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

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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 compliance is decreased, as in congestive heart fail-
the atria. Seventy-five percent of this blood flows ure, structures within the ventricles vibrate, leading
into both ventricles even before an atrial contraction to a third heart sound (SJ. It occurs in early diastole.
occurs. Decremental conduction in the AV node (ie, An S, heart sound may be normal in people less than
conduction in which the impulse decreases progres- 30 years of age.lx A fourth heart sound (S,) may be
sively) causes the impulse to be delayed long enough heard during atrial systole (ie, atrial kick) if hyper-
for the atrial contraction to contribute to ventricular trophy or other damage to the ventricular wall is pre-
filling. The atrial contraction or atrial kick con- sent. It is identified by its close proximity to S I.
tributes the remaining 25% to ventricular filling; Auscultatory areas. The places where valvular
thus, the atria function as primer pumps for the ven- movement can be heard are not the actual anatomic
tricles. The heart can function effectively at rest locations of the valves. Rather, the sounds represent
without this priming action because it can pump 300 the direction of blood flow.LyThe aortic valve sound
to 400 times more blood than is needed by the body. can be heard best at the second intercostal space near
If the atria fail, however, a patient may exhibit signs the right sternal border. The second aortic sound
of heart failure during exercise.16 may be heard at Erb’s point at the third intercostal
Heart sounds. The integrity of the heart valves space, just left of the sternum. The pulmonic sound
can be determined by listening to the sounds they is best heard at the second intercostal space near the
make as they open and close. Two sounds are clearly left sternal border. The tricuspid valve sound is best
heard with each heartbeat. The first sound (S,) is heard at the left lower sternal border, and the mitral
longer and lower in pitch than the second (S,) and valve sound is best heard at the fifth intercostal space
sounds like the word “lubb.” It corresponds closely at the apex of the heart. Figure 2 depicts these aus-
to each carotid pulsation. Deceleration of blood asso- cultation areas on the chest.
ciated with closure of the mitral and tricuspid valves
causes S,. It has two high-frequency sounds-the CORONARY ARTERIAL CIRCULATION
mitral (MI) sound and the tricuspid ( T I ) sound. The coronary arteries (CA) supply the capillar-
Events in the right heart follow those in the left; ies of the myocardium with blood. The left coronary
therefore, the tricuspid valve closes a little later than artery (LCA) and right coronary artery (RCA) arise
does the mitral valve. Consequently, TI follows M,. from the sinuses of Valsalva (ie, outpouchings of the
The split of S, into MI and T I is heard clearly in chil- aortic wall that prevent occlusion of the coronary
dren, however, it is more difficult to hear this split in orifice by the open semilbnar valve) just above the
adults. aortic valve. The LCA has two main branches-the
The second heart sound (S,) is higher pitched left anterior descending (LAD) and the left circum-
and shorter than S, and is due to closure of the aortic flex (LCX) arteries. The coronary arteries course
and pulmonic semilunar valves. It sounds like the around the heart in two grooves-the atrioventricular
word “dup.” The designations A, and P, are used for groove and the interventricular groove. These two
the aortic and pulmonic sounds. The pulmonic sound grooves meet on the posterior aspect of the heart at
is usually louder than the aortic.17 the important landmark known as the crux of the
If the cardiac valves do not close tightly (ie, heart.*” The AV node is located at the crux and is
valvular insufficiency) or are narrowed (ie, stenosis) nourished by either the RCA or the LCA. Right or
turbulence will be heard on auscultation. For exam- left coronary dominance is determined by the artery
ple, in mitral insufficiency, blood leaks back into the that crosses the crux. Fifty percent of people are
left atrium during ventricular contraction. This right coronary artery dominant, 10% to 15% are left
results in a systolic murmur. In mitral stenosis, as the coronary dominant, and 35% to 40% have mixed
atrium pumps blood through a constricted valve, a right and left dominance. Lesions of the RCA pro-
presystolic murmur is heard. In aortic insufficiency, duce AV node disturbances, and lesions of the LCA
blood leaks back into the left ventricle from the aorta can interfere with ventricular pumping. Individuals
during diastole; this results in a diastolic murmur. who are LCA dominant are more likely to die from a
When blood is forced through a stenotic aortic valve, blockage of this coronary artery.
a systolic murmur is heard. Generally, the RCA supplies the right atrium,
The tricuspid and pulmonary valves may be right ventricle, and inferior wall of the left ventricle.
affected by disease similarly. If ventricular wall 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 depolarization of atrial muscle cells and measures
to prevent cardiac output from dropping to danger- less than 0.11 of a second.
ous levels. Damage to the AV node (eg, lack of oxy- The P-R interval is an isoelectric line that
gen) can result in too few impulse transmissions or extends from the P wave to the beginning of the
complete block. QRS complex. It represents the time necessary for
The cardiac impulse travels from the AV node the cardiac impulse to spread from the atria through
to the bundle of His and then divides into the right the AV node to the ventricles. Its duration is 0.12 to
and left bundle branches. Each bundle branch termi- 0.2 of a second.
nates in a network of fibers called the Purkinje sys- The QRS complex represents ventricular depo-
tem, which stimulate ventricular contraction. Some larization. It is measured from the end of the PR seg-
individuals have “bypass” tracts that directly connect ment to where the QRS complex ends, and measures
the atria and ventricles and bypass the AV node. An 0.04 to 0.14 of a second.
example of this is Wolff-Parkinson-White syndrome, The ST segment is normally an isoelectric line
which results in premature ventricular excitation. and represents the time between ventricular depolar-
Figure 5 depicts the normal electrical conduction of ization and repolarization. It is measured from the
the heart. end of the QRS complex to the beginning of the T
Normal electrocardiogram. The electrical wave.
activity of the heart can be seen on an electrocardio- The T wave represents ventricular repolariza-
gram (ECG). The ECG is recorded from a horizontal tion. It varies in amplitude and duration and can be
baseline called an isoelectric (straight) line. Positive affected by ionic imbalances, ischemia, and medica-
waves are upright and negative waves are inverted tions. The T wave represents a vulnerable cardiac
relative to the baseline. The waves are designated by period. If an ectopic beat occurs during this time,
the letters P, Q, R, S, T and represent one complete known as R on T phenomenon, cardiac arrest can
heartbeat. result.
The P wave represents atrial depolarization. The The Q-T interval is measured from the begin-
P wave originates in the SA node; however, the ning of the QRS complex to the end of the T wave. It
amount of current generated by the node is too small usually measures 0.36 to 0.44 of a second. Figure 6
to be seen on the tracing. The P wave correlates with 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-
Figure 6 A normal electrocardiogram. The yellow area ical events in the cardiac cycle.27Since then, many
represents the absolute refractory period of the heart, physiologists and cardiologists have outlined the
and the red area represents the relative refractory peri- componenis of this cardiac event. Figure 8 shows the
od, which is the vulnerable period of the cardiac cycle cardiac cycle diagrammed sequentially beginning on
(ie, R on T phenomenon). the left with systole and progressing to diastole. It

