THE CARDIOVASCULAR

SYSTEM
THE HEART AND CIRCULATION
INTRODUCTION

• The heart is actually two separate pumps: a right heart that pumps blood through the
lungs, and a left heart that pumps blood through the peripheral organs. (Fig. 1)
• In turn, each of these hearts is a pulsatile two-chamber pump composed of an atrium and a
ventricle. Each atrium is a weak primer pump for the ventricle, helping to move blood into
the ventricle.
• The ventricles then supply the main pumping force that propels the blood either:
1. Through the pulmonary circulation by the right ventricle or
2. Through the peripheral circulation by the left ventricle.
• Special mechanisms in the heart cause a continuing succession of heart contractions called
cardiac rhythmicity, transmitting action potentials throughout the heart muscle to cause the
heart’s rhythmical beat.
FIGURE 1: NORMAL HUMAN HEART.
This image shows the components
that comprise the human heart as
well as the direction of blood flow
from the heart to the lungs, back to
the heart and to the rest of the body.
• The heart is composed of three major types of cardiac muscle: atrial muscle, ventricular
muscle, and specialized excitatory and conductive muscle fibres.
• 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 fibres contract only feebly because
they contain few contractile fibrils; 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.
• Cardiac muscle fibres are arranged in a latticework, with the fibres dividing, recombining,
and then spreading again (fig. 2).
• One also notes immediately that cardiac muscle is striated in the same manner as in typical
skeletal muscle (fig. 3).
• Further, cardiac muscle has typical myofibrils that contain actin and myosin filaments
almost identical to those found in skeletal muscle; these filaments lie side by side and slide
along one another during contraction in the same manner as occurs in skeletal muscle.
FIGURE 2:
ANATOMY OF
CARDIAC MUSCLE.
This type of muscle
is striated and
functions in much
the same way as
skeletal muscle.
Unlike skeletal
muscle, cardiac
muscle contractions
are involuntary.
This image shows
the microscopic
appearance of
cardiac muscle.
FIGURE 3: COMPARATIVE OF TYPES OF MUSCLE FIBRES. This image compares the structures of the types
of muscle fibre found in the human body. (a) skeletal muscle, (b) smooth muscle and (c) Cardiac muscle.
• The intercalated discs are actually cell membranes that separate individual cardiac muscle
cells from one another.
• That is, cardiac muscle fibres are made up of many individual cells connected in series and in
parallel with one another.
• At each intercalated disc the cell membranes fuse with one another in such a way that they
form permeable “communicating” junctions (gap junctions) that allow almost totally free
diffusion of ions.
• Therefore, from a functional point of view, ions move with ease in the intracellular fluid
along the longitudinal axes of the cardiac muscle fibres, so that action potentials travel
easily from one cardiac muscle cell to the next, past the intercalated discs.
• Thus, cardiac muscle is a syncytium (single functioning organ) 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 fibrous 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 fibrous tissue.
• Instead, they are conducted only by way of a specialized conductive system called the A-V
bundle, a bundle of conductive fibres several millimetres in diameter.
• This division of the muscle of the heart into two functional syncytiums allows the atria to
contract a short time ahead of ventricular contraction, which is important for effectiveness
of heart pumping.
THE CARDIAC CYCLE
• The cardiac events that occur from the beginning of one heartbeat to the beginning of the
next are called the cardiac cycle.
• Each cycle is initiated by spontaneous generation of an action potential in the sinus node
(sinoatrial node).
• This node is located in the superior lateral wall of the right atrium near the opening of the
superior vena cava, and the action potential travels from here rapidly through both atria and
then through the A-V bundle into the ventricles. (Fig. 4)
• Because of this special arrangement of the conducting system from the atria into the
ventricles, there is a delay of more than 0.1 seconds 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 body’s vascular system.
FIGURE 4: CONDCTION
THROUGH THE HEART.
This image shows the
locations of the nerve
bundles that transmit
signals though the cardiac
muscles, causing
contractions of the heart,
which allow the circulation
of blood.
• The cardiac cycle consists of a period of relaxation called diastole, during which the heart fills
with blood, followed by a period of contraction called systole.
