APRIL 1998, VOL 67, NO 4

Home Study Program

CARDIAC A N A T O W AND PHVSIOLOGV: A R M E W

T he article “Cardiac anatomy and physiology: A review” is the

basis for this AORN Journal independent study. The behavioral
objectives and examination for this program were prepared by
Helen Starbuck Pashley, RN, MA, CNOR, with consultation
from Trish O’Neill, RN, MS, professional education specialist,
Center for Perioperative Education.
A minimum score of 70% on the multiple-choice examination is
necessary to earn three contact hours for this independent study. Partic-
ipants receive feedback on incorrect answers. Each applicant who suc-
cessfully completes this study will receive a certificate of completion.
The deadline for submitting this study is May 31, 1999.
Send the completed application form, multiple-choice examina-
tion, learner evaluation, and appropriate fee to
AORN Customer Service
c/o Home Study Program
2170 S Parker Rd, Suite 300
Denver, CO 80231-571 1

BEHAVIOW OBJECTIVES
After reading and studying the article on cardiac anatomy and
physiology, the nurse will be able to
(1) distinguish significant cardiac anatomy,
(2) describe the major heart sounds,
(3) explain the electrophysiology of the heart, and
(4) discuss factors affecting cardiac output.

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9

Cardiac Anatomv
and Physiology: A Riview

F or it is the heart by whose virtue and pulse

the blood is moved, perfected, made apt to
nourish and is preservedfrom corruption and
coagulation. . . . Zr is indeed the fountain of
life, the source of all action. William Harvey
(1578-1697)'

FUNCTIONAL ANATOMY
AND PHYSIOLOGY OF THE HEART
sists of a visceral and parietal portion. The visceral
portion, also known as the epicardium, covers the
entire heart and great vessels and folds over to form
the parietal pericardium. The parietal portion also
lines the fibrous pericardium.
The pericardial cavity is a potential space
between the parietal and visceral pericardium. It nor-
mally contains 30 mL to 50 mL of serous fluid that
acts as a lubricant to decrease friction as the heart
The human heart is a hollow muscular organ, contracts and relaxes.6 The pericardial cavity can
nearly the size of a closed fist, that weighs approxi- hold up to one liter of fluid in some chronic diseases
mately 300 grams in the adult male and 250 grams in without compromising the heart. If the buildup of
the adult female.* Weight and size varies depending fluid occurs gradually, the pericardium can stretch
on age, sex, height, nutritional status, and epicardial without affecting the heart. If the fluid accumulates
fat.3 The heart lies within the central area of the tho- rapidly, however, even small amounts (ie, SO mL to
racic cavity, in the mediastinal space, with two thirds 100 mL) can cause compression of the heart (ie, car-
of it extending to the left of midline. The heart is an diac tamponade).
inverted cone-shaped organ that tilts forward and to The pressure of a cardiac effusion can equal
the left within the thoracic cavity. The apex of the diastolic pressure within the heart chambers and
cone lies inferiorly and the great vessels (ie, superior interfere with filling. Thmight atrium and ventricle
vena cava, inferior vena cava) are affected first because the
enter the base of the cone superi- pressure in these chambers is
. ~ apex lies between the A B S T R A C T
~ r l y The lower than the pressure on the
fifth and sixth ribs when one is This article reviews the nor- left side of the heart. Disruption
lying down and between the sixth ma1 anatomy and physiology of in cardiac filling occurs first in
and seventh ribs when one is sit- the heart. Understanding the the right atria and leads to
ting or standing5 normal anatomic and physiolog- increased venous pressure and
Pericardium. The heart is ic relationships described in this systemic congestion. Signs of
enclosed in a double-walled, article will help perioperative right heart failure are distention
fibroserous, inelastic sac called nurses care for patients who are of the Jugular veins, edema, and
the pericardium. The outer fibrous undergoing cardiac procedures. hepatomegaly. Decreased atrial
layer of the pericardium is Such knowledge also assists filling leads to inadequate filling,
attached to the great vessels, the nurses in educating patients reduced cardiac output, and
sternum, and diaphragm. This about cardiac procedures and potential circulatory collapse.
fibrous layer of the pericardium is about activities that can pre- Pulsus paradoxus, in which arter-
very resistant to distention and vent, reverse, or improve car- ial blood pressure during expira-
helps to prevent dilation of the diac illness. AORN J 67 (April tion exceeds arterial pressure
heart. The inner serous layer con- 1998) 802-822. during inspiration by more than

M A R Y GAVVAGHAN. HN

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10 mm Hg, is a key indicator of cardiac tamponade.
Normally, inspiration has little effect on cardiac
flow or volume. A “water bottle” cardiac silhouette
on a chest x-ray, dyspnea on exertion, dull chest
pain, and muffled heart sounds are other signs of
cardiac tamponade.’
The parietal pericardium is innervated by the
phrenic nerve, which contains pain fibers; however,
the visceral pericardium is insensitive to pain.8 The
fibrous pericardium anchors the heart to the great
veins and arteries at its base. It anchors the heart to
the sternum anteriorly and to the diaphragm inferior-
ly. The pericardium receives its blood supply
through branches of the internal thoracic arteries and
phrenic arteries. Venous drainage is through the azy-
gous and pericardiophrenic veins.
Layers of the heart. The heart wall consists of
three layers. The outermost layer of the heart, the
epicardium, also known as the visceral pericardium,
consists of epithelial cells that form a serous mem-
brane that covers the entire heart. The innermost
layer of the heart is known as the endocardium. It is
a serous membrane that lines the inner surface of the
heart, its valves, and the chordae tendineae, which
are the cords that connect the free edges of the atri-
oventricular valves with the papillary muscles. The
papillary muscles are muscle eminences on the walls
of the ventricles. The endocardium is continuous
with the intima (eg, the inner lining of arteries).
The middle layer of the heart is the muscular
layer known as the myocardium. It is responsible for
the major pumping action of the ventricles. The
myocardial cells have an intrinsic ability to contract
in the absence of stimuli (ie, automaticity) and in a
rhythmic manner (ie, rhythmicity), and to transmit
nerve impulses (ie, conductivity). The myocardium
does not undergo mitotic activity and cannot replace
injured cells.9
Heart chambers. The heart has four chambers,
two atria and two ventricles. It is helpful to look at
each chamber in the order in which blood flows
within the heart: right atrium to the right ventricle,
from the lungs into the left atrium, and finally into
the left ventricle.
Right atrium. The right atrium has a thin muscle
wall. It receives deoxygenated (ie, venous) blood
from the head and upper extremities via the superior
vena cava, from the trunk and lower extremities via
the inferior vena cava, and from the coronary sinus,
which drains blood from the myocardium. The coro-
nary sinus empties into the right atrium just above
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the tricuspid valve. Most blood flow into the right
atrium occurs during inspiration when right atrium
pressure drops below that in the inferior and superior
venae cavae, causing the blood to flow from an area
of higher to lower pressure. There are no true valves
in the venae cavae; thus, when right atrium pressure
rises, congestion occurs in the systemic circulation.
Normal filling pressure for the right atrium ranges
from 0 to 8 mm Hg.
Right ventricle. The right ventricle may be
divided into the body of the right ventricle (ie, an
inflow region consisting of the tricuspid valve, the
chordae tendineae, the papillary muscle, and a heavi-
ly trabeculated myocardium), and the infundibulum,
a smooth outflow region. The inflow and outflow
portions of the right ventricle are separated by four
muscular bands: the infundibulum septum, the pari-
etal band, the septa1 band, and the moderator band.
The infundibulum septum and parietal band make up
the crista supraventricularis. l o Blood flows around
the crista supraventricularis and is mixed by passing
through the strands of the trabeculae carnae.l’
The right ventricle receives blood from the right
atrium through the tricuspid valve and ejects it
through the pulmonic valve into the pulmonary
artery where it travels to the lungs. The resistance of
the pulmonary circulation is approximately one tenth
that of the systemic circulation. In addition, the vas-
cular pathways of the lungs offer very low resistance
to ejection pressure; therelbre, very little pressure is
needed to pump blood to the lungs.I2Normal systolic
pressure in the right ventricle ranges from 15 to 28
mm Hg and end-diastolic pressure is 0 to 8 mm Hg.
The right ventricle generates less than one fourth the
stroke work of the left ventricle.
Left atrium. The left atrium receives oxygenated
(ie, arterial) blood from the lungs through the right
and left inferior and superior pulmonary veins. The
wall of the left atrium is slightly thicker than that of
the right atrium and breathing does not affect its fill-
ing. Normal filling pressure ranges from 4 to 12 mm
Hg.
Left ventricle. The left ventricle has a thick
muscular wall. It receives blood from the left atrium
through the mitral valve and ejects it through the
aortic valve to the systemic circulation via the aorta.
Pressure in the left ventricle is high. Normal systolic
pressure is 90 to 140 mm Hg and normal end-dias-
tolic pressure is 4 to 12 mm Hg. The ventricular
septum, a thick muscular area that becomes mem-
branous as it nears the atrioventricular (AV) valves,
 APRIL 1998, VOL 69, NO 7
Gavaghan *

