The Anatomy and

Physiology of the
Cardiovascular System

AN INDEPENDENT CE/CME STUDY COURSE

FOR HEALTHCARE PROFESSIONALS

BY
RALPH M. MYERSON, M.D.

Tallahassee, Florida and Tinton Falls, New Jersey

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ABOUT THE AUTHOR

Ralph M. Myerson is a board-certified internist with over 50 years experience in patient care,
teaching, and clinical research. He is a graduate of Tufts College School of Medicine and received his
post-graduate training at the Boston City Hospital. Following three years of duty as an Army Medical
Officer in North Africa and Italy during World War II, he joined the Veterans Administration, serving
at the Wilmington and Philadelphia VA Hospitals as Chief of Medicine and Chief of Staff. He served
as Group Director and consultant in gastroenterology at Smith, Kline & French Laboratories and,
during his tenure there from 1975 to 1985, was instrumental in the post-marketing medical aspects
of Tagamet®.
During his professional career, Dr. Myerson has been very active in medical writing and has
authored over 150 publications, including eight textbooks and numerous textbook chapters. Since
1985 he has confined most of his activities to medical writing, serving as a consultant to many
pharmaceutical companies. He has been active as a contributor to lay periodicals and in the
dissemination of educational material to lay audiences.
Dr. Myerson is a member of Phi Beta Kappa, Alpha Omega Alpha, and numerous medical and civic
organizations. He has held the faculty position of Professor or Clinical Professor of Medicine at the
Medical College of Pennsylvania (now part of the Allegheny University Health Sciences Center)
since 1957, and was formerly Adjunct Professor of Medicine at the University of Pennsylvania School
of Medicine.

© 1998 Arc Mesa Educators/Dr. Ralph M. Myerson, M.D.

All rights reserved. This CME course,
or any part thereof, may not be duplicated
or reproduced without the permission of the author.

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TABLE OF CONTENTS

About The Author . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 2

Course Instructions . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 4

Course Objectives . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 5

Overview of the cardiovascular system . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 6

Structure of the Heart . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 7

The size and position of the heart . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 7
The wall of the ventricles . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 7
The chambers of the heart . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 7
The valves of the heart . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 8
The flow of blood through the heart . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 8
The systemic circulation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .9
The coronary circulation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 10
The nervous system of the heart . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 10

The Cardiac Cycle . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 11

Systole and diastole of the heart chambers . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 11
Regulation of the cardiac cycle . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 12
The conducting system of the heart . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 12

The Hemodynamics of the Cardiac Cycle . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 13

Pulse . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 13
Blood pressure . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 13
Cardiac output . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 14
Systemic peripheral resistance . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 14
Cardiac wall tension: preload and afterload . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 15
The Frank-Starling principle . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 16

The Vascular System . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 17

The arterial system . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 17
The venous system . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 20
The capillary system . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 21

References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 23

Course Examination . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 24

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Course Instructions

1. Read the course material carefully. For internet users, you may ‘download’ the course or study
‘on screen’ but start when you are fresh and take your time.

2. This is an "open book" exam; review the text at any time as a learning aid or as a check on your
responses prior to completing the examination. Review the chapter summaries, if applicable.

3. Be sure to answer each exam question; blanks are counted as incorrect answers.
A minimum score of 75% is required for successful completion of this course.

4. Following the exam is a brief "course evaluation form" that we encourage you to complete. We
value your evaluation responses and suggestions so that we can upgrade our procedures and
course materials to serve you even better in the future.

5. The processing fee for this course entitles one person only to receive certification of
completion. All course completions and certifications will be on file and maintained by Arc
Mesa for six years.

6. After successful completion of the course exam your Certificate of Completion will be mailed to
you within 48 hours. (If you have not received your certificate within two weeks, please call us
at the number below and we will re-ship.)

7. If you fail the exam you may retest for a $10.00 processing fee. Arc Mesa will send you
notification of the failing grade and a home study booklet and/or exam for re-testing.
Note: Re-testing on the internet will incur the full course charge!

Problems or Questions

If you have any questions about your examination or your Certificate of Completion, please call
Arc Mesa at: 1-800-597-6372.

Your Certificate of Completion will reflect the following data: Date of completion, name,
profession/occupation, license number (if provided), course title, CE/CME hours awarded, exam
score, provider name and approval number.

Thank you for choosing Arc Mesa Educators!

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COURSE OBJECTIVES

1. To learn the basics of the anatomy of the heart:

A. Size, weight and location within the body
B. The chambers of the heart
C. The valves of the heart
D. Structure of the heart wall
E. The coronary circulation
F. The conducting system of the heart

2. To learn the hemodynamic properties of the cardiac cycle:

A. Systole and diastole
B. The components and the chronological events in the cardiac cycle
C. Cardiac output

3. To become acquainted with cardiovascular hemodynamics:

A. Pulse
B. Blood pressure
C. Systemic peripheral resistance

4. To learn the basic anatomy, physiology, and function of the components of the vascular system:
A. Arterial system
B. Venous system
C. Capillary system

