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Saladin 5e Extended Outline
Chapter 19
The Circulatory System: The Heart
I. Overview of the Cardiovascular System (pp. 720–722)
A. The cardiovascular system consists of the heart and the blood vessels. (p. 684) (Fig. 19.1)
1. The broader term circulatory system also includes the blood.
2. Some authorities use the term circulatory system to include the lymphatic system.
B. The cardiovascular system has two major divisions: a pulmonary circuit and a systemic circuit.
(p. 721)
1. The right side of the heart furnishes blood to the pulmonary circuit, which carries
blood to the lungs and returns it to the heart.
a. It receives blood that has circulated through the body and has high CO 2 and
wastes.
b. It pumps the blood into the pulmonary trunk, which divides into the right and
left pulmonary arteries.
c. These transport blood to the air sacs (alveoli) of the lungs where CO 2 is
unloaded and O2 is picked up.
d. The O2-rich blood then flows by way of the pulmonary veins to the left side
of the heart.
2. The left side supplies the systemic circuit, which carries blood to the body’s tissues
and returns it to the heart.
a. It receives blood from the pulmonary veins.
b. It pumps the blood into the aorta; the aorta makes a U-turn at the aortic arch,
which supplies the head, neck, and upper limbs, and passes downward.
c. The aorta travels through the thoracic and abdominal cavities and issues
smaller arteries to organs before branching into the lower limbs.
d. After circulating, the deoxygenated systemic blood returns to the right side of
the heart via the superior vena cava and the inferior vena cava.
C. The heart is located in the thoracic cavity in the mediastinum, between the lungs and deep to
the sternum. (pp. 721–722)
1. It is tilted toward the left from superior to inferior midpoints, so about two-thirds of the
heart lies to the left of the median plane. (Figs. 19.2, A.18–A.19)
2. The broad superior portion is called the base and is the point of attachment for the
great vessels (aorta, pulmonary arteries and veins, and venae cavae).
3. The inferior end tapers to a blunt point, the apex, just above the diaphragm.
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4. The adult heart is about 9 cm (3.5 in.) wide at the base, 13 cm (5 in.) from base to
apex, and 6 cm (2.5 in.) from anterior to posterior—about the size of one’s fist; it weighs
about 300 g (10 oz.).
D. The pericardium is a double-walled sac that encloses the heart. (p. 722) (Fig. 19.3)
1. The outer wall is the pericardial sac (parietal pericardium) that has a tough, fibrous
layer of dense irregular connective tissue and a deep, thin serous layer.
2. The serous layer turns inward at the base of the heart to form the epicardium (visceral
pericardium) covering the heart surface.
3. The pericardial sac is anchored by ligaments to the diaphragm and sternum, and by
fibrous connective tissue to the mediastinal tissue.
4. Between the parietal and visceral membranes is a space called the pericardial cavity.
(Figs. 19.2b, 19.3)
a. This cavity contains 5 to 30 mL of pericardial fluid, exuded by the serous
pericardium; this fluid lubricates the membranes and reduces friction when the
heart beats.
b. In pericarditis, inflammation of the pericardium, the membranes may produce
a painful friction rub with each heartbeat.
5. The pericardium isolates the heart from other thoracic organs and allows it room to
expand, while resisting excessive expansion.
II. Gross Anatomy of the Heart (pp. 722–730)
A. The heart wall consists of three layers: epicardium, myocardium, and endocardium. (pp. 772–
725)
1. The epicardium (visceral pericardium) is a serous membrane on the heart surface.
a. It is mainly simple squamous epithelium overlying a thin layer of areolar
tissues.
b. In some places it has a thick layer of adipose tissue but in other areas is fat
free and translucent. (Figs. 19.4a, 19.5)
c. The largest branches of coronary blood vessels travel through the epicardium.
2. The endocardium is similar and lines the interior of the heart chambers. (Figs. 19.3,
19.4b)
a. It has similar structure but has no adipose tissue.
b. Endocardium covers the valve surfaces and is continuous with the
endothelium of blood vessels.
3. The myocardium between the other two layers is composed of cardiac muscle and is
the thickest layer; it performs the work of the heart.
a. Its thickness varies from one heart chamber to another and is proportional to
the workload.
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b. Its muscle spirals around the heart so that upon contraction a twisting or
wringing motion occurs. (Fig. 19.6)
4. The heart also has a framework of collagenous and elastic fibers that make up the
fibrous skeleton.
a. This tissue is especially concentrated in the walls between the heart chambers,
in fibrous rings (anuli fibrosi) around the valves, and in sheets of tissue that
interconnect these rings. (Fig. 19.8)
b. The fibrous skeleton has multiple functions.
i. It provides structural support, especially around the valves and
openings of the great vessels.
ii. It anchors the cardiac muscle cells (cardiocytes) and provides
leverage.
iii. It serves as electrical insulation between atria and ventricles.
iv. Its elastic recoil may aid in refilling the heart with blood after each
beat.
B. The heart has four chambers best seen in frontal section. (p. 725) (Figs. 19.4b, 19.7)
1. The two chambers at the superior pole (base) are the right and left atria.
a. They are thin walled and receive blood returning to the heart by way of the
great veins.
b. Most of the mass is on the posterior side of the heart, and in the anterior view,
each has a small earlike extension called an auricle that increase volume
slightly. (Fig. 19.5a)
2. The inferior chambers, the right and left ventricles, are pumps that eject blood into the
arteries.
a. The right ventricle constitutes most of the anterior aspect of the heart.
b. The left ventricle forms the apex and inferoposterior aspect.