separates the right and left ventricles. It houses elec-

trical conduction tissue and provides stability for the
ventricles during contraction.
Cardiac skeleton. The heart’s fibrous skeleton,
the anulus fibrosus, is a firm anchor to which most
of the heart’s muscles and valves are attached. The
anulus fibrosus gives structure to the heart and acts
as an insulator to ensure that electrical impulses
move through the AV node and bundle only, thus
helping prevent dysrhythmias.I3 It consists of tough
fibrous rings surrounding the AV valves, and the
bases of the aortic and the pulmonary trunks (the
aortic and pulmonary anuli) which are connected by
the tendon of the conus, a fibrous band. The aortic
anulus and the AV anuli are connected by the left
and right fibrous trigone.
Cardiac valves. Figure 1 illustrates the valves
and chambers of the heart. The mitral or bicuspid
valve lies between the left atrium and left ventricle.
It has two leaves that slightly overlap each other
when the valve is closed. The tricuspid valve lies
between the right atrium and right ventricle. It has Figure 1 Illustration showing the chambers and
three valves that are thinner than those of the mitral valves of the heart. Blue arrows indicate venous blood
valve. The leaves of both valves are attached to flow, red arrows indicate arterial blood flow. (///ustrotions
strong fibrous strands called the chordae tendineae. by Mark Kotnik, Denver)
These cords arise from the trabeculae carnae muscle
bundles in the inner ventricles. Two groups of papil-
lary muscles arise from the trabeculae cameae in the other characteristics include carditis, chorea (ie, St
left ventricle and three arise in the right ventricle. Vitus’ dance), subcutaneous nodules, erythema mar-
The aortic and pulmonary valves are called semilu- ginatum, joint pain, and ARhoff bodies (ie, sterile
nar (ie, half moon) valves because they have three lesions on the heart tissues). In the patient with
cusps that are cuplike in nature. The AV (ie, mitral severe mitral stenosis, the perioperative nurse may
and tricuspid) valves prevent backflow of blood see what is known as “mitral facies,” a pinched
from the ventricles into the atria during systole. The facial expression, malar flushing, and peripheral or
semilunar (ie, aortic and pulmonary) valves prevent central cyanosis. On surgical examination, the mitral
backflow from the aorta and pulmonary artery dur- valve may have a “fish mouth” or buttonhole appear-
ing diastole. ance. Calcium deposits may be present on the leaves
Valvular damage can result from infection of and valvular ring, which prevent effective opening
the throat with B-hemolytic, group A Streptococcus. and closing, and the chordae tendinae may appear
An autoimmune mechanism in which antibodies short and thickened.15
attack the offending organism is believed responsible
for the valvular damage. The mitral valve is most THE PUMPING MECHANISM OF THE HEART
often affected by this process known as rheumatic In basic terms, the heart consists of a right and
fever. The two cusps of the mitral valve can become left pump. The right pump (ie, the right atrium and
thick and rigid, resulting in incomplete closure, ventricle) is a low pressure system because, in a
which allows mitral regurgitation, or the valve open- healthy person, the lungs offer little resistance to
ing narrows and causes mitral stenosis. The other blood flow. The left pump (ie, the left atrium and
heart valves may be involved in a similar manner. ventricle) is a high pressure system. High pressure is
Rheumatic fever is a major cause of morbidity and necessary in the left pump to overcome systemic
mortality, and is still the most common cause of resistance to blood flow.
mitral valve disease and aortic reg~rgitati0n.l~ Its Normally, blood flows from the inferior and

