DETAILED LECTURE OUTLINE
Fundamentals of Anatomy and Physiology, 7th edition, ©2006 by Frederic H. Martini
Prepared by Professor Albia Dugger, Miami-Dade College, Miami, Florida
Please note:
 References to textbook headings, figures and tables appear in italics.
 “100 Keys” are designated by Key
 Important vocabulary terms are underlined.
Chapter 20: The Heart
I. The Organization of the Cardiovascular System, p. 670
Objective:
1. Describe the organization of the cardiovascular system and of the heart.
Figure 20-1
 The heart pumps blood through 2 separate circuits of blood vessels:
1. The pulmonary circuit:
- carries blood to and from the gas exchange surfaces of the lungs
2. The systemic circuit:
- carries blood to and from the rest of the body

Circulating blood alternates between the systemic and pulmonary systems: Blood
returning to the heart from the systemic circulation must pass through the
pulmonary circuit before returning to the systemic circuit.

There are 3 types of blood vessels:
1. Arteries carry blood away from the heart
2. Veins carry blood to the heart
3. Capillaries are networks of small, thin-walled vessels between arteries and
veins.

Capillaries are called exchange vessels because they are the location where
dissolved gases, nutrients, and wastes are exchanged between the blood and the
surrounding tissues.

The heart has 4 chambers, 2 for each circuit:
1. The right atrium collects blood from the systemic circuit.
2. The right ventricle pumps blood to the pulmonary circuit.
3. The left atrium collects blood from the pulmonary circuit.
4. The left ventricle pumps blood to the systemic circuit.
II. Anatomy of the Heart, p. 670
Objectives:
1. Describe the location and general features of the heart.
2. Describe the structure of the pericardium and explain its functions.
3. Trace the flow of blood through the heart, identifying the major blood vessels,
chambers and heart valves.
4. Identify the layers of the heart wall.
5. Describe the vascular supply to the heart.
Figure 20-2a
 The heart is located directly posterior to the sternum. The great veins and arteries
attach at the top (the base). The pointed tip is the apex.
Figure 20-2b
 The heart, surrounded by the pericardial sac, sits in the mediastinum (between the
2 pleural cavities) which also holds the great vessels, thymus, esophagus and
trachea.
The Pericardium, p. 671
Figure20-2c
 The pericardial cavity has a double lining called the pericardium.

The outer layer is the parietal pericardium. The parietal pericardium forms the
inner layer of the fibrous pericardial sac which surrounds and stabilizes the heart.

The inner layer is the visceral pericardium. The space between the 2 layers is the
pericardial cavity, which contains a small amount of lubricating pericardial fluid.

An infection of the pericardium is called pericarditis.
Superficial Anatomy of the Heart, p. 672
Figure 20-3
 The 4 cardiac chambers can be seen in the superficial view of the heart.

The atria are thin-walled, with an expandable outer portion called the auricle. A
coronary sulcus divides the atria and the ventricles. The left and right ventricles
are separated along the anterior and posterior interventricular sulci, which also
contain the blood vessels that supply the cardiac muscle.
The Heart Wall, p. 673
Figure 20-4
 The heart wall has 3 layers:
1. the outer epicardium
2. the middle myocardium
3. the inner endocardium

The epicardium is the visceral pericardium that covers the heart.

The myocardium is the muscular wall of the heart, consisting of concentric layers
of cardiac muscle tissue. The atrial myocardium wraps around the great vessels.
Superficial ventricular muscles surround the ventricles. Deep ventricular muscles
spiral around and between the ventricles.
- Cardiac Muscle Tissue
Figure 20-5
 Cardiac muscle cells are interconnected by intercalated discs which are held
together by desmosomes and linked by gap junctions. Intercalated discs convey
the force of contraction from cell to cell and propagate action potentials.

The characteristics of cardiac muscle cells include:
1. small size
2. single, central nucleus
3. branching interconnections between cells
4. intercalated discs
Table 20-1 summarizes differences between cardiac cells and skeletal fibers.
Internal Anatomy and Organization, p. 674
Figure 20-6a
 The right atrium opens to the right ventricle, and the left atrium opens to the left
ventricle. Atrioventricular (AV) valves permit blood to flow in only 1 direction:
from the atria to the ventricles.