3. On the surface three sulci (grooves) mark the boundaries of the four chambers; these
sulci are largely filled by fat and the largest of the coronary blood vessels. (Fig. 19.5a)
a. The coronary (atrioventricular) sulcus encircles the heart near the base and
separate the atria from the ventricles below.
b. The other two sulci extend obliquely down the heart from the coronary sulcus
toward the apex.
i. The one on the front is the anterior interventricular sulcus.
ii. the one on the back is the posterior interventricular sulcus.
c. These two sulci overlie an internal wall, the interventricular septum, that
divides the right ventricle from the left.
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4. The atria have thin flaccid walls corresponding to their relatively light workload of
pumping blood into the ventricles below. (Fig. 19.7)
a. They are separated by a wall called the interatrial septum.
b. The right atrium and both auricles exhibit internal ridges of myocardium
called pectinate muscles.
5. The ventricles are separated by the interventricular septum, a much more muscular,
vertical wall.
a. The right ventricle pumps blood to the lungs, and is only moderately
muscular.
b. The left ventricle wall is two to four times as thick, since it pumps blood
through the entire body.
c. Both ventricles exhibit internal ridges called trabeculae carneae.
C. The valves of the heart ensure a one-way blood flow. (pp. 725–726) (Fig. 18.4)
1. A valve lies between each atrium and its ventricle and at the exit of each ventricle into
its great artery, but no valve lies where the great veins empty into the atria. (Fig. 19.7)
2. Each valve consists of two or three flaps called cusps or leaflets, covered with
endocardium.
3. The atrioventricular (AV) valves regulate the openings between the atria and
ventricles.
a. The right AV (tricuspid) valve has three cusps, and the left AV (bicuspid) has
two. (Fig. 19.8)
b. The left AV is also known as the mitral valve.
c. Stringlike tendinous cords (chordae tendineae) connect the valve cusps to
conical papillary muscles on the floor of the ventricle and prevent the AV valves
from flipping inside out.
4. The semilunar valves (pulmonary and aortic valves) regulate the flow of blood from
the ventricles into the great arteries.
a. The pulmonary valve controls the opening from the right ventricle into the
pulmonary trunk.
b. The aortic valve controls the opening from the left ventricle into the aorta.
c. Each valve has three cusps; there are no tendinous cords.
5. The valves make no muscular effort but are simply pushed open and closed by the
chambers’ contractions.
D. Blood flow is kept entirely separate on the right and left sides of the heart. (pp. 727–728) (Fig.
19.9)
E. The blood vessels of the heart wall constitute the coronary circulation. (pp. 690–691)
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1. At rest, the coronary blood vessels supply the myocardium with about 250 mL of
blood per minute, or about 5% of the circulating blood, even though the heart is only
0.5% of the body’s weight.
2. The coronary circulation is the most variable aspect of cardiac anatomy, and its
description is the pattern seen in 70% to 85% of people.
3. The arterial supply begins immediately after the aorta leaves the left ventricle.
a. A right and a left coronary artery lead from the aorta back to the heart; their
openings lie deep in the pockets formed by two of the aortic valve cusps. (Fig.
19.8a)
b. The left coronary artery (LCA) travels through the coronary sulcus under the
left auricle and divides into two branches. (Fig. 19.10)
i. The anterior interventricular branch (left anterior descending [LAD]
branch) travels down the anterior interventricular sulcus to the apex,
rounds the bend, and travels a short distance up the posterior side of the
heart, where it joins the posterior interventricular branch.
ii. The circumflex branch continues around the left side of the heart in
the coronary sulcus and gives off a left marginal branch that passes
down the left margin and furnishes blood to the left ventricle; the
circumflex then ends on the posterior side of the heart.
c. The right coronary artery (RCA) supplies the right atrium and sinoatrial node
(pacemaker) and continues along the coronary sulcus under the right auricle; it
give off two branches of its own.
i. The right marginal branch runs toward the apex of the heart and
supplies the lateral aspect of the right atrium and ventricle.
ii. The RCA continues around the right margin, sends a small branch to
the atrioventricular node, then gives off a large posterior
interventricular branch that supplies the walls of both ventricles; it ends
by joining the anterior interventricular branch of the LCA.
d. Any interruption of the blood supply to the cardiac muscle can cause necrosis
within minutes.
i. A fatty deposit or blood clot in a coronary artery can cause a
myocardial infarction (MI), or heart attack.
ii. Some protection from MI is provided by the points where two
coronary arteries come together to form arterial anastomoses; these
provide an alternative route called collateral circulation.
e. In most organs, blood flow peaks when the ventricles contract and eject blood
into the arteries and diminishes when the ventricles relax and refill; the opposite
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is true in the coronary arteries, in which blood flow increases during ventricular
relaxation for three reasons:
i. Contraction of the myocardium compresses the arteries and obstructs
blood flow.
ii. During ventricular systole, the aortic valve is forced open and the
cusps block blood flow into the coronary artery openings.
iii. During ventricular diastole, blood in the aorta briefly surges back
toward the heart, and some of it flows into the coronary arteries.
Insight 19.1 Angina and Heart Attack
4. Venous drainage of the coronary circulation returns the blood to the heart.
a. 5% to 10% empties directly from multiple small thebesian veins into the heart
chambers, especially the right ventricle.
b. The rest of the blood returns to the right atrium by the following route. (Fig.