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superior venae cavae and the pulmonary veins into
the atria. Seventy-five percent of this blood flows
into both ventricles even before an atrial contraction
occurs. Decremental conduction in the AV node (ie,
conduction in which the impulse decreases progres-
sively) causes the impulse to be delayed long enough
for the atrial contraction to contribute to ventricular
filling. The atrial contraction or atrial kick con-
tributes the remaining 25% to ventricular filling;
thus, the atria function as primer pumps for the ven-
tricles. The heart can function effectively at rest
without this priming action because it can pump 300
to 400 times more blood than is needed by the body.
If the atria fail, however, a patient may exhibit signs
of heart failure during exercise.16
Heart sounds. The integrity of the heart valves
can be determined by listening to the sounds they
make as they open and close. Two sounds are clearly
heard with each heartbeat. The first sound (S,) is
longer and lower in pitch than the second (S,) and
sounds like the word “lubb.” It corresponds closely
to each carotid pulsation. Deceleration of blood asso-
ciated with closure of the mitral and tricuspid valves
causes S,. It has two high-frequency sounds-the
mitral (MI) sound and the tricuspid ( T I ) sound.
Events in the right heart follow those in the left;
therefore, the tricuspid valve closes a little later than
does the mitral valve. Consequently, TI follows M,.
The split of S, into MI and T I is heard clearly in chil-
dren, however, it is more difficult to hear this split in
adults.
The second heart sound (S,) is higher pitched
and shorter than S, and is due to closure of the aortic
and pulmonic semilunar valves. It sounds like the
word “dup.” The designations A, and P, are used for
the aortic and pulmonic sounds. The pulmonic sound
is usually louder than the aortic.17
If the cardiac valves do not close tightly (ie,
valvular insufficiency) or are narrowed (ie, stenosis)
turbulence will be heard on auscultation. For exam-
ple, in mitral insufficiency, blood leaks back into the
left atrium during ventricular contraction. This
results in a systolic murmur. In mitral stenosis, as the
atrium pumps blood through a constricted valve, a
presystolic murmur is heard. In aortic insufficiency,
blood leaks back into the left ventricle from the aorta
during diastole; this results in a diastolic murmur.
When blood is forced through a stenotic aortic valve,
a systolic murmur is heard.
The tricuspid and pulmonary valves may be
affected by disease similarly. If ventricular wall
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compliance is decreased, as in congestive heart fail-
ure, structures within the ventricles vibrate, leading
to a third heart sound (SJ. It occurs in early diastole.
An S, heart sound may be normal in people less than
30 years of age.lx A fourth heart sound (S,) may be
heard during atrial systole (ie, atrial kick) if hyper-
trophy or other damage to the ventricular wall is pre-
sent. It is identified by its close proximity to S I.
Auscultatory areas. The places where valvular
movement can be heard are not the actual anatomic
locations of the valves. Rather, the sounds represent
the direction of blood flow.LyThe aortic valve sound
can be heard best at the second intercostal space near
the right sternal border. The second aortic sound
may be heard at Erb’s point at the third intercostal
space, just left of the sternum. The pulmonic sound
is best heard at the second intercostal space near the
left sternal border. The tricuspid valve sound is best
heard at the left lower sternal border, and the mitral
valve sound is best heard at the fifth intercostal space
at the apex of the heart. Figure 2 depicts these aus-
cultation areas on the chest.
CORONARY ARTERIAL CIRCULATION
The coronary arteries (CA) supply the capillar-
ies of the myocardium with blood. The left coronary
artery (LCA) and right coronary artery (RCA) arise
from the sinuses of Valsalva (ie, outpouchings of the
aortic wall that prevent occlusion of the coronary
orifice by the open semilbnar valve) just above the
aortic valve. The LCA has two main branches-the
left anterior descending (LAD) and the left circum-
flex (LCX) arteries. The coronary arteries course
around the heart in two grooves-the atrioventricular
groove and the interventricular groove. These two
grooves meet on the posterior aspect of the heart at
the important landmark known as the crux of the
heart.*” The AV node is located at the crux and is
nourished by either the RCA or the LCA. Right or
left coronary dominance is determined by the artery
that crosses the crux. Fifty percent of people are
right coronary artery dominant, 10% to 15% are left
coronary dominant, and 35% to 40% have mixed
right and left dominance. Lesions of the RCA pro-
duce AV node disturbances, and lesions of the LCA
can interfere with ventricular pumping. Individuals
who are LCA dominant are more likely to die from a
blockage of this coronary artery.
Generally, the RCA supplies the right atrium,
right ventricle, and inferior wall of the left ventricle.
The LAD artery nourishes the anterior wall of the left
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Figure 2 Illustration showing auscultatory points on the chest where heart sounds can be heard.

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ventricle. The LCX artery supplies the left atrium and

lateral and posterior walls of the left ventricle. In 55%
of the population, the sinoatrial (SA) node is nourished
by the RCA. A branch of the LCX artery supplies the
SA node in the remaining 45%. The AV node is sup-
plied by the RCA in 90% of people. In the other lo%,
the AV node is supplied by the LCX artery.
Potential anastamoses (ie, intercoronary chan-
nels) exist between the arterial branches. Though not
functional during normal circulation, these anasta-
moses provide for collateral circulation if normal
coronary vasculature becomes blocked. The heart
has an extensive capillary network-approximately
3,300 capillaries per square millimeter or about one
capillary for each muscle cell-but it is not one that
changes. In conditions of cardiac hypertrophy, for
example, the capillary network does not enlarge to
accommodate the increase in heart size. This results
in lack of oxygen and nutrients to the muscle.21

CORONARY VENOUS CIRCUlAT1ON

The venous system of the heart consists of the
thebesian veins, the anterior cardiac veins, and the
coronary sinus. The thebesian veins traverse the Figure 3 IllUStratiOn showing the great Vessels, the
myocardium draining a portion of the right atrium, atria, the Ventricles, and the Coronary arteries.
right ventricle and some of the left ventricle. The
anterior cardiac veins drain a large portion of the
right ventricle and empty into the right atrium. The
coronary sinus and its branches drain most of the
myocardium through the great, middle, and small
cardiac veins and the left vein of Marshall.
The coronary sinus is located in the posterior AV
groove near the crux and collects about 85% of the
blood from the left ventricle. It opens into the right
atrium at the coronary sinus ostium near the orifice of
the inferior vena cava. The coronary sinus is often
catheterized when metabolic studies of the left ventri-
cle are needed. It may be cannulated during car-
diopulmonary bypass to deliver cardioplegia.22 Fig-
ures 3 and 4 show the coronary arteries and veins,

CORONARY BLOOD FLOW

Resting coronary blood flow in humans is about
225 mL/minute. During strenuous exercise, it
increases three to four times that amount to supply
the nutrients needed by the cardiac muscle. Blood
flow through the coronary arteries is determined by
driving pressure (ie, the pressure in the aorta minus
right atrial pressure) and vascular resistance to flow.
Vascular resistance is determined by the compres- Figure 4 Illustration showing the great veins and the
sion exerted on coronary arteries during systole as coronary veins.