• Figure 5 shows the different events during the cardiac cycle for the left side of the heart.
• The top three curves show the pressure changes in the aorta, left ventricle, and left atrium,
respectively.
• The fourth curve depicts the changes in left ventricular volume, the fifth the
electrocardiogram, and the sixth a phonocardiogram, which is a recording of the sounds
produced by the heart—mainly by the heart valves—as it pumps.
• The electrocardiogram in Figure 5 shows the P, Q, R, S, and T waves.
• They are electrical voltages generated by the heart and recorded by the electrocardiograph
from the surface of the body.
• The P wave is caused by the spread of depolarization through the atria, and this is followed
by atrial contraction, which causes a slight rise in the atrial pressure curve immediately after
the electrocardiographic P wave.
FIGURE 5: THE CARDIAC
CYCLE. This image shows the
sequence of events that
comprise the cardiac cycle.
At the bottom is a
representation of the
Electrocardiogram (ECG).
• About 0.16 second after the onset of the P wave, the QRS waves appear as a result of
electrical depolarization of the ventricles, which initiates contraction of the ventricles and
causes the ventricular pressure to begin rising, as also shown in the figure.
• Therefore, the QRS complex begins slightly before the onset of ventricular systole.
• Finally, one observes the ventricular T wave in the electrocardiogram. This represents the
stage of repolarization of the ventricles when the ventricular muscle fibres begin to relax.
• Therefore, the T wave occurs slightly before the end of ventricular contraction.
ATRIAL FUNCTION
• Blood normally flows continually from the great veins into the atria; about 80% of the blood
flows directly through the atria into the ventricles even before the atria contract.
• Then, atrial contraction usually causes an additional 20% filling of the ventricles.
• Therefore, the atria simply function as primer pumps that increase the ventricular pumping
effectiveness as much as 20%.
• However, the heart can continue to operate under most conditions even without this extra
20% effectiveness because it normally has the capability of pumping 300 to 400% 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.
• In the atrial pressure curve of Figure 5, three minor pressure elevations, called the a, c, and
v atrial pressure waves, are noted.
• The a wave is 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 backflow
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 flow 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 flow rapidly into the ventricles and causing the v wave to disappear.
VENTRICULAR FUNCTION
• 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 flow rapidly
into the ventricles, as shown by the rise of the left ventricular volume curve in Figure 5.
• This is called the period of rapid filling of the ventricles.
• The period of rapid filling lasts for about the first third of diastole.
• During the middle third of diastole, only a small amount of blood normally flows 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 inflow
of blood into the ventricles; this accounts for about 20% of the filling of the ventricles during
each heart cycle.
• Immediately after ventricular contraction begins, the ventricular pressure rises abruptly, as
shown in Figure 5, causing the A-V valves to close.
• Then an additional 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
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 fibres is occurring.
• 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 first third of the period of ejection and the remaining 30 per
cent emptying during the next two thirds.
• Therefore, the first third is called the period of rapid ejection, and the last two thirds, the
period of slow ejection.
• 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 filled 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 seconds, 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 filling of the ventricles increases the volume of each ventricle to
about 110 to 120 millilitres.
• This volume is called the end-diastolic volume.
• Then, as the ventricles empty during systole, the volume decreases about 70 millilitres,
which is called the stroke volume output.
• The remaining volume in each ventricle, about 40 to 50 millilitres, is called the end-systolic
volume.
• The fraction of the end-diastolic volume that is ejected is called the ejection fraction—
usually equal to about 60 per cent. When the heart contracts strongly, the end-systolic
volume can be decreased to as little as 10 to 20 millilitres.
• Conversely, when large amounts of blood flow into the ventricles during diastole, the
ventricular end-diastolic volumes can become as great as 150 to 180 millilitres in the healthy
heart.
• By both increasing the end-diastolic volume and decreasing the end-systolic volume, the
stroke volume output can be increased to more than double normal.
FUNCTION OF THE VALVES
• The A-V valves (the tricuspid and mitral valves) prevent backflow of blood from the
ventricles to the atria during systole, and the semilunar valves (the aortic and pulmonary
artery valves) prevent backflow from the aorta and pulmonary arteries into the ventricles
during diastole.
