercise

Time

Exercise