AHMAD, MISTLEY JANE A.

CHAPTER 9: Cardiac Muscle; The Heart as a Pump and Function

of the Heart Valves

HEART:
i IS TWO SEPARATE PUMPS:
s pumps blood through the lungs
a pumps blood through the systemic
h circulation that provides blood flow to the other
i organs and tissues of the body.
g IS COMPOSED OF:
is a weak primer pump for the ventricle,
h
helping to move blood into the ventricle. Figure 9-2 shows the histology of cardiac muscle, dem-
l then supply the main pumping force
onstrating cardiac muscle fibers arranged in a
y that propels the blood either latticework, with the fibers dividing, recombining, and
m through the pulmonary circulation by the right
then spreading again.
o ventricle or CARDIAC MUSCLE:
through the systemic circulation by the left
b is in the same manner as in skeletal muscle
ventricle has typical myofibrils that contain and
i
CARDIAC RHYTHMICITY:
l almost identical to those found in
Continuing succession of heart contractions caused
skeletal muscle
e by special mechanism of the heart.
these filaments lie side by side and slide
r
during contraction in the same manner as
e occurs in skeletal
g
i CARDIAC MUSCLE IS A SYNCYTIUM
o
n The dark areas crossing the cardiac muscle
fibers.
they are cell membranes that separate
individual cardiac muscle cells from one
another
That is, cardiac muscle fibers are made up of many
individual cells connected in series and in parallel
with one another.
At each intercalated disc the cell membranes fuse
with one another to form permeable
communicating junctions (gap junctions) that
PHYSIOLOGY OF CARDIAC MUSCLE
i 3 MAJOR TYPES OF CARDIAC MUSCLE: allow rapid diffusion of ions.
s Therefore, from a functional point of view, ions
move with ease in the intracellular fluid along the
a
longitudinal axes of the cardiac muscle fibers so
h The atrial and ventricular types of muscle
that action potentials travel easily from one
i contract in much the same way as skeletal
cardiac muscle cell to the next, past the
g muscle, except that the duration of con-
intercalated discs.
traction is much longer.
h
l CARDIAC MUSCLE:
y is a of many heart muscle cells in which
contract only feebly because they contain few
the cardiac cells are so interconnected that when
m contractile fibrils; instead, they exhibit either
one cell becomes excited, the action potential
o automatic rhythmical electrical discharge in
rapidly spreads to all of them.
b the form of action potentials or conduction of
the action potentials through the heart,
i atrial syncytium: which constitutes the walls of
providing an excitatory system that controls
l the two atria, and the
the rhythmical beating of the heart.
e ventricular syncytium: which constitutes the
walls of the two ventricles.
rPHYSIOLOGIC ANATOMY OF CARDIAC MUSCLE
This division of the muscle of the heart into
ei
two functional syncytiums allows the atria to
gs
ia
PHYSIOLOGY |CHAPTER 9: CARDIAC MUSCLE
oh
ni
 AHMAD, MISTLEY JANE A. 2