The atria are separated by the interatrial septum, and the ventricles by the
interventricular septum.

The right atrium receives blood from the systemic circuit through the superior
vena cava (head, neck, upper limbs and chest) and the inferior vena cava (trunk,
viscera and lower limbs).

The cardiac veins of the heart return blood to the coronary sinus, which opens
into the right atrium. Before birth, an opening through the interatrial septum (the
foramen ovale) connects the 2 atria. At birth, the foramen ovale seals off, leaving
a small depression called the fossa ovalis.

The anterior atrial wall and inner surfaces of the right auricle have prominent
muscular ridges called pectinate muscles.

The opening from the right atrium to the right ventricle has 3 fibrous flaps or
cusps, which are part of the right atrioventricular (AV) valve (tricuspid valve).
The free edge of each cusp is attached to connective tissue fibers (chordae
tendineae) which originate at the papillary muscles of the right ventricle and
prevent the AV valve from opening backward.

The internal surface of the right ventricle has a series of muscular ridges (the
trabeculae carneae) which includes the moderator band, a ridge that contains part
of the conducting system that coordinates the contractions of cardiac muscle
cells.

The superior part of the right ventricle (the conus arteriosus) leads to the
pulmonary trunk, which divides into the left and right pulmonary arteries of the
pulmonary circuit. Blood flows from the right ventricle to the pulmonary trunk
through the pulmonary valve, which has 3 semilunar cusps that prevent backflow.

After the blood passes through the pulmonary circuit, it is gathered into the left
and right pulmonary veins, which deliver blood into the left atrium. Blood passes
from the left atrium to the left ventricle through the left atrioventricular (AV)
valve, a 2-cusp or bicuspid valve, also known as the mitral valve.

The left ventricle holds the same amount of blood as the right ventricle, but is
larger because its muscle is thicker and more powerful. Internally, the left
ventricle is similar to the right ventricle, but has no moderator band.

Blood heading for the systemic circulation leaves the left ventricle through the
aortic valve into the ascending aorta. (The aortic valve is similar in structure to
the pulmonary valve.) The ascending aorta turns at the aortic arch and becomes
the descending aorta.
Figure 20-7
 The left and right ventricles have significant structural differences:
- The wall of the right ventricle is relatively thin and develops less pressure
than the left ventricle.
- The right ventricle is pouch-shaped, the left ventricle round.
- The Heart Valves
Figure 20-8
 The heart has a series of one-way valves that prevent backflow during
contraction.

The atrioventricular (AV) valves between the atria and the ventricles are
controlled by the chordae tendineae and the papillary muscles. When the
ventricles contract, the pressure of the blood swings the cusps together, closing
the valves to the atria. At the same time, the papillary muscles tense the chordae
tendineae and prevent the valves from swinging into the atria. Failure of the
valves causes backflow or regurgitation of blood into the atria.

The pulmonary and aortic semilunar valves prevent backflow from the pulmonary
trunk and aorta into the ventricles. Semilunar valves have no muscular support;
the 3 cusps of the valve support each other like a tripod.

The aortic sinuses at the base of the ascending aorta prevent the valve cusps from
sticking to the aorta. The right and left coronary arteries originate at the aortic
sinuses.

An inflammation of the heart (carditis) can result in valvular heart disease (VHD)
such as rheumatic fever.
Key



The heart has 4 chambers, 2 associated with the pulmonary circuit (right atrium
and right ventricle) and 2 with the systemic circuit (left atrium and left ventricle).
The left ventricle has a greater workload and is much more massive than the right
ventricle, but the two chambers pump equal amounts of blood.
AV valves prevent backflow from the ventricles into the atria, and semilunar
valves prevent backflow from the aortic and pulmonary trunks into the ventricles.
Connective Tissues and Fibrous Skeleton, p. 680

Connective tissue fibers of the heart have several functions:
1. they provide physical support for cardiac muscle fibers
2. they distribute the forces of contraction
3. they add strength and prevent overexpansion of the heart
4. elastic fibers help return the heart to its original shape after a contraction

The fibrous skeleton of the heart (4 bands around the heart valves and the bases of
the pulmonary trunk and aorta) stabilize the valves and electrically insulate
ventricular cells from atrial cells.
The Blood Supply to the Heart, p. 680
Figure 20-9
 The coronary circulation, consisting of coronary arteries and cardiac veins,
supplies blood to the muscle tissue of the heart.

