RN.

coms Assessment Series:

Cardiovascular Anatomy &
Physiology

Presented by:
RN.com
12400 High Bluff Drive
San Diego, CA 92130
This course has been approved for two (2.0) contact hours.
This course expires on September 24, 2006.
Copyright 2004 by RN.com.
All Rights Reserved. Reproduction and distribution
of these materials are prohibited without the
express written authorization of RN.com.

First Published: September 24, 2004

Acknowledgements________________________________________________________________________ 2
Purpose & Objectives _____________________________________________________________________ 3
Introduction _____________________________________________________________________________ 4
Cardiac Structures ________________________________________________________________________ 5
Layers of the Heart _____________________________________________________________________ 5
Cardiac Chambers & Blood flow through the Heart __________________________________________ 5
The Conduction System____________________________________________________________________ 9
Depolarization and Repolarization_________________________________________________________ 9
Sinoatrial (SA) Node ___________________________________________________________________ 10
Sinoatrial (SA) Node ___________________________________________________________________ 11
Atrioventricular (AV) Node and AV Junction ______________________________________________ 11
Bundle of His _________________________________________________________________________ 11
Purkinje Fibers________________________________________________________________________ 12
Summary of Pacemaker Functions________________________________________________________ 12
Coronary Circulation_____________________________________________________________________ 13
Coronary Arteries _____________________________________________________________________ 13
Coronary Blood Flow___________________________________________________________________ 14
Systemic Circulation _____________________________________________________________________ 15
Arteries ______________________________________________________________________________ 15
Capillaries ____________________________________________________________________________ 15
Venous System ________________________________________________________________________ 15
Neurohormonal Control of the Heart and Blood Vessels ________________________________________ 16
Sympathetic Nervous System of the Heart__________________________________________________ 16
Parasympathetic Nervous System of the Heart ______________________________________________ 16
Receptor Control ______________________________________________________________________ 16
Vasomotor Center _____________________________________________________________________ 17
Hormonal Influences on the Heart and Blood Vessels ________________________________________ 17
Conclusion______________________________________________________________________________ 19
References ______________________________________________________________________________ 20
Post Test Viewing Instructions _____________________________________________________________ 21

ACKNOWLEDGEMENTS
RN.com acknowledges the valuable contributions of
Lori Constantine MSN, RN, C-FNP, author of RN.coms Assessment Series: Cardiovascular Anatomy and
Physiology. Lori is a nurse of nine years with a broad range of clinical experience. She has worked as a staff
nurse, charge nurse and nurse preceptor on many different medical surgical units including vascular, neurology,
neurosurgery, urology, gynecology, ENT, general medicine, geriatrics, oncology and blood and marrow
transplantation. She received her Bachelors in Nursing in 1994 and a Masters in Nursing in 1998, both from
West Virginia University. Additionally, in 1998, she was certified as a Family Nurse Practitioner. She has
worked in staff development as a Nurse Clinician and Education Specialist since 1999 at West Virginia
University Hospitals, Morgantown, WV.

PURPOSE & OBJECTIVES

The focus of this cardiovascular anatomy and physiology course is to teach nurses about the structures and
functions of the cardiovascular system. The anatomical structures of the cardiovascular system work together to
achieve two major goals: the transport of oxygenated blood and nutrients to the cells of the body, and transport
of carbon dioxide and wastes from the cells to organs that will eliminate the waste. Understanding the
fundamental structures and functions of the cardiovascular system will allow you to provide care for all patients
you encounter and intervene effectively for those with alterations in cardiovascular status.
After successful completion of this course, you will be able to:
1. Identify the functions of various anatomical structures within the cardiovascular system.
2. Discuss the functions of the cardiovascular system.
3. Discuss the physiology of how the cardiovascular system works.

INTRODUCTION
Cardiovascular anatomy and physiology is an example of both a mechanical and an electrical organ system.
Although the heart is essentially a pump, the complex anatomy and physiology that make it able to
successfully keep a person alive is truly amazing. Add to that the hormonal influences on the cardiovascular
system and you have a truly complicated system of structures and events that need to operate correctly and
efficiently to maintain homeostasis.

