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

muscle,ventricular muscle, and specialized excitatory and conductive muscle bers.

The atrial and ventricular types of muscle contract in much the same way as
skeletal muscle, except that the duration of contraction is much longer. Conversely,
the specialized excitatory and conductive bers contract only feebly because they
contain few contractile brils;instead,they exhibit either automatic rhythmical
electrical discharge in the form of action potentials or conduction of the action
potentials through the heart,providing an excitatory system that controls the
rhythmical beating of the heart.
Thus, cardiac muscle is a syncytium of many heart muscle cells in which the
cardiac cells are so interconnected that when one of these cells becomes excited,
the action potential spreads to all of them, spreading from cell to cell throughout
the latticework interconnections.
The heart actually is composed of two syncytiums: the atrial syncytium that
constitutes the walls of the two atria, and the ventricular syncytium that constitutes
the walls of the two ventricles.The atria are separated from the ventricles by brous
tissue that surrounds the atrioventricular (A-V) valvular openings between the atria
and ventricles.Normally,potentials are not conducted from the atrial syncytium into
the ventricular syncytium directly through this brous tissue. Instead, they are
conducted only by way of a specialized conductive system called the A-V bundle, a
bundle of conductive bers several millimeters in diameter

The action potential recorded in a ventricular muscle ber, shown in Figure 93,
averages about 105 millivolts,which means that the intracellular potential rises from
a very negative value, about -85 millivolts, between beats to a slightly positive
value, about +20 millivolts,during each beat.After the initial spike, the membrane
remains depolarized for about 0.2 second, exhibiting a plateau as shown in the
gure,followed at the end of the plateau by abrupt repolarization. The presence of
this plateau in the action potential causes ventricular contraction to last as much as
15 times as long in cardiac muscle as in skeletal muscle.
What Causes the Long Action Potential and the Plateau?
In cardiac muscle, the action potential is caused by opening of two types of
channels: (1) the same fast sodium channels as those in skeletal muscle and (2)
another entirely different population of slow calcium channels, which are also called
calcium-sodium channels. This second population of channels differs from the fast
sodium channels in that they are slower to open and, even more important, remain
open for several tenths of a second.During this time,a large quantity of both calcium

and sodium ions ows through these channels to the interior of the cardiac muscle
ber,and this maintains a prolonged period of depolarization,causing the plateauin
the action potential. Further, the calcium ions that enter during this plateau phase
activate the muscle contractile process, while the calcium ions that cause skeletal
muscle contraction are derived from the intracellular sarcoplasmic reticulum.
The second major functional difference between cardiac muscle and skeletal muscle
that helps account for both the prolonged action potential and its plateau is this:
Immediately after the onset of the action potential,the permeability of the cardiac
muscle membrane for potassium ions decreases about vefold, an effect that does
not occur in skeletal muscle.This decreased potassium permeability may result from
the excess calcium inux through the calcium channels just noted. Regardless of the
cause, the decreased potassium permeability greatly decreases the outux of
positively charged potassium ions during the action potential plateau and thereby
prevents early return of the action potential voltage to its resting level.When the
slow calcium-sodium channels do close at the end of 0.2 to 0.3 second and the
inux of calcium and sodium ions ceases, the membrane permeability for potassium
ions also increases rapidly;this rapid loss of potassium from the ber immediately
returns the membrane potential to its resting level, thus ending the action potential.
The normal refractory period of the ventricle is 0.25 to 0.30 second, which is about
the duration of the prolonged plateau action potential. There is an additional
relative refractory period of about 0.05 second during which the muscle is more
difcult than normal to excite but nevertheless can be excited by a very strong
excitatory signal, as demonstrated by the early premature contraction (pag 106)
The refractory period of atrial muscle is much shorter than that for the ventricles
(about 0.15 second for the atria compared with 0.25 to 0.30 second for the
ventricles).
The term excitation-contraction coupling refers to the mechanism by which the
action potential causes the myobrils of muscle to contract.
In addition to the calcium ions that are released into the sarcoplasm from the
cisternae of the sarcoplasmic reticulum, a large quantity of extra calcium ions also
diffuses into the sarcoplasm from the T tubules themselves at the time of the action
potential. Indeed, without this extra calcium from the T tubules, 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. Conversely,
the T tubules of cardiac muscle have a diameter 5 times as great as that of the
skeletal muscle tubules, which means a volume 25 times as great.
Also, inside the T tubules is a large quantity of mucopolysaccharides that are
electronegatively charged and bind an abundant store of calcium ions, keeping

these always available for diffusion to the interior of the cardiac muscle ber when a
T tubule action potential appears.
The strength of contraction of cardiac muscle depends to a great extent on the
concentration of calcium ions in the extracellular uids.

Cardiac muscle begins to contract a few milliseconds after the action potential
begins and continues to contract until a few milliseconds after the action potential
ends. Therefore, the duration of contraction 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 ventricular muscle.

The cardiac events that occur from the beginning of one heartbeat to the beginning
of the next are called the cardiac cycle.
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 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.
pag 107
Blood normally ows continually from the great veins into the atria; about 80 per
cent of the blood ows directly through the atria into the ventricles even before the
atria contract. Then, atrial contraction usually causes an additional 20 per cent
lling of the ventricles. Therefore, the atria simply function as primer pumps that
increase the ventricular pumping effectiveness as much as 20 per cent. However,
the 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 resting body.Therefore,when the atria
fail to function, the difference is unlikely to be noticed unless a person
exercises;then acute signs of heart failure occasionally develop, especially
shortness of breath.
The a waveis caused by atrial contraction.Ordinarily, the right atrial pressure
increases 4 to 6 mm Hg during atrial contraction, and the left atrial pressure
increases about 7 to 8 mm Hg. The c wave occurs when the ventricles begin to
contract; it is caused partly by slight backow of blood into the atria at the onset of
ventricular contraction but mainly by bulging of the A-V valves backward toward the

atria because of increasing pressure in the ventricles. The v wave occurs toward the
end of ventricular contraction; it results from slow ow of blood into the atria from
the veins while the A-V valves are closed during ventricular contraction. Then, when
ventricular contraction is over, the A-V valves open, allowing this stored atrial blood
to ow rapidly into the ventricles and causing the v wave to disappear.

During ventricular systole,large amounts of blood accumulate in the right and left
atria because of the closed A-V valves. Therefore, as soon as systole is over and the
ventricular pressures fall again to their low diastolic values, the moderately
increased pressures that have developed in the atria during ventricular systole
immediately push the A-V valves open and allow blood to ow rapidly into the
ventricles, as shown by the rise of the left ventricular volume curve in Figure 9
5.This is called the period of rapid lling of the ventricles.
The period of rapid lling lasts for about the rst third of diastole. During the middle
third of diastole, only a small amount of blood normally ows into the ventricles;
this is blood that continues to empty into the atria from the veins and passes
through the atria directly into the ventricles.
During the last third of diastole, the atria contract and give an additional thrust to
the inow of blood into the ventricles;this accounts for about 20 per cent of the
lling of the ventricles during each heart cycle.
Period of Isovolumic (Isometric) Contraction. Immediately after ventricular
contraction begins, the ventricular pressure rises abruptly, as shown in Figure 95,
causing the A-V valves to close. Then an additional 0.02 to 0.03 second is required
for the ventricle to build up sufcient pressure to push the semilunar (aortic and
pulmonary) valves open against the pressures in the aorta and pulmonary
artery.Therefore,during this period, contraction is occurring in the ventricles, but
there is no emptying.This is called the period of isovolumic or isometric contraction,
meaning that tension is increasing in the muscle but little or no shortening of the
muscle bers is occurring.
Period of Ejection. When the left ventricular pressure rises slightly above 80 mm
Hg (and the right ventricular pressure slightly above 8 mm Hg), the
ventricular pressures push the semilunar valves open. Immediately, blood begins to
pour out of the ventricles, with about 70 per cent of the blood emptying occurring
during the rst third of the period of ejection and the remaining 30 per cent
emptying during the next two thirds.Therefore, the rst third is called the period of
rapid ejection, and the last two thirds, the period of slow ejection.
Period of Isovolumic (Isometric) Relaxation. At the end of systole, ventricular
relaxation begins suddenly, allowing both the right and left intraventricular

pressures to decrease rapidly.The elevated pressures in the distended large arteries

that have just been lled with blood from the contracted ventricles immediately
push blood back toward the ventricles,which snaps the aortic and pulmonary valves
closed. For another 0.03 to 0.06 second, the ventricular muscle continues to relax,
even though the ventricular volume does not change, giving rise to the period of
isovolumic or isometric relaxation. During this period, the intraventricular pressures
decrease rapidly back to their low diastolic levels. Then the A-V valves open to begin
a new cycle of ventricular pumping.
During diastole,normal lling of the ventricles increases the volume of each
ventricle to about 110 to 120 milliliters. This volume is called the end-diastolic
volume.
Then, as the ventricles empty during systole, the volume decreases about 70
milliliters, which is called the stroke volume output.