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OVERVIEW

The growth and maintenance of our body is dependent on the delivery of oxygen and nutrients to
the various tissues and organs of the body, and on the effective removal of waste products from
them. The body’s maintenance of a stable internal environment is called homeostasis.
A tissue is defined as a group or collection of similar cells and their intercellular substance that act
together in the performance of a particular function. The primary tissues are epithelial, connective,
skeletal, muscular, glandular and nervous.
An organ is a part of the body composed of several tissues and having a specialized function. The
heart, blood vessels, skin, kidneys, liver and brain are some examples of organs.
The cardiovascular system, consisting of the heart and blood vessels, plays a pivotal role in the
maintenance of homeostasis. Stated in the simplest of terms, the heart is a pump, albeit a remarkable
one and unparalleled in nature or by human hands. As with most pumps, the function of the heart
is to transport a liquid from one place to another. Of course, in the case of the heart, the liquid is
blood, the life-sustaining fluid that is essential for the survival and function of every cell, tissue and
organ in the body. Blood carries nutrients and other essential substances, but its most important
component is oxygen. Oxygen is vital; its absence for four or more minutes is usually fatal. In
addition, the cardiovascular system helps protect the body by transporting antibodies and
phagocytes to the site of tissue injury to prevent and fight infections.
The blood pumped by the heart is distributed to the tissues and organs by a complex 60,000-mile
network of blood vessels - the vascular system. The vascular system is divided into three
components. The arterial component, composed of arteries, is responsible for the delivery of blood
and oxygen from the heart to every cell, tissue and organ in the body. The venous system,
composed of veins, is responsible for returning deoxygenated (deprived of oxygen) blood and waste
products from the tissues and organs back to the heart. The capillaries are the thread-like blood
vessels that connect the arterial and venous systems and are responsible for the exchange of oxygen
for carbon dioxide and nutrients for waste products at the cellular level.

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THE HEART

THE STRUCTURE OF THE HEART

The size and position of the heart

Despite its heavy workload, the heart is not a large organ. It is about the size of the person’s
clenched fist and weighs 10 to 12 ounces. It is hollow and roughly conical in shape, with the narrow
end pointed downward, to the left, and slightly forward. Its location in the chest cavity is just to the
left of the midline, behind the sternum and between the second and sixth left ribs (see Figure 1).

Trachea

Superior
Vena Cava Aorta
Pulmonary Artery
Right Lung
Left Lung

Heart

Diaphragm

Figure 1: Position of the heart in the chest viewed from the front.

The heart wall

The wall of the heart consists of three layers: the pericardium, a fibrous sac surrounding the heart
whose inner lining is a thin, transparent membrane covering the outside of the heart muscle; the
endocardium, the delicate innermost lining of the heart; and, the myocardium, the thick muscular
layer that separates the two linings. The myocardium is a specialized type of muscle that is unique
to the heart and responsible for its contraction.
The chambers of the heart
The heart has four cavities or chambers. Two of these are thin-walled receiving chambers, the left
and right atria (singular, atrium), and two thick-walled pumping chambers, the ventricles.
Actually, the heart consists of two parallel pumps that work simultaneously. The right-sided pump
receives deoxygenated blood from the veins and pumps it to the lungs where it is re-supplied with
oxygen. The left-sided pump receives the reoxygenated blood from the lungs and pumps it through
the arteries to the rest of the body (see Figure 2).

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The valves of the heart

The heart contains four valves. There is a valve between the right atrium and right ventricle, the
tricuspid valve, and one between the left atrium and the left ventricle, the mitral valve. These
valves are open when the ventricles are filling and receiving blood from the atria, but close when the
ventricles contract and are so structured that they prevent back-flow or regurgitation of blood from
the ventricle into the atrium. The right ventricle pumps blood into the pulmonary artery on its way
to the lungs. There is a valve, the pulmonic valve, at the outflow area of the right ventricle. It opens
when the ventricle contracts, but closes during diastole, thus preventing regurgitation of blood from
the pulmonary artery back into the right ventricle. A similar valve, the aortic valve, is present at
the outflow area of the left ventricle. It is open when the left ventricle contracts sending blood into
the aorta, but closes during diastole so that blood cannot regurgitate from the aorta back into the left
ventricle. The contraction of the ventricles and the closure of the valves contribute to the sounds of
the heart, often described as lubb, the contraction or first sound, and dupp, the second cardiac
sound (see Figure 2).

Superior Vena Cava

Arch of the Aorta

Pulmonary Artery
Right Atrium

Pulmonary Valve Aortic Valve

Tricuspid Valve Mitral Valve

Right Ventricle
Left Ventricle

Figure 2: View of the opened heart from the valve showing valves and main blood vessels
entering and leaving heart.

The flow of blood through the heart

Blood enters the right atrium from the veins and passes through the tricuspid valve into the right ventricle. The
right ventricle contracts, expelling blood through the pulmonic valve into the pulmonary artery on its way to the
lungs. As the right ventricle contracts, the tricuspid valve closes, preventing regurgitation of blood into the right
atrium. Following right ventricular contraction, the pulmonic valve closes to prevent regurgitation of blood back
into the right ventricle. Reoxygenated blood returns from the lungs by way of the pulmonic veins and enters the
left atrium. Blood flows through the open mitral valve into the left ventricle. After the left ventricle fills, it contracts
sending blood through the aortic valve into the aorta and the rest of the body. As the left ventricle contracts, the
mitral valve closes to prevent regurgitation into the left atrium. After left ventricular contraction, the aortic valve
closes to prevent regurgitation of blood from the aorta back into the left ventricle.

