Human Physiology, 14th edition (2016)

452 Chapter 14

Each action potential is accompanied by contraction of the
myocardium.
Both sympathetic and parasympathetic innervations to the
heart are active to a greater or lesser degree. Norepinephrine from
sympathetic axons and epinephrine from the adrenal medulla
bind to b 1 -adrenergic receptors in the heart to stimulate the pro-
duction of cyclic AMP (chapter 7; see fig. 7.31). Cyclic AMP
acts on the HCN and Ca^21 channels of the pacemaker cells that
produce the pacemaker potential to increase the rate of diastolic
depolarization. This stimulates a faster production of action
potentials and thus a faster cardiac rate ( fig. 14.1 ).
Acetylcholine, released by vagus nerve endings, binds to
muscarinic ACh receptors and causes the opening of separate
K^1 channels in the membrane (see chapter 7, fig. 7.27; also
see chapter 9, fig. 9.11). The outward diffusion of K^1 par-
tially counters the depolarizing mechanisms that produce the
pacemaker potential. This results in a slower rate of diastolic
depolarization and action potential production, and thus in a
slower cardiac rate. The vagus nerve is tonically active to some
degree, and the ACh effects generally keep the resting cardiac
rate slower that the 90–100 beats per minute that it would be in
the absence of this inhibition ( fig. 14.1 ).
The actual pace set by the SA node at any time depends on the
net effect of these antagonistic influences (see fig. 14.5 ). Mecha-
nisms that affect the cardiac rate are said to have a chronotropic
effect ( chrono 5 time). Those that increase cardiac rate have a
positive chronotropic effect; those that decrease the rate have a
negative chronotropic effect.
Autonomic innervation of the SA node is the major means
by which cardiac rate is regulated. However, other autonomic
control mechanisms also affect cardiac rate to a lesser degree.
Sympathetic endings in the musculature of the atria and ventricles
increase the strength of contraction and cause a slight decrease in
the time spent in systole when the cardiac rate is high ( table 14.1 ).
The resting bradycardia (slow heart rate) of endurance-
trained athletes is largely due to high vagus nerve activity. During
exercise, the cardiac rate increases as a result of decreased vagus
nerve inhibition of the SA node. Further increases in cardiac rate
are achieved by increased sympathetic nerve stimulation.

The activity of the autonomic innervation of the heart

is coordinated by the cardiac control center in the medulla

oblongata of the brain stem. The cardiac control center, in turn,

is affected by higher brain areas and by sensory feedback from

pressure receptors, or baroreceptors, in the aorta and carotid

arteries. In this way, a fall in blood pressure can produce a

reflex increase in the heart rate (chapter 1; see fig. 1.6). This

baroreceptor reflex is discussed in more detail in relation to

blood pressure regulation in section 14.6.

Regulation of Stroke Volume

The stroke volume is regulated by three variables:

1. the end-diastolic volume (EDV), which is the volume of

blood in the ventricles at the end of diastole;

2. the total peripheral resistance, which is the frictional

resistance, or impedance to blood flow, in the arteries; and

3. the contractility, or strength, of ventricular contraction.

The end-diastolic volume is the amount of blood in the ven-

tricles immediately before they begin to contract. This is a work-

load imposed on the ventricles prior to contraction, and thus

is sometimes called a preload. The stroke volume is directly

proportional to the preload; an increase in EDV results in an

increase in stroke volume. (This relationship is known as the

Frank-Starling law of the heart, discussed shortly.) The stroke

volume is also directly proportional to contractility; when the

ventricles contract more forcefully, they pump more blood.

In order to eject blood, the pressure generated in a ven-

tricle when it contracts must be greater than the pressure in

the arteries (because blood flows only from higher pressure to

lower pressure). The pressure in the arterial system before the

ventricle contracts is, in turn, a function of the total peripheral

resistance—the higher the peripheral resistance, the higher the

pressure. As blood begins to be ejected from the ventricle, the

added volume of blood in the arteries causes a rise in mean arte-

rial pressure against the “bottleneck” presented by the peripheral

resistance. Ejection of blood stops shortly after the aortic pres-

sure becomes equal to the intraventricular pressure. The total

peripheral resistance thus presents an impedance to the ejection

of blood from the ventricle, or an afterload imposed on the ven-

tricle after contraction has begun. This can be medically signifi-

cant; a person with a high total peripheral resistance has a high

arterial blood pressure, and thus a high afterload imposed on the

ventricular muscle.

In summary, the stroke volume is inversely proportional

to the total peripheral resistance; the greater the peripheral

resistance, the lower the stroke volume. It should be noted

that this lowering of stroke volume in response to a raised

peripheral resistance occurs for only a few beats. Thereaf-

ter, a healthy heart is able to compensate for the increased

peripheral resistance by beating more strongly. This com-

pensation occurs by means of a mechanism described in the

next section (Frank-Starling law of the heart). An inabil-

ity of the heart to compensate can lead to congestive heart

failure.

Table 14.1 | Effects of Autonomic Nerve
Activity on the Heart

Region

Affected

Sympathetic Nerve

Effects

Parasympathetic

Nerve Effects

SA node Increased rate of diastolic

depolarization;

increased cardiac rate

Decreased rate of

diastolic depolarization;

decreased cardiac rate

AV node Increased conduction

rate

Decreased conduction

rate

Atrial muscle Increased strength

of contraction

No significant effect

Ventricular

muscle

Increased strength

of contraction

No significant effect