contract a short time ahead of ventricular potential is over within another thousandth of a
contraction, which is important for second or so.
effectiveness of heart pumping. THE ACTION POTENTIAL IS CAUSED BY
The atria are separated from the ventricles by fibrous OPENING OF TWO TYPES OF CHANNELS:
tissue that surrounds the atrioventricular (A-V) the same voltage-activated fast sodium
valvular openings between the atria and ventricles. channels as those in skeletal muscle and
Normally, potentials are not conducted from the atrial another entirely different population of L-
syncytium into the ventricular syncytium directly type calcium channels (slow calcium channels),
through this fibrous tissue. which are also called calcium-sodium channels.
Instead, they are conducted only by way of a - This second population of channels differs from
specialized conductive system called the A-V the fast sodium channels in that they:
bundle, a bundle of conductive fibers several are slower to open and, even more
millimeters in diameter. important, remain open for several tenths
of a second.
ACTION POTENTIALS IN CARDIAC MUSCLE - During this time, a large quantity of both calcium
i and sodium ions flows through these channels to
s the interior of the cardiac muscle fiber, and this
a activity maintains a prolonged period of
h depolarization, in the action
i potential.
g - Further, the calcium ions that enter during this
plateau phase activate the muscle contractile
h
process, whereas the calcium ions that cause
l skeletal muscle contraction are derived from the
y intracellular sarcoplasmic reticulum.
m
o The recorded in a ventricular muscle
b fiber, shown in Figure 9-3:
i averages about 105 millivolts, which means that the
l intracellular potential rises from a very negative
value, about 85 millivolts, between beats to a the permeability of the cardiac muscle membrane
e for potassium ions decreases about fivefold, an
slightly positive value, about +20 millivolts, during
r each beat. effect that does not occur in skeletal muscle.
e After the initial , the membrane remains This decreased potassium permeability may result
g depolarized for about 0.2 second, exhibiting a from:
plateau, followed at the end of the plateau by the excess calcium influx through the calcium
i
abrupt repolarization. channels just noted.
o
The presence of this plateau in the action decreased potassium permeability:
n decreases the outflux of positively charged
potential causes ventricular contraction to last
as much as 15 times as long in cardiac muscle potassium ions during the action potential
as in skeletal muscle. plateau and thereby prevents early return of
the action potential voltage to its resting level.
WHAT CAUSES THE LONG ACTION POTENTIAL When the slow calcium-sodium channels do close at
AND THE PLATEAU? At least two major differences the end of 0.2 to 0.3 second and the influx of
between the membrane properties of cardiac and calcium and sodium ions ceases:
skeletal muscle account for the prolonged action the membrane permeability for potassium ions
potential and the plateau in cardiac muscle. also increases rapidly;
this rapid loss of potassium from the fiber
is caused almost entirely by the sudden opening of immediately returns the membrane potential
large numbers of fast sodium channels that allow to its resting level, thus ending the action
tremendous numbers of sodium ions to enter the potential.
skeletal muscle fiber from the extracellular fluid.
These channels are called fast channels because
they remain open for only a few thousandths of a SUMMARY OF PHASES OF CARDIAC MUSCLE
second and then abruptly close. At the end of this ACTION POTENTIAL
closure, repolarization occurs, and the action

PHYSIOLOGY |CHAPTER 9: CARDIAC MUSCLE

 AHMAD, MISTLEY JANE A. 3

VELOCITY OF SIGNAL CONDUCTION IN CARDIAC

MUSCLE
The velocity of conduction of the excitatory action
potential signal along both and
is:
about 0.3 to 0.5 m/sec, or about 1/250 the velocity
in very large nerve fibers and
about 1/10 the velocity in skeletal muscle fibers.
The velocity of conduction in the specialized heart
conductive systemin the :
is as great as 4 m/sec in most parts of the system,
which allows reasonably rapid conduction of the
excitatory signal to the different parts of the
heart.

Figure 9-4 summarizes the phases of the action REFRACTORY PERIOD OF CARDIAC MUSCLE
potential in cardiac muscle and the ion flows that
occur during each phase.
PHASE 0: DEPOLARIZATION

When the cardiac cell is stimulated and

depolarizes, the membrane potential becomes
more positive.
Voltage-gated sodium channels (fast sodium
channels) open and permit sodium to rapidly flow
into the cell and depolarize it.
The membrane potential reaches about +20
millivolts before the sodium channels close.
PHASE 1: INITIAL REPOLARIZATION

