(Heart Muscle (The Heart as a Pump and Function of the Heart Valves pdf - The Heart

parallel with one another.

separate individual cardiac muscle cells from one another. That is, cardiac

in Figure 9–2 are called

The dark areas crossing the cardiac muscle fibers

cardiac muscle is quite different from skeletal muscle, as we shall see.

same manner as occurs in skeletal muscle (see Chapter 6). But in other ways,

almost identical to those found in skeletal muscle; these fila-

muscle. Further, cardiac muscle has typical myofibrils that contain

recombining, and then spreading again. One also notes immediately from this

ing cardiac muscle fibers arranged in a latticework, with the fibers dividing,

Figure 9–2 shows a typical histological picture of cardiac muscle, demonstrat-

Physiologic Anatomy of Cardiac Muscle

action potentials through the heart, providing an excitatory system that controls

they contain few contractile fibrils; instead, they exhibit either automatic rhyth-

tal muscle, except that the duration of contraction is much longer. Conversely,

fibers. The

tricular muscle,

atrial muscle, ven-

The heart is composed of three major types of cardiac muscle:

Physiology of Cardiac Muscle

operates as a pump, beginning with the special features of heart muscle itself.

system is explained in Chapter 10. In this chapter, we explain how the heart

the heart muscle to cause the heart’s rhythmical beat. This rhythmical control

tractions called cardiac rhythmicity, transmitting action potentials throughout

ventricle.

helping to move blood into the ventricle. The ventricles then supply the main

atrium is a weak primer pump for the ventricle,

ventricle.

turn, each of these hearts is a pulsatile two-chamber

that pumps blood through the peripheral organs. In

that pumps blood through the lungs, and a

9–1, is actually two separate pumps: a

and circulatory system. The heart, shown in Figure

With this chapter we begin discussion of the heart

Heart Valves

Heart Muscle; The Heart as

103

a Pump and Function of the

right heart

left heart

pump composed of an atrium and a

Each

pumping force that propels the blood either (1) through the pulmonary circu-
lation by the right ventricle or (2) through the peripheral circulation by the left

Special mechanisms in the heart cause a continuing succession of heart con-

and specialized excitatory and conductive muscle

atrial and ventricular types of muscle contract in much the same way as skele-

the specialized excitatory and conductive fibers contract only feebly because

mical electrical discharge in the form of action potentials or conduction of the

the rhythmical beating of the heart.

figure that cardiac muscle is striated in the same manner as in typical skeletal

actin and

myosin filaments
ments lie side by side and slide along one another during contraction in the

Cardiac Muscle as a Syncytium.

intercalated discs; they are actually cell membranes that

muscle fibers are made up of many individual cells connected in series and in

long in cardiac muscle as in skeletal muscle.

the end of the plateau by abrupt repolarization. The

as shown in the figure, followed at

spike,

millivolts, during each beat. After the initial

between beats to a slightly positive value, about

85 millivolts,

from a very negative value, about

volts, which means that the intracellular potential rises

fiber, shown in Figure 9–3, averages about 105 milli-

The

Action Potentials in Cardiac Muscle

important for effectiveness of heart pumping.

short time ahead of ventricular contraction, which is

functional syncytiums allows the atria to contract a

This division of the muscle of the heart into two

A-V bundle,

tissue. Instead, they are conducted only by way of a

the ventricular syncytium directly through this fibrous

tials are not conducted from the atrial syncytium into

ings between the atria and ventricles. Normally, poten-

tutes the walls of the two ventricles. The atria are sepa-

two atria, and the

The heart actually is composed of two syncytiums:

throughout the latticework interconnections.

spreads to all of them, spreading from cell to cell

of these cells becomes excited, the action potential

past the intercalated discs. Thus, cardiac muscle is a

the cardiac muscle fibers, so that action potentials

from a functional point of view, ions move with ease

allow almost totally free diffusion of ions. Therefore,

able “communicating” junctions (gap junctions) that

104

Unit III

The Heart

At each intercalated disc the cell membranes fuse

with one another in such a way that they form perme-

in the intracellular fluid along the longitudinal axes of

travel easily from one cardiac muscle cell to the next,

syncytium of many heart muscle cells in which the
cardiac cells are so interconnected that when one

the atrial syncytium that constitutes the walls of the

ventricular syncytium that consti-

rated from the ventricles by fibrous tissue that
surrounds the atrioventricular (A-V) valvular open-

specialized conductive system called the
a bundle of conductive fibers several millimeters in
diameter that is discussed in detail in Chapter 10.

action potential recorded in a ventricular muscle

+20

the

membrane remains depolarized for about 0.2 second,
exhibiting a plateau

presence of this plateau in the action potential causes
ventricular contraction to last as much as 15 times as

Aorta

Pulmonary artery

Inferior

vena cava

Superior

vena cava

Right ventricle

Tricuspid

valve

Pulmonary

valve

Right atrium

Pulmonary
vein

Left atrium

Mitral valve

Aortic valve

Left
ventricle

Lungs

HEAD AND UPPER EXTREMITY

TRUNK AND LOWER EXTREMITY

chambers and heart valves.

Structure of the heart, and course of blood flow through the heart

Figure 9–1

“Syncytial,” interconnecting nature of cardiac muscle fibers.