CARDIAC STRUCTURES
Layers of the Heart
Practice Pearl
The human heart is protected by two layers that envelope it.
The outer layer is called the pericardium. It covers the heart.
It folds in on itself at the aorta forming the epicardium of the
heart. Between these layers is a small amount of fluid (10-50
mL) that provides the layers with a non-stick surface
(American Association of Critical Care Nurses, 1998).
While the epicardium forms the outer layer of the heart, the
myocardium forms the middle layer and the endocardium the
innermost layer. The coronary arteries travel across the
epicardium. The muscular myocardium is the thickest layer
and the workhorse of the heart.

When infection is within the pericardial sac

the inner surfaces of these layers begin to
stick. This is known as pericarditis. This
causes friction and pain. A friction rub may
result.
An accumulation of relatively small
amounts of fluid in this pericardial sac is
known as a pericardial effusion. If the fluid
accumulates enough to affect the hearts
ability to contract, it is known as cardiac
tamponade.

Practice Pearl
Mural thrombi typically form when
blood is allowed to pool in these
pockets. This usually happens due to
an inability of the heart to effectively
pump blood from the atria, such as in
atrial fibrillation.

The endocardium has a smooth inner surface to allow blood to flow

easily through the hearts chambers. Within the endocardium of
the atrium are pockets known as trabiculae. These pockets are
sometimes the sites of pathologic clot formation known as mural
(wall) thrombi.
The hearts valves are covered by the endocardium. The
endocardium also has an endocrine function, releasing hormones
such as endocardin - a substance that prolongs myocardial
contraction.

Cardiac Chambers & Blood flow through the Heart

The human heart is a four-chambered pump made up of
two receiving chambers called atria and two pumping
chambers called ventricles.

Aorta

Right Atrium (RA)

Pulmonary Arteries

The Right Atrium receives oxygen-depleted blood

returning from the body through the superior and
inferior vena cava. It is a thin walled, low-pressure
system. Normal pressures in the Right Atrium are
typically 08 mmHg. It is home to the Sinoatrial, or SA
Node, the pacemaker of the heart (American
Association of Critical Care Nurses, 1998).

R Atrium
L Atrium

L Ventricle

R Ventricle

Right Ventricle (RV)

The Right Ventricle is also a thin walled, low-pressure chamber. It receives blood from the Right Atrium when
the atrioventricular valve dividing the Right Atrium and ventricle (the Tricuspid Valve) is open. When this
valve is open, and the chamber is resting (filling with blood [diastole]) typical right ventricular pressures are
equal to that in the Right Atrium, 0-8 mmHg. However, when the valve closes and contraction (systole) begins,
pressures are 15-25 mmHg, enough to pump blood forward to the lungs via the right and left pulmonary arteries.
The blood is then oxygenated in the lungs (American Association of Critical Care Nurses, 1998).

Left Atrium (LA)

Another thin walled, low-pressure chamber is the Left atrium. It receives
oxygen-rich blood from the pulmonary circuit, via the right and left
pulmonary veins. Normal resting pressures (diastolic pressures) in the Left
atrium are 4-12 mmHg, less than that of the lungs. Because pressure is less
in this chamber during diastole, blood is more easily returned from the
higher-pressure pulmonary circuit (American Association of Critical Care
Nurses, 1998).

Practice Pearl
The right and left atria and
ventricular chambers are
separated by a septal wall
or septum

Left Ventricle (LV)

The Left Ventricle is a thick walled chamber that receives blood from the Left atrium, and is approximately
three times thicker than the Right Ventricle. When the atrioventricular valve dividing the Left atrium and
ventricle (the Mitral Valve) is open and the chamber is resting, or filling with blood (diastole) typical left
ventricular pressures are equal to that in the Left atrium, 4-12 mmHg. However, when the valve closes and
contraction (systole) begins, pressures must be generated to overcome the bodys systemic vascular resistance
(SVR). These pressures are typically 110-130 mmHg (American Association of Critical Care Nurses, 1998).
When the ventricle generates enough pressure to overcome the SVR, blood moves out the semilunar valve
known as the Aortic Valve into the aorta. There it is transported throughout the body via a network of arteries,
capillaries, and veins. Eventually the blood will return to the Right Atrium where the oxygenation process starts
all over again.