19.10)
i. The great cardiac vein collects blood from the anterior aspect and
carries blood from the apex toward the coronary sulcus, then arcs
around the left side and empties into the coronary sinus.
ii. The posterior interventricular (middle cardiac) vein collects blood
from the posterior aspect and carries it from the apex upward to the
coronary sinus.
iii. The left marginal vein travels from a point near the apex up the left
margin and also empties into the coronary sinus.
iv. The coronary sinus, a large transverse vein in the coronary sulcus on
the posterior side of the heart, collects blood from all other coronary
vein sources and empties blood into the right atrium.
III. Cardiac Muscle and the Cardiac Conduction System (pp. 730–733)
A. The vertebrate heartbeat is myogenic—the signal for contraction originates within the heart
itself. (p. 730)
B. Cardiocytes are inherently autorhythmic—even solitary, isolated cells pulsate rhythmically. (p.
730)
C. In terms of structure, the heart is mostly muscle; the muscle is striated but is different from
skeletal muscle in other respects. (pp. 730–731)
1. Cardiocytes, the heart muscle cells, are relatively short, thick, and branched, about 50
to 100 μm long and 10 to 20 μm wide. (Fig. 19.11)
a. The ends of the cell are slightly branched and through the branches, each
cardiocyte contacts several others to form a network.
b. One network is in the atria, and another network is in the ventricles.
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c. The nucleus is centrally located; the sarcoplasmic reticulum is less developed
than in skeletal muscle and lacks terminal cisternae.
i. The sarcoplasmic reticulum does have footlike sacs associated with
the T tubules, which are much larger than in skeletal muscle.
ii. These T tubules admit calcium ions to activate muscle contraction.
d. Cardiocytes have especially large mitochondria.
2. Cardiocytes are joined end to end by thick connections called intercalated discs, which
are complex steplike structures with three distinctive features compared to skeletal
muscle.
a. Interdigitating folds. The plasma membrane is folded somewhat like the
bottom of an egg carton, and the folds interlock with those of adjoining cells.
b. Mechanical junctions. The cells are tightly joined by two types of junctions:
the fascia adherens and desmosomes.
i. The fascia adherens is the most extensive and is a band in which actin
of thin myofilaments is anchored to the plasma membrane and the cells
are linked via transmembrane protein.
ii. Desmosomes interrupt the fascia adherens here and there; these are
weldlike mechanical junctions between cells.
c. Electrical junctions. The intercalated discs contain gap junctions that allow
the flow of ions between cardiocytes, enabling coordinated contraction of each
network of cardiocytes.
3. Skeletal muscle contains satellite cells that can divide, but cardiac muscle does not; the
repair of damaged cardiac muscle is almost entirely by fibrosis (scarring).
a. A limited capacity for myocardial mitosis and regeneration was discovered in
2001.
D. In terms of metabolism, cardiac muscle depends almost exclusively on aerobic respiration to
make ATP. (p. 732)
1. Cardiac muscle is rich in myoglobin, a short-term source of stored oxygen.
2. Its huge mitochondria fill about 25% of the cell, compared to 2% of skeletal muscle
fibers that have smaller mitochondria.
3. Cardiac muscle is adaptable to fuel source, getting about 60% of its energy from fatty
acids, 35% from glucose, and 5% from other fuels such as ketones, lactic acid, and amino
acids.
4. It makes little use of anaerobic fermentation and is not prone to fatigue, but it is
vulnerable to oxygen deficiency.
E. The heartbeat is coordinated by a cardiac conduction system composed of an internal
pacemaker and nervelike conduction pathways through the myocardium. (pp. 732–733)
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1. The origin of the system is unclear—it may have arisen like the nervous system from
the neural crest of the embryo, or it may have formed from modified cardocytes.
2. The cardiac conduction system generates rhythmic electrical signals in the following
order. (Fig. 19.12)
a. (1) The sinoatrial (SA) node, a patch of modified cardiocytes in the right
atrium, initiates each heartbeat and determines the heart rate.
b. (2) Signals from the SA node spread throughout the atria.
c. (3) The atrioventricular (AV) node, located near the right AV valve at the
lower end of the interatrial septum, acts as an electrical gateway to the
ventricles; the fibrous skeleton prevents currents from getting to ventricles by
any other route.
d. (4) The atrioventricular (AV) bundle (bundle of His) is the pathway by which
signals leave the AV node; it forks into the right and left bundle branches that
enter the interventricular septum and descend toward the apex.
e. (5) Purkinje fibers, nervelike processes, spread upward throughout the
ventricular myocardium and distribute the electrical excitation to cardiocytes of
the ventricles.
3. When the Purkinje fibers have delivered the signals, the cardiocytes themselves
perpetuate it by passing ion flows from cell to cell via gap junctions.
F. The heart does receive both sympathetic and parasympathetic nerves that modify heart rate and
contraction strength. (p. 733)
1. Sympathetic stimulation can raise the heart rate to as high as 230 bpm;
parasympathetic stimulation can slow it to as low as 20 bpm or even stop it for a few
seconds.
2. The sympathetic pathway to the heart originates in the lower cervical to upper thoracic
segments of the spinal cord.
a. Preganglionic nerve fibers extend from the cord to adjacent sympathetic chain
ganglia, and some ascend to cervical ganglia.
b. Postganglionic fibers pass through a cardiac plexus in the mediastinum and
continue via cardiac nerves to the heart.
c. These fibers terminate in the SA and AV nodes and in the myocardia, as well
as the aorta, pulmonary trunk, and coronary arteries.
d. Stimuation increases heart rate and contraction strength and dilates coronary
arteries.