Figure 9–2

Ventricular muscle

Millivolts

+20

–100

– 80

– 60

– 40

– 20

+20

– 60

– 40

– 20

–100

– 80

Seconds

Purkinje fiber

Plateau

microelectrodes.

and from a ventricular muscle fiber, recorded by means of

Rhythmical action potentials (in millivolts) from a Purkinje fiber

Figure 9–3

There is an additional

ventricle is 0.25 to 0.30 second, which is about the

cardiac muscle. The normal refractory period of the

the left in Figure 9–4, during which a normal cardiac

period of the heart is the interval of time, as shown to

during the action potential. Therefore, the refractory

all excitable tissue, is refractory to restimulation

Cardiac muscle, like

Refractory Period of Cardiac Muscle.

as explained in Chapter 10.

system, which allows reasonably rapid conduction of

tal muscle fibers. The velocity of conduction in the

about 0.3 to 0.5 m/sec, or about

The veloci-

Velocity of Signal Conduction in Cardiac Muscle.

membrane potential to its resting level, thus ending

potassium ions also increases rapidly; this rapid loss of

sodium ions ceases, the membrane permeability for

the action potential voltage to its resting level. When

noted. Regardless of the cause, the decreased potas-

that does not occur in skeletal muscle. This decreased

about fivefold, an effect

tial, the permeability of the cardiac muscle membrane

is this: Immediately after the onset of the action poten-

The second major functional difference between

plateau phase activate the muscle contractile process,

tial. Further, the calcium ions that enter during this

muscle fiber, and this maintains a prolonged period of

for several tenths of a second. During this time, a large

to open and, even more important, remain open

This second population of channels differs

channels.

channels,

slow calcium

sodium channels

opening of two types of channels: (1) the same

cardiac muscle

is over within another thousandth of a second or so.

closure, repolarization occurs, and the action potential

of a second and then abruptly close. At the end of this

cellular fluid. These channels are called “fast” channels

channels

plateau in cardiac muscle. First, the

were presented in Chapter 5, but they merit summa-

not? The basic biophysical answers to these questions

have a plateau, whereas that of skeletal muscle does

potential of cardiac muscle so long, and why does it

this point, we must ask the questions: Why is the action

Heart Muscle; The Heart as a Pump and Function of the Heart Valves

Chapter 9

105

What Causes the Long Action Potential and the Plateau?

rizing here as well.

At least two major differences between the mem-

brane properties of cardiac and skeletal muscle
account for the prolonged action potential and the

action potential of

skeletal muscle is caused almost entirely by sudden
opening of large numbers of so-called fast sodium

that allow tremendous numbers of sodium

ions to enter the skeletal muscle fiber from the extra-

because they remain open for only a few thousandths

, the action potential is caused by

fast

as those in skeletal muscle and (2)

another entirely different population of

which are also called calcium-sodium

from the fast sodium channels in that they are slower

quantity of both calcium and sodium ions flows
through these channels to the interior of the cardiac

depolarization, causing the plateau in the action poten-

while the calcium ions that cause skeletal muscle con-
traction are derived from the intracellular sarcoplas-
mic reticulum.

cardiac muscle and skeletal muscle that helps account
for both the prolonged action potential and its plateau

for potassium ions decreases

potassium permeability may result from the excess
calcium influx through the calcium channels just

sium permeability greatly decreases the outflux of
positively charged potassium ions during the action
potential plateau and thereby prevents early return of

the slow calcium-sodium channels do close at the end
of 0.2 to 0.3 second and the influx of calcium and

potassium from the fiber immediately returns the

the action potential.

ty of conduction of the excitatory action potential
signal along both atrial and ventricular muscle fibers is

250

the velocity in very

large nerve fibers and about

the velocity in skele-

specialized heart conductive system—in the Purkinje
fibers—is as great as 4 m/sec in most parts of the

the excitatory signal to the different parts of the heart,

impulse cannot re-excite an already excited area of

duration of the prolonged plateau action potential.

relative refractory period of

Seconds

Relative refractory

period

Refractory period

Early premature

contraction

Later premature

contraction

Force of contraction

Note that premature contractions

effect of premature contraction.

relative refractory period, plus the

tion of the refractory period and

Force of ventricular heart muscle

Figure 9–4

contraction, showing also dura-

do not cause wave summation, as
occurs in skeletal muscle.

depicts the changes in left ventricular volume, the fifth

tricle, and left atrium, respectively. The fourth curve

curves show the pressure changes in the aorta, left ven-

cardiac cycle for the left side of the heart.The top three

Figure 9–5 shows the different events during the

systole.

diastole,

The cardiac cycle consists of a period of relaxation

power for moving blood through the body’s vascular

for the ventricles, and

before the strong ventricular contraction begins. Thus,

traction, thereby pumping blood into the ventricles

cardiac impulse from the atria into the ventricles. This

system from the atria into the ventricles, there is a

and then through the A-V bundle into the ventricles.

opening of the superior vena cava, and the action

, as explained in Chapter 10. This node is located

Each cycle is initiated by sponta-

cardiac cycle.

The cardiac events that occur from the beginning of

The Cardiac Cycle

tricular muscle.

action potential ends. Therefore, the duration of con-

comes along.

and the T tubule–extracellular fluid space. As a result,

the muscle fiber is suddenly cut off, and the calcium

potential, the influx of calcium ions to the interior of

the skeletal muscle fiber itself.)

(By way of contrast, the strength of skeletal muscle

tubule system—that is, the availability of calcium ions

Consequently, the quantity of calcium ions in the T

interstitium to percolate through the T tubules as well.

extracellular spaces surrounding the cells, allowing the

this is that the openings of the T tubules pass directly

calcium ions in the extracellular fluids. The reason for

The strength of contraction of cardiac muscle

when a T tubule action potential appears.

store of calcium ions, keeping these always available

means a volume 25 times as great. Also, inside the T

great as that of the skeletal muscle tubules, which

calcium to provide full contraction. Conversely, the T

without this extra calcium from the T tubules, the

selves at the time of the action potential. Indeed,

diffuses into the sarcoplasm from the T tubules them-

reticulum, a large quantity of extra calcium ions also

there is a second effect that is quite different. In addi-

coupling is the same as that for skeletal muscle, but

Thus far, this mechanism of excitation-contraction

myosin filaments along one another; this produces the

another few thousandths of a second, these calcium

muscle sarcoplasm from the sarcoplasmic reticulum. In

(T) tubules. The T tubule action potentials in turn act

tial passes over the cardiac muscle membrane, the

As is true for skeletal muscle, when an action poten-

for skeletal muscle in Chapter 7. Once again, there are

the myofibrils of muscle to contract. This was discussed

The term “excitation-contraction coupling” refers to

Transverse Tubules

second example of Figure 9–4. The refractory period

strated by the early “premature” contraction in the

excited by a very strong excitatory signal, as demon-

106

Unit III

The Heart

about 0.05 second during which the muscle is more dif-
ficult than normal to excite but nevertheless can be

of atrial muscle is much shorter than that for the ven-
tricles (about 0.15 second for the atria compared with
0.25 to 0.30 second for the ventricles).