The remaining volume in each ventricle,about 40 to 50 milliliters,is called the endsystolic volume.
The fraction of the end-diastolic volume that is ejected is called the ejection
fraction usually equal to about 60 per cent.
The A-V valves (the tricuspid and mitral valves) prevent backow of blood from the
ventricles to the atria during systole, and the semilunar valves (the aortic and
pulmonary artery valves) prevent backow from the aorta and pulmonary arteries
into the ventricles during diastole
These valves, close and open passively. That is, they close when a backward
pressure gradient pushes blood backward, and they open when a forward pressure
gradient forces blood in the forward direction. For anatomical reasons, the thin,
lmy A-V valves require almost no backow to cause closure, whereas the much
heavier semilunar valves require rather rapid backow for a few milliseconds.
The papillary muscles contract when the ventricular walls contract, but contrary to
what might be expected, they do not help the valves to close.Instead,they pull the
vanes of the valves inward toward the ventricles to prevent their bulging too far
backward toward the atria during ventricular contraction. If a chorda tendinea
becomes ruptured or if one of the papillary muscles becomes paralyzed, the valve
bulges far backward during ventricular contraction, sometimes so far that it leaks
severely and results in severe or even lethal cardiac incapacity.

When the left ventricle contracts,the ventricular pressure increases rapidly until the
aortic valve opens. Then,after the valve opens,the pressure in the ventricle rises
much less rapidly, as shown in Figure 95, because blood immediately ows out of
the ventricle into the aorta and then into the systemic distribution arteries. The
entry of blood into the arteries causes the walls of these arteries to stretch and the
pressure to increase to about 120 mm Hg. Next, at the end of systole, after the left
ventricle stops ejecting blood and the aortic valve closes, the elastic walls of the
arteries maintain a high pressure in the arteries, even during diastole. A so-called
incisura occurs in the aortic pressure curve when the aortic valve closes.This is
caused by a short period of backward ow of blood immediately before closure of
the valve,followed by sudden cessation of the backow. After the aortic valve has
closed,the pressure in the aorta decreases slowly throughout diastole because the
blood stored in the distended elastic arteries ows continually through the
peripheral vessels back to the veins. Before the ventricle contracts again, the aortic
pressure usually has fallen to about 80 mm Hg (diastolic pressure), which is two
thirds the maximal pressure of 120 mm Hg (systolic pressure) that occurs in the
aorta during ventricular contraction. The pressure curves in the right ventricle and
pulmonary artery are similar to those in the aorta,except that the pressures are only
about one sixth as great
When the ventricles contract, one rst hears a sound caused by closure of the A-V
valves.The vibration is low in pitch and relatively long-lasting and is known as the
rst heart sound.When the aortic and pulmonary valves close at the end of
systole, one hears a rapid snap because these valves close rapidly,and the
surroundings vibrate for a short period. This sound is called the second heart
sound.
The stroke work output of the heart is the amount of energy that the heart
converts to work during each heartbeat while pumping blood into the arteries
Work output of the heart is in two forms.First,by far the major proportion is used to
move the blood from the low-pressure veins to the high-pressure arteries. This is
called volume-pressure work or external work. Second, a minor proportion of the
energy is used to accelerate the blood to its velocity of ejection through the aortic
and pulmonary valves. This is the kinetic energy of blood ow component of the
work output
pag 110
For the normal right ventricle, the maximum systolic pressure is between 60 and 80
mm Hg.
The red lines in Figure 97 form a loop called the volume-pressure diagram of
the cardiac cycle for normal function of the left ventricle.It is divided into four
phases.

Phase I: Period of lling. This phase in the volumepressure diagram begins at a

ventricular volume of about 45 milliliters and a diastolic pressure near 0 mm Hg.
Forty-ve milliliters is the amount of blood that remains in the ventricle after the
previous heartbeat and is called the end-systolic volume. As venous blood ows into
the ventricle from the left atrium, the ventricular volume normally increases to
about 115 milliliters, called the end-diastolic volume, an increase of 70
milliliters.Therefore, the volume-pressure diagram during phase I extends along the
line labeled I, with the volume increasing to 115 milliliters and the diastolic
pressure rising to about 5 mm Hg.
Phase II: Period of isovolumic contraction. During isovolumic contraction, the
volume of the ventricle does not change because all valves are closed. However,
the pressure inside the ventricle increases to equal the pressure in the aorta, at a
pressure value of about 80 mm Hg, as depicted by the arrow end of the line labeled
II.
Phase III: Period of ejection. During ejection, the systolic pressure rises even
higher because of still more contraction of the ventricle.At the same time, the
volume of the ventricle decreases because the aortic valve has now opened and
blood ows out of the ventricle into the aorta.Therefore, the curve labeled III
traces the changes in volume and systolic pressure during this period of ejection.
Phase IV: Period of isovolumic relaxation. At the end of the period of ejection,
the aortic valve closes, and the ventricular pressure falls back to the diastolic
pressure level.The line labeled IV traces this decrease in intraventricular pressure
without any change in volume.Thus, the ventricle returns to its starting point, with
about 45 milliliters of blood left in the ventricle and at an atrial pressure near 0 mm
Hg. Readers well trained in the basic principles of physics should recognize that the
area subtended by this functional volume-pressure diagram (the tan shaded area,
labeled EW) represents the net external work output of the ventricle during its
contraction cycle.In experimental studies of cardiac contraction, this diagram is
used for calculating cardiac work output. When the heart pumps large quantities of
blood, the area of the work diagram becomes much larger.That is, it extends far to
the right because the ventricle lls with more blood during diastole,it rises much
higher because the ventricle contracts with greater pressure, and it usually extends
farther to the left because the ventricle contracts to a smaller volumeespecially if
the ventricle is stimulated to increased activity by the sympathetic nervous system.
Concepts of Preload and Afterload. In assessing the contractile properties of
muscle, it is important to specify the degree of tension on the muscle when it
begins to contract,which is called the preload,and to specify the load against which
the muscle exerts its contractile force, which is called the afterload. For cardiac
contraction, the preload is usually considered to be the end-diastolic pressure when
the ventricle has become lled. The afterload of the ventricle is the pressure in the
artery leading from the ventricle.In Figure 97,this corresponds to the systolic

pressure described by the phase III curve of the volume-pressure diagram.

(Sometimes the afterload is loosely considered to be the resistance in the
circulation rather than the pressure.)

Preload
Preload, also known as the left ventricular end-diastolic pressure (LVEDP), is the
amount of ventricular stretch at the end of diastole. Think of it as the heart loading
up for the next big squeeze of the ventricles during systole. Some people remember
this by using an analogy of a balloon blow air into the balloon and it stretches; the
more air you blow in, the greater the stretch.

Afterload
Afterload, also known as the systemic vascular resistance (SVR), is the amount of
resistance the heart must overcome to open the aortic valve and push the blood
volume out into the systemic circulation. If you think about the balloon analogy,
afterload is represented by the knot at the end of the balloon. To get the air out, the
balloon must work against that knot.

Cardiac Output & Cardiac Index

Cardiac output is the volume of blood the heart pumps per minute. Cardiac output is
calculated by multiplying the stroke volume by the heart rate; normal cardiac
output is about 4 to 8 L/min, but varies depending on the bodys metabolic needs.
Cardiac index is a calculation of the cardiac output divided by the persons body
surface area (BSA).
During heart muscle contraction, most of the expended chemical energy is
converted into heat and a much smaller portion into work output. The ratio of work
output to total chemical energy expenditure is called the efciency of cardiac
contraction, or simply efciency of the heart. Maximum efciency of the normal
heart is between 20 and 25 per cent.In heart failure,this can decrease to as low as 5
to 10 per cent.
The basic means by which the volume pumped by the heart is regulated are (1)
intrinsic cardiac regulation of pumping in response to changes in volume of blood
owing into the heart and (2) control of heart rate and strength of heart pumping by
the autonomic nervous system.