Cardiac Output (CO)

About two-thirds of the atrial blood flows passively from the atria into the ventricles. When atrial contraction
occurs, the atrial blood is pushed down into the ventricles. This atrial contribution is called atrial kick and
accounts for approximately thirty percent of the cardiac output (American Association of Critical Care Nurses,
1998).
Cardiac output is the amount of blood ejected by the Left Ventricle every minute. Cardiac output equals the
stroke volume times the heart rate.
The heart rate is the number of times that the heart beats per minute. Heart rate increases or decreases based
upon the metabolic and oxygen demands of the body. The stroke volume is the amount of blood pumped by the
heart per cardiac cycle. It is measured in ml/beat. A decreased stroke volume may indicate impaired cardiac
contractility or valve dysfunction and may result in heart failure. It may also indicate decreased circulating
volume. Increased stroke volume may be caused by an increase in circulating volume or an increase in inotropy,
the contractile force of the ventricle.

When the heart rate or the stroke volume (amount of blood ejected with each contraction) increases, cardiac
output increases. When the heart rate or the stroke volume decreases, cardiac output decreases. Cardiac output
varies according to body mass, but is typically between 4-8 liters per minute.

Cardiac index is cardiac output normalized for body surface area. There are several methods for measuring
cardiac output. Typical cardiac indices are between 2.5-4.0 liters of blood per minute per meter2 (American
Association of Critical Care Nurses, 1998).

Cardiac Valves
When blood flows through the heart, it follows a
unidirectional pattern. There are four different valves
within the myocardium and their functions are to
assure blood flows from the right to left side of the
heart and always in a forward direction.

Aortic Valve

Pulmonic Valve

The two valves found between the atria and ventricles

are appropriately called atrioventricular (A-V) valves.
The Tricuspid Valve separates the Right Atrium from
the Right Ventricle. The Tricuspid Valve is named so
because of its three (tri) leaflets (cusps). Similarly, the
Mitral Valve separates the Left atrium from the Left
Ventricle. The Mitral Valve is a two-leaflet valve,
named after a bishops miter.

Mitral Valve

Tricuspid Valve

The two remaining valves are called semilunar valves (because they look like half moons). The valve located
where the pulmonary artery meets the Right Ventricle is called the Pulmonic Valve. The Aortic Valve is located
at the juncture of the Left Ventricle and aorta. Both semilunar valves prevent backflow of blood into the
ventricles.

Valve Type
Atrioventricular (AV)

Valve Name
Tricuspid
Mitral

Semilunar

Pulmonic
Aortic

(Sherwood, 1997).

Location
Separates Right Atrium and
Right Ventricle
Separates Left atrium and Left
Ventricle
Between Right Ventricle and
pulmonary artery
Between Left Ventricle and aorta

Cardiac Cycle
Correlation with Heart Sounds
The first heart sound is called S1 (The Lub of the Lub-Dub sound). It results from of closure of the tricuspid
and Mitral Valves during ventricular contraction. The second heart sound is called S2 (The Dub of the LubDub sound). It occurs at the end of ventricular contraction due to the closure of the Aortic and Pulmonic
Valves.

Atrial
Contraction or
Atrial Kick

Slow Passive
Ventricular
Filling AV
Valves are open

DIASTOLE

Rapid
ventricular
filling

AV Valves
Close &
Produce S1

SYSTOLE
Semilunar
valves close
produce S2

Semi-lunar
valves open and
ventricles begin
ejection

THE CONDUCTION SYSTEM

Depolarization and Repolarization
In a cardiac cell, two primary chemicals provide the electrical charges: sodium (Na+) and potassium (K+). In the
resting cell, the potassium is mostly on the inside, while the sodium is mostly on the outside. This results in a
negatively charged cell at rest (the interior of the cardiac cell is mostly negative or polarized at rest). When
depolarized, the interior cell becomes positively charged and the cardiac cell will contract.
In summary, the polarized or resting cell will carry a
negative charge on the inside. When depolarized, the
opposite will occur. This is due to the movement of
sodium and potassium across the cell membrane.
Depolarization moves an electrical wave through the
myocardium. As the wave of depolarization stimulates
the hearts cells, they become positive and begin to
contract. This cell-to-cell conduction of depolarization
through the myocardium is carried by the fast moving
sodium ions.
Repolarization is the return of electrical charges to
their original state. This process must happen before
the cells can be ready conduct again.
Note the depolarization and repolarization phases as
they are represented on the ECG.