Excitation-Contraction Coupling—Function
of Calcium Ions and the

the mechanism by which the action potential causes

differences in this mechanism in cardiac muscle that
have important effects on the characteristics of cardiac
muscle contraction.

action potential spreads to the interior of the cardiac
muscle fiber along the membranes of the transverse

on the membranes of the longitudinal sarcoplasmic
tubules to cause release of calcium ions into the

ions diffuse into the myofibrils and catalyze the chemi-
cal reactions that promote sliding of the actin and

muscle contraction.

tion to the calcium ions that are released into the
sarcoplasm from the cisternae of the sarcoplasmic

strength of cardiac muscle contraction would be
reduced considerably because the sarcoplasmic re-
ticulum of cardiac muscle is less well developed than
that of skeletal muscle and does not store enough

tubules of cardiac muscle have a diameter 5 times as

tubules is a large quantity of mucopolysaccharides that
are electronegatively charged and bind an abundant

for diffusion to the interior of the cardiac muscle fiber

depends to a great extent on the concentration of

through the cardiac muscle cell membrane into the

same extracellular fluid that is in the cardiac muscle

to cause cardiac muscle contraction—depends to a
great extent on the extracellular fluid calcium ion
concentration.

contraction is hardly affected by moderate changes in
extracellular fluid calcium concentration because
skeletal muscle contraction is caused almost entirely
by calcium ions released from the sarcoplasmic retic-
ulum inside

At the end of the plateau of the cardiac action

ions in the sarcoplasm are rapidly pumped back out of
the muscle fibers into both the sarcoplasmic reticulum

the contraction ceases until a new action potential

Duration of Contraction.

Cardiac muscle begins to contract

a few milliseconds after the action potential begins and
continues to contract until a few milliseconds after the

traction of cardiac muscle is mainly a function of the
duration of the action potential, including the plateau—
about 0.2 second in atrial muscle and 0.3 second in ven-

one heartbeat to the beginning of the next are called
the
neous generation of an action potential in the sinus
node
in the superior lateral wall of the right atrium near the

potential travels from here rapidly through both atria

Because of this special arrangement of the conducting

delay of more than 0.1 second during passage of the

allows the atria to contract ahead of ventricular con-

the atria act as primer pumps
the ventricles in turn provide the major source of

system.

Diastole and Systole

called

during which the heart fills with blood,

followed by a period of contraction called

ventricles. Therefore, the atria simply function as

before the atria contract. Then, atrial contraction

into the atria; about 80 per cent of the blood flows

Function of the Atria as Primer Pumps

fibers begin to relax. Therefore, the T wave occurs

electrocardiogram. This represents the stage of repo-

ventricular T wave

Finally, one observes the

lar systole.

rising, as also shown in the figure. Therefore, the QRS

tion of the ventricles, which initiates contraction of the

About 0.16 second after the onset of the P wave, the

P wave.

traction, which causes a slight rise in the atrial pres-

through the atria, and this is followed by atrial con-

The

the surface of the body.

12, and 13. They are electrical voltages generated by

T waves,

R, S,

P, Q,

The electrocardiogram in Figure 9–5 shows the

Relationship of the Electrocardiogram

the heart—mainly by the heart valves—as it pumps. It

gram, which is a recording of the sounds produced by

the electrocardiogram, and the sixth a phonocardio-

Heart Muscle; The Heart as a Pump and Function of the Heart Valves

Chapter 9

107

is especially important that the reader study in detail
this figure and understand the causes of all the events
shown.

to the Cardiac Cycle

and

which are discussed in Chapters 11,

the heart and recorded by the electrocardiograph from

P wave is caused by spread of depolarization

sure curve immediately after the electrocardiographic

QRS waves appear as a result of electrical depolariza-

ventricles and causes the ventricular pressure to begin

complex begins slightly before the onset of ventricu-

in the

larization of the ventricles when the ventricular muscle

slightly before the end of ventricular contraction.

Blood normally flows continually from the great veins

directly through the atria into the ventricles even

usually causes an additional 20 per cent filling of the

1st

2nd

3rd

120

100

Pressure (mm Hg)

130

Volume (ml)

Systole

Diastole

Phonocardiogram

Electrocardiogram

Ventricular volume

Ventricular pressure

Atrial pressure

Aortic pressure

A-V valve

opens

A-V valve

closes

Aortic valve

closes

Aortic

valve

opens

Isovolumic

contraction

Ejection

Isovolumic

relaxation

Rapid inflow

Diastasis

Atrial systole

ventricular volume, the electrocardiogram, and the phonocardiogram.

aortic pressure,

Events of the cardiac cycle for left ventricular function, showing changes in left atrial pressure, left ventricular pressure,

Figure 9–5

volume, the stroke volume output can be increased to

milliliters in the healthy heart. By both increasing the

into the ventricles during diastole, the ventricular end-

liters. Conversely, when large amounts of blood flow

When the heart contracts strongly, the end-systolic

The fraction of the end-diastolic

end-systolic volume.

in each ventricle, about 40 to 50 milliliters, is called the

The remaining volume

the volume decreases about 70 milliliters, which is

Then, as the ventricles empty during systole,

volume.

120 milliliters. This volume is called the

During diastole, normal filling of the ventricles

End-Diastolic Volume, End-Systolic Volume, and Stroke Volume

new cycle of ventricular pumping.

diastolic levels. Then the A-V valves open to begin a

During this period, the intraven-

isovolumic

change, giving rise to the period of

relax, even though the ventricular volume does not

to 0.06 second, the ventricular muscle continues to

aortic and pulmonary valves closed. For another 0.03

push blood back toward the ventricles, which snaps the

to decrease rapidly. The elevated pressures in the dis-

systole, ventricular relaxation begins suddenly, allow-

slow ejection.

and the last two thirds, the

thirds. Therefore, the first third is called the

ately, blood begins to pour out of the ventricles, with

pressures push the semilunar valves open. Immedi-

lar pressure slightly above 8 mm Hg), the ventricular

rises slightly above 80 mm Hg (and the right ventricu-

When the left ventricular pressure

Period of Ejection.

of the muscle fibers is occurring.

there is no emptying. This is called the period of

period, contraction is occurring in the ventricles, but

the aorta and pulmonary artery. Therefore, during this

causing the A-V valves to close. Then an additional

ular pressure rises abruptly, as shown in Figure 9–5,

ately after ventricular contraction begins, the ventric-

Period of Isovolumic (Isometric) Contraction.