under most conditions, the amount of blood pumped by the heart each minute is
determined almost entirely by the rate of blood ow into the heart from the
veins,which is called venous return.
This intrinsic ability of the heart to adapt to increasing volumes of inowing blood is
called the FrankStarling mechanism of the heart, in honor of Frank and Starling,two

great physiologists of a century ago.Basically, the Frank-Starling mechanism means

that the greater the heart muscle is stretched during lling, the greater is the force
of contraction and the greater the quantity of blood pumped into the aorta.Or,stated
another way:Within physiologic limits,the heart pumps all the blood that
returns to it by the way of the veins.
When an extra amount of blood ows into the ventricles, the cardiac muscle itself is
stretched to greater length.This in turn causes the muscle to contract with
increased force because the actin and myosin laments are brought to a more
nearly optimal degree of overlap for force generation.Therefore, the ventricle,
because of its increased pumping, automatically pumps the extra blood into the
arteries.
Stretch of the right atrial wall directly increases the heart rate by 10 to 20 per cent;
this, too, helps increase the amount of blood pumped each minute, although its
contribution is much less than that of the Frank-Starling mechanism.
pag 112

Strong sympathetic stimulation can increase the heart rate in young adult humans
from the normal rate of 70 beats per minute up to 180 to 200 and,rarely, even 250
beats per minute.Also,sympathetic stimulation increases the force of heart
contraction to as much as double normal, thereby increasing the volume of blood
pumped and increasing the ejection pressure
The vagal bers are distributed mainly to the atria and not much to the ventricles,
where the power contraction of the heart occurs.This explains the effect of vagal
stimulation mainly to decrease heart rate rather than to decrease greatly the
strength of heart contraction. Nevertheless, the great decrease in heart rate
combined with a slight decrease in heart contraction strength can decrease
ventricular pumping 50 per cent or more.
Excess potassium in the extracellular uids causes the heart to become dilated and
accid and also slows the heart rate. Large quantities also can block conduction of
the cardiac impulse from the atria to the ventricles through the A-V bundle.
An excess of calcium ions causes effects almost exactly opposite to those of
potassium ions, causing the heart to go toward spastic contraction.This is caused by
a direct effect of calcium ions to initiate the cardiac contractile process, as
explained earlier in the chapter. Conversely,deciency of calcium ions causes
cardiac accidity, similar to the effect of high potassium. Fortunately, however,
calcium ion levels in the blood normally are regulated within a very narrow range.

Therefore, cardiac effects of abnormal calcium concentrations are seldom of clinical

concern.
Note that the resting membrane potential of the sinus nodal ber between
discharges has a negativity of about -55 to -60 millivolts,in comparison with -85 to
-90 millivolts for the ventricular muscle ber.
The cause of this lesser negativity is that the cell membranes of the sinus bers are
naturally leaky to sodium and calcium ions, and positive charges of the entering
sodium and calcium ions neutralize much of the intracellular negativity.
At this level of -55 millivolts, the fast sodium channels mainly have already become
inactivated, which means that they have become blocked.
Therefore, only the slow sodium-calcium channels can open (i.e., can become
activated) and thereby cause the action potential. As a result, the atrial nodal
action potential is slower to develop than the action potential of the ventricular
muscle. Also, after the action potential does occur, return of the potential to its
negative state occurs slowly as well, rather than the abrupt return that occurs for
the ventricular ber.
threshold voltage of about -40 millivolts, the sodium-calcium channels become
activated,thus causing the action potential.
The slow conduction in the transitional,nodal,and penetrating A-V bundle bers is
caused mainly by diminished numbers of gap junctions between successive cells in
the conducting pathways,so that there is great resistance to conduction of
excitatory ions from one conducting ber to the next. Therefore,it is easy to see why
each succeeding cell is slow to be excited.
pag 120
The A-V nodal bers, when not stimulated from some outside source, discharge at
an intrinsic rhythmical rate of 40 to 60 times per minute,and the Purkinje bers
discharge at a rate somewhere between 15 and 40 times per minute.These rates
are in contrast to the normal rate of the sinus node of 70 to 80 times per minute.
Thus, the sinus node controls the beat of the heart because its rate of rhythmical
discharge is faster than that of any other part of the heart.Therefore,the sinus node
is virtually always the pacemaker of the normal heart.
A pacemaker elsewhere than the sinus node is called an ectopic pacemaker.

When A-V block occursthat is, when the cardiac impulse fails to pass from the
atria into the ventricles through the A-V nodal and bundle systemthe atria
continue to beat at the normal rate of rhythm of the sinus node, while a new
pacemaker usually develops in the Purkinje system of the ventricles and drives the
ventricular muscle at a new rate somewhere between 15 and 40 beats per
minute.After sudden A-V bundle block, the Purkinje system does not begin to emit
its intrinsic rhythmical impulses until 5 to 20 seconds later because, before the
blockage, the Purkinje bers had been overdriven by the rapid sinus impulses and,
consequently, are in a suppressed state. During these 5 to 20 seconds,the
ventricles fail to pump blood,and the person faints after the rst 4 to 5 seconds
because of lack of blood ow to the brain.This delayed pickup of the heartbeat is
called Stokes-Adams syndrome. If the delay period is too long, it can lead to death.
The parasympathetic nerves (the vagi) are distributed mainly to the S-A and A-V
nodes, to a lesser extent to the muscle of the two atria, and very little directly to the
ventricular muscle. The sympathetic nerves,conversely,are distributed to all parts of
the heart, with strong representation to the ventricular muscle as well as to all the
other areas.

Stimulation of the parasympathetic nerves to the heart (the vagi) causes the
hormone acetylcholine to be released at the vagal endings. This hormone has two
major effects on the heart. First, it decreases the rate of rhythm of the sinus node,
and second, it decreases the excitability of the A-V junctional bers between the
atrial musculature and the A-V node, thereby slowing transmission of the cardiac
impulse into the ventricles. Weak to moderate vagal stimulation slows the rate of
heart pumping,often to as little as one half normal. And strong stimulation of the
vagi can stop completely the rhythmical excitation by the sinus node or block
completely transmission of the cardiac impulse from the atria into the ventricles
through the A-V mode.In either case,rhythmical excitatory signals are no longer
transmitted into the ventricles. The ventricles stop beating for 5 to 20 seconds,but
then some point in the Purkinje bers, usually in the ventricular septal portion of the
A-V bundle, develops a rhythm of its own and causes ventricular contraction at a
rate of 15 to 40 beats per minute.This phenomenon is called ventricular escape.
Thus,the process of ventricular repolarization extends over a long period, about
0.15 second.For this reason,the T wave in the normal electrocardiogram is a
prolonged wave,but the voltage of the T wave is considerably less than the voltage
of the QRS complex, partly because of its prolonged length.

The normal P-Q interval is about 0.16 second. (Often this interval is called the P-R
interval because the Q wave is likely to be absent.)

A vector is an arrow that points in the direction of the electrical potential generated
by the current ow, with the arrowhead in the positive direction. Also, by
convention, the length of the arrow is drawn proportional to the voltage of the
potential.
Each lead is actually a pair of electrodes connected to the body on opposite sides
of the heart,and the direction from negative electrode to positive electrode is called
the axis of the lead. Lead I is recorded from two electrodes placed respectively on
the two arms.Because the electrodes lie exactly in the horizontal direction, with the
positive electrode to the left, the axis of lead I is 0 degrees.
In recording lead II, electrodes are placed on the right arm and left leg. The right
arm connects to the torso in the upper right-hand corner and the left leg connects in
the lower left-hand corner.Therefore, the direction of this lead is about +60 degrees.
By similar analysis, it can be seen that lead III has an axis of about +120
degrees;lead aVR,+210 degrees; aVF,+90 degrees;and aVL-30 degrees.The
directions of the axes of all these leads are shown in Figure 123, which is known as
the hexagonal reference system.The polarities of the electrodes are shown by the
plus and minus signs in the gure.