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The systemic circulation

After returning from the pulmonary circulation, the oxygenated blood begins its systemic
circulation. Systemic (peripheral) circulation is that part of circulation in which blood is transported
to all body tissues and returned to the heart. It begins when oxygenated blood leaves the left
ventricle. When the ventricles relax, oxygenated blood flows from the left atrium through the mitral
valve into the left ventricle. When the ventricles subsequently contract, this blood is pumped with
considerable force through the aortic valve into the major artery of the body, the aorta.
As the aorta descends, it branches into several smaller arteries. Some of these arteries, such as the
carotid arteries, carry blood to the head and neck. Other arteries, such as the subclavian arteries
and the femoral arteries, carry blood to the upper and lower extremities, respectively.
From these arteries, blood enters the arterioles and then the capillaries, where oxygen is exchanged for
carbon dioxide and nutrients for metabolic wastes. The deoxygenated blood that has been used by the body
then travels back to the heart by way of the venules and veins. It finally empties into two principal veins:
the superior vena cava, which carries blood from the upper portion of the body; and the inferior vena
cava, which carries blood from the lower portion of the body. Blood from both the superior and inferior
vena cavae enters the right atrium, where systemic circulation ends. With the next heart relaxation, the
blood again flows from the right atrium through the tricuspid valve into the right ventricle, and the cycle
of pulmonary circulation to systemic circulation is repeated.
The following diagram summarizes the flow of blood through the body, tracing it from the
peripheral venous system into the heart, through the pulmonary circulation, back to the heart, to
the systemic circulation, and back again to the heart (see Figure 3).

Venous blood enters right atrium from venae cavae

Blood enters right ventricle through tricuspid valve

Right ventricle contracts, sending blood through the pulmonic valve into pulmonary artery

Blood enters pulmonary capillary system, where gas exchange takes place

CO2 in pulmonary venous capillaries exchanges for O2 in pulmonary alveoli (air spaces)

Oxygenated blood returns to left atrium via pulmonic veins

Blood enters left ventricle through mitral valve

Left ventricle contracts, sending blood through the aortic valve into systemic circulation

Gas exchange occurs within capillary system of peripheral circulation; O2 is released into tissues and
CO2 enters the deoxygenated venous circulation for return to the heart.

Figure 3: Tracing the flow of blood through the heart and the pulmonary and systemic circulation.

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The circulation of the heart (coronary circulation)

The heart also has its own important blood supply, the coronary circulation. The two main
coronary arteries, the left and the right coronary arteries, branch from the aorta as it leaves the
heart. The left coronary artery then divides into the circumflex artery and the left descending
artery. These three arteries are the principal coronary arteries and they, in turn, give rise to numerous
branches guaranteeing the heart a rich supply of blood and oxygen (see Figure 4).
The major coronary arteries lie on the surface of the heart. From them, smaller arteries pass into
the myocardium, ultimately forming arterioles and capillaries and comprising the collateral
circulation. When needed, coronary arterioles have the ability to increase the size and number of
collateral vessels. This forms a valuable increase in the blood supply in the event of an occlusion of
a coronary artery.

Superior Vena Cava

Arch of the Aorta

Pulmonary Artery

Right Coronary Artery

Branch of Left
Coronary Artery

Figure 4: The Coronary Circulation.

A decrease in the oxygen supply to the heart as a result of narrowing or complete obstruction of a
coronary artery results in angina pectoris if the obstruction is incomplete and transient. When a
portion of the myocardium is deprived of blood permanently, that portion of the myocardium
sustains myocardial infarction due to death of that portion of the myocardial muscle.
The nervous system of the heart
Although the heart has the remarkable property of automaticity and is capable of contracting on
its own, it is supplied with two sets of nerves to augment its work. There are sympathetic nerves
that stimulate the heart causing it to beat faster and with greater strength, and parasympathetic
nerves that calm the heart and slow its rate. These nervous systems carry impulses from the brain
and elsewhere in the body that help the body respond and adjust to internal and external factors.
Both systems respond to a variety of drugs that may be used in the treatment of various cardiac
disorders and hypertension.

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THE CARDIAC CYCLE

The cardiac cycle is defined as the series of events that occur during a single heartbeat. It consists
of two phases: systole and diastole. Systole refers to a period of contraction by the heart muscle,
whereas diastole refers to a period of relaxation by the heart muscle. The heart does not undergo the
cardiac cycle as one unit. Rather, the atria and ventricles act as separate units, entering systole and
diastole at different times. However, both atria and both ventricles act simultaneously.
The duration of these events during a typical cardiac cycle is approximately 0.8 seconds. Because
the series of contractions and relaxations of the different chambers of the heart occur cyclically, there
is no real "beginning" or "ending" of the cardiac cycle. However, for the purpose of discussion, we
will artificially label atrial systole, or atrial contraction, as the "beginning" of the cycle.

Atrial Contraction
Just prior to atrial contraction, both the atria and ventricles are relaxed. The pulmonic and aortic
valves connecting the ventricles to the major arteries are closed. However, the atrioventricular valves
that connect the atria to the ventricles are open. During this period of relaxation, blood flows
continually from the veins into the atria, filling these chambers. Some of this blood passes through
the open atrioventricular valves to the ventricles. When the atria contract, they force the remaining
blood contained in them to flow into the ventricles. By the end of atrial contraction, the ventricles
contain a full supply of blood, while the atria contain virtually none.

Ventricular Systole
Ventricular systole occurs only a fraction of a second after atrial contraction. As the ventricles
begin to contract, the pressure within them quickly exceeds that within the atria, forcing the
atrioventricular valves to close. This action prevents a backward flow of blood (regurgitation) from
being forced into the atria from the ventricles.
As ventricular contraction continues, the pressure within the ventricles reaches a point where it
exceeds that in the aorta and the pulmonary arteries. At this point, the aortic and pulmonic valves
open, and the blood from the ventricles is ejected through these valves into the aorta and pulmonary
artery, respectively.
At about the same time that the ventricles enter systole, the atria begin to relax. During this period,
blood flows into the left atrium from the pulmonary veins and into the right atrium from the
superior and inferior vena cavae. However, this blood remains in the atria during ventricular systole,
since the high pressure in the ventricles during its contraction forces the atrioventricular valves to
remain closed.