Emptying of the Ventricles During Systole

of the filling of the ventricles during each heart cycle.

into the ventricles; this accounts for about 20 per cent

During the last third of diastole, the atria contract

directly into the ventricles.

ventricles; this is blood that continues to empty into

third of diastole. During the middle third of diastole,

The period of rapid filling lasts for about the first

rapid filling of the ventricles.

in Figure 9–5. This is called the

ventricles, as shown by the rise of the left

during ventricular systole immediately push the A-V

again to their low diastolic values, the moderately

because of the closed A-V valves. Therefore, as soon

During ventricular systole, large

Filling of the Ventricles.

Function of the Ventricles as Pumps

causing the v wave to disappear.

contraction is over, the A-V valves open, allowing this

during ventricular contraction. Then, when ventricular

atria from the veins while the A-V valves are closed

contraction; it results from slow flow of blood into the

The

ventricles.

but mainly by bulging of the A-V valves backward

contract; it is caused partly by slight backflow of blood

The

about 7 to 8 mm Hg.

atrial contraction, and the

atrial pressure increases 4 to 6 mm Hg during

is caused by atrial contraction. Ordinarily,

The

v atrial pressure waves,

a, c,

elevations, called the

atrial pressure curve of Figure 9–5, three minor pressure

Pressure Changes in the Atria—The a, c, and v Waves.

develop, especially shortness of breath.

exercises; then acute signs of heart failure occasionally

resting body. Therefore, when the atria fail to function,

effectiveness as much as 20 per cent. However, the

108

Unit III

The Heart

primer pumps that increase the ventricular pumping

heart can continue to operate under most conditions
even without this extra 20 per cent effectiveness
because it normally has the capability of pumping 300
to 400 per cent more blood than is required by the

the difference is unlikely to be noticed unless a person

In the

and

are

noted.

a wave

the right

left atrial pressure increases

c wave occurs when the ventricles begin to

into the atria at the onset of ventricular contraction

toward the atria because of increasing pressure in the

v wave occurs toward the end of ventricular

stored atrial blood to flow rapidly into the ventricles and

amounts of blood accumulate in the right and left atria

as systole is over and the ventricular pressures fall

increased pressures that have developed in the atria

valves open and allow blood to flow rapidly into the

ventricular

volume curve

period of

only a small amount of blood normally flows into the

the atria from the veins and passes through the atria

and give an additional thrust to the inflow of blood

Immedi-

0.02 to 0.03 second is required for the ventricle to build
up sufficient pressure to push the semilunar (aortic
and pulmonary) valves open against the pressures in

iso-

volumic or isometric contraction, meaning that tension
is increasing in the muscle but little or no shortening

about 70 per cent of the blood emptying occurring
during the first third of the period of ejection and the
remaining 30 per cent emptying during the next two

period of

rapid ejection,

period of

Period of Isovolumic (Isometric) Relaxation.

At the end of

ing both the right and left intraventricular pressures

tended large arteries that have just been filled with
blood from the contracted ventricles immediately

or iso-

metric relaxation.
tricular pressures decrease rapidly back to their low

Output.

increases the volume of each ventricle to about 110 to

end-diastolic

called the stroke volume output.

volume that is ejected is called the ejection fraction—
usually equal to about 60 per cent.

volume can be decreased to as little as 10 to 20 milli-

diastolic volumes can become as great as 150 to 180

end-diastolic volume and decreasing the end-systolic

more than double normal.

When listening to the heart with a stethoscope, one does

Sounds to Heart Pumping

Relationship of the Heart

that the pressures are only about one sixth as great, as

are similar to those in the aorta, except

The pressure curves in the

sure of 120 mm Hg (systolic pressure) that occurs in

tolic pressure), which is two thirds the maximal pres-

pressure usually has fallen to about 80 mm Hg (dias-

veins. Before the ventricle contracts again, the aortic

After the aortic valve has closed, the pressure in the

tion of the backflow.

before closure of the valve, followed by sudden cessa-

curve when the aortic valve closes. This is caused by a

the arteries, even during diastole.

stops ejecting blood and the aortic valve closes, the

Next, at the end of systole, after the left ventricle

to about 120 mm Hg.

The entry of blood into the arteries causes the walls

arteries.

cle rises much less rapidly, as shown in Figure 9–5,

Then, after the valve opens, the pressure in the ventri-

sure increases rapidly until the aortic valve opens.

When the left ventricle contracts, the ventricular pres-

stresses.

valve at the bottom of Figure 9–6) that they must be

lunar valves. It is obvious from the anatomy of the

the chordae tendineae, which is not true for the semi-

A-V valves. Finally, the A-V valves are supported by

because of the rapid closure and rapid ejection, the

than that through the much larger A-V valves. Also,

of smaller openings, the velocity of blood ejection

much softer closure of the A-V valves. Second, because

valves to snap to the closed position, in contrast to the

ently from the A-V valves. First, the high pressures in

The aortic and pul-

Aortic and Pulmonary Artery Valves.

incapacity.

tricular contraction, sometimes so far that it leaks

paralyzed, the valve bulges far backward during ven-

ventricular contraction. If a chorda tendinea becomes

help the valves to close. Instead, they pull the vanes of

but contrary to what might be expected, they

The papillary

chordae tendineae.

Figure 9–6 also

Function of the Papillary Muscles.

milliseconds.

cause closure, whereas the much heavier semilunar

thin, filmy A-V valves require almost no backflow to

in the forward direction. For anatomical reasons, the

pressure gradient pushes blood backward, and they

That is, they close when a backward

passively.

shown in Figure 9–6 for the left ventricle, close and

teries into the ventricles during diastole. These valves,

ventricles to the atria during systole, and the

The

Atrioventricular Valves.