3. The parasympathetic pathway beings with nuclei of the vagus nerves in the medulla
oblongata.
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a. Preganglionic fibers extend through the vagus nerves to the cardiac plexus
where they mingle with the sympathetic fibers; they continue to the heart via the
cardiac nerves.
b. They synapse with postganglionic neurons in the epicardial surface and heart
wall.
c. Postganglionic fibers from the right vagus nerve lead mainly to the SA node.
d. Postganglionic fiber from the left vagus nerve lead mainly to the AV node—
but both right and left have some fibers that cross over.
e. Little or no vagal parasympathetic innervation occurs in the myocardium.
f. Parasympathetic stimulation reduces heart rate.
4. The cardiac nerves carry both sympathetic and parasympathetic efferent fibers, and
they also carry sensory (afferent) fibers to the CNS; these latter are important in
cardiovascular reflexes and transmission of pain signals.
IV. Electrical and Contractile Activity of the Heart (pp. 733–739)
A. Contraction of the heart is called systole, and relaxation is diastole.
B. The sinus rhythm, triggered by the SA node, is a cycle of 70–80 bpm in adults, although rates
of 60–100 bpm are not unusual. (pp. 733–734)
1. Stimuli such as hypoxia, electrolyte imbalances, caffeine, nicotine, and other drugs can
cause other parts of the conduction system to fire before the SA node does.
a. This firing sets off an extra heartbeat called a premature ventricular
contraction (PVC), or extrasystole.
2. Any region of spontaneous firing other than the SA node is called an ectopic focus.
a. If the SA node is damaged, an ectopic focus may take over the governance of
the heart rhythm.
b. The most common ectopic focus is the AV node, which produces a nodal
rhythm of 40 to 50 bpm.
3. Any abnormal cardiac rhythm is called arrhythmia.
a. One cause of arrhythmia is a heart block, the failure of any part of the cardiac
conduction system to transmit signals.
b. It is usually a result of disease and degeneration of conduction system fibers.
i. A bundle branch block is due to damage to one or both bundle
branches.
ii. Damage to the AV node causes total heart block, in which signals
from the atria fail to reach the ventricles, which then beat at their
intrinsic rhythm of 10 to 40 bpm.
Insight 19.2 Cardiac Arrhythmias
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C. The cells of the SA node do not have a stable resting potential; instead their membrane
potential starts at about –60 mV and drifts upward in a gradual depolarization called the
pacemaker potential. (p. 734) (Fig. 19.13)
1. The slow drift results from a slow inflow of Na + without a compensating outflow of
K+.
2. When the pacemaker potential reaches –40 mV, voltage regulated fast calcium–sodium
channels open, and both ions flow in from the extracellular fluid.
a. This produces the rising phase of the action potential, which peaks at slightly
above 0 mV.
b. At this point, K+ channels open and K+ leaves the cell, bringing about
repolarization.
c. K+ channels then close and the cycle begins again.
3. Each depolarization of the SA node sets off one heartbeat; at rest, the SA node
typically fires every 0.8 second or so, or 75 bpm.
D. Impulse conduction to the myocardium begins when the SA node fires. (pp. 734–735)
1. Firing of the SA node excites atrial cardiocytes, stimulating atrial contraction.
2. The signal travels at 1 m/sec through the atrial myocardium and reaches the AV node
in about 50 msec.
3. In the AV node, the signal slows down to about 0.05 m/sec.
a. The slowing is primarily due to fewer gap junctions in cardiocytes in this
region.
b. The signal is delayed for about 100 msec, which allows the ventricles to fill.
4. The ventricular myocardium has a conduction speed of only 0.3 to 0.5 m/sec, but
signals travel through the AV bundle and Purkinje fibers at a speed of 4 m/sec.
5. As a result, the entire ventricular myocardium depolarizes within 200 msec after the
SA node fires, causes contraction of the ventricles in near unison.
6. Signals reach the papillary muscles before the rest of the myocardium, so that these
take up slack in the tendinous cords an instant before ventricular contraction.
7. Ventricular systole begins at the apex of the heart and moves upward, pushing blood
toward the semilunar valves.
E. The action potentials of cardiocytes are significantly different from those of neurons and
skeletal muscle fibers. (pp. 735–736) (Fig. 19.14)
1. Cardiocytes have a stable resting potential of –90 mV and normally depolarize only
when stimulated, unlike SA node cells.
2. A stimulus opens voltage-regulated sodium gates, allowing Na+ inflow and
depolarization of the cell to threshold.
3. The threshold voltage opens more Na+ gates and triggers a positive feedback cycle.
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4. The action potential peaks at nearly +30 mV, at which point the Na + gates close
quickly.
5. As action potentials spread over the membrane, they open voltage-regulated slow
calcium channels that admit Ca2+.
a. The Ca2+ binds to ligand-regulated calcium channels on the sarcoplasmic
reticulum (SR), opening them and releasing Ca2+ from the SR.
b. This second wave of Ca2+ binds to troponin and triggers contraction just as in
skeletal muscle.
c. The SR provides 90% to 98% of the Ca2+ needed for myocardial contraction.