The left and right coronary arteries originate at the aortic sinuses. High blood
pressure and elastic rebound force blood through the coronary arteries between
contractions.

The right coronary artery supplies blood to the right atrium, portions of both
ventricles, and cells of the sinoatrial (SA) and atrioventricular nodes that regulate
the heartbeat. The right coronary artery supplies marginal arteries on the surface
of the right ventricle, and the posterior interventricular artery.

The left coronary artery supplies blood to the left ventricle, left atrium and
interventricular septum. The 2 main branches of the left coronary artery are the
circumflex artery (on the left around the coronary sulcus) and the anterior
interventricular artery.

The anterior and posterior interventricular arteries are interconnected by arterial
anastomoses, which stabilize the blood supply to the cardiac muscle.

The great cardiac vein drains blood from the region of the anterior interventricular
artery into the coronary sinus. Other cardiac veins that empty into the great
cardiac vein or coronary sinus include the posterior cardiac vein, the middle
cardiac vein, and the small cardiac vein. The anterior cardiac vein empties into the
right atrium.
III The Heartbeat, p. 684
Objectives:
1. Describe the events of an action potential in cardiac muscle and explain the
importance of calcium ions to the contractile process.
2. Discuss the differences between nodal cells and conducting cells, and describe the
components and functions of the conducting system of the heart.
3. Identify the electrical events associated with a normal electrocardiogram.
4. Explain the events of the cardiac cycle, including atrial and ventricular systole
and diastole, and relate the heart sounds to specific events in the cycle.
Cardiac Physiology, p. 684
Figure 20-11
 In a single contraction or heartbeat, the entire heart contracts in series: first the
atria, then the ventricles.

Two types of cardiac muscle cells are involved in the heartbeat:
1. the conducting system:
- controls and coordinates the heartbeat
2. the contractile cells:
- produce contractions

The cardiac cycle begins with an action potential at the SA node, which is
transmitted through the conducting system. This produces action potentials in the
cardiac muscle cells (contractile cells) which cause the contraction.

The electrical events in the cardiac cycle can be recorded on an electrocardiogram
(ECG).
The Conducting System, p. 684
Figure 20-12
 Cardiac muscle tissue contracts automatically (automaticity). A system of
specialized cardiac muscle cells (the conducting system) initiates and distributes
the electrical impulses that stimulate contraction.

The conducting system includes:
- the sinoatrial (SA) node
- the atrioventricular (AV) node
- conducting cells

Conducting cells interconnect the SA and AV nodes and distribute the contractile
stimulus through the heart. In the atria, conducting cells are found in internodal
pathways that distribute the impulse to atrial cells and the AV node. Ventricular
conducting cells are found in the AV bundle, bundle branches and Purkinje fibers.

Conducting cells of the SA and AV nodes cannot maintain a stable resting
potential; after repolarization they gradually drift toward threshold (prepotential
or pacemaker potential). The SA node depolarizes first, establishing a heart rate of
about 80-100 beats per minute. Normal heart rate is slowed by parasympathetic
stimulation. The AV node generates 40-60 action potentials per minute
Figure 20-13
- Impulse Conduction Through the Heart
1. The Sinoatrial (SA) Node
- in posterior wall of right atrium
- contains pacemaker cells
- connected to AV node by internodal pathways
- begins atrial activation (Step 1)
2. The Atrioventricular (AV) Node
- in floor of right atrium
- receives impulse from SA node (Step 2)
- delays impulse (Step 3)
- atrial contraction begins
3. The AV Bundle
- in the septum
- carries impulse to left and right bundle branches:
- which conduct to Purkinje fibers (Step 4)
- and to the moderator band:
- which conducts to papillary muscles
4. The Purkinje Fibers
- distribute impulse through ventricles (Step 5)
- atrial contraction is completed
- ventricular contraction begins

Abnormal pacemaker function changes the heart rate:
- bradycardia is an abnormally slow heart rate.
- tachycardia is an abnormally fast heart rate.