Function of the Valves

Heart Muscle; The Heart as a Pump and Function of the Heart Valves

Chapter 9

109

A-V valves (the tricuspid

and mitral valves) prevent backflow of blood from the

semilu-

nar valves (the aortic and pulmonary artery valves)
prevent backflow from the aorta and pulmonary ar-

open

open when a forward pressure gradient forces blood

valves require rather rapid backflow for a few

shows papillary muscles that attach to the vanes of the
A-V valves by the
muscles contract when the ventricular walls contract,

do not

the valves inward toward the ventricles to prevent
their bulging too far backward toward the atria during

ruptured or if one of the papillary muscles becomes

severely and results in severe or even lethal cardiac

monary artery semilunar valves function quite differ-

the arteries at the end of systole cause the semilunar

through the aortic and pulmonary valves is far greater

edges of the aortic and pulmonary valves are subjected
to much greater mechanical abrasion than are the

aortic and pulmonary valves (as shown for the aortic

constructed with an especially strong yet very pliable
fibrous tissue base to withstand the extra physical

Aortic Pressure Curve

because blood immediately flows out of the ventricle
into the aorta and then into the systemic distribution

of these arteries to stretch and the pressure to increase

elastic walls of the arteries maintain a high pressure in

A so-called incisura occurs in the aortic pressure

short period of backward flow of blood immediately

aorta decreases slowly throughout diastole because
the blood stored in the distended elastic arteries flows
continually through the peripheral vessels back to the

the aorta during ventricular contraction.

right ventricle and pul-

monary artery

discussed in Chapter 14.

not hear the opening of the valves because this is a

Cusp

MITRAL VALVE

AORTIC VALVE

Papillary muscles

Chordae tendineae

Mitral and aortic valves (the left ventricular valves).

Figure 9–6

0 mm Hg. Forty-five milliliters is the amount of

This phase in the volume-

Period of filling.

four phases.

ventricle. It is divided into

of the cardiac cycle

The red lines in Figure 9–7 form a loop

Work Output.

“Volume-Pressure Diagram” During the Cardiac Cycle; Cardiac

80 mm Hg.

ventricle,

by cardiac nerves. For the normal

person’s heart strength and degree of heart stimulation

250 and 300 mm Hg, but this varies widely with each

volumes, the actin and myosin filaments of the cardiac

pressure curve in Figure 9–7, because at these great

some conditions, as demonstrated by the falling systolic

further, the systolic pressure actually decreases under

170 milliliters. Then, as the volume increases still

During ventricular contraction, the “systolic” pres-

increases rapidly, partly because of fibrous tissue in the

Above 150 milliliters, the ventricular diastolic pressure

does not increase greatly. Therefore, up to this volume,

above about 150 milliliters, the “diastolic” pressure

contraction at each volume of filling.

The systolic pressure curve is determined by record-

of the ventricle.

before ventricular contraction occurs, which is the

The diastolic pressure curve is determined by filling

curves.

“systolic pressure.” These curves are volume-pressure

the two curves labeled “diastolic pressure” and

The most important components of the diagram are

ventricle.

Figure 9–7 shows a diagram that is especially useful in

Graphical Analysis of Ventricular

create kinetic energy of blood flow.

great velocity through the stenosed valve, more than

ditions, such as aortic stenosis, in which blood flows with

total stroke work output. But in certain abnormal con-

Ordinarily, the work output of the left ventricle

that the two ventricles pump. The additional work

energy of blood flow

the aortic and pulmonary valves. This is the

Second, a minor proportion of the energy is used to

This is called

the low-pressure veins to the high-pressure arteries.

Work output of the heart is in two forms. First, by far

times the heart rate per minute.

work in 1 minute; this is equal to the stroke work output

heartbeat while pumping blood into the arteries.

The

Work Output of the Heart

tion to listening to the sounds with the stethoscope.

sounds are discussed more fully in Chapter 23, in rela-

The precise causes of the heart

vibrate for a short period. This sound is called the

because these valves close rapidly, and the surroundings

close at the end of systole, one hears a rapid snap

When the aortic and pulmonary valves

caused by closure of the A-V valves. The vibration is low

When the ventricles contract, one first hears a sound

of sudden pressure changes, giving off sound that travels

However, when the valves close, the vanes of the valves

relatively slow process that normally makes no noise.

110

Unit III

The Heart

and the surrounding fluids vibrate under the influence

in all directions through the chest.

in pitch and relatively long-lasting and is known as the
first heart sound.

second heart sound.

stroke work output of the heart is the amount of

energy that the heart converts to work during each

Minute

work output is the total amount of energy converted to

the major proportion is used to move the blood from

volume-pressure work or external work.

accelerate the blood to its velocity of ejection through

kinetic

component of the work output.

Right ventricular external work output is normally

about one sixth the work output of the left ventricle
because of the sixfold difference in systolic pressures

output of each ventricle required to create kinetic
energy of blood flow is proportional to the mass of
blood ejected times the square of velocity of ejection.

required to create kinetic energy of blood flow is only
about 1 per cent of the total work output of the ventri-
cle and therefore is ignored in the calculation of the

50 per cent of the total work output may be required to

Pumping

explaining the pumping mechanics of the left

the heart with progressively greater volumes of blood
and then measuring the diastolic pressure immediately

end-

diastolic pressure

ing the systolic pressure achieved during ventricular

Until the volume of the noncontracting ventricle rises

blood can flow easily into the ventricle from the atrium.

heart that will stretch no more and partly because the
pericardium that surrounds the heart becomes filled
nearly to its limit.

sure increases even at low ventricular volumes and
reaches a maximum at a ventricular volume of 150 to

muscle fibers are pulled apart far enough that the
strength of each cardiac fiber contraction becomes less
than optimal.