when the vector in the heart is in a direction almost perpendicular to the axis of the
lead, the voltage recorded in the electrocardiogram of this lead is very low.
Conversely, when the heart vector has almost exactly the same axis as the lead
axis,essentially the entire voltage of the vector will be recorded.
When the cardiac impulse enters the ventricles through the atrioventricular bundle,
the rst part of the ventricles to become depolarized is the left endocardial surface
of the septum. Then depolarization spreads rapidly to involve both endocardial
surfaces of the septum
pag 134
the septum and other endocardial areas have a longer period of
contraction than most of the external surfaces of the heart.Therefore, the
greatest portion of ventricular muscle mass to repolarize rst is the entire
outer surface of the ventricles,especially near the apex of the heart.The

endocardial areas, conversely, normally repolarize last. This sequence of

repolarization is postulated to be caused by the high blood pressure inside
the ventricles during contraction, which greatly reduces coronary blood
ow to the endocardium, thereby slowing repolarization in the endocardial
areas.
Because the outer apical surfaces of the ventricles repolarize before the inner
surfaces, the positive end of the overall ventricular vector during repolarization is
toward the apex of the heart.As a result,the normal T wave in all three bipolar limb
leads is positive,which is also the polarity of most of the normal QRS complex.
T wave 0.15 s
Spread of depolarization through the atrial muscle is much slower than in the
ventricles because the atria have no Purkinje system for fast conduction of the
depolarization signal. Therefore, the musculature around the sinus node becomes
depolarized a long time before the musculature in distal parts of the atria.Because
of this, the area in the atria that also becomes repolarized rst is the sinus nodal
region, the area that had originally become depolarized rst.
Therefore,the atrial repolarization vector is backward to the vector of
depolarization.
the so-called atrial T wave follows about 0.15 second after the atrial P wave, but
this T wave is on the opposite side of the zero reference line from the P wave;that
is,it is normally negative rather than positive in the three standard bipolar limb
leads.
It has been noted in the discussion up to this point that the vector of current ow
through the heart changes rapidly as the impulse spreads through the myocardium.
It changes in two aspects: First, the vector increases and decreases in length
because of increasing and decreasing voltage of the vector. Second, the vector
changes direction because of changes in the average direction of the electrical
potential from the heart
pag 137
This preponderant direction of the potential during depolarization is called
the mean electrical axis of the ventricles. The mean electrical axis of the
normal ventricles is 59 degrees. In many pathological conditions of the
heart, this direction changes markedly sometimes even to opposite
poles of the heart.
Although the mean electrical axis of the ventricles averages about 59 degrees, this
axis can swing even in the normal heart from about 20 degrees to about 100

degrees. The causes of the normal variations are mainly anatomical differences in
the Purkinje distribution system or in the musculature itself of different hearts.
When one ventricle greatly hypertrophies, the axis of the heart shifts toward the
hypertrophied ventricle for two reasons. First, a far greater quantity of muscle exists
on the hypertrophied side of the heart than on the other side,and this allows excess
generation of electrical potential on that side. Second, more time is required for the
depolarization wave to travel through the hypertrophied ventricle than through the
normal ventricle. Consequently, the normal ventricle becomes depolarized
considerably in advance of the hypertrophiedventricle,and this causes a strong
vector from the normal side of the heart toward the hypertrophied side,which
remains strongly positively charged.Thus, the axis deviates toward the
hypertrophied ventricle.
A similar picture of left axis deviation occurs when the left ventricle hypertrophies
as a result of aortic valvular stenosis,aortic valvular regurgitation,or any number of
congenital heart conditionsin which the left ventricle enlarges while the right
ventricle remains relatively normal in size.
he right axis deviation demonstrated in this gure was caused by hypertrophy of
the right ventricle as a result of congenital pulmonary valve stenosis. Right axis
deviation also can occur in other congenital heart conditions that cause hypertrophy
of the right ventricle,such as tetralogy of Fallotand interventricular septal defect.
The cause of high-voltage QRS complexes most often is increased muscle mass of
the heart, which ordinarily results from hypertrophy of the muscle in response to
excessive load on one part of the heart or the other. For example, the right ventricle
hypertrophies when it must pump blood through a stenotic pulmonary valve, and
the left ventricle hypertrophies when a person has high blood pressure.The
increased quantity of muscle causes generation of increased quantities of electricity
around the heart.As a result, the potentials are greater than normal
Decreased Voltage Caused by Cardiac Myopathies. One of the most common
causes of decreased voltage of the QRS complex is a series of old myocardial artery
infarctionswith resultant diminished muscle mass.This also causes the
depolarization wave to move through the ventricles slowly and prevents major
portions of the heart from becoming massively depolarized all at once.
Consequently, this condition causes some prolongation of the QRS complex along
with the decreased voltage
Decreased Voltage Caused by Conditions Surrounding the Heart. One of the
most important causes of decreased voltage in electrocardiographic leads is uid in
the pericardium.Because extracellular uid conducts electrical currents with great

ease, a large portion of the electricity owing out of the heart is conducted from one
part of the heart to another through the pericardial uid.Thus,this effusion
effectively short-circuits the electrical potentials generated by the heart,
decreasing the electrocardiographic voltages that reach the outside surfaces of the
body. Pleural effusion, to a lesser extent, also can short-circuit the electricity
around the heart,so that the voltages at the surface of the body and in the
electrocardiograms are decreased. Pulmonary emphysema can decrease the
electrocardiographic potentials, but by a different method from that of pericardial
effusion.In pulmonary emphysema, conduction of electrical current through the
lungs is depressed considerably because of excessive quantity of air in the
lungs.Also, the chest cavity enlarges, and the lungs tend to envelop the heart to a
greater extent than normally.Therefore,the lungs act as an insulator to prevent
spread of electrical voltage from the heart to the surface of the body,and this
results in decreased electrocardiographic potentials in the various leads.
The normal QRS complex lasts 0.06 to 0.08 second,whereas in hypertrophy or
dilatation of the left or right ventricle, the QRS complex may be prolonged to 0.09 to
0.12 second.
Bizarre patterns of the QRS complex most frequently are caused by two conditions:
(1) destruction of cardiac muscle in various areas throughout the ventricular
system,with replacement of this muscle by scar tissue, and (2) multiple small local
blocks in the conduction of impulses at many points in the Purkinje system. As a
result, cardiac impulse conduction becomes irregular,causing rapid shifts in voltages
and axis deviations.This often causes double or even triple peaks in some of the
electrocardiographic leads
Many different cardiac abnormalities,especially those that damage the heart muscle
itself, often cause part of the heart to remain partially or totally depolarized all the
time. When this occurs, current ows between the pathologically depolarized and
the normally polarized areas even between heartbeats. This is called a current of
injury. Note especially that the injured part of the heart is negative, because this is
the part that is depolarized and emits negative charges into the surrounding uids,
whereas the remainder of the heart is neutral or positive polarity.
The causes of the cardiac arrhythmias are usually one or a combination of the
following abnormalities in the rhythmicity-conduction system of the heart:
1. Abnormal rhythmicity of the pacemaker
2. Shift of the pacemaker from the sinus node to another place in the heart
3. Blocks at different points in the spread of the impulse through the heart
4. Abnormal pathways of impulse transmission through the heart

5. Spontaneous generation of spurious impulses in almost any part of the heart

The term tachycardia means fast heart rate, usually dened in an adult person as
faster than 100 beats per minute.
The term bradycardia means a slow heart rate, usually dened as fewer than 60
beats per minute.
Sinus arrhythmia can result from any one of many circulatory conditions that alter
the strengths of the sympathetic and parasympathetic nerve signals to the heart
sinus node. In the respiratory type of sinus arrhythmia, as shown in Figure 133,
this results mainly from spillover of signals from the medullary respiratory center
into the adjacent vasomotor center during inspiratory and expiratory cycles of
respiration.The spillover signals cause alternate increase and decrease in the
number of impulses transmitted through the sympathetic and vagus nerves to the
heart.
In rare instances, the impulse from the sinus node is blocked before it enters the
atrial muscle. This phenomenon is demonstrated in Figure 134, which shows
sudden cessation of P waves,with resultant standstill of the atria.However,the
ventricles pick up a new rhythm, the impulse usually originating spontaneously in
the atrioventricular (A-V) node,so that the rate of the ventricular QRS-T complex is
slowed but not otherwise altered.
Prolonged P-R (or P-Q) IntervalFirst Degree Block. The usual lapse of time between
beginning of the P wave and beginning of the QRS complex is about 0.16 second
when the heart is beating at a normal rate. This socalled P-R interval usually
decreases in length with faster heartbeat and increases with slower heartbeat.In
general,when the P-R interval increases to greater than 0.20 second,the P-R interval
is said to be prolonged,and the patient is said to have rst degree incomplete heart
block.