Ventricular Diastole
When ventricular diastole begins, the ventricles start to relax and the pressure within the ventricles
decreases. Once the ventricular pressure becomes lower than the pressure in the aorta and the
pulmonary artery, the pulmonic and aortic valves close, preventing regurgitation of blood into the
ventricles. As the ventricles fully relax, the ventricular pressure becomes lower than the pressure in
the atria. This allows the atrioventricular (mitral and tricuspid) valves to open.

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Because the ventricles are now in diastole and the atrioventricular valves are open, some of the
blood that has been flowing into the atria flows through the open valves into the ventricles. The
ventricles reach about 80% of their capacity before the atria begin to contract and the cardiac cycle
is repeated.

Regulation of the Cardiac Cycle

In order for the heart to effectively complete each cardiac cycle, cardiac muscle cells must contract
more or less simultaneously. The coordination of cardiac muscle contractions is made possible by
two factors. First, the cells in cardiac muscle are tightly interwoven, so that muscle contraction
spreads rapidly throughout the heart. Second, the heart contains specialized cardiac muscle cells
that are organized into a conducting system, spreading muscle contraction impulses throughout the
heart at regular intervals.
The heart has the unique ability to beat (contract) on its own. Although in real life it is assisted in
this function by nerves and hormones in the blood, it still functions even when removed from these
influences. This is best illustrated by the donor organ in heart transplantations.
The mechanism by which the heart generates and transmits the signal to contract is quite complex.
Actually, a minute electrical current of about 2 millivolts is generated and passes down from its origin
through the conducting system of the heart, causing muscular contraction of each chamber as it
passes through it. The impulse or action potential normally arises in a specialized group of cells
located in the wall of the right atrium called the sinoatrial (SA) node. Normally, an electrical
difference (potential difference) exists between the inside and outside of all cells, which is due to the
differences in electrical charges inside the cell from those outside the cell. The impulse is initiated by
passage of electrical charges across the membrane (covering) of the cell, causing a change in the
potential difference and creating an action potential.
Leaving the SA node, the impulse passes through both atria causing them to contract thus helping
blood pass into their respective ventricles. On its way to the ventricles, the action potential next
encounters the atrioventricular (AV) node, another group of specialized cells. From there the
impulse passes down an anatomical pathway called the Bundle of His which branches out and
spreads throughout both ventricles (Purkinje fibers), resulting in contraction of the ventricles.
Figure 5 illustrates the components of the conducting system of the heart.

The Purkinje fibers conduct the

4
impulse through the ventricles.

1 A heartbeat begins about once every

second in the sinoatrial (SA) node.
These specialized cells are the heart’s
natural pacemaker, regulating the rate
and rhythm of the heartbeat.

2 The impulse spreads throughout both

atria, reaching the atrioventricular
The impulse continues to the
(AV) node. The AV node is located at 3
Bundle of His, a conduction
the junction of the atria and the
pathway that spreads out into
ventricles.
the ventricles.

Figure 5: The Conducting System of the Heart

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THE HEMODYNAMICS OF THE CARDIAC CYCLE: VITAL SIGNS

Left ventricular systole produces a surge of blood through the blood vessels that gives rise to two
important vital signs. Vital signs are readily available indices used to monitor the general state of
health of an individual and include pulse, blood pressure, body temperature, and rate of
respirations. In hospitalized patients, these are the measurements the physician or nurse records on
the patient's chart and which provide an indication of the patient's general condition. Of the vital
signs, two, pulse and blood pressure, are generated by left ventricular systole.

Pulse
The pulse is a direct result of the surge of blood produced by left ventricular systole. It is a ready
means of recognizing the rate of the heart and its regularity. The strength of the pulse is also of
importance; a weak, thready pulse may be an indication of a serious problem. The pulse can be taken
at any point where a large artery runs close to the skin. Common sites for this are the temple, neck,
armpit, groin and foot. For convenience, the pulse is usually "taken" at the wrist at the base of the
thumb, where the large radial artery to the hand is close to the skin. In case of doubt, the pulse can
be verified by listening to the heart with a stethoscope, a procedure referred to as auscultation.

Blood pressure
The blood pressure is the second of the vital signs that is related to the heart. It is a measurement
of the outward pressure exerted on arterial walls by the blood and consists of two components; the
systolic (SBP) and the diastolic blood pressure (DSP). The systolic blood pressure is the pressure
generated by left ventricular systole. The diastolic pressure is the residual pressure in the arterial
system during the diastolic phase of ventricular relaxation and refilling. It is important to remember
that there is always a supply of blood in the vascular system, both during systole and diastole. Blood
pressure is measured by various types of sphygmomanometers which register the pressure in terms
of the height of a column of mercury expressed in millimeters - mm/Hg (mercury is a liquid element
13 times heavier than water and provides an easy and useful means of measurement). The blood
pressure is expressed as the ratio of systolic to diastolic pressures (systolic/diastolic).
Normally, the systolic pressure is 140 millimeters of mercury (mm/Hg) or less and the diastolic is
90 mm/Hg or less. Hypertension (high blood pressure) exists when either the systolic or diastolic
readings are above 140 and 90 respectively. There are no set standards for hypotension (low blood
pressure) since it is relative to the patient's known normal blood pressure. Thus a systolic blood
pressure of 120 mm/Hg, considered normal under usual conditions, might represent hypotension in
an individual who had a systolic blood pressure of 180 mm/Hg. Generally speaking, however, a
systolic blood pressure of 100 mm/Hg or below suggests hypotension. The diagnosis is usually made
in the presence of other confirmatory signs and symptoms.
According to guidelines set by the JNC (Joint National Committee) on Detection, Evaluation, and
Treatment of High Blood Pressure, blood pressure under 140/90 mmHg is considered normal.
Systolic readings between 130-139 mmHg and diastolic readings from 85-89 mmHg are high normal,
while blood pressure under 120/80 mmHg is optimal.
Arterial blood pressure is determined by two primary factors: the total amount or volume of blood pumped by
the heart (cardiac output) and the resistance arterioles present to blood flow (total peripheral resistance). In turn,
each of these primary factors is influenced by a number of secondary factors.