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well as the diameters of these vessels. During sys-

tole, the strong compression exerted by the contract-
ing muscle causes coronary arterial blood flow to
fall. During diastole, when the muscle relaxes, blood
flows rapidly in these arteries. Anything that
decreases diastolic time (eg, tachycardia), however,
will decrease coronary perfusion.
The diameter of coronary arteries is autoregulat-
ed by tissue needs. Increased activity results in
increased blood flow. The metabolic hypothesis used
to explain this proposes that a decrease in the ratio of
oxygen supply to oxygen demand releases a
vasodilator substance from the myocardium, which
results in relaxation of coronary v e ~ s e l s . ~Most
3
experts believe that the type of vasodilator released
is adenosine because it has the greatest vasodilator
propensity. Low oxygen concentrations in muscle
cells cause adenosine triphosphate (ATP) to degrade
to adenosine, which results in vasodilation of the
coronary arteries. After vasodilation, the adenosine
is reabsorbed to the cardiac cells and reused. Other
substances considered as possible coronary dilators Figure 5 The electrical conduction system of the
include potassium and hydrogen ions, carbon diox- heart.
ide, bradykinin, and prostaglandin^.^^ Recent
research suggests that factors produced by intact
endothelial cells cause relaxation or contraction of gic and beta-adrenergic receptors exist in the coro-
vascular smooth muscle. These factors are called nary vessels. Stimulation of alpha-receptors pro-
endothelial-derived relaxing factor and endothelial- duces constriction, and stimulation of beta-receptors
derived contracting factor. produces dilation. The epicardial vessels have most-
The coronary arteries also are influenced by the ly alpha-receptors and thds constrict. The intramus-
sympathetic and parasympathetic divisions of the cular arteries have mostly beta-receptors and thus
autonomic nervous system. This influence can be dilate.15
direct or indirect. The direct effect results from the
norepinephrine secreted by the sympathetic system ELECTROPHYSIOLOGY OF THE HEART
and acetylcholine secreted by the parasympathetic The cardiac impulse arises in the sinoatrial (SA)
system. Sympathetic stimulation results in vasocon- node, which is located in the posterior wall of the
striction; parasympathetic stimulation results in right atrium near the entrance of the superior vena
slight vasodilation. cava. It is known as the cardiac pacemaker because it
The indirect effect of the autonomic nervous has the fastest rate of impulse generation (ie, 60 to
system occurs when increased or decreased metabol- 100 bpm). When it is generated, the impulse spreads
ic activity resulting from changes in heart rate takes to three conduction pathways-the anterior inter-
place. For example, sympathetic stimulation increas- nodal tract of Bachnian, the middle internodal tract
es the heart rate and its contractility, resulting in of Wenkebach, and the posterior internodal tract of
increased metabolism and oxygen consumption. Thorel-that carry the impulse to the AV node.26
These metabolic events result in activation of local The AV node is in the right atrium near the
blood flow regulatory mechanisms, which dilate the opening of the coronary sinus. The AV node serves
coronary arteries. The opposite effect (ie, slowing of two very important functions: it delays the cardiac
the heart rate, decreased metabolism and oxygen impulse for .08 to .12 seconds to allow for the “atrial
consumption) occurs with parasympathetic stimula- kick” that aids in the filling of the ventricles, and it
tion, thus the parasympathetic division indirectly controls the number of impulses reaching the ventri-
constricts the coronary vessels. Both alpha-adrener- cles. The AV node prevents impulses of more than

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180 per minute to allow the ventricles time to fill and
to prevent cardiac output from dropping to danger-
ous levels. Damage to the AV node (eg, lack of oxy-
gen) can result in too few impulse transmissions or
complete block.
The cardiac impulse travels from the AV node
to the bundle of His and then divides into the right
and left bundle branches. Each bundle branch termi-
nates in a network of fibers called the Purkinje sys-
tem, which stimulate ventricular contraction. Some
individuals have “bypass” tracts that directly connect
the atria and ventricles and bypass the AV node. An
example of this is Wolff-Parkinson-White syndrome,
which results in premature ventricular excitation.
Figure 5 depicts the normal electrical conduction of
the heart.
Normal electrocardiogram. The electrical
activity of the heart can be seen on an electrocardio-
gram (ECG). The ECG is recorded from a horizontal
baseline called an isoelectric (straight) line. Positive
waves are upright and negative waves are inverted
relative to the baseline. The waves are designated by
the letters P, Q, R, S, T and represent one complete
heartbeat.
The P wave represents atrial depolarization. The
P wave originates in the SA node; however, the
amount of current generated by the node is too small
to be seen on the tracing. The P wave correlates with
Figure 6 A normal electrocardiogram. The yellow area
represents the absolute refractory period of the heart,
and the red area represents the relative refractory peri-
od, which is the vulnerable period of the cardiac cycle
(ie, R on T phenomenon).
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depolarization of atrial muscle cells and measures
less than 0.11 of a second.
The P-R interval is an isoelectric line that
extends from the P wave to the beginning of the
QRS complex. It represents the time necessary for
the cardiac impulse to spread from the atria through
the AV node to the ventricles. Its duration is 0.12 to
0.2 of a second.
The QRS complex represents ventricular depo-
larization. It is measured from the end of the PR seg-
ment to where the QRS complex ends, and measures
0.04 to 0.14 of a second.
The ST segment is normally an isoelectric line
and represents the time between ventricular depolar-
ization and repolarization. It is measured from the
end of the QRS complex to the beginning of the T
wave.
The T wave represents ventricular repolariza-
tion. It varies in amplitude and duration and can be
affected by ionic imbalances, ischemia, and medica-
tions. The T wave represents a vulnerable cardiac
period. If an ectopic beat occurs during this time,
known as R on T phenomenon, cardiac arrest can
result.
The Q-T interval is measured from the begin-
ning of the QRS complex to the end of the T wave. It
usually measures 0.36 to 0.44 of a second. Figure 6
represents a normal ECG.
CARDIAC CYCLE
The cardiac cycle is defined as the period from
the beginning of one heartbeat to the beginning of
the next beat. It includes systole (ie, contraction),
diastole (ie, relaxation), and a short pause called the
diastasis cordis (ie, when both atria and ventricles
relax). The duration of a cardiac cycle depends on
the heart rate. For example, with a heart rate of 75
beats/minute the cardiac cycle is 0.8 seconds (eg, 60
seconds/minute divided by 75 beatslminute = 0.8).
During this 0.8 seconds, the atria are in systole for
0.1 seconds and in diastole 0.7 seconds; the ventri-
cles are in systole 0.3 seconds and in diastole 0.5
seconds. The entire heart rests for about 0.4 seconds.
Figure 7 depicts a cardiac cycle for a heart rate of 75
beats a minute.
In 1915, Wiggers first diagrammed the mechan-
ical events in the cardiac cycle.27Since then, many
physiologists and cardiologists have outlined the
componenis of this cardiac event. Figure 8 shows the
cardiac cycle diagrammed sequentially beginning on
the left with systole and progressing to diastole. It
 APRIL 1998, VOL 67, NO 4
* Gavaghan *
Figure 7 The cardiac cycle for a heart rate of 75
beats per minute. The inner circle (ie, pinklblue area)
represents the atria and the outer circle (ie, white/blue
area) represents the ventricles. Systole is represented
by the blue sections and diastole is seen in the white
and pink sections of the diagram. (Adapted from Basic
Physiology and Anatomy [I9691€ € Caffee and
Greisheimer, with permission from Lippincott Publica-
tions, P ~ i l u d e l ~ ~ i u ~
also shows how venous pressure waves, ECG trac-
ings, and heart sounds relate to the cardiac cycle.**
Ventricular systole. The first section of the dia-
gram in Figure 8 represents ventricular systole,
which is divided into three phases: isometric con-
traction, rapid ejection, and slow ejection.*’
Isometric Contraction phase. This phase repre-
sents the beginning of ventricular contraction. The
resulting increase in pressure within the ventricle
causes the AV valves to close. The beginning of ven-
tricular contraction is seen on an ECG as the R
wave, and closure of the AV valves can be heard as
S, on a phonocardiogram (PCG) or through ausculta-
tion. The isometric contraction phase is also called
the isovolumetric contraction phase because all the
valves are closed and there is no ejection of blood.
The ventricular pressure curve on Figure 8 rises
above the aortic pressure curve. The atrial pressure
curve (broken line) also is rising because the atria are
filling with blood.3O
Rapid ejection phase. When left ventricular
pressure exceeds 80 mm Hg and right ventricular
pressure exceeds 8 mm Hg, the aortic and pulmonic
valves open. Blood pours out of the ventricles into
the aorta. It is called the rapid ejection phase because
70% of the ventricle’s blood is emptied during the
813
AORN JOURNAL
first third of the ejection period. The aortic pressure
curve (ie, the dotted line) rises sharply because of
blood flow into the a0rta.3~
Slow ejection phase. The ventricle’s remaining
30% of blood is emptied during the latter two thirds
of the ejection phase, and is called the slow ejection
phase. Very little blood is ejected toward the end of
systole even though the ventricles remain contracted.
The C wave on the venous pulse curve is caused by
closure of the tricuspid valve and the subsequent
increase in ventricular, atrial, and central venous
pressures.32
As ventricular systole occurs, right atrial pres-
sure drops, producing a decline in the venous pulse
curve on Figure 8. The T wave appears toward the
end of ventricular contraction. It represents repolar-
ization of the ventricles, at which time the ventricu-
lar muscle begins to relax. The electrical activity
demonstrated on the ECG momentarily precedes the
mechanical events3,
Ventricular diastole. Ventricular diastole can be
divided into four phases: isometric interval, rapid
ventricular filling, slow ventricular filling, and atrial
systole.34
Isometric interval phase. The isometric or iso-
volumetric interval is a relaxation phase and is the
beginning of diastole. During diastole, ventricular
pressure is lower than that in the aorta and the pul-
monary artery and results in momentary backflow of
blood. This backflow snaps the semilunar aortic and
pulmonic valves shut. This pressure reversal, back-
flow of blood, and closure of the semilunar valves
produces the second heart sound (S,) as depicted on
the PCG and seen on the incisura (indentation) or
dicrotic notch on the aortic pressure curve. During
this time, the ventricular pressure curve drops close
to 0 mm Hg. The upslope of the V wave on the
venous pressure curve represents increased atrial
pressure before the AV valves open. The peak of the
V wave occurs just before the AV valves open. If a
large V wave is present it may indicate inadequate
closure of the AV valve and regurgitation of blood.35
Rapid ventricular filling phase. When ventricu-
lar pressure falls below atrial pressure, the AV
valves open and blood rushes rapidly from the atria
into the ventricles. This is represented by the down-
ward slope of the V wave on the venous pressure
curve and by the third heart sound (S,) on the PCG.36
Slow ventricular filling phase. The slow ven-
tricular filling phase is also known as diastasis or
the last part of diastole. In this phase, a small
 9Gavaghan -
APRIL 1998, VOL 67, NO 4