Second Degree Block. When conduction through the A-V bundle is slowed enough to
increase the P-R interval to 0.25 to 0.45 second, the action potential sometimes is
strong enough to pass through the bundle into the ventricles and sometimes is not
strong enough. In this instance, there will be an atrial P wave but no QRS-T
wave,and it is said that there are dropped beatsof the ventricles. This condition is
called second degree heart block. At times, every other beat of the ventricles is
dropped,so that a 2:1 rhythmdevelops,with the atria beating twice for every single
beat of the ventricles.At other times, rhythms of 3:2 or 3:1 also develop.
Complete A-V Block (Third Degree Block). When the condition causing poor

conduction in the A-V node or A-V bundle becomes severe, complete block of the
impulse from the atria into the ventricles occurs.In this instance, the ventricles
spontaneously establish their own signal, usually originating in the A-V node or A-V
bundle. Therefore, the P waves become dissociated from the QRS-T complexes
Each time A-V conduction ceases,the ventricles often do not start their own beating
until after a delay of 5 to 30 seconds. This results from the phenomenon called
overdrive suppression. This means that ventricular excitability is at rst in a
suppressed state because the ventricles have been driven by the atria at a rate
greater than their natural rate of rhythm. However, after a few seconds, some part
of the Purkinje system beyond the block,usually in the distal part of the A-V node
beyond the blocked point in the node, or in the A-V bundle, begins discharging
rhythmically at a rate of 15 to 40 times per minute and acting as the pacemaker of
the ventricles.This is called ventricular escape.
Because the brain cannot remain active for more than 4 to 7 seconds without blood
supply,most patients faint a few seconds after complete block occurs because the
heart does not pump any blood for 5 to 30 seconds, until the ventricles
escape.After escape,however,the slowly beating ventricles usually pump enough
blood to allow rapid recovery from the faint and then to sustain the person.These
periodic fainting spells are known as the Stokes-Adams syndrome.
Causes of Premature Contractions. Most premature contractions result from ectopic
fociin the heart,which emit abnormal impulses at odd times during the cardiac
rhythm. Possible causes of ectopic foci are (1) local areas of ischemia (2) small
calcied plaques at different points in the heart,which press against the adjacent
cardiac muscle so that some of the bers are irritated; and (3) toxic irritation of the
A-V node, Purkinje system,or myocardium caused by drugs,nicotine,or caffeine.
Ventricular brillation-partial contraction
First,block of the impulses in some directions but successful transmission in other
directions creates one of the necessary conditions for a re-entrant signal to develop
that is, transmission of some of the depolarization waves around the heart in only
some directions but not other directions. Second,the rapid stimulation of the heart
causes two changes in the cardiac muscle itself, both of which predispose to circus
movement:(1) The velocity of conduction through the heart muscle decreases,
which allows a longer time interval for the impulses to travel around the heart. (2)
The refractory period of the muscle is shortened, allowing re-entry of the impulse
into previously excited heart muscle within a much shorter time than normally.
Third, one of the most important features of brillation is the division of impulses,as
demonstrated in heart A. When a depolarization wave reaches a refractory area in
the heart, it travels to both sides around the refractory area. Thus, a single impulse
becomes two impulses. Then, when each of these reaches another refractory area,

it, too, divides to form two more impulses.In this way,many new wave fronts are
continually being formed in the heart by progressive chain reactions
until,nally,there are many small depolarization waves traveling in many directions
at the same time.
Pressures in the Various Portions of the Circulation. Because the heart pumps blood
continually into the aorta, the mean pressure in the aorta is high,averaging about
100 mm Hg.Also, because heart pumping is pulsatile, the arterial pressure
alternates between a systolic pressure level of 120 mm Hg and a diastolic pressure
level of 80 mm Hg,as shown on the left side of Figure 142. As the blood ows
through the systemic circulation, its mean pressure falls progressively to about 0
mm Hg by the time it reaches the termination of the venae cavae where they empty
into the right atrium of the heart. The pressure in the systemic capillaries varies
from as high as 35 mm Hg near the arteriolar ends to as low as 10 mm Hg near the
venous ends, but their average functional pressure in most vascular beds is about
17 mm Hg, a pressure low enough that little of the plasma leaks through the minute
pores of the capillary walls,even though nutrients can diffuse easily through these
same pores to the outlying tissue cells.
pulmonary artery systolic pressure averages about 25 mm Hg and diastolic pressure
8 mm Hg,with a mean pulmonary arterial pressure of only 16 mm Hg. The mean
pulmonary capillary pressure averages only 7 mm Hg.
Basic Theory of Circulatory Function
1. The rate of blood ow to each tissue of the body is almost always precisely
controlled in relation to the tissue need.
2. The cardiac output is controlled mainly by the sum of all the local tissue ows.
the heart acts as an automaton, responding to the demands of the tissues.
3. In general the arterial pressure is controlled independently of either local blood
ow control or cardiac output control.
Blood ow through a blood vessel is determined by two factors: (1) pressure
difference of the blood between the two ends of the vessel,also sometimes called
pressure gradientalong the vessel,which is the force that pushes the blood
through the vessel, and (2) the impediment to blood ow through the vessel,which
is called vascular resistance.
Blood ow means simply the quantity of blood that passes a given point in the
circulation in a given period of time.
When blood ows at a steady rate through a long,smooth blood vessel,it ows in
streamlines, with each layer of blood remaining the same distance from the vessel
wall. Also, the central most portion of the blood stays in the center of the
vessel.This type of ow is called laminar ow or streamline ow, and it is the

opposite of turbulent ow, which is blood owing in all directions in the vessel and
continually mixing within the vessel, as discussed subsequently.

the parabolic prole for velocity of blood ow. The cause of the parabolic prole is
the following:The uid molecules touching the wall barely move because of
adherence to the vessel wall.The next layer of molecules slips over these, the third
layer over the second, the fourth layer over the third, and so forth.Therefore, the
uid in the middle of the vessel can move rapidly because many layers of slipping
molecules exist between the middle of the vessel and the vessel wall; thus, each
layer toward the center ows progressively more rapidly than the outer layers.
When the rate of blood ow becomes too great, when it passes by an obstruction in
a vessel, when it makes a sharp turn, or when it passes over a rough surface, the
ow may then become turbulent, or disorderly, rather than streamline
When eddy currents are present,the blood ows with much greater resistance than
when the ow is streamline because eddies add tremendously to the overall friction
of ow in the vessel.
Actually,blood pressure means the force exerted by the blood against any unit area
of the vessel wall.
Resistance is the impediment to blood ow in a vessel, but it cannot be measured
by direct means
Note particularly in this equation that the rate of blood ow is directly proportional
to the fourth power of the radius of the vessel, which demonstrates once again that
the diameter of a blood vessel (which is equal to twice the radius) plays by far the
greatest role of all factors in determining the rate of blood ow through a vessel.
an increase in arterial pressure not only increases the force that pushes blood
through the vessels but also distends the vessels at the same time, which decreases
vascular resistance.
Anatomically,the walls of the arteries are far stronger than those of the
veins.Consequently,the arteries, on average, are about eight times less distensible
than the veins.That is, a given increase in pressure causes about eight times as
much increase in blood in a vein as in an artery of comparable size.
Vascular distensibility normally is expressed as the fractional increase in volume
for each millimeter of mercury rise in pressure.
compliance is equal to distensibility times volume.

In aortic stenosis, the diameter of the aortic valve opening is reduced signicantly,
and the aortic pressure pulse is decreased signicantly because of diminished blood
ow outward through the stenotic valve.
In patent ductus arteriosus, one half or more of the blood pumped into the aorta by
the left ventricle ows immediately backward through the wide-open ductus into the
pulmonary artery and lung blood vessels,thus allowing the diastolic pressure to fall
very low before the next heartbeat.
In aortic regurgitation, the aortic valve is absent or will not close
completely.Therefore, after each heartbeat, the blood that has just been pumped
into the aorta ows immediately backward into the left ventricle.As a result,the
aortic pressure can fall all the way to zero between heartbeats.Also, there is no
incisura in the aortic pulse contour because there is no aortic valve to close.
Blood from all the systemic veins ows into the right atrium of the
heart;therefore,the pressure in the right atrium is called the central venous
pressure.

The normal right atrial pressure is about 0 mm Hg, which is equal to the
atmospheric pressure around the body.
The hydrostatic pressure in the capillaries tends to force uid and its dissolved
substances through the capillary pores into the interstitial spaces. Conversely,
osmotic pressure caused by the plasma proteins (called colloid osmotic pressure)
tends to cause uid movement by osmosis from the interstitial spaces into the
blood.
This osmotic pressure exerted by the plasma proteins normally prevents signicant
loss of uid volume from the blood into the interstitial spaces.

1. The capillary pressure (Pc), which tends to force uid outward through the
capillary membrane.
2. The interstitial uid pressure (Pif), which tends to force uid inward through the
capillary membrane when Pif is positive but outward when Pif is negative.
3. The capillary plasma colloid osmotic pressure (Pp), which tends to cause osmosis
of uid inward through the capillary membrane.

4. The interstitial uid colloid osmotic pressure (Pif), which tends to cause osmosis
of uid outward through the capillary membrane.
If the sum of these forces,the net ltration pressure, is positive,there will be a net
uid ltration across the capillaries.If the sum of the Starling forces is negative,
there will be a net uid absorption from the interstitial spaces into the capillaries
As discussed later, the NFP is slightly positive under normal conditions, resulting in
a net ltration of uid across the capillaries into the interstitial space in most
organs.
Filtration K NFP
The average capillary pressure at the arterial ends of the capillaries is 15 to 25 mm
Hg greater than at the venous ends. Because of this difference, uid lters out of
the capillaries at their arterial ends,but at their venous ends uid is reabsorbed
back into the capillaries. Thus, a small amount of uid actually ows through the
tissues from the arterial ends of the capillaries to the venous ends.The dynamics of
this ow are as follows.