The sodium channels close, the cell begins to repo-

larize, and potassium ions leave the cell through
Cardiac muscle, like all excitable tissue, is refractory
open potassium channels.
to restimulation during the action potential.
PHASE 2: PLATEAU
REFRACTORY PERIOD:
is the interval of time during which a normal
cardiac impulse cannot re-excite an already
A brief initial repolarization occurs and the action
excited area of cardiac muscle.
potential then plateaus as a result of:
increased calcium ion permeability and
decreased potassium ion permeability
is 0.25 to 0.30 second
The voltage-gated calcium ion channels open slowly
which is about the duration of the prolonged
during phases 1 and 0, and calcium enters the cell.
plateau action potential
Potassium channels then close, and the combination
of decreased potassium ion efflux and increased
calcium ion influx causes the action potential to
about 0.05 second during which the muscle is
plateau.
more difficult to excite than normal but never-
PHASE 3: RAPID REPOLARIZATION
theless can be excited by a very strong
excitatory signal, as demonstrated by the
early premature contraction in the second
The closure of calcium ion channels and increased
example of Figure 9-5.
potassium ion permeability, permitting potassium

ions to rapidly exit the cell, ends the plateau and
about 0.15 second
returns the cell membrane potential to its resting
level.
EXCITATION-CONTRACTION COUPLING FUNCTION OF
PHASE 4: RESTING MEMBRANE POTENTIAL i CALCIUM IONS AND THE TRANSVERSE TUBULES
averages about 90 millivolts s
a
h
i PHYSIOLOGY |CHAPTER 9: CARDIAC MUSCLE
g
 AHMAD, MISTLEY JANE A. 4

EXCITATION-CONTRACTION COUPLING The reason for this response is that the openings
refers to the mechanism by which the action of the T tubules pass directly through the cardiac
potential causes the myofibrils of muscle to muscle cell membrane into the extracellular spaces
contract surrounding the cells, allowing the same
As is true for skeletal muscle, when an action potential extracellular fluid that is in the cardiac muscle
passes over the cardiac muscle membrane: interstitium to percolate through the T tubules.
the action potential spreads to the interior of the Consequently, the quantity of calcium ions in the T
cardiac muscle fiber along the membranes of the tubule system (i.e., the availability of calcium ions to
transverse (T) tubules. cause cardiac muscle contraction) depends to a great
The T tubule action potentials in turn act on: extent on the extracellular fluid calcium ion
the membranes of the longitudinal sarcoplasmic concentration.
tubules In contrast, the strength of skeletal muscle
to cause release of calcium ions into the muscle contraction is hardly affected by moderate changes in
sarcoplasm from the sarcoplasmic reticulum. extracellular fluid calcium concentration because
In another few thousandths of a second, these skeletal muscle contraction is caused almost entirely by
calcium ions diffuse into the myofibrils and calcium ions released from the sarcoplasmic reticulum
catalyze the chemical reactions that promote inside the skeletal muscle fiber.
sliding of the actin and myosin filaments along one At the end of the plateau of the cardiac action poten-
another, which produces the muscle contraction. tial, the influx of calcium ions to the interior of the
Thus far, this mechanism of excitation-contraction muscle fiber is suddenly cut off, and calcium ions in the
coupling is the same as that for skeletal muscle, but sarcoplasm are rapidly pumped back out of the muscle
there is a second effect that is quite different. fibers into both the sarcoplasmic reticulum and the T
In addition to the calcium ions that are released into tubule extracellular fluid space.
the sarcoplasm from the cisternae of the sarcoplasmic Transport of calcium back into the sarcoplasmic
reticulum, calcium ions also diffuse into the sarcoplasm reticulum is achieved with the help of a calcium
from the T tubules themselves at the time of the action adenosine triphosphatase (ATPase) pump (see Figure 9-
potential, which opens voltage-dependent calcium 6).
channels in the membrane of the T tubule (Figure 9-6). Calcium ions are also removed from the cell by a sodium-
Calcium entering the cell then activates calcium release calcium exchanger.
channels, also called ryanodine receptor channels, in the The sodium that enters the cell during this exchange is
sarcoplasmic reticulum membrane, triggering the then transported out of the cell by the sodium-
release of calcium into the sarcoplasm. potassium ATPase pump.
Calcium ions in the sarcoplasm then interact with As a result, the contraction ceases until a new action
troponin to initiate cross-bridge formation and potential comes along.
contraction by the same basic mechanism as described
for skeletal muscle.