Na+

+
+

Na

Depolarization
(cell will contract)

V e n tr ic u la r
r e p o la r iz a tio n

V e n tr ic u la r
d e p o la r iz a t io n

Polarization
(cell at rest)

Na

A tr ia l
d e p o la r iz a t io n

K+

Repolarization
(return to baseline)

These electrical cells in the heart are arranged in a system of pathways called the conduction system. These
specialized electrical cells and structures guide the wave of myocardial depolarization. Two distinct components
must occur for the heart to be able to contract and pump blood. These components are an electrical impulse and
a mechanical response to the impulse
Electrical Impulse

Mechanical Response

The electrical impulse tells the heart to

beat.
This property is called
automaticity. Automaticity means that
these specialized cells within the heart can
discharge an electrical current without an
external pacemaker, or stimulus from the
brain via the spinal cord.

The mechanical beating or contraction

of the heart occurs after the electrical
stimulation.
When the mechanical
contraction occurs, the person will have
both a heart rate and a blood pressure.

The heart also has two distinct types of cells. There are electrical (conductive) cells, which initiate electrical
activity and conduct it through the heart. There are also mechanical (contracting) cells, which respond to the
electrical stimulus and contract to pump blood.
The electrical cells are responsible for
conducting
impulses
through
the
myocardial tissue and electrical pathways
of the heart. They are responsible for the
heart rate and rhythm. An ECG tracing is
designed to give a graphic display of the
electrical activity in the heart.

The contracting or myocardial working

cells contain contractile filaments. When
these cells are electrically stimulated,
these filaments slide together and the
myocardial cell contracts and the atria or
ventricular chambers contract. This is
how we get our pulse and blood pressure.

The physical layout of the conduction system is shown in the picture below. It is important that you understand
the sequence of events within this conduction system. Knowledge of the layout helps you to understand normal
and abnormal rhythms.
The conduction system consists of the Sinoatrial Node (SA Node), Atrioventricular Node (AV Node), Bundle of
His (also called the AV Junction), Right and Left Bundle Branches, and Purkinje Fibers.

10

Sinoatrial (SA) Node

The Sinoatrial Node (also called the SA Node or Sinus Node) is a group of specialized cells located in the
posterior wall of the Right Atrium. The SA Node normally depolarizes or paces more rapidly than any other
part of the conduction system. It sets off impulses that trigger atrial depolarization and contraction. Because the
SA Node discharges impulses quicker than any other part of the heart, it is commonly known as the natural
pacemaker of the heart. The SA Node normally fires at a rate of 60-100 beats per minute.
After the SA Node fires, a wave of cardiac cells begin to depolarize. Depolarization occurs throughout both the
right and left atria (similar to the ripple effect when a rock is thrown into a pond). This impulse travels through
the atria by way of inter-nodal pathways down to the next structure, which is called the AV Node.
Do you remember the term mentioned before called atrial kick? Atrial kick occurs when the atria contract and
dump their blood into the ventricles. This atrial contraction contributes up to 30% of the cardiac output, which
is obviously an important element toward maintaining our blood pressure. So remember... the SA Node is not
only the primary pacemaker of the heart but also triggers atrial depolarization and the contribution of the atrial
kick.
The heart is truly an amazing organ. Not only does it have one dominant pacemaker (the SA Node) it also has
two back-up pacemakers. A back-up pacer is located in the area near the Bundle of His. The final back-up
pacer is located in the ventricles along the Purkinje fibers. More interesting information on this later.

