586
UNIT FOUR
traction at a given preload, is influenced by autonomic
innervation and hormones (epinephrine, norepinephrine,
thyroid hormones). Sympathetic stimulation contracts the
ventricles more forcefully, increasing the volume ejected and
decreasing the ESV. Decreased sympathetic stimulation pro-
duces the opposite effect. The amount of force the ventricle
must produce to open the semilunar valves to eject blood
is the
afterload.
Increased arterial pressure (hypertension)
increases afterload. As the afterload increases, stroke volume
decreases and ESV increases.
Recall that baroreceptors in the walls of the aortic arch
and carotid sinuses sense changes in blood pressure. If arte-
rial pressure increases, nerve impulses travel from the recep-
tors to the
cardiac center
of the medulla oblongata. This
center relays parasympathetic impulses to the SA node in
the heart, and heart rate decreases in response. As a result
of this
cardioinhibitor refl
ex,
cardiac output falls, and blood
pressure decreases toward the normal level.
Figure 15.37
summarizes this mechanism.
Conversely, decreasing arterial blood pressure initiates
the
cardioaccelerator refl
ex,
in which sympathetic impulses
go to the SA node. The heart then beats faster. This response
increases cardiac output, increasing arterial pressure.
Recall that epinephrine increases heart rate (chapter 13,
p. 506) and consequently alters cardiac output and blood
pressure. Other factors that increase heart rate and blood
pressure include emotional responses, such as fear and
anger; physical exercise; and a rise in body temperature.
Changes in arteriole diameters regulate peripheral resis-
tance. Blood vessels with smaller diameters offer a greater
resistance to blood flow, so factors that cause arteriole
normal contraction, so increasing the force of ventricular
contraction may increase that fraction and help maintain
stroke volume if venous return should decrease.
RECONNECT
To Chapter 9, Recording a Muscle Contraction,
pages 296–297.
Another mechanism increases stroke volume indepen-
dently of sympathetic stimulation. As blood enters the ven-
tricles, myocardial F bers are mechanically stretched. This
constitutes the
preload.
The greater the EDV, the greater the
preload. Within limits, the longer these F
bers, the greater the
force with which they contract. This relationship between
fiber length (due to stretching of the cardiac muscle cell
just before contraction) and force of contraction is called
the
Frank-Starling law of the heart,
or Starling’s law of the
heart. This becomes important, for example, during exercise,
when venous return increases. The more blood that enters
the heart from the veins, the greater the ventricular disten-
sion, the stronger the contraction, the greater the stroke vol-
ume, and the greater the cardiac output.
Conversely, the less blood that returns from the veins, the
less the ventricle distends, the weaker the ventricular contrac-
tion, and the lesser the stroke volume and cardiac output. This
mechanism ensures that the volume of blood discharged from
the heart is equal to the volume entering its chambers.
Some blood remains in the ventricles after contrac-
tion and stroke volume ejection. This ESV is influenced
by preload, contractility of the ventricle, and afterload.
Contractility,
the amount of force produced during a con-
Decreased cardiac output
Increased cardiac output
Increased blood pressure
Decreased blood pressure
Blood pressure maintained
Decreased heart rate
Decreased stroke volume
Increased heart rate
Increased stroke volume
Decreased peripheral resistance
Increased peripheral resistance
FIGURE 15.36
Controlling cardiac output and peripheral resistance regulates blood pressure.
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