.
Figure 8 Representation of the cardiac cycle combining systole, diastole, venous pressure waves, electrocardio-
gram tracing, and heart sounds. (Adapted from Cardiovascular Nursing: Holistic Nursing Practice [I9921C E
Guzzena, B M Dossey, with permission from Mosby-Year Book, Inc, St Louis)

814
AORN JOURNAL
 APRIL 1998, VOL 67, NO 4
* Gavaghun *
amount of blood drains from the lungs and periph-
eral circulation into the atria and is added to the
blood in the ventricles. Toward the end of this
phase, depolarization of the atria begins, as evi-
denced by the P wave on the ECG. After the begin-
ning of the P wave, there is a slight increase in the
atrial c ~ n t r a c t i o n . ~ ~
Atrial systole phase. The atrial contraction or
atrial kick during the last phase of ventricular dias-
tole contributes 25% more blood to the ventricles.
The beginning of atrial contraction correlates with
the peak of the P wave. The A wave of the venous
pulse curve corresponds to atrial contraction just
before closure of the AV valves. The S, heart sound
(abnormal in adults and also known as atrial gallop)
occurs during atrial contraction. It is a low-pitched,
soft, diastolic sound heard close to S, in presystole.
The S, and S, sounds are normal in children and
young adults. In people more than 30 years of age
these sounds are abnormal and maybe heard as gal-
lop sounds or rhythms. In the adult, the S, sound rep-
resents ventricular volume overload, as in congestive
heart failure, and S, may represent the presence of a
stiff v e n t r i ~ l e . ~ ~
CARDIAC VOLUMES
Toward the end of diastole, the blood volume in
the ventricles (ie, end-diastolic volume) is approxi-
mately 120 mL. At the end of systole, blood volume
in the ventricles (ie, end-systolic volume) is approxi-
mately 50 mL. The difference between the end-dias-
tolic volume and the end-systolic volume (approxi-
mately 70 mL) is known as stroke volume (SV) and
is the amount of blood ejected from the ventricles
each time they contract. To determine ejection frac-
tion (EF), stroke volume is divided by end-diastolic
volume (EDV). An SV of 70 divided by an EDV of
120 equals an EF of .58, or about 60%. Alterations
in these volumes reflect cardiac disorders that occur
in low output or high output heart failure. The EF
indicates the pumping efficiency of the ventricle. It
is reduced in patients with myocardial infarction and
is a good indicator of ventricular function.
Cardiac output. Cardiac output (CO) is the
amount of blood in liters that is ejected from the
heart per minute, and is equal to the SV multiplied
by the heart rate. A person with a heart rate of 70
beats/minute and a SV of 70 mL has a CO of 4,900
mL; however, during heavy exercise this may
increase to 35 liters a minute.39
Clinically, CO can be assessed by checking for
816
AORN JOURNAL
the presence and the quality of the of peripheral puls-
es (eg, weak, strong, thready, full); assessing the
location and quality of heart sounds by auscultation;
monitoring and assessing the patient’s blood pres-
sure; and by assessing the patient’s ECG.40
Cardiac index. The cardiac index (CI) is a mea-
surement used by clinicians to adjust for individual
differences in body size. It is the CO in terms of
liters per/minute per square meter (m2) of body sur-
face area. The CI gives a better indication of how
well tissues are perfused than does CO alone because
it addresses the actual size of the body and its blood
supply needs. The normal CI is 2.5 to 4.0 liters/
minute/m2 of body surface. Both CO and CI are
means of assessing the ability of a patient’s heart to
pump effectively.
FACTORS AFFECTING CARDIAC OUTPUT
There are four interrelated factors that govern
cardiac output: preload (ie, ventricular filling), after-
load (ie, resistance to ejection of blood), contractili-
ty, and heart rate.
Preload. Preload refers to the volume of blood
that fills the ventricles during diastole. It is influ-
enced by the total volume of circulating blood. The
greater the venous return to the heart, the more the
myocardial fibers will stretch, to accommodate that
load. According to the Frank-Starling law, the
greater the myocardial fiber stretch the greater will
be the force of contractibn. This mechanism has
been compared to the increased recoil of a rubber
band when stretched. The increase in contractile
force is related to an increase in sarcomere length
(the contractile unit of a striated muscle) that pro-
duces increased cross-bridge formation (a cellular
aid to contraction) that regulates the amount of calci-
um released into the myocyte and thus regulates con-
t r a ~ t i o n . ~In’ conditions of decreased filling (eg,
hypovolemia), there is overlap of the actin-myosin
filaments (amino acid chains that aid in contraction),
and in conditions of excessive filling (eg, congestive
failure), the filaments are pulled too far apart; these
conditions prevent effective contractions.
Clinically, preload can be determined by pul-
monary capillary wedge pressure and pulmonary
artery diastolic pressure. The ventricular function
curves as depicted in Figure 9 show the relationship
between fiber length and the force of contraction.
Increasing ventricular end-diastolic volume
increases the force of contraction and stroke vol-
ume to a point. Eventually, the curve flattens, and
 APRIL 1998, VOL 67, NO 4
Gavaghan
Figure 9 Ventricular function curve showing the
relationship between fiber length and the force of
contraction.
more volume will not help. A shift of the curve up
and to the left indicates improvement in ventricular
function; a shift downward and to the right indi-
cates worsening. Substances that improve ventricu-
lar function include calcium and catecholamines,
which will shift the curve to the left. Factors that
negatively affect the ventricles are hypoxia and its
subsequent acidosis. These conditions will shift the
curve to the right.
Afterloud. Afterload is the amount of tension
the ventricles must develop to eject the blood
through the semilunar valves. In other words, after-
load is the resistance against which the heart must
pump the blood to all parts of the body. Some resis-
tance is always present. Examples of factors causing
higher than normal resistance include the systemic
and pulmonary arterioles, increased blood viscosity,
aortic and pulmonary valve stenosis, and arterial
hypertension.
Many things can affect resistance. According
to La Place’s law, ventricular wall tension is a
function of intraventricular systolic pressure, divid-
ed by ventricular wall thickness, and multiplied by
intraventricular radius.42 For example, an increase
in arterial pressure necessitates increased tension in
ventricular walls to eject the blood, thus raising
resistance. Similarly, an increase in chamber size
(increased radius) necessitates more tension to eject
the blood and raises resistance. These two factors
(pressure and size) are offset by the thickness of
the ventricular wall. The thicker the ventricular
wall is, the less tension is needed to eject the blood
and resistance is lowered.
818
AORN JOURNAL
CARDIAC CONTRACTILITY
Cardiac contractility depends on many factors
including the amount of contractile proteins (ie,
actin, myosin, troponin, tropomyosin) present in car-
diac muscle, the presence of ATP and calcium, sym-