Atrioventricular (AV) Node and AV Junction

The next area of conductive tissue along the conduction pathway is at the site of the atrioventricular (AV) Node.
This node is a cluster of specialized cells located in the lower portion of the Right Atrium, above the base of the
Tricuspid Valve. The AV Node itself possesses no pacemaker cells.
The AV Node has two functions. The first function is to DELAY the electrical impulse in order to allow the
atria time to contract and complete filling of the ventricles. The second function is to receive an electrical
impulse and conduct it down to the ventricles via the AV junction and Bundle of His.

Bundle of His
After passing through the AV Node, the electrical impulse enters
the Bundle of His (also referred to as the common bundle). The
Bundle of His is located in the upper portion of the
interventricular septum and connects the AV Node with the two
bundle branches. If the SA Node should become diseased or fail
to function properly, the Bundle of His has pacemaker cells,
which are capable of discharging at an intrinsic rate of 40-60
beats per minute. This back-up pacemaker function can really
come in handy!
The AV Node and the bundle of His are referred to collectively
as the AV junction. The Bundle of His conducts the electrical
impulse down to the right and left bundle branches.
The right bundle branch spreads the wave of depolarization to the Right Ventricle. Likewise, the left bundle
branch spreads the wave of depolarization to both the interventricular septum and the Left Ventricle. The left
bundle further divides into 3 branches or fascicles. The bundle branches further divide into Purkinje fibers.
11

Purkinje Fibers
We are now coming to the end of this amazing cardiac conduction system. At the terminal ends of the bundle
branches, smaller fibers distribute the electrical impulses to the muscle cells, which stimulate contraction. This
web of fibers is called the Purkinje fibers. The Purkinje fibers penetrate about 1/4 to 1/3 of the way into the
ventricular muscle mass and then become continuous with the cardiac muscle fibers. The electrical impulse
spreads rapidly through the right and left bundle branches and Purkinje fibers to reach the ventricular muscle,
causing ventricular contraction, or systole.
These Purkinje fibers within the ventricles also have intrinsic pacemaker ability. This third and final pacemaker
site of the myocardium can only pace at a rate of 20-40 beats per minute. You have probably noticed that the
further you travel away from the SA Node, the slower the backup pacemakers become. As common sense tells
you, if you only have a heart rate of 30 (from the ventricular back-up pacemaker), your blood pressure is likely
to be low and you might be quite symptomatic.

Summary of Pacemaker Functions

The heart is designed with a system of one dominant and two back-up pacing systems.

Pacemaker Hierarchy
Level 1 (normal)

Summary of Pacemaker Function

Location
SA Node

Level II (back-up system)

Bundle of His/ AV Node/ Junction

Pacing Rate
60-100
beats/minute
40-60
beats/minute

Level III (lowest back-up Purkinje Fibers within Ventricles (typically called 20-40
system)
the Ventricular Pacemaker)
beats/minute

12

CORONARY CIRCULATION
Coronary Arteries
The coronary arteries receive their name for the crown they form over the heart. Two main arteries arise off the
aorta at the Sinus of Valsava. These arteries are named the Right Coronary Artery (RCA) and Left Coronary
Artery (LCA)
When the Aortic Valve closes at the beginning of diastole, the Sinus of Valsalva distends and blood flows into
the RCA and LCA.

RCA (Right Coronary Artery)

The RCA arises from right side of aorta and follows a groove between Right Ventricle and Left Ventricle. It
extends to back of heart, forming the posterior descending artery. The RCA is the main blood supply to Right
Atrium and Right Ventricle, much of conduction system and the inferior and posterior Left Ventricle. The RCA
supplies blood to the SA Node (in fifty-five percent of the population) and the AV Node (in ninety percent of
the population). Occlusion of the Right Coronary Artery leads to inferior and posterior myocardial infarctions
(MI). Bradycardia and arrhythmias are commonly seen in these MIs.
Occlusions of RCA

Inferior or Posterior MI

13

LCA (Left Coronary Artery)

The LCA arises off of the left side of the aorta. It quickly forms the left main that divides into the left anterior
descending (LAD) artery and the circumflex artery.
LCA