6. In cardiac muscle the depolarization is prolonged for 200 to 250 msec, as compared to
2 msec in skeletal muscle and neurons.
a. This long plateau in the action potential may result because Ca2+ channels are
slow to close, or because SR is slow to remove Ca2+.
7. As long as the action potential is in its plateau, the cardiocytes contract.
a. Cardiac muscle does not have the brief twitch of skeletal muscle, but a more
sustained contraction for blood expulsion.
b. Both atrial and ventricular cardiocytes exhibit plateaus, but they are more
pronounced in the ventricles.
8. At the end of the plateau, Ca2+ channels close and K+ channels open; membrane
voltage drops rapidly and muscle tension declines soon afterward.
9. Cardiac muscle has an absolute refractory period of 250 msec, compared with 1 to 2
msec in skeletal muscle, preventing wave summation and tetanus.
F. A machine called an electrocardiograph detects the heart’s electrical current and produces a
graph called an electrocardiogram (ECG or EKG). (pp. 736–738) (Fig. 19.14)
1. To record an ECG, electrodes are attacked to wrists, ankles, and six locations on the
chest.
2. An ECG is a composite recording of all the action potentials produced by the nodal
and myocardial cells, not a single action potential.
3. A typical ECG shows a P wave, a QRS complex, and a T wave. (Fig. 19.15)
4. These correspond to the regions of the heart undergoing depolarization and
repolarization. (Fig. 19.16)
a. The P wave is produced when a signal from the SA node spreads through the
atria and depolarizes them.
b. Atrial systole begins about 100 msec after the P wave begins, during the PQ
segment.
i. This segment is about 160 msec long and is the time required from
impulses to travel from the SA node to the AV node.
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c. The QRS complex consists of a small downward deflection (Q), a tall sharp
peak (R), and a final downward deflection (S).
i. It is produced when the signal from the AV node spreads through the
ventricular myocardium and depolarizes the muscle.
ii. Its shape is due to the different sizes of the two ventricles and the
different times required from them to depolarize.
iii. Atrial repolarization and diastole also occur during the QRS
interval, but the signal is obscured by ventricular activity.
d. Ventricular systole begins after the QRS complex, in the ST segment.
i. The ST segment corresponds to the plateau in the myocardial action
potential and is the time during which ventricles contract and eject
blood.
e. The T wave is generated by the ventricular repolarization immediately before
diastole.
i. The ventricles take longer to repolarize than to depolarize, and so the
T wave is smaller and more spread out than the QRS complex and is
rounder.
ii. Even when the T wave is taller than the QRS complex, it can be
recognized by its relatively rounded peak.
5. The ECG is useful for diagnosing abnormalities in conduction pathways, myocardial
infarction, enlargement of the heart, and electrolyte and hormone imbalances.
a. Some abnormal ECGs are given in Table 19.1 and Fig. 19.17.
V. Blood Flow, Heart Sounds, and the Cardiac Cycle (pp. 739–745)
A. A cardiac cycle consists of one complete contraction and relaxation of all four heart chambers.
(p. 739)
B. Certain principles of pressure and flow apply to movement of a fluid. (pp. 740–741)
1. A fluid is a state of matter that can flow in bulk from place to place, including both
liquids and gases.
2. Fluid dynamics is the term for principles that govern flow.
3. The main variables are pressure, which impels a fluid to move, and resistance, which
opposes flow.
4. Pressure is measured by a device called a manometer.
a. Typically this is a J-shaped glass tube partially filled with mercury.
b. The sealed end, above the mercury, contains a vacuum, and the lower end is
open.
c. Pressure applied at the lower end is measured in terms of how high it can push
the mercury column up the tube.
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d. Thus pressures are expressed in millimeters of mercury (mm Hg).
5. Blood pressure is usually measured with a sphygmomanometer, which has its open end
attached to an inflatable pressure cuff that is wrapped around the arm.. (Fig. 18.20a)
6. Flow occurs when a fluid is subjected to more pressure at one point than at another,
which creates a pressure gradient.
a. Fluids always flow down their pressure gradients.
b. An analogy that demonstrates this is an air-filled syringe. (Fig. 19.18)
i. Pressure is inversely proportional to the volume of a container.
ii. As the plunger on a syringe is pulled back, the volume increases,
lowering the air pressure in the barrel and pulling in air from the
outside.
iii. As the plunger is depressed, the volume decreases, raising the
pressure in the barrel, and forcing air out.
c. A heart chamber such as the left ventricle is like a syringe barrel.
i. When the ventricle is expanding, pressure falls, and blood flows into
the ventricle.
ii. When the ventricle contracts, pressure rises, and when the aortic
valve opens, blood is ejected into the aorta.
d. The opening and closing of heart valves are governed by pressure changes,
since they have no muscle and are passive.
3. When the ventricles are relaxed, the AV valve cusps hang down limply and both
valves are open (Fig. 19.19a)
a. Blood flows freely into the ventricles even before the atria contract.
b. As the ventricles fill with blood, the cusps float upward toward the closed
position.
4. When the ventricles contract, their internal pressure rises sharply, pushing the cusps of
the AV valves together to seal the openings.
a. The papillary muscles contract slightly before the rest of the ventricular
myocardium, pulling on the tendinous cords and preventing the valves from
bulging into the atria.
5. The rising pressure also opens the aortic and pulmonary valves.
a. Pressure in the aorta and pulmonary trunk oppose opening, but when
ventricular pressure exceeds arterial pressure, the valves open.
e. As ventricles relax, arterial blood briefly flows backward and fills the
pocketlike cusps of the semilunar valves, sealing the opening.