pathetic stimulation, and pharmacologic agents. The
primary factor that detemiines whether a contraction
occurs is the presence of free calcium. Positive
inotropes increase free calcium levels and promote
contractions. Positive inotropes include cate-
cholamines from the sympathetic system and the
adrenal medulla glands, digitalis, thyroid hormone,
and sympathomimetics (eg, caffeine). Agents that
reduce intracellular calcium and inhibit contraction
are called negative inotropes and include calcium
channel blockers, parasympathomimetics, and states
such as hypoxemia and metabolic acidosis.
Heart rate. Heart rate is influenced by many
factors. Exercise increases the heart rate to provide
for extra oxygen and elimination of carbon dioxide.
A person’s physical size affects his or her heart rate.
The larger a person’s size, the slower the heart rate;
for example, infants have higher rates than adults in
part due to size differences. Age affects heart rate,
too; heart rates are higher in young people because
of their increased metabolism. Gender differences
also affect heart rates. Men, in general, have slower
heart rates than women because of size differences.
Hypotension increases heart rate and hyperten-
sion decreases it because of the aortic reflex. This
reflex is a response to changes in blood pressure that
stimulates baroreceptors (pressoreceptors) in the aor-
tic arch and carotid sinuses. These baroreceptors
stimulate the cardioregulatory center in the medulla,
causing a reflex slowing or quickening of the heart.
Hormones, especially epinephrine and thyroxine,
increase heart rate. Increased temperature greatly
increases the heart rate, and decreased temperature
decreases the rate. It is believed that heat causes an
increased permeability of muscles to ions, which
results in acceleration of the excitation process.
The autonomic nervous system influences heart
rate via the sympathetic and parasympathetic
branches. The sympathetic branch supplies all areas
of the heart. The sympathetic branch increases heart
rate (ie, chronotropic effect), induces the heart to
contract more forcefully (ie, inotropic effect), and
increases its speed of conduction (ie, dromotropic
effect). These effects are the result of cate-
cholamines binding to receptor sites on the cardiac
cell membrane and activating channels that allow
 APRIL 1998, VOL 67, NO 4
Gavaghan
the entry of the sodium and calcium necessary for
contraction.
The parasympathetic branch releases acetyl-
choline, which binds to other receptor sites on the
cell membrane. Acetylcholine increases the perme-
ability of the cell membrane to potassium, allowing
it to leak from the cell. This results in hyperpolariza-
tion, which makes it more difficult for the impulse to
reach threshold and inhibits an action potential,
slowing the heart rate. The parasympathetic branch
affects primarily the S h and AV nodes.
REFLEXES THAT AFFECT CARDIAC OUTPUT
The aortic reflex. As previously mentioned,
this reflex is a response to a rise in blood pressure
that stimulates baroreceptors or pressoreceptors in
the aortic arch and carotid sinuses. These barore-
ceptors stimulate the cardioregulatory center in the
medulla, causing a reflex slowing of the heart. If
the blood pressure decreases, the baroreceptors are
less stimulated and there is an increase in heart
rate.43
The Bainbridge reflex. This reflex is triggered
by high venous blood pressure that stimulates
venous pressoreceptors in the venae cavae and right
atrium. This results in stimulation of the cardioaccel-
eratory center in the medulla and depression of the
cardioinhibitory center and results in an increase in
heart rate. An increase in heart rate reduces the time
spent in diastole. This contributes to decreased fill-
ing and decreased stroke volume, which results in
decreased cardiac
The Valsalva maneuver. The Valsalva maneu-
ver consists of forced expiration against a closed
glottis. This maneuver increases intrathoracic pres-
sure, which affects the baroreceptors in the aortic
arch and carotid bodies. Afferent impulses traveling
in the glossopharyngeal nerve (ie, Hemng’s nerve)
from the carotid sinus or from the vagus (via the aor-
tic arch) travel to the vasomotor center in the medul-
la, where they stimulate parasympathetic fibers that
decrease heart rate, blood pressure, and cardiac out-
put. The increased intrathoracic pressure resulting
from the Valsalva maneuver decreases venous return
and cardiac output.45
Oculocardiac reflex. The oculocardiac reflex
occurs when there is traction on orbital structures,
the conjunctiva, or the extraocular muscles; trauma
to the eye; presence of a retrobulbar block (ie, anes-
thesia of multiple cranial nerves); and pressure on
remaining orbital tissue after enucleation. This reflex
820
AORN JOURNAL
produces hypotension, which results in decreased
cardiac
Celiac reflex. The celiac reflex results from trac-
tion on the mesentery or gallbladder or from vagal
stimulation. It results in bradycardia and hypotension,
which leads to decreased cardiac
Diving reflex. The diving reflex occurs during
immersion of the face in water and is a protective
mechanism that guards against asphyxia. It results in
apnea, intense vagal slowing of the heart rate, and
vasoconstriction of all blood vessels except the coro-
nary and cerebral vessels. It occurs in humans when
diving or on application of cold or iced water to the
face. It occurs most often in birds and submerged
vertebrates, enabling them to remain under water for
long periods. Clinically, the diving reflex can be
used to terminate supraventricular paroxysmal tachy-
cardia. The reflex is very potent in the neonate and is
considered a survival mechanism during the birth
process. It is also believed to aid in the survival of
children who are accidentally submerged in cold
water for long periods?* The central hypervolemia
that results from vasoconstriction increases cardiac
output by improving stroke volume through
enhanced preload.49
THE EFFECTS OF MEDICATIONS ON THE HEART
Medications are used to affect the heart in vari-
ous ways. Some of the more common medications
are discussed here. .e
Digitalis. Digitalis increases the force of con-
traction (positive inotropy) by inhibiting the sodi-
um/potassium pump, thus increasing intracellular
sodium. Sodium is then exchanged for calcium,
which results in a buildup of intracellular calcium.
Increased calcium results in more excitation-contrac-
tion coupling and heightened contractility. Digitalis
also prolongs the heart’s refractory period and slows
conduction at the AV node.50
Antiarrhythmics. The effects of these medica-
tions vary depending on the class of medication
used. Class I medications (eg, quinidine) have local
anesthetic properties and will depress the fast-inward
sodium current, reducing the rate of depolarization
and increasing the threshold of excitability by mak-
ing the resting membrane potential more negative.
Conduction velocity is slowed and the refractory
period is prolonged. Class I1 medications, the beta-
adrenergic blockers (eg, propranalol), reduce sympa-
thetic stimulation and depress the slope of sponta-
neous depolarization of slow-response cells. Class
 AI’KIL 1998. VOL 67. SO 1
G u ~ ~ l l ~ ‘l ~ u l l

