Regulation of cardiac output • Figure 11.8
Several factors influence cardiac output by changing stroke volume and/or heart rate.
a.
Autonomic nervous system activity changes
heart rate
and stroke volume
During exercise or emotional stress,
cardiac output rises to supply working
tissues with increased amounts
of oxygen and nutrients.
Baroreceptors sense changes in
blood pressure and send signals
to
the
brain.
Baroreceptors •— ' V
in carotid sinus
Baroreceptors
in arch of aorta
SA node
AV node
Cardiac accelerator
nerves increase
heart rate.
Cardiac accelerator nerves in the sympathetic nervous
system stimulate the SA and AV nodes of the heart to
increase heart rate. In addition, these nerves increase
the contractility of the atria and ventricles, which
increases stroke volume.
Vagus nerve activity slows
heart rate.
Parasympa-
thetic nerves, primarily the vagus nerves, decrease the
stimulation of the nodes when the demand for cardiac
output decreases.
Cardiac
output
(CO)
Stroke Volume
(SV)
Heart Rate (HR)
Measured in L/min
Measured in mL/beat
X
Measured in beats/min
b. Three factors regulate stroke volume under
normal
conditions:
Degree of stretch in
heart
before
contraction (preload)
• Increased blood flow into the heart
increases the force of contraction
(Frank-Starling Law of the heart)
and increases SV
Force of contraction
• Increased force of contraction
increases SV
• Increased Ca2+ increases contractility
• Hormones (epinephrine and
norepinephrine) increase contractility
Pressure required to eject blood
from ventricles (afterload):
• Increased aortic and/or pulmo-
nary artery pressures reduce the
time that semilunar valves are
open, reducing SV
Decreased blood flow has the
opposite effect
Many Factors Affect Cardiac Output
The work done by the heart, called the cardiac output
(CO), is defined as the volume of blood ejected from the
ventricle per minute. The same amount of blood is ejected
from the right and left ventricles. Cardiac output is the
product of stroke volume (SV; the amount of blood eject-
ed during each beat) and the heart rate (HR; number
of beats per minute). For example, in a resting adult, the
stroke volume is typically 70 mL per beat and the heart
rate is 72 beats/min. So, the cardiac output is as follows:
CO = SV x HR
= 70 mL/beat x 72 beats/min
= 5040 mL/min,
or slightly over 5 L/min. You may recall that this is the
typical blood volume for an individual.
Decreased force of contraction
• Decreased pressures have the
decreases SV
opposite effect
Increased Na+ and K+ decrease
contractility
Decreased temperature decreases
contractility
Cardiac output is affected by factors that influence
stroke volume and/or heart rate (
). Stroke
volume can be influenced by the amount of blood present
in the ventricle at the end of diastole
(preload
), the force
of contraction
(co n tra ctility ),
or the vascular pressures that
the ventricles must overcome to push the blood out of
the chamber
(afterload).
The force of contraction is influ-
enced by how much the heart has been stretched before
it contracts. The more blood that enters the heart dur-
ing diastole, the stronger the subsequent contraction will
be; this principle is called the Frank-Starling Law of the
heart. While the heart rate is set by an intrinsic pacemak-
er called the sinoatrial node, which initiates regular waves
of depolarization across the atria, it can also be influenced
by other factors:
318 CHAPTER 11
The Cardiovascular System: Heart, Blood Vessels, and Circulation
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