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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
Figure 7 The cardiac cycle for a heart rate of 75 curve on Figure 8. The T wave appears toward the
beats per minute. The inner circle (ie, pinklblue area) end of ventricular contraction. It represents repolar-
represents the atria and the outer circle (ie, white/blue ization of the ventricles, at which time the ventricu-
area) represents the ventricles. Systole is represented lar muscle begins to relax. The electrical activity
by the blue sections and diastole is seen in the white demonstrated on the ECG momentarily precedes the
and pink sections of the diagram. (Adapted from Basic mechanical events3,
Physiology and Anatomy [I9691€ € Caffee and Ventricular diastole. Ventricular diastole can be
Greisheimer, with permission from Lippincott Publica- divided into four phases: isometric interval, rapid
tions, P ~ i l u d e l ~ ~ i u ~ ventricular filling, slow ventricular filling, and atrial
systole.34
Isometric interval phase. The isometric or iso-
also shows how venous pressure waves, ECG trac- volumetric interval is a relaxation phase and is the
ings, and heart sounds relate to the cardiac cycle.** beginning of diastole. During diastole, ventricular
Ventricular systole. The first section of the dia- pressure is lower than that in the aorta and the pul-
gram in Figure 8 represents ventricular systole, monary artery and results in momentary backflow of
which is divided into three phases: isometric con- blood. This backflow snaps the semilunar aortic and
traction, rapid ejection, and slow ejection.*’ pulmonic valves shut. This pressure reversal, back-
Isometric Contraction phase. This phase repre- flow of blood, and closure of the semilunar valves
sents the beginning of ventricular contraction. The produces the second heart sound (S,) as depicted on
resulting increase in pressure within the ventricle the PCG and seen on the incisura (indentation) or
causes the AV valves to close. The beginning of ven- dicrotic notch on the aortic pressure curve. During
tricular contraction is seen on an ECG as the R this time, the ventricular pressure curve drops close
wave, and closure of the AV valves can be heard as to 0 mm Hg. The upslope of the V wave on the
S, on a phonocardiogram (PCG) or through ausculta- venous pressure curve represents increased atrial
tion. The isometric contraction phase is also called pressure before the AV valves open. The peak of the
the isovolumetric contraction phase because all the V wave occurs just before the AV valves open. If a
valves are closed and there is no ejection of blood. large V wave is present it may indicate inadequate
The ventricular pressure curve on Figure 8 rises closure of the AV valve and regurgitation of blood.35
above the aortic pressure curve. The atrial pressure Rapid ventricular filling phase. When ventricu-
curve (broken line) also is rising because the atria are lar pressure falls below atrial pressure, the AV
filling with blood.3O valves open and blood rushes rapidly from the atria
Rapid ejection phase. When left ventricular into the ventricles. This is represented by the down-
pressure exceeds 80 mm Hg and right ventricular ward slope of the V wave on the venous pressure
pressure exceeds 8 mm Hg, the aortic and pulmonic curve and by the third heart sound (S,) on the PCG.36
valves open. Blood pours out of the ventricles into Slow ventricular filling phase. The slow ven-
the aorta. It is called the rapid ejection phase because tricular filling phase is also known as diastasis or
70% of the ventricle’s blood is emptied during the the last part of diastole. In this phase, a small