Ill medications (cg, amiodaronc) prolong the action
potential and the refractory period. Class IV niedica-
tions. calcium channel blockcrs (cg. vcrapamil),
block the slow-inward calcium channcls. They sup-
press firing of the SA node and prolong the effective
rcfractory period in thc AV node.5’
MEeABOUSM OF CARDIAC CELLS
Myocardial cells contain many morc niito-
chondria (ic. sarcosomcs) than d o o t h e r cells.
Myocardial cells arc mostly aerobic and cannot tol-
crate oxygen dcficicncy. T h i s is i n contrast to
skeletal musclc cclls, which can function well aero-
bically o r anaerobically. Energy for cellular life is
dcrived from ATP. Intracellular supplies of ATP
arc so small that, without replenishment, they
would be exhausted in a second.’? Each cell must
manufacture its own supply of ATP almost contin-
uously because ATP docs not cross the cell mem-
brane. Myocardial cells can storc some ATP in the
form of crcatinc phosphatc (CP). The enzyme crea-
tinc kinasc (CK) niakcs this storage possible. When
ATP lcvcls arc low, adenosine diphosphate (ADP)
combines with C P to foim ATP.
If inadequate oxygen is present, anaerobic
metabolism via the Embyden Meyerhoff glycolytic
pathway must be used to generate ATP. This is a
very inefficient method of energy gcncration when
compared to the A T P generatcd acrobically by
oxidative phosphorylation of fatty acids through the
Krcb’s cycle. Seventy percent of the heart’s fuel
source comes from fatty acids. A further disadvan-
tage of the glycolytic pathway is the production of
lactic acid, which has been idcntificd as thc main
cause of pain during a myocardial infarct.
Exercise improves thc ability of the h e a t to use
fatty acids f o r fuel generation. T h i s results in
improved exercise capacity, reduced lactate accumu-
lation. and the ability to work at a higher maximum
aerobic capacity.53
ENDOCRINE FUNCTIONS OF THE I
IH
The heart secrctcs two endocrine hormoncs:
atrial natriuretic pcptidc and brain natriurctic pcp-
tide. Atrial natriurctic pcptidc is synthcsizcd in thc
atrial myocytc and is secreted i n response to atrial
stretch rcsulting from increased blood volume.
This hormone causes the body to excrete sodium
a n d w a t e r a n d o p p o s e s the renin-angiotensin
mechanism. Brain natriurctic pcptidc is produced
in the ventricles and is sccreted into the circulation
through the coronal-y sinus. It exerts several diuret-
ic, natriurctic, and hypotcnsive effects similar to
atrial natriurctic pcptidc.”
SUMMARY
Thc heart is a powerful muscular organ that
pumps more than 3,000 gallons of blood every day
to supply the body‘s cells with the nutrients nceded
for survival. It bcats nonstop every minute of evcry
hour, resting only for a fraction of a second betwccn
cach contraction. When contracting at a rate of 70 to
75 times a minute. it totals more than four billion
contractions in a lifetime.
It is important to maintain a healthy heart. Nurs-
es are in a primary position to help patients maintain
their cardiac health through education and by being
positive role models. Cardiac health can, in most
instances, bc attained by adhering to the recommen-
dations of thc American Heart Association to control
high blood pressure, refrak from tobacco use, be
physically fit, and eat foods low in fat. Striving to
maintain a healthy hcart and addrcssing any unusual
alterations in its activity in a timely manner help pre-
vent the morbidity and mortality that arise if i t
becomes diseased. A
Mary Gavaghan,RN.EdD. is an associate professor in
the department of nursing at Bloomsburg (Pal Universi-
ty. Rloonisburg.