Insight 19.3 Valvular Insufficiency
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C. Two or three heart sounds are audible with a stethoscope during the cardiac cycle. (pp. 742–
743)
1. Listening to sounds made by the body is called auscultation.
2. The first (S1) and second (S2) heart sounds are often described as a “lubb-dupp,” with
S1 louder and longer and S2 a little softer and sharper.
3. In children and adolescents it is normal to hear a third heart sound (S 3); it is rarely
audible in people older than 30 but when it is, it is called a triple rhythm or gallop.
4. The cause of each sound is not known with certainty because the valves operate
silently; turbulence in blood flow may be the cause.
D. The cardiac cycle can be described as having four phases, all of which are completed in less
than 1 second. (pp. 742–744) (Fig. 19.20)
1. Ventricular filling.
a. As the ventricles relax and expand during diastole, the AV valves open;
ventricular filling occurs in three phrases:
i. Rapid ventricular filling is the first one-third, when blood enters
quickly.
ii. Diastasis is the second on-third and is marked by slower filling; the
P wave of the electrocardiogram occurs at the end of diastasis as the
atria depolarize.
iii. Atrial systole is the last one-third, during which the atria contract
and filling of the ventricles is completed.
b. At the end of ventricular filling, each ventricle contains an end-diastolic
volume (EDV) of about 130 mL of blood; only 40mL (31%) is contributed by
atrial systole.
2. Isovolumetric contraction.
a. The atria repolarize, relax, and remain in diastole for the rest of the cardiac
cycle.
b. The ventricles depolarize, generate the QRS complex, and begin to contract,
and pressure rises sharply.
c. AV valves close and heart sound S1 occurs, produced mainly by the left
ventricle.
d. This phase is called isovolumetric because even though the ventricles
contract, they do not eject blood yet; there is no change in their volume.
i. Pressures in the aorta (80 mm Hg) and pulmonary trunk (10 mm Hg)
are still greater than the pressures in the ventricles.
ii. With all four valves closed, blood cannot go anywhere.
3. Ventricular ejection.
Saladin Outline Ch.19
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a. Ejection of blood begins when ventricular pressure exceeds arterial pressure,
forcing the semilunar valves open.
i. The pressure peaks at 120 mm Hg in the left ventricle and 25 mm Hg
in the right.
ii. Blood spurts out rapidly at first (rapid ejection) and the flows more
slowly (reduced ejection.
b. Ventricular ejection lasts 200 to 250 msec, corresponding to the plateau of the
myocardial action potential but lagging somewhat.
c. The T wave occurs late in this phase.
d. The ventricles do not expel all their blood.
i. Each ventricle in an average resting heart contains an EDV of 130
mL.
ii. The amount ejected, about 70 mL, is called the stroke volume (SV).
iii. The percentage of EDV ejected, about 54%, is the ejection fraction.
iv. The blood remaining behind, about 60 mL, is called the end-systolic
volume (ESV); EDV – SV = ESV.
v. In vigorous exercise, the ejection fraction may be as high as 90%.
vi. A diseased heart may eject much less than 50%.
4. Isovolumetric relaxation.
a. This phase, early ventricular diastole, occurs when the T wave ends and
ventricles begin to expand.
b. Two hypotheses seek to explain ventricular expansion.
i. One is that blood flowing into the ventricles “inflates” them.
ii. Another is that contraction of the ventricles deforms the fibrous
skeleton, which springs back, sucking blood into the ventricles.
c. At the beginning of ventricular diastole, blood briefly flows backward through
the semilunar valves.
i. This backflow quickly fills the cusps and closes them, creating a
slight pressure rebound that appears as the dicrotic notch of the aortic
pressure curve. (Fig. 19.20)
ii. Heart sound S2 occurs as blood rebounds from the closed semilunar
valves and ventricles expand.
d. This phase is called isovolumetric because the semilunar valves are closed,
the AV valves have not yet opened, and the ventricles are therefore taking in no
blood.
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e. When the AV valves open, phase 1 begins again; heart sound S3, if it occurs,
is thought to occur from the transition from expansion of empty ventricles to
their sudden filling with blood.
5. In a resting person, atrial systole lasts about 0.1 sec; ventricular systole, 0.2 sec; and
the quiescent period, 0.4 sec; total duration is therefore 0.8 sec in a heart beating at 75
bpm.
E. Volume changes during the cardiac cycle give an additional perspective. (pp. 744–745)
1. The summary of changes is as follows.
a. End-systolic volume (ESV) is 60 mL.
b. Passive addition to the ventricle is +30 mL, and active addition by atrial
diastole is +40 mL.
c. Total end-diastolic volume (EDV) is therefore 60 + 30 + 40 = 130 mL.
d. Stroke volume (SV) ejected is –70 mL.
e. End-systolic volume (ESV) is therefore 130 – 70 = 60mL.