If an abnormal conducting cell or ventricular muscle cell begins generating a high
rate of action potentials, they can override the SA and AV nodes and bypass the
conducting system, disrupting ventricular contractions. The origin of these
abnormal impulses is called an ectopic pacemaker.
The Electrocardiogram, p. 687
Figure 20-14a
 The electrocardiogram (ECG or EKG) is a recording of electrical events in the
heart, obtained by placing electrodes at specific locations on the body. Abnormal
ECG patterns are used to diagnose damage to specific nodal, conducting and
contractile components of the heart.

The basic features of an ECG include:
1. The P wave: A small wave produced when the atria depolarize.
2. The QRS complex: A complex signal produced when the ventricles
depolarize. The ventricles begin contracting just after the peak of the R
wave.
3. The T wave: A small wave produced when the ventricles repolarize.

The time intervals between waves are also important. Time intervals commonly
used in clinical diagnosis include:
1. P-R interval: The time from the start of atrial depolarization to the start of
the QRS complex.
2. Q-T interval: The time from ventricular depolarization to ventricular
repolarization.

Abnormal patterns of cardiac electrical activity are called cardiac arrhythmias.
Key


The heart rate is normally established by cells of the SA node, but that rate can be
modified by autonomic activity, hormones and other factors.
From the SA node the stimulus is conducted to the AV node, the AV bundle, the
bundle branches and Purkinje fibers before reaching the ventricular muscle cells.

The electrical events associated with the heartbeat can be monitored in an
electrocardiogram (ECG).
Contractile Cells, p. 688

Purkinje fibers distribute the stimulus to the contractile cells, which make up most
of the muscle cells in the heart.
Figure 20-15
 Action potentials in cardiac muscle are different than action potentials in skeletal
muscle. The resting potential of a ventricular cell is about -90mV, an atrial cell
about -80 mV.

Once threshold is reached, the action potential proceeds in 3 steps:
1. Rapid depolarization: Voltage-regulated sodium channels (fast channels)
open.
2. As sodium channels close, voltage-regulated calcium channels (slow
channels) open, balancing the Na+ ions being pumped out and holding the
membrane at a 0 mV plateau.
3. Repolarization: As the plateau continues, slow calcium channels close,
and slow potassium channels open, resulting in rapid repolarization that
restores the resting potential.

Cardiac muscle cells then undergo an absolute refractory period, when they
cannot respond, followed by a shorter relative refractory period. The total time for
a cardiac action potential in a ventricular cell is 250-300 msecs -- 30 times longer
than a skeletal muscle fiber. The long refractory period prevents summation and
tetany in cardiac tissues.

Contraction of a cardiac muscle cell is produced by an increase in calcium ion
concentration around the myofibrils, which occurs in 2 steps:
1. 20% of the calcium ions required for a contraction enter the cell
membrane during the plateau phase.
2. The arrival of extracellular Ca++ triggers the release of calcium ion
reserves from the sarcoplasmic reticulum.

As the slow calcium channels close, intracellular Ca++ is absorbed by the SR or
pumped out of the cell. Cardiac muscle tissue is very sensitive to extracellular
Ca++ concentrations.
The Cardiac Cycle, p. 690

The period between the start of one heartbeat and the beginning of the next is one
cardiac cycle, including both contraction and relaxation.

Within any one chamber, the cycle is divided into 2 phases: systole (contraction)
and diastole (relaxation). Pressure in the chamber rises during systole and falls
during diastole. Blood flows from high pressure to low pressure, controlled by the
timing of contractions and directed by one-way valves.
Figure 20-16
 The cardiac cycle is divided into 4 phases: atrial systole, atrial diastole,
ventricular systole and ventricular diastole.