NOTES (Norwalk, Conn: Applcton & I.ange, C Brown. 1994) 226.

I . M H Swartz. ?e.vthook of P t i w
i d Diugriosis: tli.stor:v und E.~-unii-
ntrtion. second ed (Philadelphia: W B
Saunders Co, 1994)223.
2. J R Turner, Cor.dio~~o.sculu~~
Reurtiviry orirl Stress: Patterxs of
Phvsiologii~olResponse (New York:
Plenum Press, 1994)22.
3. L 0 Burrell, Adult Nursing in
Ilo.spitol or id Conim~iniiySettings
1992)34 1. 6. C M Poith. Putlri~p~r~.siolo,s~:
4. J M Black. E M Jacobs, L u c ~ - Coticqits of‘Altc~retlIleulth Srarcs,
i n n m irnd Sorvnson ’ .Y Mrrliccil Sui;qi- fourth ed (Philadelphia: J B 1.ippin-
m l Nirrsirig:A Ps~c~Iiopliq.siolo~ic~uIcott Co. 1994) 404.
Approach, fouith cd (Philadelphia: 7. K L McCancc. S E Huether.
W B Saundcrs Co, 1993) 1094. P t r t l i o i ~ l i ~ s i o l o?he
, ~ ~Biologic,
: 6cr.si.s
5 . T J Nvwak. A Ci Handford. f i n . Di.rc~i.ve in Adirlis und Chilil~-c~n,
Es.seniir11.c of Prrilio~~h~.siolo~~y:
Coil- second ed (St Louis: Mosby-Year
ccpts und Ap/~lic~rrtiorisfi~i.Heulth Book, Inc. 1994) 1033.
Cuw P r~fk.ssionn1.s(Dubuque. Ia: W 8. Swartz, Te.\-ihooX C!f PhJ.vii,~I

82 1
AOKh’ J O U R N A L
 APRIL 1998, VOL 67, NO 1
Gavughun

Diagnosis: History and Examination,
second ed, 224.
9. Porth, Pathophysiology: Con-
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10. A Farb, A P Burke, R Vir-
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the right ventricle (including
acquired tricuspid and pulmonic
valve disease ),” Cardiology Clinics
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the heart,” in Hurst’s The Heart,
eighth ed, R C Schlant, R W
Alexander, eds (New York:
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11. McCance, Huether, Patho-
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12. F A Lee, “Hemodynamics of
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(February 1992) 59-67.
13. J J Naglehout, K L Zaglan-
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14. C E Guzzetta, B M Dossey,
CardiovascularNursing: Holistic
Nursing (St Louis: Mosby-Year
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15. Ibid, 359.
16. A C Guyton, Human Physiolo-
g y and Mechanisms of Disease, fifth
ed (Philadelphia: W B Saunders Co,
1992) 83.
17. Guzzetta, Dossey, Cardiovascu-
lar Nursing: Holistic Nursing, 65,68.
18. Black, Jacobs, Luckman and
Sorensen’s Medical Surgical Nurs-
ing: A Psychophysiological
Approach, fourth ed, 1100.
19. Burrell, Adult Nursing in Hos-
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20. S A Price, L M Wilson, Patho-
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21. McCance, Huether, Patho-
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12. Naglehout, Zaglaniczny, Nurse
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23. R M Beme, M N Levy, Physi-
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24. A C Guyton, Textbook of Med-
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25. Ibid, 239.
26. Guyton, Human Physiology and
Mechanisms ofDisease, fifth ed, 80.
17. Ganong, Review of Medical
Physiology, 498; Schlant, Alexander,
Hurst’s The Heart, eighth ed, 96.
18.L H Opie. “Mechanisms of
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29. Guzzetta, Dossey, Cardiovas-
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65.
30. Ibid.
31. Ibid.
32. Guyton, Textbook of Medical
Physiology, eighth ed, 103.
33. Guzzetta, Dossey, Cardiovas-
cular Nursing: Holistic Nursing, 61,
65.
34. Guyton, Textbook of Medical
Physiology, eighth ed, 101.
35. Guzzetta, Dossey, Cardiovas-
cular Nursing: Holistic Nursing, 66.
36. Ibid, 61.65.
37. Ibid, 61,65-66.
38. Ibid, 65-66.
39. Ibid, 65; Swartz, Textbook of
Physical Diagnosis: History and
Examination, second ed, 230.
40. Nowack, Handford, Essentials
of Pathophysiology: Concepts and
Applicationsfor Health Care Profes-
sionals, 226.
41. S A Sedlock “Nursing care of
the surgical cardiac patient,” in The
Cardiac Patient: A Comprehensive
Approach. Saunders Monographs in
Clinical NursinAL2, ed R G Sander-
son (Philadelphia: W B Saunders Co,
1972) 474.
42. Schlant, Alexander, Hurst’s
The Heart, 527.
43. Price, Wilson, Pathophysiolo-
gy: Clinical Concepts of Disease
Process, 389.
44. Nagelhout, Zaglaniczny,
Nurse Anesthesia, 139, 140.
45. Ibid.
46. Ibid.
47. h i d .
48. Ibid.
49. Porth, Pathophysiology: Con-
cepts of Altered Health States, 416.
SO. D K Moser, “Maximizing ther-
apy in the advanced heart failure
patient,” The Journal of Cardiovascu-
lar Nursing I0 (January 1996) 29-46.
5 1. W.G Clark, D C Brater, A R
Johnson, Goth’s Medical Plzarmacol-
ogy, 13th ed (St Louis: Mosby-Year
Book, Inc, 1992) 423-424.
52. H Taegtmeyer, R Russell,
“Biochemistry of the heart,’’in Cur-
rent Concepts in Cardioiiascular
Physiology, ed 0 B Garfin (San
Diego: Academic Press, 1990) 3.
53. A Margherita, “Effects of exer-
cise and training in cardiovascular
function,” Physical Medicine and
Rehabilitation Clinics of North
America6 (May 1995) 225-241.
54. M Kohno et al, “Brain natriuret-
ic peptide as a marker for hypertensive
left ventricular hypertrophy: Changes
during 1-year antihypertensivetherapy
with angiotensin-convertingenzyme
inhibitor,” American Journal of Medi-
cine 93 (March 1995)257-262; M
Mukoyama et al, “Human brain natri-
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mone,” [letter] Lancet 335 (March 31,
1990) 801-802.

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Professional nurses are invited to submit manuscripts for the
Home Study Program. Manuscripts or queries should be sent to
the Edifoc AORN Journal, 21 70 S Parker Rd, Suite 300, Denver,
CO 80231-571 1. As with all manuscr@fs sent to the Journal,
papers submitted for Home Study Programs should not have
been previously published or submitted simultaneously to any
other publication.

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AORN JOURNAL