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Cardiac output (CO) is the volume of blood that is pumped each minute from the left ventricle to
the tissues. If all other variables remain equal, increased cardiac output leads to increased arterial
blood pressure. Resistance to blood flow is determined by the diameter of every arteriole in the body
and is called Total Peripheral Resistance (TPR) or systemic vascular resistance. TPR is controlled by
arterioles because their diameters, under control of the autonomic nervous system, can vary
according to the body's needs.
If expressed mathematically, the relationship between CO, TPR, and arterial blood pressure can be
represented with the following equation:

CO x TPR = BP

According to this equation, a change in cardiac output or peripheral resistance will result in a
proportional change in arterial blood pressure (i.e., if CO or TPR increase, BP will also increase).
Numerous factors influence cardiac output and peripheral resistance.

Cardiac Output
Cardiac output can be calculated by multiplying the heart rate by the stroke volume. Heart rate
(HR) is the number of ventricular contractions per minute, regulated by the autonomic nervous
system. The normal range for heart rate is 60-100 contractions per minute. Stroke volume (SV) is
the volume of blood ejected by the left ventricle each time it contracts. It is determined by
calculating the difference between the volume of the ventricle at the end of systole and the end of
diastole. Stroke volume is influenced largely by venous return, the volume of blood returned to the
heart by the veins. The normal range for left ventricular stroke volume is 60-130 mL per contraction.

HR x SV = CO

(It is important not to confuse stroke volume with the term ejection fraction. The ejection fraction
is the ratio of the stroke volume to the volume of the left ventricle at the end of diastole. In other
words, the ejection fraction is the percentage of the end diastolic volume. That is the volume of
blood present in the ventricle at the end of diastole that is actually forced out of the left ventricle
into the aorta during contraction. Typically, ejection fraction averages around 67%.)
Since changes in stroke volume or heart rate can alter cardiac output, these variables can also affect
arterial blood pressure. For example, an increase in heart rate, with no compensating decrease in
other parameters, will increase cardiac output and thus increase overall blood pressure. Similarly, if
stroke volume increases, but heart rate does not drop accordingly, overall blood pressure will rise.

Peripheral Resistance
Peripheral resistance can be changed by both chronic and temporary factors. Chronic changes in arteriolar
diameter, such as the narrowing caused by atherosclerosis, can produce a constant change in resistance to blood
flow. Temporary changes may occur from either vasodilation (relaxation of smooth muscle in the arteriolar walls,
which causes the vessel diameter to increase and resistance to blood flow to drop) or vasoconstriction (contraction
of smooth muscle in the arteriolar walls, which causes the vessel diameter to decrease and resistance to rise). If
peripheral resistance increases or decreases while cardiac output remains unchanged, overall blood pressure will
rise or fall accordingly.

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The relationship between heart rate and cardiac work is fairly simple. If the heart beats more
quickly (during exercise, for example), it performs more work. However, the ways in which cardiac
wall tension and myocardial contractility affect cardiac work are somewhat more complex.

Cardiac Wall Tension

Cardiac wall tension is the force cardiac muscle fibers exert to contain the blood and to contract
against it. As blood enters the heart, it exerts an outward pressure on the cardiac walls. To prevent
the heart from expanding like a balloon filling with air, the heart fibers are able to resist excessive
stretching and thus exert the pressure necessary to contain the blood. When the heart contracts to
pump the blood, the cardiac walls must exert even greater pressure to expel the blood into the
circulation. Increasing the wall tension increases the total effort that must be exerted by the heart
muscle and it must work harder to contract.
Two factors play a significant role in determining cardiac wall tension. These factors are:
1. preload
2. afterload

Preload and Cardiac Wall Tension

Preload refers to the pressure exerted by the blood against the ventricular wall the instant prior to
contraction. Preload is synonymous with venous return to the heart, and this is often monitored as
left ventricular end diastolic pressure (LVEDP). Any change in the body that increases the return
of blood to the heart will increase the preload.
Increases in preload increase myocardial work. To understand this relationship, imagine two
bicycle tires, with one containing more air than the other. If you try to compress each tire with your
hand, you must squeeze harder on the tire with the higher air pressure to push the wall inward. In
a similar way, the heart must work harder to "push" its walls inward during contraction if the preload
has been increased.
Two factors can increase preload: increased blood/fluid volumes and constriction of blood vessels.
Increases of blood/fluid volume means that more fluid is available in the cardiovascular system to
enter the heart prior to each contraction. Constriction of blood vessels affects preload by reducing
the area in the vascular system through which blood can flow. Vasoconstriction decreases the
capacity of the veins and venules to hold blood. This reduces the amount of blood that is allowed
to pool in the veins, thus forcing more blood back into the heart. Vasoconstriction is primarily
controlled by activation of the sympathetic nervous system, which stimulates vasoconstriction
through the action of norepinephrine.