At 75 beats per minute, a cardiac cycle lasts about 800 msecs. When heart rate
increases, all phases of the cardiac cycle shorten, particularly the diastole.
Figure 20-17
 Pressure and volume change during the cardiac cycle: 8 steps are shown in the
figure.
1. Atrial Systole: Atrial contraction begins. Right and left AV valves are
open.
2. Atria eject blood into the ventricles, filling the ventricles.
3. Atrial systole ends: AV valves close. Ventricles contain maximum volume
(end-diastolic volume, EDV).
4. Ventricular systole: Isovolemic ventricular contraction. Pressure in
ventricles rises, AV valves shut.
5. Ventricular ejection: Semilunar valves open, blood flows into pulmonary
and aortic trunks. Stroke volume (SV) = 60% of end-diastolic volume.
6. Ventricular pressure falls, semilunar valves close. Ventricles contain endsystolic volume (ESV), about 40% of end-diastolic volume.
7. Ventricular diastole: Ventricular pressure is higher than atrial pressure. All
heart valves are closed. Ventricles relax (isovolumetric relaxation).
8. Atrial pressure is higher than ventricular pressure. AV valves open;
passive atrial filling occurs. Passive ventricular filling. Cardiac cycle ends.

Lack of adequate blood flow to peripheral tissues and organs due to ventricular
damage is called heart failure.
Figure 20-18
 There are 4 heart sounds (S1 through S4): S1, produced by the AV valves, and S2,
produced by the semilunar valves, are loud sounds that can be detected using a
stethoscope. The stethoscope is placed in different locations to detect the sounds
of each valve.

S3 and S4, produced by blood flowing into the ventricles and atrial contraction,
are very soft sounds.

The sound produced by regurgitation through the valves is called a heart murmur.

The heart obtains energy from the aerobic (mitochondrial) breakdown of fatty
acids and glucose. In addition to oxygen obtained from circulating hemoglobin,
cardiac muscles store oxygen bound to myoglobin molecules for times of
increased oxygen demand.
IV. Cardiodynamics, 695
Objectives:
1. Define cardiac output, and describe the factors that influence this variable.
2. Describe the variables that influence heart rate.
3. Describe the variables that influence stroke volume.
4. Explain how adjustments in stroke volume and cardiac output are coordinated at
different levels of activity.

Cardiodynamics is the movement and force generated by cardiac contractions.

Important terms used in cardiodynamics are:
- end-diastolic volume (EDV)
- end-systolic volume (ESV)
- stroke volume (SV):
SV=EDV-ESV
- ejection fraction:
- % of EDV represented by SV
- cardiac output (CO):
- the volume pumped by each ventricle in 1 minute
Figure 20-19
 Stroke volume is the volume (ml) of blood ejected per beat.

Cardiac output (CO) ml/min = heart rate (HR) beats/min X stroke volume (SV)
ml/beat

The body adjusts cardiac output to provide adequate circulation in a variety of
conditions.
Overview: The Control of Cardiac Output, p. 697
Figure 20-20
 Cardiac output can be adjusted by either changes in heart rate or stroke volume.

Heart rate is adjusted by the autonomic nervous system or by hormones.

Stroke volume is adjusted by changing EDV or ESV.
Factors Affecting the Heart Rate, p. 697
Figure 20-21
- Autonomic Innervation:





The cardiac plexuses innervate the heart.
The vagus nerves (X) carry parasympathetic preganglionic fibers to small ganglia
in the cardiac plexus.
Cardiac centers of the medulla oblongata contain autonomic controls:
 cardioacceleratory center controls sympathetic neurons that
increase heart rate
- cardioinhibitory center controls parasympathetic neurons that slow
heart rate
Cardiac reflexes:
- The cardiac centers monitor baroreceptors (blood pressure) and
chemoreceptors (arterial oxygen and carbon dioxide levels).
- Cardiac centers adjust cardiac activity.
Autonomic tone:
- The heart’s dual innervation maintains resting autonomic tone by
releasing ACh and NE.
- Can make fine adjustments to meet needs of other systems.
Figure 20-22
 The effects of sympathetic and parasympathetic stimulation are greatest at the SA
node, which affects the heart rate:
- Membrane potential of pacemaker cells is lower than other cardiac
cells.
- Rate of spontaneous depolarization depends on (1) resting
membrane potential and (2) rate of depolarization.
- ACh (parasympathetic stimulation) slows the heart
- NE (sympathetic stimulation) speeds the heart

The atrial reflex (Bainbridge reflex) adjusts heart rate in response to the venous
return. Stretching the right atrium, stretch receptors trigger an increase in heart
rate through increased sympathetic activity. An increase in venous return
stimulates the atrial reflex.
- Hormones:
 Epinephrine, norepinephrine and thyroid hormone increase the heart rate by their
sympathetic effect on the SA node.
Factors Affecting the Stroke Volume, p. 699
Figure 20-23
 Changes in either EDV or ESV can change the stroke volume.