the strength of cardiac muscle contraction would

be reduced considerably because the sarcoplasmic
reticulum of cardiac muscle is less well developed
than that of skeletal muscle and does not store
enough calcium to provide full contraction.
The T tubules of cardiac muscle, however, have a
diameter five times as great as that of the skeletal
muscle tubules, which means a volume 25 times as
DURATION OF CONTRACTION
great. Cardiac muscle begins to contract a few milliseconds
Also, inside the T tubules is a large quantity of
after the action potential begins and continues to
mucopolysaccharides that are electronegatively
contract until a few milliseconds after the action
charged and bind an abundant store of calcium ions,
potential ends.
keeping them available for diffusion to the interior
duration of contraction of cardiac muscle:
of the cardiac muscle fiber when a T tubule action
is mainly a function of the duration of the action
potential appears. potential, including the plateau about 0.2 second
The strength of contraction of cardiac muscle depends
in atrial muscle and 0.3 second in ventricular
to a great extent on the concentration of calcium ions
muscle.
in the extracellular fluids.
In fact, a heart placed in a calcium-free solution will
CARDIAC CYCLE
quickly stop beating. i
s
a PHYSIOLOGY |CHAPTER 9: CARDIAC MUSCLE
h
 AHMAD, MISTLEY JANE A. 5

CARDIAC CYCLE: At a normal heart rate of 72 beats/min, systole

The cardiac events that occur from the beginning comprises about 0.4 of the entire cardiac cycle. At
of one heartbeat to the beginning of the next. three times the normal heart rate, systole is about 0.65
Each cycle is initiated by spontaneous generation of the entire cardiac cycle.
of an action potential in the sinus node. This means that the heart beating at a very fast
is located in the superior lateral rate does not remain relaxed long enough to allow
wall of the right atrium near the opening of the complete filling of the cardiac chambers before
superior vena cava, and the action potential travels the next contraction.
from here rapidly through both atria and then
through the A-V bundle into the ventricles.
Because of this special arrangement of the
conducting system from the atria into the
ventricles:
there is a delay of more than 0.1 second during
passage of the cardiac impulse from the atria
into the ventricles.
This delay allows the atria to contract ahead
of ventricular contraction, thereby pumping
blood into the ventricles before the strong
ventricular contraction begins.
Thus, the atria act as primer pumps for the
ventricles, and the ventricles in turn provide the
major source of power for moving blood through
the bodys vascular system.

DIASTOLE AND SYSTOLE

i The cardiac cycle consists of:

s DIASTOLE: a period of relaxation, during which

a the heart fills with blood followed by
h SYSTOLE: period of contraction
i TOTAL DURATION OF THE CARDIAC CYCLE:
including systole and diastole
g
is the reciprocal of the heart rate.
h For example, if heart rate is 72 beats/min, the
l duration of the cardiac cycle is 1/72
y min/beatabout 0.0139 minutes per beat, or
m 0.833 second per beat.
o

b Figure 9-7 shows the different events during the

cardiac cycle for the left side of the heart.
i
- The top three curves show the pressure changes in the
l
aorta, left ventricle, and left atrium, respectively.
-e The fourth curve depicts the changes in left ventricular
volume,
r the fifth depicts the electrocardiogram, and the
sixth
e depicts a phonocardiogram, which is a recording of the
sounds
g produced by the heartmainly by the heart valves
as it pumps.
i
o
INCREASING HEART RATE DECREASES DURATION
n OF CARDIAC CYCLE

WHEN HEART RATE INCREASES:

the duration of each cardiac cycle decreases,
including the contraction and relaxation phases.
The duration of the action potential and the period
of contraction (systole) also decrease, but not by
as great a percentage as does the relaxation phase
(diastole).

PHYSIOLOGY |CHAPTER 9: CARDIAC MUSCLE