2. Both ventricles eject the same amount of blood even though pressure in the right
ventricle is only about one-fifth the pressure in the left.
a. Blood pressure in the pulmonary trunk is relatively low compared to the aortic
pressure, so not as much force is needed.
b. It is essential that both ventricles have the same output; if the right ventricle
pumped more blood, the blood would accumulate in the lungs causing
pulmonary hypertension and edema. (Fig. 19.21a)
c. If the left ventricle pumped out more blood, blood would accumulate in the
systemic circuit and cause hypertension and edema there. (Fig. 19.21b)
Insight 19.4 Congestive Heart Failure
VI. Cardiac Output (pp. 745–750)
A. The amount of blood ejected by each ventricle in 1 minute is called the cardiac output (CO). (p.
745)
1. If HR is heart rate and SV is stroke volume, then CO = HR × SV.
2. The body’s total volume of blood, 4–6 L, passes through the heart every minute; CO at
75 beats per minute × 70 mL/beat = 5,250 mL/min.
B. Cardiac output varies with activity. (p. 745)
1. Vigorous exercise increases CO to 21 L/min in someone in good condition, and up to
35 L/min in world-class athletes.
2. The difference between max CO and resting CO is the cardiac reserve.
3. CO can be changed by alterations in heart rate or in stroke volume; these usually are
somewhat interdependent and inversely related.
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C. Heart rate is most easily measured by taking a person’s pulse at a point where an artery runs
close to the surface. (pp. 745–747)
1. Heart rate can be obtained by counting the number of pulses in 15 seconds and
multiplying by 4 to get beats per minute.
2. In newborns, the resting heart rate is commonly 120 bpm or greater, then declines to
average 72 to 80 in young adult females and 64 to 72 in young adult males; it rises again
in the elderly.
3. Tachycardia is a persistent, resting adult heart rate above 100 bpm.
a. It can be caused by stress, anxiety, drugs, heart disease, or fever.
b. Heart rate also rises to compensate for a drop in stroke volume, so the heart
races when significant blood has been lost or the myocardium has been
damaged.
4. Bradycardia is a persistent, resting adult heart rate below above 60 bpm.
a. It is common during sleep and in endurance-trained athletes.
b. Hypothermia also slows the heart rate and may be deliberately induced for
cardiac surgery.
c. Diving mammals exhibit bradycardia during the dive, as do humans to some
extent when the face is immersed in cool water.
5. Factors that raise the heart rate are called positive chronotropic agents, and those that
lower it are negative chronotropic agents. (Table 19.2)
6. The autonomic nervous system can have chronotropic effects.
a. The reticular formation of the medulla oblongata contains cardiac centers that
initiate autonomic output to the heart.
i. Some neurons have a cardiostimulatory effect and transmit signals to
the heart by way of the sympathetic pathways.
ii. Others have a cardioinhibitory effect communicated by way of the
vagus nerves.
b. The sympathetic postganglionic fibers are adrenergic and release
norepinephrine that binds to β-adrenergic fibers in the heart.
i. Binding activates the cAMP second-messenger system in cardiocytes
and nodal cells.
ii. cAMP activates a phosphorylase that opens a calcium channel in the
plasma membrane, allowing influx of Ca2+ that accelerates
depolarization of the SA node and contraction of the cardiocytes, so it
speed up the heart.
iii. In addition, cAMP accelerates the uptake of Ca2+ by the
sarcoplasmic reticulum, enabling cardiocytes to relax more quickly.
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c. Adrenergic stimulation can raise heart rate as high as 230 bpm.
i. The limit is set by the refractory period of the SA node.
ii. Cardiac output peaks at a heart rate of 160 to 180 bpm; at higher
rates the ventricles do not have sufficient time to fill between
contractions.
d. The parasympathetic vagus nerves have cholinergic, inhibitory effects on the
SA and AV nodes.
i. Acetylcholine (ACh) binds to muscarinic receptors and opens K +
gates in the nodal cells.
ii. As K+ exits, the cells become hyperpolarized and fire less frequently,
so the heart slows down.
iii. The vagus nerves have a faster-acting effect on the heart than the
sympathetic nerves because ACh acts directly on ion channels.
e. If all sympathetic and parasympathetic stimulation of the heart is blocked, or
if the cardiac nerves are severed, the heart beats at about 100 bpm, the intrinsic
rate of the SA node.
i. With intact innervation, the resting heart rate is held down to about
70 to 80 bpm by vagal tone, the background firing rate of the vagus
nerves.
ii. More extreme vagal stimulation can reduce the heart rate to as low
as 20 bpm or even stop the heart briefly.
f. Placing the heart rate under the influence of cardiac centers in the medulla
allows input and integration of stimuli into the heart rate.
i. Sensory and emotional stimuli can increase heart rate in anticipation
of an event.
ii. Emotions such as love and anger also affect heart rate.
g. The medulla also receives input from receptors in the muscles, joints, arteries,
and brainstem.
i. Proprioceptors in muscles and joints provide information on changes
in physical activity, allowing heart rate to increase even before the
metabolic demands rise.
ii. Baroreceptors (pressoreceptors) in the aorta and internal carotid
arteries send a continual stream of signals to the medulla, providing
information on heart rate and blood pressure, to which the medulla
responds by altering sympathetic output in a negative feedback loop.
iii. Chemoreceptors in the aortic arch, carotid arteries, and medulla
oblongata provide information about blood pH, and CO2 and O2 levels;
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Page 19
hypercapnia (excess CO2) and acidosis lead to an increase in heart rate,
and hypoxemia (O2 deficiency) leads to a drop.
iv. Responses to fluctuations in blood chemistry and pressure are called
chemoreflexes and baroreflexes.