EDV is affected by 2 factors:
1. filling time: the duration of ventricular diastole
2. venous return: the rate of blood flow during ventricular diastole

The degree of ventricular stretching during ventricular diastole is called preload,
which is directly proportional to EDV. Preload affects the ability of muscle cells
to produce tension. At rest, myocardial muscle doesn’t stretch much; EDV is low,
and stroke volume is low. With exercise, EDV increases, the myocardium
stretches more, and stroke volume increases.

The relationship between increasing EDV and increasing stroke volume is known
as the Frank-Starling principle.

Ventricular expansion is limited by myocardial connective tissue, the fibrous
skeleton, and the pericardial sac.

The amount of blood that remains in the ventricle at the end of ventricular systole
is the ESV. The 3 factors that affect ESV are:
1. preload:
- degree of ventricular stretching during ventricular diastole
2. contractility:
- the force produced during a contraction, at a given preload
3. afterload:
- the amount of tension the contracting ventricle must produce to
force the semilunar valve open and eject blood

Contractility is affected by both autonomic activity and hormones.

Autonomic activity includes:
1. sympathetic stimulation (the release of NE by postganglionic fibers of
cardiac nerves and the release of epinephrine and NE by the adrenal
medullae) causes the ventricles to contract with more force, increasing
ejection fraction and decreasing ESV.
2. parasympathetic activity (acetylcholine released by vagus nerves) reduces
the force of cardiac contractions.

Many hormones affect heart contraction, and pharmaceutical drugs have been
developed that mimic the actions of hormones by stimulating or blocking beta
receptors on cardiac muscle cells; or by affecting calcium ion action. Dopamine
and digitalis elevate intracellular calcium ion concentrations by different methods.
Calcium channel blockers have a negative ionotropic effect.

Afterload is increased by any factor that restricts blood flow through the arterial
system. As afterload increases, stroke volume decreases.
Summary: The Control of Cardiac Output, p. 702
Figure 20-24 summarizes the factors that affect heart rate and stroke volume.

Heart rate is controlled by:
1. the autonomic nervous system: sympathetic and parasympathetic
stimulation
2. circulating hormones
3. venous return and stretch receptors

Stroke volume is determined by EDV and ESV:
- EDV is determined by:
1. filling time
2. rate of venous return
- ESV is determined by:
1. preload
2. contractility
3. afterload

The difference between resting and maximal cardiac output is the cardiac reserve.
Key



Cardiac output is the amount of blood pumped by the left ventricle each minute.
It is adjusted on a moment-to-moment basis by the ANS, and in response to
circulating hormones, changes in blood volume, and alterations in venous return.
Most healthy people can increase cardiac output by 300-500 percent.
V. The Heart and the Cardiovascular System, p. 703

The purpose of cardiovascular regulation is to provide adequate circulation to the
body tissues.

Cardiovascular centers control not only the heart but also the peripheral blood
vessels.

The cardiovascular system responds to changing activity patterns and circulatory
emergencies.
SUMMARY
In Chapter 20 we learned about:
- The organization of the cardiovascular system (pulmonary and systemic circuits)
- The 3 types of blood vessels (arteries, veins and capillaries)
- The 4 chambers of the heart (left and right atria and ventricles)
- The pericardium, mediastinum and pericardial sac.
- The coronary sulcus and superficial anatomy of the heart
- The structures and cells of the heart wall
- The internal anatomy and structures of the heart:
- the septa, muscles and blood vessels
- The valves of the heart and direction of blood flow
- The connective tissues of the heart
- The coronary blood supply
- Contractile cells and the conducting system
- pacemaker calls, nodes, bundles and Purkinje fibers
- The electrocardiogram and its wave forms
- The refractory period of cardiac cells
- The cardiac cycle (atrial and ventricular systole and diastole)
- Cardiodynamics (stroke volume and cardiac output)
- The control of cardiac output