Left Main

LAD

Circumflex

LAD (Left Anterior Descending) Artery

The LAD travels down the heart between the Right Ventricle and Left Ventricle to the apex and turns back up
the heart. It is the main blood supply to Left Ventricle, septum, and anterior wall. Diagonal arteries arise off of
the LAD.
Occlusions of LAD

anterior MIs

Circumflex (CFX) Artery

The circumflex artery curves around the left side of the heart between the Left Atrium and the Left Ventricle. It
supplies blood to the posterior surface of the heart. It supplies blood to the SA Node (in forty-five percent of the
population) and the AV Node (in ten percent of the population). Its marginal branches provides the left lateral
ventricle and the posterior Left Ventricle with its blood supply.
Occlusions of Circumflex

Lateral or Posterior MI

Coronary Blood Flow

Two-thirds of coronary blood flow occurs during diastole, or when the
heart is at rest. Five percent of cardiac output goes to the coronary
arteries. Seventy percent of oxygen is extracted by the myocardial
tissues of the heart, in comparison to the rest of the body at twentyfive percent. During times of extreme demand, the coronary arteries
can dilate up to four times greater than normal to increase supply of
oxygen to the myocardial tissues.

Practice Pearl
Bradycardias increase diastolic
filling time. This is why cardiac
patients can tolerate
bradycardias better than
tachycardias.

Practice Pearl
Patients with Coronary Artery Disease have fixed
lesions that cannot dilate to meet increased
demand. This leads to angina and coronary
dysfunction, which may eventually lead to
myocardial infarction.

The de-oxygenated blood from the myocardium is

collected in the coronary sinus. This large vein then
returns the de-oxygenated blood to the Right Atrium.

14

SYSTEMIC CIRCULATION
Arteries
The arterial system carries about thirteen percent of the bodys blood
volume at any given time. The heart pumps blood out through one major
artery the aorta. The aorta branches and these branches further divide
into smaller arteries known as arterioles. Arterioles contain smooth
muscle. They are innervated by the autonomic nervous system and can
constrict and dilate to regulate blood supply to tissues. Arterioles are
largely responsible for our systemic vascular resistance (SVR).
Eventually, the arterioles divide enough that they become capillaries
where the exchange of oxygen, carbon dioxide, and nutrients occurs.

Practice Pearl
Coronary Artery Disease
(CAD) is characterized by
damage to the intima, or
internal layer of arteries.

Arteries are composed of three layers: the intima (the inner layer of epithelial cells), the media (the muscular
middle layer), and the adventitia (the tough outer layer). The media layer helps the heart pump the blood.
When the heart beats, the artery expands as it fills with blood. When the heart relaxes, the artery contracts
exerting a force that it strong enough to push the blood forward. This rhythm between the heart and the artery
results in successful circulation of the blood to the body.

Capillaries
Blood spends only 0.5 seconds in capillaries. Our capillaries are only one
cell thick. The exchange of oxygen, carbon dioxide, and nutrients takes
place through this very thin wall. At this cellular level, the red blood cells
inside the capillaries free their oxygen. This oxygen then passes through
the wall and into the surrounding tissue. Simultaneously, the tissues free
their waste products, like carbon dioxide. These wastes pass through the
wall and into the red blood cells, where the red blood cells transport the
wastes to the lungs, liver and other cleansing organs for their excretion.
Additionally, capillaries have both pre and post capillary sphincters that
have a high degree of intrinsic tone and are independent of neurohormonal
controls. Capillaries auto-regulate to meet metabolic needs of surrounding
tissues.

Venous System

Practice Pearl
In shock, pre-capillary
sphincters dilate and postcapillary sphincters contract in
an attempt to supply cells with
more needed nutrients due to
decreased blood supply.

