Measurement of Cardiac Output
In experimental settings, cardiac output can
be measured by electromagnetic or Dop-
pler flowmeters placed around the pulmo-
nary artery. Obviously, this approach cannot
be used in humans; therefore, indirect tech-
niques are used. The most commonly used is
the thermodilution technique, which uses a
special multilumen, thermistor-tipped cath-
eter (Swan-Ganz) that is inserted into the pul-
monary artery from a peripheral vein. A cold
saline solution of known temperature and
volume is injected into the right atrium from a
proximal port on the catheter. The cold injec-
tate mixes into the blood and cools the blood,
which then passes through the right ventricle
and into the pulmonary artery. The thermistor
at the catheter tip measures the blood temper-
ature, and a cardiac output computer is used
to calculate flow (cardiac output). Doppler
echocardiography can be used to estimate
real-time changes in flow within the heart,
pulmonary artery, or ascending aorta. Echo-
cardiography and various radionuclide tech-
niques can also be used to measure changes
in ventricular dimensions during the cardiac
cycle in order to calculate SV, which, when
multiplied by heart rate, gives cardiac out-
put. Although used less frequently, the Fick
method permits time-averaged cardiac output
(CO; mL/min) calculations from measure-
ments of arterial and venous blood oxygen
content (CaO2 and CvO2, respectively; mL O2/
mL blood), and whole body oxygen consump-
tion (VO2; mL O2/min). This method is based
on the following relationship (Fick Principle):
CO =
V O2
(CaO2 - CvO2)
Influence of Heart Rate and
Stroke Volume on Cardiac Output
Although cardiac output is determined by
both heart rate and SV, changes in heart rate
are generally more important quantitatively
in producing changes in cardiac output. For
example, heart rate may increase by 100%
to 200% during exercise, whereas SV may
increase by <50%. These changes in heart rate
are brought about primarily by changes in
sympathetic and parasympathetic nerve activ-
ity at the SA node (see Chapter 2).
A change in heart rate does not necessar-
ily result in a proportionate change in cardiac
output. The reason is that changes in heart
rate can inversely affect SV. For example, dou-
bling heart rate from 70 to 140 beats/min by
pacemaker stimulation alone does not double
cardiac output because SV falls when heart
rate is elevated. This occurs because the ven-
tricular filling time decreases as the length of
diastole shortens, thereby resulting in less ven-
tricular filling. However, when normal physi-
ological mechanisms during exercise cause the
heart rate to double, cardiac output more than
doubles because SV actually increases. This
increase in SV, despite the elevation in heart
rate, is brought about by several mechanisms
acting on the heart and systemic circulation
(see Chapter 9). When these mechanisms fail,
SV cannot be maintained at elevated heart rates.
Therefore, it is important to understand the
mechanisms that regulate SV because impaired
SV regulation can lead to a state of heart failure
and limited exercise capacity (see Chapter 9).
is the initial stretching of the cardiac
myocytes prior to contraction; therefore, it is
related to the sarcomere length at the end of dias-
. Sarcomere length cannot be determined in
the intact heart, so indirect indices of preload,
such as ventricular EDV or pressure, must be
used. These measures of preload are not ideal
because they may not always reflect sarcomere
length because of changes in the structure and
mechanical properties of the heart. Despite these
acute changes
in end-diastolic pres-
sure and volume are useful indices for examin-
ing the effects of acute preload changes on SV.
Effects of Ventricular Compliance
on Preload
As the ventricle fills with blood, the pressure
generated at a given volume is determined
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