• These valves, shown in Figure 6, 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, filmy A-V valves require almost no backflow to cause
closure, whereas the much heavier semilunar valves require rather rapid backflow for a few
milliseconds.
• Figure 6 also shows papillary muscles that attach to the vanes of the A-V valves by the
chordae tendineae.
• The papillary muscles contract when the ventricular walls contract, but contrary to what
might be expected, they do not help the valves to close.
FIGURE 6: CARDIAC VALVES.
This image shows the
positioning and appearance
of the valves that regulate
the directionality of blood
flow within the chambers of
the heart.
• 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 tendineae 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.
• The aortic and pulmonary artery semilunar valves function quite differently from the A-V
valves.
• First, the high pressures in the arteries at the end of systole cause the semilunar valves to
snap to the closed position, in contrast to the much softer closure of the A-V valves.
• Second, because of smaller openings, the velocity of blood ejection through the aortic and
pulmonary valves is far greater than that through the much larger A-V valves.
• Also, because of the rapid closure and rapid ejection, the edges of the aortic and pulmonary
valves are subjected to much greater mechanical abrasion than are the A-V valves.
• Finally, the A-V valves are supported by the chordae tendineae, which is not true for the
semilunar valves.
• It is obvious from the anatomy of the aortic and pulmonary valves that they must be
constructed with an especially strong yet very pliable fibrous tissue base to withstand the
extra physical stresses.
• 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 5, because blood immediately flows 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 flow of blood immediately before closure of the
valve, followed by sudden cessation of the backflow.
• After the aortic valve has closed, the pressure in the aorta decreases slowly throughout
diastole because the blood stored in the distended elastic arteries flows 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 listening to the heart with a stethoscope, one does not hear the opening of the valves
because this is a relatively slow process that normally makes no noise.
• However, when the valves close, the vanes of the valves and the surrounding fluids vibrate
under the influence of sudden pressure changes, giving off sound that travels in all directions
through the chest.
• When the ventricles contract, one first 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 first 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.
CARDIAC WORK OUTPUT
• 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.
• Minute work output is the total amount of energy converted to work in 1 minute; this is
equal to the stroke work output times the heart rate per minute.
• 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 flow 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 six-fold difference in systolic pressures that the two ventricles
pump.
• The additional work 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.
• Ordinarily, the work output of the left ventricle required to create kinetic energy of blood
flow is only about 1 per cent of the total work output of the ventricle and therefore is
ignored in the calculation of the total stroke work output.
• But in certain abnormal conditions, such as aortic stenosis (narrowing of the aorta), in which
blood flows with great velocity through the stenosed valve, more than 50 per cent of the
total work output may be required to create kinetic energy of blood flow.
• 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 filled.
• The afterload of the ventricle is the pressure in the artery leading from the ventricle.
• The importance of the concepts of preload and afterload is that in many abnormal functional
states of the heart or circulation, the pressure during filling of the ventricle (the preload), the
arterial pressure against which the ventricle must contract (the afterload), or both are
severely altered from normal.
• Heart muscle, like skeletal muscle, uses chemical energy to provide the work of contraction.
• This energy is derived mainly from oxidative metabolism of fatty acids and, to a lesser extent,
of other nutrients, especially lactate and glucose.
• Therefore, the rate of oxygen consumption by the heart is an excellent measure of the
chemical energy liberated while the heart performs its work.
• 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 efficiency of
cardiac contraction, or simply efficiency of the heart.
• Maximum efficiency 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.
REGULATION OF HEART PUMPING
• When a person is at rest, the heart pumps only 4 to 6 litres of blood each minute.
• During severe exercise, the heart may be required to pump four to seven times this amount.
• The basic means by which the volume pumped by the heart is regulated are:
• Intrinsic cardiac regulation of pumping in response to changes in volume of blood flowing into the heart
and
• 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 flow into the heart from the veins, which is
called venous return.
• That is, each peripheral tissue of the body controls its own local blood flow, and all the local
tissue flows combine and return by way of the veins to the right atrium.
• The heart, in turn, automatically pumps this incoming blood into the arteries, so that it can
flow around the circuit again.