Afterload and Cardiac Wall Tension

Afterload is the pressure that the ventricles must work against to pump blood into the aorta and
pulmonary artery. It varies with arteriolar resistance to the flow of blood (peripheral resistance). An
increase in afterload increases cardiac work by forcing the ventricles to pump against a higher
pressure in the arteries.
If afterload remains increased for a long period of time, the heart must work harder to pump the
blood through the arterial system. To compensate for this, the muscles of the heart increase in size
(hypertrophy). Eventually, this compensatory mechanism fails and the heart is no longer capable of

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pumping blood against the elevated arterial pressure and its pump action begins to fail. This
condition is known as congestive heart failure (CHF), and requires therapy.

Myocardial contractility and cardiac work

Myocardial contractility is the strength or forcefulness of contraction of individual cardiac muscle
fibers. Depending on its health, the heart may contract vigorously or weakly. A strong contraction
allows expulsion of a greater volume of blood. Thus, if a heart's contractions are strong, it has to
pump fewer times (i.e., it does less work) than it would if its contractions were weakened by disease.
Myocardial contractility can be augmented by sympathetic nervous stimulation. This is mediated
by the actions of epinephrine (adrenaline) and norepinephrine on muscle fibers. In periods of stress,
fright, or other conditions that initiate sympathetic activity, myocardial contractility and the work
performed by the heart increase. Certain drugs, called inotropic agents, have the capability of
increasing the force of myocardial contraction and are valuable therapeutic agents.

The Frank-Starling Principle and Myocardial Contractility

One further concept important to understanding cardiac function is the Frank-Starling Principle.
The Frank-Starling Principle states that the output of the heart increases in proportion to the
amount of stretch in the cardiac muscle fibers. In other words, if the heart is forced to stretch to
accommodate higher volumes of blood, myocardial contractility will increase. Thus, the amount
of blood pumped out of the heart per beat will increase if the amount of stretch of the
ventricle increases.
Increased preload can cause cardiac muscle fibers to stretch. An increased volume of blood
returning to the heart can fill the heart's chambers to the point where muscle fibers have to stretch
more than normal to expel the blood. As the Frank-Starling Principle states, the increased stretch
provides increased force for contraction. However, if the myocardium is stretched too far or too
frequently, it can lose the ability to return to its original contracted state. If the heart muscle is
stretched excessively, it can eventually lose its ability to contract with its normal force.

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THE VASCULAR SYSTEM

The vascular system is divided into three components. The arterial system is responsible for
the delivery of blood and oxygen to every cell, tissue and organ in the body. The arteries carry blood
away from the heart. Veins comprise the venous system that is responsible for returning
deoxygenated (deprived of oxygen) blood from the tissues and organs back to the heart. The
capillary system links the two systems together and is responsible for the exchange of oxygen for
carbon dioxide at the cellular level.
The vascular system is not a passive system of pipes, but actually plays a critical role in
supplementing the action of the heart in the distribution of blood. Its status also plays a major role
in the determination of the blood pressure.
The arterial system
The arterial component of the vascular system is responsible for the transportation of oxygenated
blood from the heart to the cells, tissues and organs. During left ventricular systole, blood leaves the
heart and passes into the aorta, the largest blood vessel in the body. The aortic valve is situated at
the entrance to the aorta. During left ventricular systole, the valve opens, allowing the free flow of
blood into the aorta. During diastole, the relaxation and refilling stage of the cardiac cycle, the aortic
valve snaps shut, preventing regurgitation of blood from the aorta back into the left ventricle. Anatomically, the
aortic valve consists of three cusps (posterior, right, and left) that come together during diastole to completely
occlude the valve and prevent regurgitation. Because the edge of each cusp is in the shape of a half moon, the
valve is sometimes called the semilunar valve (see Figure 6).

Right coronary artery

Right semilunar cusp

of aortic valve
Aorta

Posterior cusp of Left coronary

aortic valve artery

Left semilunar
Ventricular wall cusp of aortic
valve

Figure 6: Base of the aorta showing anatomy of the aortic valve.

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Within the cavities formed by the right and left aortic cusps are the origins of the left and right
coronary arteries. These are the arteries which branch to form the coronary circulation of the heart
muscle and provide oxygenated blood to the heart muscle. Shortly after leaving the heart, the aorta
arches to the left and sends large branches to the neck and head and to the upper extremities. The
large arteries supplying the neck, head and brain with blood are called the carotid arteries. Their
strong pulsations can be felt in the neck on both sides of the larynx. The aorta then descends down
the back of the body in front of the spine, supplying branches to the chest and to the organs in the
abdomen. In the pelvis, the aorta splits into two large branches, each supplying one of the legs with
blood.
Figure 7 illustrates the major components of the arterial system.

