Various intrinsic, neural, and
hormonal factors act to influence
the rhythm control and impulse
conduction within the heart. The
rhythmic control of the cardiac
cycle and its accompanying
heartbeat relies on the regulation
of impulses generated and
conducted within the heart.
Regulation of the cardiac cycle is
also achieved via the autonomic
nervous system. The sympathetic
and parasympathetic divisions of
the autonomic system regulate
heart rhythm by affecting the
same intrinsic impulse
conducting mechanisms that lie
within the heart in opposing
ways.
Cardiac muscle is self-contractile
because it is capable of
generating a spontaneous
electrochemical signal as it
contracts. This signal induces
surrounding cardiac muscle
tissue to contract and a wave-
like contraction of the heart can
result from the initial contraction
of a few localized cardiac cells.
The cardiac cycle describes the
normal rhythmic series of cardiac
muscular contractions. The
cardiac cycle can be subdivided
into the systolic and diastolic
phases. Systole occurs when the
ventricles of the heart contract
and diastole occurs between
ventricular contractions when
the right and left ventricles relax
and fill. The sinoatrial node (S-A
node) and atrioventricular node
(AV node) of the heart act as
pacemakers of the cardiac cycle.
The contractile systolic phase
begins with a localized
contraction of specialized cardiac
muscle fibers within the sino-
atrial node. The S-A node is
composed of nodal tissue that
contains a mixture of muscle and
neural cell properties. The
contraction of these fibers
generates an electrical signal that
then propagates throughout the
surrounding cardiac muscle
tissue. In a contractile wave
originating at the S-A node, the
right atrium muscle contracts
(forcing blood into the right
ventricle) and then the left atrium
contracts (forcing blood into the
left ventricle).
Intrinsic regulation is achieved
by delaying the contractile signal
at the atrioventricular node. This
delay also allows the complete
contraction of the atria so that
the ventricles receive the
minimum amount of blood to
make their own contractions
efficient. A specialized type of
neuro-muscular cells, named
Purkinje cells, form a system of
fibers that covers the heart and
which conveys the contractile
signal from S-A node (which is
also a part of the Purkinje system
or subendocardial plexus).
Because the Purkinje fibers are
slower in passing electrical
signals (action potentials) than
are neural fibers, the delay allows
the atria to finish their
contractions prior to ventricular
contractions. The signal delay by
the AV node lasts about a tenth
(0.1) of a second.
The contractile signal then
continues to spread across the
ventricles via the Purkinje system.
The signal travels away from the
AV node via the bundle of His
before it divides into left and
right bundle branches that travel
down their respective ventricles.
Extrinsic control of the heart rate
and rhythm is achieved via
autonomic nervous system (ANS)
impulses (regulated by the
medulla oblongata) and specific
hormones that alter the
contractile and or conductive
properties of heart muscle. ANS
sympathetic stimulation via the
cervical sympathetic chain
ganglia acts to increase heart
rate and increase the force of
atrial and ventricular
contractions. In contrast,
parasympathetic stimulation via
the vagal nerve slows the heart
rate and decreases the vigor of
atrial and ventricular
contractions. Sympathetic
stimulation also increases the
conduction velocity of cardiac
muscle fibers. Parasympathetic
stimulation decreases
conduction velocity.
The regulation in impulse
conduction results from the fact
that parasympathetic fibers
utilize acetylcholine, a
neurotransmitter hormone that
alters the transmission of an
action potential by altering
membrane permeability to
specific ions (e.g., potassium ions
[K+]). In contrast, sympathetic
postganglionic neurons secrete
the neurotransmitter
norepinephrine that alters
membrane permeability to
sodium (Na+) and calcium ions
(Ca2+).
The ion permeability changes
result in parasympathetic
induced hypopolarization and
sympathetic induced
hyperpolarization.
Additional hormonal control is
achieved principally by the
adrenal glands (specifically the
adrenal medulla) that release
both epinephrine and
norepinephrine into the blood
when stimulated by the
sympathetic nervous system. As
part of the fight or flight reflex,
these hormones increase heart
rate and the volume of blood
ejected during the cardiac cycle.
The electrical events associated
with the cardiac cycle are
measured with an
electrocardiogram (EKG).
Disruptions in the impulse
conduction system of the heart
result in arrhythmias.
Variations in the electrical system
can lead to serious, even
dangerous, consequences. When
that occurs an artificial electrical
stimulator, called a pacemaker,
must be implanted to take over
regulation of the heartbeat. The
small pacemaker can be
implanted under the skin near
the shoulder and long wires
from it are fed into the heart and
implanted in the heart muscle.
The pacemaker can be regulated
for the number of heartbeats it
will stimulate per minute. Newer
pacemakers can detect the need
for increased heart rate when
the individual is under exertion
or stress and will respond.