7. Chemicals also have chronotropic effects.
a. Blood-borne epinephrine and norepinerphine from the adrenal medulla have
the same effect as epinephrine from sympathetic nerves.
b. Chronotropic action of other chemicals are also related to their impact on the
catecholamine–cAMP mechanism.
i. Nicotine accelerates the heart by stimulating catecholamine secretion.
ii. Thyroid hormone stimulates up-regulation of adrenergic receptors,
so hyperthyroidism commonly produces tachycardia.
iii. Caffeine and related stimulants in tea and chocolate inhibit cAMP
breakdown, prolonging adrenergic effects.
c. The electrolyte with the greatest chronotropic effect is potassium (K +).
i. In hyperkalemia, excess K+ diffuses into cardiocytes, keeping
membrane voltage elevated and inhibiting repolarization; heart rate
becomes slow and irregular, and the heart may arrest in diastole.
ii. In hypokalemia, a potassium deficiency, K+ diffuses out of the
cardiocytes and they become hyperpolarized and harder to stimulate.
iii. Potassium imbalances are very dangerous and require emergency
medical treatment.
d. Calcium also affects heart rate.
i. Hypercalcemia, a calcium excess, causes a slow heartbeat, whereas
hypocalcemia, calcium deficiency, elevates it.
ii. They are rare, but when they do occur, their primary effect is on
contraction strength.
D. Stroke volume is governed by three variables: preload, contractility, and afterload; increases in
the first two increase stroke volume, whereas increased afterload reduces stroke volume. (pp. 747–
748)
1. Preload is the amount of tension in the ventricular myocardium immediately before it
begins to contract.
a. As active muscles massage veins, they drive more blood to the heart
increasing venous return.
i. Increased venous return stretches the myocardium, and because of the
length–tension relationship, moderate stretch enables cardiocytes to
generate more tension upon contraction.
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ii. More forceful contraction expels more blood.
b. The Frank-Starling law of the heart states that SV is proportional to the
EDV—ventricles tend to eject as much blood as they receive.
c. This effect helps balance the output of the two ventricles.
2. Contractility refers to how hard the myocardium contracts for a given preload.
a. Factors that increase contractility are called positive inotropic agents, and
those that reduce it are negative inotropic agents. (Table 19.2)
b. Calcium has a strong positive inotropic effect, increasing the strength of each
contraction.
i. In hypercalcemia, extra Ca2+ diffuses into cardiocytes and produces
strong prolonged contractions, and in extreme cases can cause cardiac
arrest in systole.
ii. In hypcalcemia, cardiocytes lose Ca2+ to the ECF, leading to a weak
heartbeat and potentially to cardiac arrest in diastole; it is more likely to
kill through skeletal muscle paralysis, however.
c. Agents that affect calcium also have inotropic effects as a result.
i. Norepinephrine increases calcium levels in the sacroplasm; it
increases not only heart rate but also contraction strength, as does
epinephrine.
ii. Glucagon exerts an inotropic effect by stimulating cAMP
production.
iii. A solution of glucagon and calcium chloride is sometimes used for
emergency treatment of heart attacks.
iv. Digitalis, from the foxglove plant, also raises the intracellular
calcium level; it is used to treat congestive heart failure.
d. Hyperkalemia has a negative inotropic effect because it reduces the strength
of myocardial action potentials and thus the release of Ca2+ into the sarcoplasm.
e. The vagus nerves have a negative inotropic effect on the atria, but no
significant effect on the ventricles.
3. Afterload is the blood pressure in the aorta and pulmonary trunk immediately distal to
the semilunar valves.
a. Afterload opposes the opening of the valves and thereby limits stroke volume.
b. Hypertension therefore increase afterload and opposes ventricular ejection.
c. Anything that impedes arterial circulation also increases afterload, such as
scar tissue from some lung diseases.
i. Increased afterload in the pulmonary truck causes the right ventricle
to work harder, and it gets larger.
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ii. Hypertrophy can eventually cause the ventricle to weaken and fail.
iii. Right ventricular failure is called cor pulmonale and is a common
complication of emphysema, chronic bronchitis, and black lung
disease.
E. Exercise makes the heart work harder, and this increases cardiac output.
1. At the beginning of exercise, proprioceptors in muscles and joints signal cardiac
centers that muscles are active, and sympathetic output then increases cardiac output.
2. As exercise progresses, muscular activity increases venous return.
3. As heart rate and stroke volume rise, cardiac output rises to compensate for increased
venous return.
4. A sustained program of exercise causes hypertrophy of the ventricles, such that the
heart can beat more slowly and still maintain a normal resting cardiac output.
a. Endurance athletes commonly have resting heart rates as low as 40 to 60 bpm.
b. Champion cyclist Lance Armstrong has a resting heart rate of only 32 to 34
bpm.
c. With a greater cardiac reserve, athletes can tolerate more exertion than can a
sedentary person.
5. Some common heart disease are listed in Table 19.3.
Insight 19.5 Coronary Artery Disease (Fig. 19.22)
Cross References
Additional information on topics mentioned in Chapter 19 can be found in the chapters listed below.
Chapter 7: Effects of hypocalcemia
Chapter 18: Disorders of the blood
Chapter 20: Role of pressure and resistance in flow of blood through vessels.
Chapter 20: Blood pressure
Chapter 20: Chemoreflexes and baroreflexes
Chapter 20: Disorders of the blood vessels.
Chapter 21: Lymphatic system
Chapter 22: Respiratory airflow
Chapter 22: Chronic lung diseases
Chapter 24: Causes and effects of electrolyte imbalances