Cerebral arteries

Internal carotid artery

External carotid artery
Right common carotid artery
Vertebral artery
Left common carotid
Brachiocephalic trunk aorta
Subclavian artery
Ascending aorta
Brachial artery

Thorocic aorta
Celiac trunk artery

Left renal artery

Abdominal aorta
Ulnar artery
Common iliac artery
Radial artery
Internal iliac artery

External iliac artery

Popliteal artery
Femeral artery

Anterior tibial artery

Posterier tibial artery

Figure 7: The arterial system

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As the arteries approach their goals, they get increasingly smaller and are called arterioles. Finally,
they attain a thread-like diameter and are called capillaries.
If one examines the wall of an artery under the microscope, three layers are apparent. The intima
is the innermost layer of the artery and is composed of endothelium, the delicate inner lining of the
blood vessel. It is the endothelium that becomes involved with atherosclerosis, commonly referred
to as hardening of the arteries. The middle layer of the arterial wall, the media has a layer of elastic
tissue which is capable of decreasing and increasing the caliber of the blood vessel and thus
controlling the flow of blood through it. The media of the large arteries also have a layer of
muscular tissue. The arterial elastic and muscular tissues play important roles in supplementing the
heart in the propulsion of blood through the vascular system. The nervous system and circulating
hormones also play important roles in this action. The outer arterial wall layer, the adventitia, is
composed of protective fibrous tissue.
Figure 8 depicts a microscopic view of the wall of an artery.

Media elastic Layer

Intima

Adventitia

Media-Muscular Layer

Figure 8: Microscopic view of the wall of an artery

Vasoconstriction is the term applied to constriction of a blood vessel. Vasoconstrictor substances

are formed within the body, especially in the kidneys and adrenal glands. They play an important
role in the control of blood pressure. Vasoconstriction causes an increase in blood pressure by
increasing the resistance against which the heart has to work. The administration of vasoconstrictors
is helpful in raising blood pressure and in the control of bleeding.
Vasodilatation is the term applied to dilatation of the blood vessels. This also occurs within the
body under certain circumstances, causing a fall in blood pressure. Vasodilatation plays a role in the
development of circulatory shock. Vasodilators are important therapeutic agents in the treatment
of hypertension.
Both vasoconstriction and vasodilatation are under the control of ner-vous and hormonal
influences over which we have little or no voluntary control.

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The venous system

The venous system is responsible for the return of blood from the tissues and organs of the body
to the heart. The blood carried by the venous system has been depleted of oxygen in exchange for
carbon dioxide (CO2). The transport of the blood from the heart to the lungs for replenishment of
oxygen is considered by some as part of the venous system.
For the most part, arteries and veins travel and branch out through the body side-by-side, similar to the opposite
sides of a highway with the traffic (or blood) flowing in opposite directions. In many instances, arteries and veins
share the some name. All venous channels from the head and chest lead into the superior vena cava. Blood from
below the chest drains into the inferior vena cava. Both of these large veins empty into the right atrium from
which their contents are passed into the right ventricle. Right ventricular systole then pumps the blood to the
lungs by way of the pulmonary arteries.
There are striking anatomical and physiological differences between arteries and veins. Whereas arteries are
strong, muscular and elastic, veins are more delicate in structure and to a significant degree, lack the elasticity and
muscular power of the arteries. They have a limited capability for vasoconstriction, but have a prominent capacity
for vasodilatation. Arterial blood flow is much faster than venous blood flow because it reflects the power of the
left ventricular contraction as well as the artery's own capability for contraction. Arterial bleeding is pulsatile, again
reflecting the contraction of the left ventricle, whereas venous bleeding is slower and steady in character. In some
of the major arteries, blood moves at a rate of over a foot a second, whereas the flow rate in veins is about 4 inches
per second. Contraction of the muscles surrounding a vein assists in promoting venous blood flow. This
mechanism is sometimes referred to as the venous pump. The venous pressure varies throughout the body,
depending on the position of the individual and the site of measurement. It averages 50 to 100 mm of water,
much lower than the pressure of 120 mm of mercury seen in arteries during systole. Arterial blood is much
brighter and redder than venous blood because of its oxygen content.
To prevent the reversal of the flow of venous
blood, veins have valves that prevent this from
Venous Valves
happening. For example, standing in the
upright position for a prolonged period would
be expected to increase the pressure in the
veins of the leg and promote backflow of blood
(See Figure 9). The venous valves prevent this.
Unfortunately, the valves are prone to damage
and this may result in edema (swelling), and
the presence of permanently dilated veins
(varicose veins).

Figure 9: Venous valves

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The veins have a greater capacity to widen or dilate than do arteries. Because of this, the volume
of blood in our venous system is 2 to 2 1/2 times that in the arterial system. This pool of blood acts
as an important reservoir that becomes available if the circumstances require more blood. When the
venous circulation makes more blood available, there is a resultant important increase in cardiac
output. Thus, the venous circulation, once thought to play a rather passive role in the circulation
and serve only as a passageway for the flow of blood, is now recognized as playing an important,
active role in the circulation.