Note especially in the figure that the maximum sys-

tolic pressure for the normal left ventricle is between

right

the maximum systolic pressure is between 60 and

called the volume-pressure diagram
for normal function of the left

Phase I:

pressure diagram begins at a ventricular volume of
about 45 milliliters and a diastolic pressure near

100

150

200

250

Left ventricular volume (ml)

Intraventricular pressure (mm Hg)

250

200

150

100

300

Isovolumic

relaxation

Isovolumic

contraction

Systolic pressure

III

Diastolic

pressure

Period of ejection

Period of filling

normal cardiac cycle. EW, net external work.

changes in intraventricular volume and pressure during the

red lines is the “volume-pressure diagram,” demonstrating

pressure during diastole and systole. Also shown by the heavy

Figure 9–7

Relationship between left ventricular volume and intraventricular

in honor of Frank and

Starling mechanism of the heart,

Frank-

This intrinsic ability of the heart to adapt to increas-

pumps this incoming blood into the arteries, so that it

the right atrium. The heart, in turn, automatically

body controls its own local blood flow, and all the local

That is, each peripheral tissue of the

blood flow into the heart from the veins, which is called

tions, the amount of blood pumped by the heart each

In Chapter 20, we will learn that under most condi-

Intrinsic Regulation of Heart

this amount. The basic means by which the volume

liters of blood each minute. During severe exercise,

When a person is at rest, the heart pumps only 4 to 6

Regulation of Heart Pumping

cent. In heart failure, this can decrease to as low as 5 to

efficiency of the normal heart is between 20 and 25 per

efficiency of cardiac

. The ratio of work output to total chemical

traction, most of the expended chemical energy is con-

energy are discussed in Chapters 67 and 68.

work. The different chemical reactions that liberate this

lactate and glucose. Therefore, the rate of oxygen con-

and, to a lesser extent, of other nutrients, especially

to provide the work of contraction. This energy is

Heart muscle, like skeletal muscle, uses chemical energy

the Heart

for Cardiac Contraction:

Chemical Energy Required

which the ventricle must contract (the afterload), or

ventricle (the preload), the arterial pressure against

heart or circulation, the pressure during filling of the

The importance of the concepts of preload and after-

in the circulation rather than the pressure.)

III curve of the volume-pressure diagram. (Sometimes

artery leading from the ventricle. In Figure 9–7, this cor-

The

For cardiac contraction, the

against which the muscle exerts its contractile force,

tract, which is called the

tile properties of muscle, it is important to specify the

the ventricle contracts with greater pressure, and it

more blood during diastole, it rises much higher because

area of the work diagram becomes much larger. That is,

When the heart pumps large quantities of blood, the

tal studies of cardiac contraction, this diagram is used

the ventricle during its contraction cycle. In experimen-

0 mm Hg.

starting point, with about 45 milliliters of blood

change in volume. Thus, the ventricle returns to its

pressure level. The line labeled “IV” traces this

of the period of ejection, the aortic valve closes, and

Period of isovolumic relaxation.

Phase IV:

labeled “III” traces the changes in volume and

the ventricle into the aorta. Therefore, the curve

more contraction of the ventricle. At the same time,

During ejection, the

Period of ejection.

end of the line labeled “II.”

value of about 80 mm Hg, as depicted by the arrow

to equal the pressure in the aorta, at a pressure

However, the pressure inside the ventricle increases

isovolumic contraction, the volume of the ventricle

Period of isovolumic contraction.

diastolic pressure rising to about 5 mm Hg.

during phase I extends along the line labeled “I,”

milliliters. Therefore, the volume-pressure diagram

end-diastolic volume,

normally increases to about 115 milliliters, called

from the left atrium, the ventricular volume

volume.

Heart Muscle; The Heart as a Pump and Function of the Heart Valves

Chapter 9

111

blood that remains in the ventricle after the
previous heartbeat and is called the end-systolic

As venous blood flows into the ventricle

the

an increase of 70

with the volume increasing to 115 milliliters and the

Phase II:

During

does not change because all valves are closed.

Phase III:

systolic pressure rises even higher because of still

the volume of the ventricle decreases because the
aortic valve has now opened and blood flows out of

systolic pressure during this period of ejection.

At the end

the ventricular pressure falls back to the diastolic

decrease in intraventricular pressure without any

left in the ventricle and at an atrial pressure near

Readers well trained in the basic principles of physics
should recognize that the area subtended by this func-
tional volume-pressure diagram (the tan shaded area,
labeled EW) represents the net external work output of

for calculating cardiac work output.

it extends far to the right because the ventricle fills with

usually extends farther to the left because the ventricle
contracts to a smaller volume—especially if the ventri-
cle is stimulated to increased activity by the sympathetic
nervous system.

Concepts of Preload and Afterload.

In assessing the contrac-

degree of tension on the muscle when it begins to con-

preload, and to specify the load

which is called the afterload.

preload is usually con-

sidered to be the end-diastolic pressure when the ven-
tricle has become filled.

afterload of the ventricle is the pressure in the

responds to the systolic pressure described by the phase

the afterload is loosely considered to be the resistance

load is that in many abnormal functional states of the

both are severely altered from normal.

Oxygen Utilization by

derived mainly from oxidative metabolism of fatty acids

sumption by the heart is an excellent measure of the
chemical energy liberated while the heart performs its

Efficiency of Cardiac Contraction.

During heart muscle con-

verted into heat and a much smaller portion into work
output
energy expenditure is called the
contraction, or simply efficiency of the heart. Maximum

10 per cent.

the heart may be required to pump four to seven times

pumped by the heart is regulated are (1) intrinsic
cardiac regulation of pumping in response to changes
in volume of blood flowing into the heart and (2)
control of heart rate and strength of heart pumping by
the autonomic nervous system.

Pumping—The Frank-Starling
Mechanism

minute is determined almost entirely by the rate of

venous return.

tissue flows combine and return by way of the veins to

can flow around the circuit again.

ing volumes of inflowing blood is called the

blood pumped and increasing the ejection pressure.

as double normal, thereby increasing the volume of

even 250 beats per minute. Also, sympathetic stimula-

rate of 70 beats per minute up to 180 to 200 and, rarely,

Nerves.

per cent by sympathetic stimulation. By contrast, the

(cardiac output)

pressure, the amount of blood pumped each minute

shown in Figure 9–10. For given levels of input atrial

nerves, which abundantly supply the heart, as

The pumping effectiveness of the heart also is con-

Parasympathetic Nerves

Control of the Heart by the Sympathetic and

arteries.

cardiac muscle contraction increase, causing the

pressures, each ventricular volume and strength of

That is, as the ventricles fill in response to higher atrial

expressing the Frank-Starling mechanism of the heart.