Forces tending to move uid outward: Capillary pressure (arterial end of capillary)
30 Negative interstitial free uid pressure 3 Interstitial uid colloid osmotic pressure
8 total outward force 41 Forces tending to move uid inward: Plasma colloid osmotic
pressure 28 total inward force 28 Summation of forces: Outward 41 Inward 28 net
outward force (at arterial end) 13

Forces tending to move uid inward: Plasma colloid osmotic pressure 28 total
inward force 28 Forces tending to move uid outward: Capillary pressure (venous
end of capillary) 10 Negative interstitial free uid pressure 3 Interstitial uid colloid
osmotic pressure 8 total outward force 21 Summation of forces: Inward 28 Outward
21 net inward force 7

The reabsorption pressure causes about nine tenths of the uid that has ltered out
of the arterial ends of the capillaries to be reabsorbed at the venous ends. The
remaining one tenth ows into the lymph vessels and returns to the circulating
blood.

Mean forces tending to move uid outward: Mean capillary pressure 17.3 Negative
interstitial free uid pressure 3.0 Interstitial uid colloid osmotic pressure 8.0 total
outward force 28.3 Mean force tending to move uid inward: Plasma colloid osmotic
pressure 28.0 total inward force 28.0 Summation of mean forces: Outward 28.3
Inward 28.0 net outward force 0.3
Local blood ow control can be divided into two phases: (1) acute control and (2)
long-term control. Acute control is achieved by rapid changes in local vasodilation or
vasoconstriction of the arterioles, metarterioles, and precapillary sphincters,
occurring within seconds to minutes to provide very rapid maintenance of
appropriate local tissue blood ow. Long-term control, however,means
slow,controlled changes in ow over a period of days, weeks, or even months. In
general, these long-term changes provide even better control of the ow in
proportion to the needs of the tissues. These changes come about as a result of an
increase or decrease in the physical sizes and numbers of actual blood vessels
supplying the tissues.

Vasodilator Theory for Acute Local Blood Flow RegulationPossible

Special Role of Adenosine. According to this theory, the greater the rate of
metabolism or the less the availability of oxygen or some other nutrients to a tissue,
the greater the rate of formation of vasodilator substances in the tissue cells. The
vasodilator substances then are believed to diffuse through the tissues to the
precapillary sphincters, metarterioles,and arterioles to cause dilation.Some of the
different vasodilator substances that have been suggested are adenosine, carbon
dioxide, adenosine phosphate compounds, histamine, potassium ions, and hydrogen
tons.
Oxygen Lack Theory for Local Blood Flow Control
When the blood supply to a tissue is blocked for a few seconds to as long an hour or
more and then is unblocked, blood ow through the tissue usually increases
immediately to four to seven times normal; this increased ow will continue for a
few seconds if the block has lasted only a few seconds but sometimes continues for
as long as many hours if the blood ow has been stopped for an hour or more.This
phenomenon is called reactive hyperemia.
Active Hyperemia. When any tissue becomes highly active, such as an exercising
muscle, a gastrointestinal gland during a hypersecretory period, or even the brain
during rapid mental activity, the rate of blood ow through the tissue increases.

Mechanism of Long-Term Regulation Change in Tissue Vascularity The

mechanism of long-term local blood ow regulation is principally to change the
amount of vascularity of the tissues. For instance, if the metabolism in a given
tissue is increased for a prolonged period, vascularity increases; if the metabolism is
decreased, vascularity decreases.
Role of Oxygen in Long-Term Regulation.
Importance of Vascular Endothelial Growth Factor in Formation of New Blood Vessels

Humoral Control of the Circulation

Norepinephrine and Epinephrine. Norepinephrine is an especially powerful
vasoconstrictor hormone; epinephrineis less so and in some tissues even causes
mild vasodilation. (A special example of vasodilation caused by epinephrine occurs
to dilate the coronary arteries during increased heart activity.)
Angiotensin II. Angiotensin II is another powerful vasoconstrictor substance
Vasopressin. Vasopressin, also called antidiuretic hormone,is even more powerful
than angiotensin II as a vasoconstrictor, thus making it one of the bodys most
potent vascular constrictor substances.
EndothelinA Powerful Vasoconstrictor in Damaged Blood Vessels.
Bradykinin. Several substances called kininscause powerful vasodilation when
formed in the blood and tissue uids of some organs
Histamine. Histamine is released in essentially every tissue of the body if the tissue
becomes damaged or inamed or is the subject of an allergic reaction
distribution of sympathetic nerve bers to the blood vessels, demonstrating that in
most tissues all the vessels except the capillaries, precapillary sphincters, and
metarterioles are innervated.
Role of the Nervous System in Rapid Control of Arterial Pressure
1. Almost all arterioles of the systemic circulation are constricted. This greatly
increases the total peripheral resistance, thereby increasing the arterial pressure.
2. The veins especially (but the other large vessels of the circulation as well) are
strongly constricted. This displaces blood out of the large peripheral blood vessels
toward the heart, thus increasing the volume of blood in the heart chambers.The

stretch of the heart then causes the heart to beat with far greater force and
therefore to pump increased quantities of blood.This, too, increases the arterial
pressure.
3. Finally, the heart itself is directly stimulated by the autonomic nervous system,
further enhancing cardiac pumping.
Atrial Reex Control of Heart Rate (the Bainbridge Reex). An increase in atrial
pressure also causes an increase in heart rate,sometimes increasing the heart rate
as much as 75 per cent.
at low levels of blood ow to the vasomotor center, the local concentration of
carbon dioxide increases greatly and has an extremely potent effect in stimulating
the sympathetic vasomotor nervous control areas in the brains medulla.
emergency pressure control system that acts rapidly and very powerfully to prevent
further decrease in arterial pressure whenever blood ow to the brain decreases
dangerously close to the lethal level.
Special Features of Nervous Control of Arterial Pressure
Role of the Skeletal Nerves and Skeletal Muscles in Increasing Cardiac Output and
Arterial Pressure

Abdominal Compression Reex. When a baroreceptor or chemoreceptor reex is

elicited,nerve signals are transmitted simultaneously through skeletal nerves to
skeletal muscles of the body, particularly to the abdominal muscles. This
compresses all the venous reservoirs of the abdomen, helping to translocate blood
out of the abdominal vascular reservoirs toward the heart
Increased Cardiac Output and Arterial Pressure Caused by Skeletal Muscle
Contraction During Exercise.
With each cycle of respiration, the arterial pressure usually rises and falls 4 to 6 mm
Hg in a wavelike manner, causing respiratory waves in the arterial pressure. The
waves result from several different effects, some of which are reex in nature, as
follows: 1. Many of the breathing signals that arise in the respiratory center of the
medulla spill over into the vasomotor center with each respiratory cycle. 2. Every
time a person inspires, the pressure in the thoracic cavity becomes more negative
than usual, causing the blood vessels in the chest to expand. This reduces the
quantity of blood returning to the left side of the heart and thereby momentarily
decreases the cardiac output and arterial pressure. 3. The pressure changes caused
in the thoracic vessels by respiration can excite vascular and atrial stretch
receptors.

The cause of vasomotor waves is reex oscillation of one or more nervous

pressure control mechanisms,

The renalbody uid system for arterial pressure control is a simple one:When the
body contains too much extracellular uid, the blood volume and arterial pressure
rise.The rising pressure in turn has a direct effect to cause the kidneys to excrete
the excess extracellular uid,thus returning the pressure back toward normal.
arterial pressurearterial pressure equals cardiac output times total peripheral
resistance

The overall mechanism by which increased extracellular uid volume elevates

arterial pressure is given in the schema of Figure 196.The sequential events are (1)
increased extracellular uid volume (2) increases the blood volume, which (3)
increases the mean circulatory lling pressure, which (4) increases venous return of
blood to the heart, which (5) increase
Renin is a protein enzyme released by the kidneys when the arterial pressure falls
too low. In turn, it raises the arterial pressure in several ways, thus helping to
correct the initial fall in pressure.
During its persistence in the blood, angiotensin II has two principal effects that can
elevate arterial pressure. The rst of these, vasoconstriction in many areas of the
body, occurs rapidly. Vasoconstriction occurs intensely in the arterioles and much
less so in the veins. Constriction of the arterioles increases the total peripheral
resistance,thereby raising the arterial pressure,as demonstrated at the bottom of
the schema in Figure 199.Also,the mild constriction of the veins promotes
increased venous return of blood to the heart, thereby helping the heart pump
against the increasing pressure. The second principal means by which angiotensin
increases the arterial pressure is to decrease excretion of both salt and water by the
kidneys. This slowly increases the extracellular uid volume, which then increases
the arterial pressure during subsequent hours and days. This long-term effect,
acting through the extracellular uid volume mechanism, is even more powerful
than the acute vasoconstrictor mechanism in eventually raising the arterial
pressure.