The capillary system

It is the function of the capillaries, the thread-like blood vessels that link the arterial with the
venous system, to exchange fluid, oxygen, carbon dioxide, nutrients, electrolytes, hormones, and
other substances between the blood and the interstitial space, the space outside the capillaries and
separating the cells. In the lungs, the capillary system exchanges oxygen and carbon dioxide with
the alveoli, the tiny air spaces of the lungs.
Every cell must be in close proximity to a capillary in order to survive. In addition, the capillary
walls are very thin, consisting of a single layer of cells, in order to allow the passage of small
molecular-sized substances through its wall. There are tiny pores or clefts in the capillary wall which
allow passage of molecules from the interior to the exterior of the capillary wall and vice versa. In
addition, substances can be transported through the wall with the help of small bubbles, called
vesicles, which carry the substance to be transferred within them.
By far, the most important means by which substances are transferred from the plasma, the liquid
portion of the blood, and the interstitial fluid surrounding the cells is the process of diffusion.
Diffusion allows the passage of substances through the capillary wall without the necessity of pores,
clefts or vesicles. Diffusion occurs from an area of high concentration to an area of low
concentration. The method of transportation that is used depends on many complex factors
including the size of the particle, pressure and concentration differences between the interior and
exterior of the capillary, and the solubility of the substance in water and lipids (fats).
The body’s most essential task is the continuous transport of oxygen from the blood to the tissues
and the return of oxygen to the blood in exchange for carbon dioxide (CO2). This is the exchange
process that occurs in the pulmonary capillary circulation. In the lung, the capillary system takes
up oxygen from the alveoli (air sacs) and releases carbon dioxide to be exhaled.
The blood has special carriers for the oxygen it delivers to the tissues; they are the red blood cells,
tiny concave discs. Red blood cells are so small that about 75 billion of them would fit into a one-
inch cube. Red cells get their color from hemoglobin, a protein that contains iron and is capable of
carrying, releasing, and retrieving oxygen.
In the tissues, oxygen leaves the blood for the interstitial fluid by the process of diffusion. The
concentration or partial pressure of oxygen in the interstitial fluid is low because it has been used by
the cells. On the other hand, the content of oxygen in the capillary is high. Thus, by the process
of diffusion, oxygen passes from the area of high concentration to the area of low concentration.
Simultaneously, by the same process, carbon dioxide, a waste product of the cells is picked up by the
blood and carried by way of the venous circulation to the right atrium and right ventricle and sent
to the lungs. The exchange of carbon dioxide for oxygen occurs between the pulmonary capillary
system and the alveolus, that tiny air sac in the lungs, which has received oxygen from inhaled air.

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The process again is one of diffusion across the delicate membrane that separates the pulmonary
capillary from the alveolus.
These processes of gas exchange are continuous and essential for survival. Impairment of the
process by any mechanism (tissue, lung, or blood) leads to serious consequences. The body does not
tolerate continuous low concentrations of oxygen and high concentrations of carbon dioxide for a
prolonged period of time.

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REFERENCES

1. Hurst, J.W. (editor-in-chief). The Heart, 6th edition, McGraw-Hill, New York; 1986.

2. Gray, H. Anatomy of the Human Body, 29th edition, Lea & Febiger, Philadelphia; 1973.

3. Myerson, RM. How Your Heart Works, Ziff-Davis Press, Emeryville, CA; 1994.

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COURSE EXAMINATION

Please select the most appropriate answer for each of the following examination questions.

1. Which chamber of the heart pumps blood to the lungs?

A. left atrium
B. right atrium
C. left ventricle
D. right ventricle
E. all of the above

2. Blood is supplied to the heart muscle by the:

A. superior vena cava
B coronary arteries
C. internal carotid arteries
D. external carotid arteries
E. inferior vena cava

3. Which of the following statements does not describe pulmonary circulation?

A. During pulmonary circulation deoxygenated blood becomes oxygenated.
B. Pulmonary circulation begins as blood leaves the right ventricle and enters the
pulmonary artery.
C. Pulmonary circulation ends as blood returns through the pulmonary veins to the
left atrium.
D. Pulmonary circulation begins when oxygenated blood leaves the left ventricle.
E. The pulmonic valve prevents regurgitation from the pulmonary artery to the right
ventricle.

4. Which of the following substances are not normally carried by the circulatory system?
A. Oxygen
B. Carbon monoxide
C. Hormones
D. White blood cells

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5. The muscular layer of the wall of the heart is called the:

A. Endocardium
B. Pericardium
C. Myocardium
D. Adventitia
E. Serosa

6. The exchange of gases occurs in which component of the vascular system?

A. venules
B. capillaries
C. veins
D. arterioles
E. lymphatics

7. The conducting system throughout the ventricles is called the:

A. Purkinje system
B. Sino-atrial node
C. Bundle of His
D. Atrioventricular node
E. Parasympathetic nervous system

8. In most individuals the cardiac output changes with the cardiac rate.
True False

9. A cardiac rate in excess of 100/minute is referred to as a bradycardia.

True False

10. The pulmonary artery carries deoxygenated blood.

True False

11. Valves exist in the veins of the lower extremities.

True False

12. The valve between the left atrium and left ventricle is the tricuspid valve.
True False

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13. The normal pacemaker of the heart is the sinoatrial node.

True False

14. The inner lining of the heart wall is called the endocardium.
True False

15. Peripheral vascular resistance plays little or no role in the determination and maintenance
of blood pressure.
True False

16. Cardiac output can be calculated by multiplying the heart rate by the stroke volume.
True False

17. Ventricular systole is associated with relaxation and decreased intra-ventricular pressure.
True False

18. Veins have a greater capacity to dilate than do arteries.

True False

19. The Frank-Starling principle relates to the relationship of heart muscle stretching
to cardiac output.
True False

20. An increased preload can cause cardiac muscle fibers to stretch.

True False

21. Myocardial contractility is depressed by sympathetic nervous system stimulation.

True False

22. Afterload is the pressure that the ventricles must work against to pump blood into the
aorta and pulmonary artery.
True False

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Examination Answer Sheet
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The Anatomy and Physiology of the Cardiovascular System

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4. (A) (B) (C) (D) 15. True False

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6. (A) (B) (C) (D) (E) 17. True False

7. (A) (B) (C) (D) (E) 18. True False

8. True False 19. True False

9. True False 20. True False

10. True False 21. True False

11. True False 22. True False

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