Practice Pearl

Blood leaving the capillaries returns to the heart through the venous
system. The path begins with the venules and progresses to larger and
larger veins which lead to the superior and inferior vena cavae which then
enter the Right Atrium. Veins are highly distensible, thin walled vessels.
They act as a volume reservoir for circulatory systems. At any given time,
the veins carry about fifty percent of the blood volume of the body. Veins
are very much like arteries, however they transport blood at a lower
pressure than arteries. The veins transport blood back to the lungs and
heart. Veins have valves that are located inside the veins that keep blood
moving back to the heart. The vein valves also provide footholds for the
blood as it travels against gravity towards the heart. For example, blood
returning to the heart from the foot has to travel against gravity. The
venous valves and muscle contractions of the leg prevents backflow of
blood (American Association of Critical Care Nurses, 1998).
15

Drugs that increase venous capacity

(diuretics, morphine, and
nitroglycerin) will decrease
preload, thus decreasing the amount
of blood returning to the right side
of the heart. High fowlers also
increases venous capacity &
decreases preload. The supine
position decreases venous capacity
and increases preload, or the
amount of blood returning to the
right side of the heart.

NEUROHORMONAL CONTROL OF THE HEART AND

BLOOD VESSELS
The brain and central nervous system control the body through two pathways - the somatic & autonomic
nervous systems. The somatic nervous system is typically under voluntary control. In contrast, the autonomic
nervous system is not voluntary. Due to this involuntary system, we dont have to think about every heart beat,
the amount of blood delivered to specific tissues, the dilation of our pupils, and how much digestive motility our
GI tract needs. In other words, the autonomic nervous system regulates the activities of the internal organs.
The autonomic nervous system has two main parts, the sympathetic and the parasympathetic systems. These
two opposite systems often operate in opposition to each other. Many internal organs are stimulated by both
systems. When one stimulates an organ, the other tends to depress the organ. The sympathetic nervous system
is responsible for the fight-or-flight" response. This response prepares us for emergency situations. The
parasympathetic nervous system, oppositely, tends to inhibit these reactions. The response of our body depends
on the proportionate strength of stimulation supplied by each system at any given instance.

Sympathetic Nervous System of the Heart

Activation of the sympathetic nervous system increases heart rate (positive chronotropy), increases contractility
(positive inotropy), and increases conduction velocity (positive dromotropy). Additionally, in blood vessels,
sympathetic activation constricts arteries and arterioles. This increases systemic vascular resistance (SVR,
increases central blood flow and decreases distal blood flow. In other words blood is shunted away from the
periphery to the heart, brain and skeletal muscles. Sympathetic stimulation also produces an effect on the
bodys venous system. It decreases venous blood volume, and increases venous pressure (Tortora, 1987).
The overall effect of sympathetic activation is to increase cardiac output, systemic vascular resistance (both
arteries and veins), and arterial blood pressure. Enhanced sympathetic activity is particularly important during
exercise, emotional stress, and during hemorrhagic shock.

Parasympathetic Nervous System of the Heart

When the parasympathetic system is activated it works to decrease heart rate (negative chronotropy), decrease
contractility (negative inotropy), and decrease conduction velocity (negative dromotropy) via the Vagus Nerve.
Most blood vessels in the body do not have parasympathetic innervation. However, parasympathetic nerves do
innervate salivary glands, gastrointestinal glands, and genital erectile tissue where they cause vasodilation
(Tortora, 1987).

Receptor Control
Baroreceptors
Baroreceptors are located in the aortic arch, the carotid bodies of the external carotid arteries, the pulmonary
artery, and the atria. They respond to changes in blood pressure. The baroreceptors of the aortic arch have a
high threshold pressure and are less sensitive than the carotid sinus receptors.

16

The baroreceptors of the carotid sinus typically respond to pressures ranging from 60-180 mmHg. These
receptors are the dominant receptors. These receptors work by sensing the mean arterial blood pressure. This
"set point" changes during hypertension, heart failure, and other chronic disease states. However, when there is
an acute increase or decrease in mean arterial pressure, the baroreceptors alter their firing rate. Under normal
physiological conditions, decreased pressure leads to decreased baroreceptor firing. This also inhibits
sympathetic stimulation from the brain (medulla) (American Association of Critical Care Nurses, 1998).
For example, hypotension decreases the firing rate of the carotid baroreceptors. The brains normal inhibition of
sympathetic response decreases, thereby increasing sympathetic activity which leads to increased blood pressure
by increasing vasoconstriction (increased SVR), increasing heart rate, and increasing the force of contraction of
the heart. These changes result in the net effect of increased arterial pressure. Alternatively, an acute increase
in arterial pressure increases the firing rate of the baroreceptors. This increases the inhibition of sympathetic
activity in the brain (medulla). When sympathetic stimulation is inhibited, bradycardia, decreased conductivity,
and decreased contractility of the myocardium result.