Angiotensin causes the kidneys to retain both salt and water in two major ways: 1.
Angiotensin acts directly on the kidneys to cause salt and water retention. 2.

Angiotensin causes the adrenal glands to secrete aldosterone, and the aldosterone
in turn increases salt and water reabsorption by the kidney tubules.
Occasionally a tumor of the renin-secreting juxtaglomerular cells (the JG cells)
occurs and secretes tremendous quantities of renin; in turn, equally large quantities
of angiotensin II are formed.In all patients in whom this has occurred, severe
hypertension has developed. Also, when large amounts of angiotensin are infused
continuously for days or weeks into animals, similar severe long-term hypertension
develops.
Rapidly Acting Pressure Control Mechanisms, Acting Within Seconds or
Minutes.
(1) the baroreceptor feedback mechanism, (2) the central nervous system ischemic
mechanism, and (3) the chemoreceptor mechanism.
Pressure Control Mechanisms That Act After Many Minutes.
(1) the renin-angiotensin vasoconstrictor mechanism, (2) stress-relaxation of the
vasculature, and (3) shift of uid through the tissue capillary walls in and out of the
circulation to readjust the blood volume as needed.
The stress-relaxation mechanism is demonstrated by the following example: When
the pressure in the blood vessels becomes too high, they become stretched and
keep on stretching more and more for minutes or hours;as a result,the pressure in
the vessels falls toward normal.This continuing stretch of the vessels, called stressrelaxation, can serve as an intermediate-term pressure buffer.
The capillary uid shift mechanism means simply that any time capillary pressure
falls too low, uid is absorbed through the capillary membranes from the tissues
into the circulation,thus building up the blood volume and increasing the pressure in
the circulation. Conversely,when the capillary pressure rises too high, uid is lost
out of the circulation into the tissues, thus reducing the blood volume as well as
virtually all the pressures throughout the circulation.
Long-Term Mechanisms for Arterial Pressure Regulation.
Kidneys
Cardiac outputis the quantity of blood pumped into the aorta each minute by the
heart. This is also the quantity of blood that ows through the circulation
Venous return is the quantity of blood owing from the veins into the right atrium
each minute. The venous return and the cardiac output must equal each other
except for a few heartbeats at a time when blood is temporarily stored in or
removed from the heart and lungs.

cardiac index, which is the cardiac output per square meter of body surface area.
When one states that cardiac output is controlled by venous return,this means that
it is not the heart itself that is the primary controller of cardiac output.
Instead, it is the various factors of the peripheral circulation that affect ow of blood
into the heart from the veins, called venous return, that are the primary controllers.
The main reason peripheral factors are usually more important than the heart itself
in controlling cardiac output is that the heart has a built-in mechanism that normally
allows it to pump automatically whatever amount of blood that ows into the right
atrium from the veins. This mechanism, called the Frank-Starling law of the heart
To summarize, cardiac output is determined by the sum of all the various factors
throughout the body that control local blood ow. All the local blood ows summate
to form the venous return, and the heart automatically pumps this returning blood
back into the arteries to ow around the system again.

when the total peripheral resistance increases above normal, the cardiac output
falls; conversely,when the total peripheral resistance decreases, the cardiac output
increases.
Cardiac Output
Arterial Pressure Total Peripheral Resistance

Factors That Can Cause Hypereffective Heart Only two types of factors
usually can make the heart a better pump than normal.They are (1)
nervous stimulation and (2) hypertrophy of the heart muscle.
Effect of Nervous Excitation to Increase Heart Pumping. In Chapter 9, we saw
that a combination of (1) sympathetic stimulation and (2) parasympathetic
inhibition does two things to increase the pumping effectiveness of the heart: (1) it
greatly increases the heart rate sometimes, in young people, from the normal
level of 72 beats/min up to 180 to 200 beats/minand (2) it increases the strength
of heart contraction (which is called increased contractility) to twice its normal
strength.
Increased Pumping Effectiveness Caused by Heart Hypertrophy. A longterm increased workload, but not so much excess load that it damages the

heart,causes the heart muscle to increase in mass and contractile strength in the
same way that heavy exercise causes skeletal muscles to hypertrophy

the cause is vibration of the taut valves immediately after closure, along
with vibration of the adjacent walls of the heart and major vessels around
the heart.
The duration of each of the heart sounds is slightly more than 0.10 secondthe
rst sound about 0.14 second, and the second about 0.11 second.The reason for the
shorter second sound is that the semilunar valves are more taut than the A-V
valves,so that they vibrate for a shorter time than do the A-V valves.
A valve in which the leaets adhere to one another so extensively that blood cannot
ow through it normally is said to be stenosed.Conversely,when the valve edges are
so destroyed by scar tissue that they cannot close as the ventricles contract,
regurgitation (backow) of blood occurs when the valve should be closed. Stenosis
usually does not occur without the coexistence of at least some degree of
regurgitation,and vice versa.
Systolic Murmur of Aortic Stenosis
Diastolic Murmur of Aortic Regurgitation.
Systolic Murmur of Mitral Regurgitation
Diastolic Murmur of Mitral Stenosis
t the aortic stenotic lesion causes the loudest murmur, and the mitral stenotic lesion
causes the weakest.
With even moderately strenuous exercise,the person is likely to become weak and
may even faint from momentary heart failure. Botalli
The high pressures in the pulmonary vessels caused by excess ow through the
lungs often lead to pulmonary congestion and pulmonary edema.As a result of the
excessive load on the heart, and especially because the pulmonary congestion
becomes progressively more severe with age,most patients with uncorrected patent
ductus die from heart disease between ages 20 and 40 years.
Tetralogy of Fallot A Right-to-Left Shunt
1. The aorta originates from the right ventricle rather than the left, or it overrides a
hole in the septum, as shown in Figure 235, receiving blood from both ventricles.

2. The pulmonary artery is stenosed, so that much lower than normal amounts of
blood pass from the right ventricle into the lungs; instead, most of the blood passes
directly into the aorta, thus bypassing the lungs.

3. Blood from the left ventricle ows either through a ventricular septal hole into the
right ventricle and then into the aorta or directly into the aorta that overrides this
hole.
4. Because the right side of the heart must pump large quantities of blood against
the high pressure in the aorta, its musculature is highly developed, causing an
enlarged right ventricle.
It is readily apparent that the major physiological difculty caused by tetralogy of
Fallot is the shunting of blood past the lungs without its becoming oxygenated. As
much as 75 per cent of the venous blood returning to the heart passes directly from
the right ventricle into the aorta without becoming oxygenated.
0.1
0.3
0.4

Augmented limb leads, designated by the letter a (aVR, aVL, aVF), are generally
used. The augmented limb leads are recordings between one limb and the other two
limbs. This increases the size of the potentials by 50% without any change in
conguration from the nonaugmented record.

PR interval 0.18 0.120.20 Atrial depolarization and conduction through AV node

QRS duration 0.08 to 0.10 Ventricular depolarization and atrial repolarization

QT interval 0.40 to 0.43 Ventricular depolarization plus ventricular repolarization

ST interval (QT minus QRS)
0.32 . . . Ventricular repolarization (during T wave)

When conduction from the atria to the ventricles is completely interrupted,

complete (third-degree) heart block results, and the ventricles beat at a low rate
(idioventricular rhythm) independently of the atria
The block may be due to disease in the AV node (AV nodal block) or in the
conducting system below the node (infranodal block). In patients with AV nodal
block, the remaining nodal tissue becomes the pacemaker and the rate of the
idioventricular rhythm is approximately 45 beats/min. In patients with infranodal
block due to disease in the bundle of His, the ventricular pacemaker is located more
peripherally in the conduction system and the ventricular rate is lower; it averages
35 beats/min, but in individual cases it can be as low as 15 beats/min. In such
individuals, there may also be periods of asystole lasting a minute or more. The
resultant cerebral ischemia causes dizziness and fainting (StokesAdams
syndrome). Causes of third-degree heart block include septal myocardial infarction
and damage to the bundle of His during surgical correction of congenital
interventricular septal defects.
When conduction between the atria and ventricles is slowed but not completely
interrupted, incomplete heart block is present. In the form called rst-degree heart
block, all the atrial impulses reach the ventricles but the PR interval is abnormally
long. In the form called second-degree heart block, not all atrial impulses are
conducted to the ventricles. For example, a ventricular beat may follow every
second or every third atrial beat (2:1 block, 3:1 block, etc).
Sometimes one branch of the bundle of His is interrupted, causing right or left
bundle branch block. In bundle branch block, excitation passes normally down the
bundle on the intact side and then sweeps back through the muscle to activate the
ventricle on the blocked side.
Ventricular brillation can be produced by an electric shock or an extrasystole
during a critical interval, the vulnerable period. The vulnerable period coincides in
time with the midportion of the T wave; that is, it occurs at a time when some of the
ventricular myocardium is depolarized, some is incompletely repolarized, and some
is completely repolarized. These are excellent conditions in which to establish
reentry and a circus movement. The brillating ventricles cannot pump blood
effectively, and circulation of the blood stops. Therefore, in the absence of
emergency treatment, ventricular brillation that lasts more than a few minutes is

fatal. The most frequent cause of sudden death in patients with myocardial infarcts
is ventricular brillation.