• This intrinsic ability of the heart to adapt to increasing volumes of inflowing blood is called
the Frank-Starling mechanism of the heart, in honour of Frank and Starling.
• The Frank-Starling mechanism means that the greater the heart muscle is stretched during
filling, 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 flows 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
filaments 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.
• This ability of stretched muscle, up to an optimal length, to contract with increased work
output is characteristic of all striated muscle.
• In addition to the important effect of lengthening the heart muscle, still another factor
increases heart pumping when its volume is increased.
• 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.
• The pumping effectiveness of the heart also is controlled by the sympathetic and
parasympathetic (vagus) nerves, which abundantly supply the heart.
• The pumping effectiveness of the heart also is controlled by the sympathetic and
parasympathetic (vagus) nerves, which abundantly supply the heart, as shown in Figure 7.
• For given levels of input atrial pressure, the amount of blood pumped each minute (cardiac
output) often can be increased more than 100 per cent by sympathetic stimulation.
• By contrast, the output can be decreased to as low as zero or almost zero by vagal
(parasympathetic) stimulation.
• 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.
FIGURE 7: CARDIAC INNERVATION.
This image shows the sympathetic
and parasympathetic nerve fibres
that aid in the regulation of blood
circulation.
• 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.
• Thus, sympathetic stimulation often can increase the maximum cardiac output as much as
twofold to threefold, in addition to the increased output caused by the Frank-Starling
mechanism already discussed.
• Conversely, inhibition of the sympathetic nerves to the heart can decrease cardiac pumping
to a moderate extent in the following way:
• Under normal conditions, the sympathetic nerve fibres to the heart discharge continuously at a slow rate
that maintains pumping at about 30 per cent above that with no sympathetic stimulation.
• Therefore, when the activity of the sympathetic nervous system is depressed below normal,
this decreases both heart rate and strength of ventricular muscle contraction, thereby
decreasing the level of cardiac pumping as much as 30 per cent below normal.
• Strong stimulation of the parasympathetic nerve fibres in the vagus nerves to the heart can
stop the heartbeat for a few seconds, but then the heart usually “escapes” and beats at a
rate of 20 to 40 beats per minute as long as the parasympathetic stimulation continues.
• In addition, strong vagal stimulation can decrease the strength of heart muscle contraction
by 20 to 30 per cent.
• The vagal fibres 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.
• Potassium ions have a marked effect on membrane potentials and calcium ions play an
especially important role in activating the muscle contractile process.
• Therefore, it is to be expected that the concentration of each of these two ions in the
extracellular fluids should also have important effects on cardiac pumping.
• Excess potassium in the extracellular fluids causes the heart to become dilated and flaccid 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.
• 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.
• These effects result partially from the fact that a high potassium concentration in the extracellular
fluids decreases the resting membrane potential in the cardiac muscle fibres.
• As the membrane potential decreases, the intensity of the action potential also decreases, which
makes contraction of the heart progressively weaker.
• 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.
• Conversely, deficiency of calcium ions causes cardiac flaccidity, 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.
• Temperature also has an effect on the pumping of the heart.
• Increased body temperature, as occurs when one has fever, causes a greatly increased heart
rate, sometimes to as fast as double normal. Decreased temperature causes a greatly
decreased heart rate, falling to as low as a few beats per minute when a person is near death
from hypothermia in the body temperature range of 16-21 °C.
• These effects presumably result from the fact that heat increases the permeability of the
cardiac muscle membrane to ions that control heart rate, resulting in acceleration of the self-
excitation process.
• Contractile strength of the heart often is enhanced temporarily by a moderate increase in
temperature, as occurs during body exercise, but prolonged elevation of temperature
exhausts the metabolic systems of the heart and eventually causes weakness.
• Therefore, optimal function of the heart depends greatly on proper control of body
temperature by the temperature control mechanisms
• Increasing the arterial pressure in the aorta does not decrease the cardiac output until the
mean arterial pressure rises above about 160 mm Hg.
• In other words, during normal function of the heart at normal systolic arterial pressures (80
to 140 mm Hg), the cardiac output is determined almost entirely by the ease of blood flow
through the body’s tissues, which in turn controls venous return of blood to the heart.