Chemoreceptors
Chemoreceptors are located both peripherally and centrally. Their role in the body is to detect abnormal
changes in oxygen, carbon dioxide, and hydrogen ion concentration in the blood stream.
The bodys major chemoreceptors are located in the carotid bodies of the external carotid arteries near the
bifurcation of the internal carotid arteries. These carotid bodies continually sense oxygen, carbon dioxide and
hydrogen ion concentration in the blood. When these receptors are stimulated, respiratory activity is incited to
change to correct the sensed disturbance.
Respiratory arrest and circulatory shock dramatically increase chemoreceptor activity leading to increased
sympathetic stimulation to the heart and vasculature via activation of the vasomotor center.

Vasomotor Center
The vasomotor center in the medulla of the brain is responsible for the overall control of blood distribution and
pressure throughout the body. Impulses from the vasomotor center typically cause vasoconstriction everywhere
except for the coronary and skeletal arteries, where they cause vasodilation.

Hormonal Influences on the Heart and Blood Vessels

Certain hormones and substances help the body auto-regulate its blood pressure.
Vasopressin or Anti Diuretic Hormone (ADH) is released from the pituitary gland in the brain when the
baroreceptors sense a fall in blood pressure. Its effect on vessels is to cause vasoconstriction which usually
results in an increased blood pressure.
Endothelin is released from the endothelial cells of the vasculature after vascular damage.
vasoconstriction of the underlying vascular smooth muscle and prevents blood loss

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It produces

Atrial natriuretic peptide (ANP) is released from the atria of the

heart and endothelium due to an increase in pressure or venous
return to the atria and excess stretching of the vessels. Its net
effect is to relax vascular smooth muscle and decrease blood
pressure.
Nitric oxide is also released from the endothelium of the
vasculature when stretching increases, producing a net effect of
vasodilation
Renin Angiotension System
When the kidneys sense a decrease on blood pressure the reninangiotension system is activated. This system has the net effect of
increasing organ perfusion and arterial blood pressure. This
system is very effective when there is blood loss. However, when
the system is activated due to a pathologic condition such as heart
failure, the system itself is pathologic to the body, resulting in
increased blood pressure that may be detrimental. The mechanism
of the system is summarized below.

Practice Pearl
Nitric Oxide is the basis of the
therapeutic action of nitroglycerine. It
vasodilates coronary arteries.
It also acts as the basis of action for the
drug Viagra. It blocks the destruction
of the chemical messenger that is
produced when nitric oxide dilates the
vascular smooth muscles of the penis
net effect vasoconstriction of the
vessels of the penis and subsequently
an erection.

Decreased renal blood flow

Renin Release
Angiotensin

Angiotensin I
Angiotensin II

Vasoconstriction

Aldosterone Release

Sodium & water retention

Practice Pearl
The mechanisms of actions
of many drugs we use to
control hypertension work
by interfering with specific
pathways within this
system, such as ACE
Inhibitors and Beta
Blockers.

Increased Blood Pressure

Increased Organ Perfusion

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CONCLUSION
Knowledge of the anatomy and physiology of the complex structures and mechanisms of the cardiovascular
system involves not only the physical structures but also the electrical and hormonal influences that make them
work. This knowledge will help you assess and care for all your patients.

Please Read:
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REFERENCES
American Association of Critical Care Nurses (1998). The Cardiovascular System. In J. Alspach (Ed.), Core curriculum for
critical care nursing (5th ed., Rev., pp. 137-338). Philadelphia: Saunders.
Sherwood, L. (Ed.). (1997). Human physiology: From cells to systems (3rd ed.). Belmont, California: Wadsworth.
Tortora, G. (1989). The autonomic nervous system. In E. Dollinger (Ed.), Principals of human anatomy (5th ed., pp. 533547). New York: Harper & Row.

Copyright 2004, AMN Healthcare, Inc.

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