Individuals with WolffParkinsonWhite syndrome have an additional aberrant

muscular or nodal tissue connection (bundle of Kent) between the atria and
ventricles. This conducts more rapidly than the slowly conducting AV node, and one
ventricle is excited early.
This period of isovolumetric (isovolumic, isometric) ventricular contraction lasts
about 0.05 s, until the pressures in the left and right ventricles exceed the pressures
in the aorta (80 mm Hg; 10.6 kPa) and pulmonary artery (10 mm Hg) and the aortic
and pulmonary valves open. During isovolumetric contraction, the AV valves bulge
into the atria, causing a small but sharp rise in atrial pressure
When the aortic and pulmonary valves open, the phase of ventricular ejection
begins. Ejection is rapid at rst, slowing down as systole progresses. The
intraventricular pressure rises to a maximum and then declines somewhat before
ventricular systole ends. Peak pressures in the left and right ventricles are about
120 and 25 mm Hg, respectively
The amount of blood ejected by each ventricle per stroke at rest is 70 to 90 mL.
The end-diastolic ventricular volume is about 130 mL. Thus, about 50 mL of blood
remains in each ventricle at the end of systole (end-systolic ventricular volume),
and the ejection fraction, the percent of the end-diastolic ventricular volume that is
ejected with each stroke, is about 65%.
Once the ventricular muscle is fully contracted, the already falling ventricular
pressures drop more rapidly. This is the period of protodiastole, which lasts about
0.04 s. It ends when the momentum of the ejected blood is overcome and the aortic
and pulmonary valves close, setting up transient vibrations in the blood and blood
vessel walls.
After the valves are closed, pressure continues to drop rapidly during the period of
isovolumetric ventricular relaxation. Isovolumetric relaxation
ends when the ventricular pressure falls below the atrial pressure and the AV valves
open, permitting the ventricles to ll. Filling is rapid at rst, then slows as the next
cardiac contraction approaches. Atrial pressure continues to rise after the end of
ventricular systole until the AV valves open, then drops and slowly rises again until
the next atrial systole.

However, the duration of systole is much more xed than that of diastole, and
when the heart rate is increased, diastole is shortened to a much greater degree.
This fact has important physiologic and clinical implications. It is during diastole that
the heart muscle rests, and coronary blood ow to the subendocardial portions of
the left ventricle occurs only during diastole (see Chapter 34). Furthermore, most of
the ventricular lling occurs in diastole. At heart rates up to about 180, lling is
adequate as long as there is ample venous return, and cardiac output per minute is
increased by an increase in rate. However, at very high heart rates, lling may be
compromised to such a degree that cardiac output per minute falls.
The blood forced into the aorta during systole not only moves the blood in the
vessels forward but also sets up a pressure wave that travels along the arteries. The
pressure wave expands the arterial walls as it travels, and the expansion is palpable
as the pulse.
One of the loudest murmurs is that produced when blood ows backward in
diastole through a hole in a cusp of the aortic valve.
In patients with congenital interventricular septal defects, ow from the left to the
right ventricle causes a systolic murmur. Soft murmurs may also be heard in
patients with interatrial septal defects, although they are not a constant nding.
CARDIAC OUTPUT METHODS OF MEASUREMENT
The Fick principle states that the amount of a substance taken up by an organ (or by
the whole body) per unit of time is equal to the arterial level of the substance minus
the venous level (A-V difference) times the blood ow. This principle can be applied,
of course, only in situations in which the arterial blood is the sole source of the
substance taken up. The principle can be used to determine cardiac output by
measuring the amount of O2 consumed by the body in a given period and dividing
this value by the A-V difference across the lungs.
In the indicator dilution technique, a known amount of a substance such as a dye or,
more commonly, a radioactive isotope is injected into an arm vein and the
concentration of the indicator in serial samples of arterial blood is determined. The
output of the heart is equal to the amount of indicator injected divided by its
average concentration in arterial blood after a single circulation through the heart
The amount of blood pumped out of the heart per beat, the stroke volume, is about
70 mL from each ventricle in a resting man of average size in the supine position.
The output of the heart per unit of time is the cardiac output. In a resting, supine
man, it averages about 5.0 L/min (70 mL 72 beats/min). There is a correlation
between resting cardiac output and body surface area. The output per minute per
square meter of body surface (the cardiac index) averages 3.2 L.

Predictably, changes in cardiac output that are called for by physiologic conditions
can be produced by changes in cardiac rate or stroke volume or both (Figure 315).
The cardiac rate is controlled primarily by the autonomic nerves, with sympathetic
stimulation increasing the rate and parasympathetic stimulation decreasing it (see
Chapter 30). Stroke volume is also determined in part by neural input, with
sympathetic stimuli making the myocardial muscle bers contract with greater
strength at any given length and parasympathetic stimuli having the opposite
effect.
The force of contraction of cardiac muscle depends on its preloading and its
afterloading.
Regulation of cardiac output as a result of changes in cardiac muscle ber length is
sometimes called heterometric regulation, whereas regulation due to changes in
contractility independent of length is sometimes called homometric regulation.

energy of contraction is proportional to the initial length of the cardiac muscle ber
(Starlings law of the heart or the FrankStarling law).
The pulse pressure, the difference between the systolic and diastolic pressures, is
normally about 50 mmHg
The rate of ltration at any point along a capillary depends on a balance of forces
sometimes called the Starling forces, after the physiologist who rst described their
operation in detail. One of these forces is the hydrostatic pressure gradient (the
hydrostatic pressure in the capillary minus the hydrostatic pressure of the interstitial
uid) at that point. The other force is the osmotic pressure gradient across the
capillary wall (colloid osmotic pressure of plasma minus colloid osmotic pressure of
interstitial uid). This component is directed inward.
Fluid movement = k[(Pc Pi) (c i)]
where k = capillary ltration coefficient Pc = capillary hydrostatic pressure Pi =
interstitial hydrostatic pressure c = capillary colloid osmotic pressure i =
interstitial colloid osmotic pressure
i is usually negligible, so the osmotic pressure gradient (c i) usually equals the
oncotic pressure. The capillary ltration coefficient takes into account, and is
proportional to, the permeability of the capillary wall and the area available for
ltration.
Blood ows through the blood vessels, including the veins, primarily because of the
pumping action of the heart. However, venous ow is aided by the heartbeat, the

increase in the negative intrathoracic pressure during each inspiration, and

contractions of skeletal muscles that compress the veins (muscle pump).
The pressure in the venules is 12 to 18 mm Hg. It falls steadily in the larger veins to
about 5.5 mm Hg in the great veins outside the thorax. The pressure in the great
veins at their entrance into the right atrium (central venous pressure) averages 4.6
mm Hg, but uctuates with respiration and heart action.

Impulses in the sympathetic nerves to the heart increase the cardiac rate
(chronotropic effect), rate of transmission in the cardiac conductive tissue
(dromotropic effect), and the force of contraction (inotropic effect).
(forced expiration against a closed glottis: the Valsalva maneuver). Valsalva
maneuvers occur regularly during coughing, defecation, and heavy lifting.
It is probably due in part to the intrinsic contractile response of smooth muscle to
stretch (myogenic theory of autoregulation). As the pressure rises, the blood vessels
are distended and the vascular smooth muscle bers that surround the vessels
contract.
Vasodilator substances tend to accumulate in active tissues, and these
metabolites also contribute to autoregulation (metabolic theory of
autoregulation). When blood ow decreases, they accumulate and the vessels
dilate; when blood ow increases, they tend to be washed away.
The all-or-none law is the principle that the strength by which a nerve or muscle
ber responds to a stimulus is independent of the strength of the stimulus. If that
stimulus exceeds the threshold potential, the nerve or muscle ber will give a
complete response; otherwise, there is no response.