Thus,

volume outputs per minute also increase.

atrial pressures increase, the respective ventricular

extrapolated from lower animals. As the right and left

The two curves of this figure represent function of the

ventricular volume output curve.

Figure 9–9 shows another type of ventricular func-

limit of the ventricle’s pumping ability.

pressure for each side of the heart increases, the stroke

stroke work output curve.

as shown in Figures 9–8 and 9–9. Figure

tion curves,

Ventricular Function Curves

tion is much less than that of the Frank-Starling

of blood pumped each minute, although its contribu-

10 to 20 per cent; this, too, helps increase the amount

pumping when its volume is increased. Stretch of the

the heart muscle, still another factor increases heart

6, and is not simply a characteristic of cardiac muscle.

acteristic of all striated muscle, as explained in Chapter

length, to contract with increased work output is char-

This ability of stretched muscle, up to an optimal

pumps the extra blood into the arteries.

because of its increased pumping, automatically

overlap for force generation. Therefore, the ventricle,

length. This in turn causes the muscle to contract with

cles, the cardiac muscle itself is stretched to greater

When an extra amount of blood flows into the ventri-

all the blood that returns to it by the way of the veins.

Within physiologic limits, the heart pumps

the quantity of blood pumped into the aorta. Or, stated

greater the heart muscle is stretched during filling,

cally, the Frank-Starling mechanism means that the

Starling, two great physiologists of a century ago. Basi-

112

Unit III

The Heart

the greater is the force of contraction and the greater

another way:

What Is the Explanation of the Frank-Starling Mechanism?

increased force because the actin and myosin filaments
are brought to a more nearly optimal degree of

In addition to the important effect of lengthening

right atrial wall directly increases the heart rate by

mechanism.

One of the best ways to express the functional ability
of the ventricles to pump blood is by ventricular func-

9–8 shows a type of ventricular function curve called
the

Note that as the atrial

work output for that side increases until it reaches the

tion curve called the

two ventricles of the human heart based on data

ventricular function curves are another way of

heart to pump increased quantities of blood into the

trolled by the sympathetic and parasympathetic
(vagus)

often can be increased more than 100

output can be decreased to as low as zero or almost
zero by vagal (parasympathetic) stimulation.

Mechanisms of Excitation of the Heart by the Sympathetic

Strong sympathetic stimulation can increase

the heart rate in young adult humans from the normal

tion increases the force of heart contraction to as much

Left mean atrial

pressure

(mm Hg)

Left ventricular

stroke work

(gram meters)

Right mean atrial

pressure

(mm Hg)

Right ventricular

stroke work

(gram meters)

Sarnoff SJ: Myocardial contractility as described by ventricular

right mean atrial pressures. (Curves reconstructed from data in

ventricular stroke work output

Left and right ventricular function curves recorded from dogs,

Figure 9–8

depicting

as a function of left and

function curves. Physiol Rev 35:107, 1955.)

+ 4

+12

+16

+ 8

Ventricular output (L

/min)

Atrial pressure (mm Hg)

–

Left ventricle

Right ventricle

data obtained in dogs and data from human beings.

for the normal resting human heart as extrapolated from

Approximate normal right and left

Figure 9–9

ventricular volume output

curves

pumping.

process. Therefore, it is to be expected that the con-

marked effect on membrane potentials, and in Chapter

5, it was pointed out that potassium ions have a

Effect of Potassium and Calcium Ions

changes in contractile strength of the heart

changes in heart rate

tion. These changes in output caused by nerve stimu-

given right atrial pressure, the cardiac output increases

The curves of Figure 9–11 demonstrate that at any

tricle; they show the relation between right atrial pres-

function curves of Figure 9–9. However, they represent

function curves. They are similar to the ventricular

Figure 9–11 shows four cardiac

Cardiac Function Curve.

or more.

tion. Nevertheless, the great decrease in heart rate

traction of the heart occurs. This explains the effect of

and not much to the ventricles, where the power con-

The vagal fibers are distributed mainly to the atria

addition, strong vagal stimulation can decrease the

as the parasympathetic stimulation continues. In

few seconds, but then the heart usually “escapes” and

Parasympathetic (Vagal) Stimulation of the Heart.

muscle contraction, thereby decreasing the level of

nervous system is depressed below normal, this

lation. Therefore, when the activity of the sympathetic

extent in the following way: Under normal conditions,

Conversely,

Frank-Starling mechanism already discussed.

fold, in addition to the increased output caused by the

Thus, sympathetic stimulation often can increase the

Heart Muscle; The Heart as a Pump and Function of the Heart Valves

Chapter 9

113

maximum cardiac output as much as twofold to three-

inhibition of the sympathetic nerves to

the heart can decrease cardiac pumping to a moderate

the sympathetic nerve fibers to the heart discharge
continuously at a slow rate that maintains pumping at
about 30 per cent above that with no sympathetic stimu-

decreases both heart rate and strength of ventricular

cardiac pumping as much as 30 per cent below normal.

Strong

stimulation of the parasympathetic nerve fibers in the
vagus nerves to the heart can stop the heartbeat for a

beats at a rate of 20 to 40 beats per minute as long

strength of heart muscle contraction by 20 to 30
per cent.

vagal stimulation mainly to decrease heart rate rather
than to decrease greatly the strength of heart contrac-

combined with a slight decrease in heart contraction
strength can decrease ventricular pumping 50 per cent

Effect of Sympathetic or Parasympathetic Stimulation on the

function of the entire heart rather than of a single ven-

sure at the input of the right heart and cardiac output
from the left ventricle into the aorta.

during increased sympathetic stimulation and
decreases during increased parasympathetic stimula-

lation result both from

and from

because

both change in response to the nerve stimulation.

on Heart Function

In the discussion of membrane potentials in Chapter

6 it was noted that calcium ions play an especially
important role in activating the muscle contractile

centration of each of these two ions in the extracellu-
lar fluids should also have important effects on cardiac

Effect of Potassium Ions.

Excess potassium in the extra-

cellular fluids causes the heart to become dilated and

Sympathetic

nerves

Sympathetic

nerves

Vagi

S-A

node

A-V

node

Sympathetic chains

nerves to the heart are parasympathetic nerves.)

Cardiac

Figure 9–10

sympathetic and parasympathetic nerves. (The vagus

+ 8

Cardiac output (L

/min)

Right atrial pressure (mm Hg)

–

+ 4

Maximum sympathetic

stimulation

Normal sympathetic

stimulation

Zero sympathetic

stimulation

(Parasympathetic

stimulation)

Effect on the cardiac output curve of different degrees of sympa-

Figure 9–11

thetic or parasympathetic stimulation.

York: Oxford University Press, 2002.

sec 2: The Cardiovascular System, vol 1: The Heart. New

Page E, Fozzard HA, Solaro JR: Handbook of Physiology,

Med 10:467, 2004.

Olson EN: A decade of discoveries in cardiac biology. Nat

coupling: a cellular update. Adv Physiol Educ 27:192, 2003.

Korzick DH: Regulation of cardiac excitation-contraction

17:202, 2002.

heart rate by nitric oxide is site specific. News Physiol Sci

Herring N, Danson EJ, Paterson DJ: Cholinergic control of

WB Saunders, 1973.

Cardiac Output and Its Regulation, 2nd ed. Philadelphia:

Guyton AC, Jones CE, Coleman TG: Circulatory Physiology:

Rev 35:123, 1955.

venous return curves with cardiac response curves. Physiol

Guyton AC: Determination of cardiac output by equating

Starling relationship. News Physiol Sci 16:5, 2001.

Fuchs F, Smith SH: Calcium, cross-bridges, and the Frank-

of excitatory currents. Cardiovasc Res 55:1, 2002.

Fozzard HA: Cardiac sodium and calcium channels: a history

mutations to clinical syndromes. J Clin Invest 110:1075,

Clancy CE, Kass RS: Defective cardiac ion channels: from

micity. Physiol Rev 83:59, 2003.

role in cardiac growth, contractile performance, and rhyth-

Brutsaert DL: Cardiac endothelial-myocardial signaling: its

myocytes. Circ Res 92:1182, 2003.

Brette F, Orchard C: T-tubule function in mammalian cardiac

415:198, 2002.

Bers DM: Cardiac excitation-contraction coupling. Nature

blood to the heart. This is the principal subject of

tissues, which in turn controls

entirely by the ease of blood flow through the body’s

140 mm Hg), the cardiac output is determined almost

160 mm Hg. In other words, during normal function of

Note in Figure 9–12 that increasing the arterial pres-

(up to a Limit) Does Not Decrease the

Increasing the Arterial Pressure Load

heart and eventually causes weakness. Therefore,

occurs during body exercise, but prolonged elevation

temporarily by a moderate increase in temperature, as

process.

rate, resulting in acceleration of the self-excitation

60° to 70°F. These effects presumably result from

causes a greatly decreased heart rate, falling to as low

to as fast as double normal. Decreased temperature

fever, causes a greatly increased heart rate, sometimes

Increased body temperature, as occurs when one has

Effect of Temperature on

Therefore, cardiac effects of abnormal calcium con-

normally are regulated within a very narrow range.

Fortunately, however, calcium ion levels in the blood

, similar to the effect of high potassium.

Conversely, deficiency of calcium ions causes cardiac

earlier in the chapter.

initiate the cardiac contractile process, as explained

tion. This is caused by a direct effect of calcium ions to

ions, causing the heart to go toward spastic contrac-

traction of the heart progressively weaker.

the action potential also decreases, which makes con-

As the membrane potential decreases, the intensity of

the cardiac muscle fibers, as explained in Chapter 5.

These effects result partially from the fact that a

the atria to the ventricles through the A-V bundle.

flaccid and also slows the heart rate. Large quantities

114

Unit III

The Heart

also can block conduction of the cardiac impulse from

Elevation of potassium concentration to only 8 to
12 mEq/L—two to three times the normal value—can
cause such weakness of the heart and abnormal
rhythm that this can cause death.

high potassium concentration in the extracellular
fluids decreases the resting membrane potential in

Effect of Calcium Ions.

An excess of calcium ions causes

effects almost exactly opposite to those of potassium

flaccidity

centrations are seldom of clinical concern.

Heart Function

as a few beats per minute when a person is near death
from hypothermia in the body temperature range of

the fact that heat increases the permeability of the
cardiac muscle membrane to ions that control heart

Contractile strength of the heart often is enhanced

of temperature exhausts the metabolic systems of the

optimal function of the heart depends greatly on
proper control of body temperature by the tempera-
ture control mechanisms explained in Chapter 73.

Cardiac Output

sure in the aorta does not decrease the cardiac output
until the mean arterial pressure rises above about

the heart at normal systolic arterial pressures (80 to

venous return of

Chapter 20.

References

2002.

200

250

100

Cardiac output (L

/min)

Arterial pressure (mm Hg)

150

Normal range

significantly.

the increasing pressure load cause the cardiac output to fall

Only when the arterial pressure rises above this normal limit does

Constancy of cardiac output up to a pressure level of 160 mm Hg.

Figure 9–12

and nitric oxide. Prog Biophys Mol Biol 84:217, 2004.

thetic outflow in heart failure: the roles of angiotensin II

Zucker IH, Schultz HD, Li YF, et al: The origin of sympa-

where have the stem cells gone? Annu Rev Physiol 66:29,

Sussman MA, Anversa P: Myocardial aging and senescence:

London: Longmans Green, 1918.

Starling EH: The Linacre Lecture on the Law of the Heart.

tricular function curves. Physiol Rev 35:107, 1955.

Sarnoff SJ: Myocardial contractility as described by ven-

cardiac excitation. Ann Biomed Eng 28:945, 2000.

Rudy Y: From genome to physiome: integrative models of

Heart Muscle; The Heart as a Pump and Function of the Heart Valves

Chapter 9

115

2004.