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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)

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* Gavaghun *

amount of blood drains from the lungs and periph- the presence and the quality of the of peripheral puls-
eral circulation into the atria and is added to the es (eg, weak, strong, thready, full); assessing the
blood in the ventricles. Toward the end of this location and quality of heart sounds by auscultation;
phase, depolarization of the atria begins, as evi- monitoring and assessing the patient’s blood pres-
denced by the P wave on the ECG. After the begin- sure; and by assessing the patient’s ECG.40
ning of the P wave, there is a slight increase in the Cardiac index. The cardiac index (CI) is a mea-
atrial c ~ n t r a c t i o n . ~ ~ surement used by clinicians to adjust for individual
Atrial systole phase. The atrial contraction or differences in body size. It is the CO in terms of
atrial kick during the last phase of ventricular dias- liters per/minute per square meter (m2) of body sur-
tole contributes 25% more blood to the ventricles. face area. The CI gives a better indication of how
The beginning of atrial contraction correlates with well tissues are perfused than does CO alone because
the peak of the P wave. The A wave of the venous it addresses the actual size of the body and its blood
pulse curve corresponds to atrial contraction just supply needs. The normal CI is 2.5 to 4.0 liters/
before closure of the AV valves. The S, heart sound minute/m2 of body surface. Both CO and CI are
(abnormal in adults and also known as atrial gallop) means of assessing the ability of a patient’s heart to
occurs during atrial contraction. It is a low-pitched, pump effectively.
soft, diastolic sound heard close to S, in presystole.
The S, and S, sounds are normal in children and FACTORS AFFECTING CARDIAC OUTPUT
young adults. In people more than 30 years of age There are four interrelated factors that govern
these sounds are abnormal and maybe heard as gal- cardiac output: preload (ie, ventricular filling), after-
lop sounds or rhythms. In the adult, the S, sound rep- load (ie, resistance to ejection of blood), contractili-
resents ventricular volume overload, as in congestive ty, and heart rate.
heart failure, and S, may represent the presence of a Preload. Preload refers to the volume of blood
stiff v e n t r i ~ l e . ~ ~ that fills the ventricles during diastole. It is influ-
enced by the total volume of circulating blood. The
CARDIAC VOLUMES greater the venous return to the heart, the more the
Toward the end of diastole, the blood volume in myocardial fibers will stretch, to accommodate that
the ventricles (ie, end-diastolic volume) is approxi- load. According to the Frank-Starling law, the
mately 120 mL. At the end of systole, blood volume greater the myocardial fiber stretch the greater will
in the ventricles (ie, end-systolic volume) is approxi- be the force of contractibn. This mechanism has
mately 50 mL. The difference between the end-dias- been compared to the increased recoil of a rubber
tolic volume and the end-systolic volume (approxi- band when stretched. The increase in contractile
mately 70 mL) is known as stroke volume (SV) and force is related to an increase in sarcomere length
is the amount of blood ejected from the ventricles (the contractile unit of a striated muscle) that pro-
each time they contract. To determine ejection frac- duces increased cross-bridge formation (a cellular
tion (EF), stroke volume is divided by end-diastolic aid to contraction) that regulates the amount of calci-
volume (EDV). An SV of 70 divided by an EDV of um released into the myocyte and thus regulates con-
120 equals an EF of .58, or about 60%. Alterations t r a ~ t i o n . ~In’ conditions of decreased filling (eg,
in these volumes reflect cardiac disorders that occur hypovolemia), there is overlap of the actin-myosin
in low output or high output heart failure. The EF filaments (amino acid chains that aid in contraction),
indicates the pumping efficiency of the ventricle. It and in conditions of excessive filling (eg, congestive
is reduced in patients with myocardial infarction and failure), the filaments are pulled too far apart; these
is a good indicator of ventricular function. conditions prevent effective contractions.
Cardiac output. Cardiac output (CO) is the Clinically, preload can be determined by pul-
amount of blood in liters that is ejected from the monary capillary wedge pressure and pulmonary
heart per minute, and is equal to the SV multiplied artery diastolic pressure. The ventricular function
by the heart rate. A person with a heart rate of 70 curves as depicted in Figure 9 show the relationship
beats/minute and a SV of 70 mL has a CO of 4,900 between fiber length and the force of contraction.
mL; however, during heavy exercise this may Increasing ventricular end-diastolic volume
increase to 35 liters a minute.39 increases the force of contraction and stroke vol-
Clinically, CO can be assessed by checking for ume to a point. Eventually, the curve flattens, and

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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
Figure 9 Ventricular function curve showing the are called negative inotropes and include calcium
relationship between fiber length and the force of channel blockers, parasympathomimetics, and states
contraction. such as hypoxemia and metabolic acidosis.
Heart rate. Heart rate is influenced by many
more volume will not help. A shift of the curve up factors. Exercise increases the heart rate to provide
and to the left indicates improvement in ventricular for extra oxygen and elimination of carbon dioxide.
function; a shift downward and to the right indi- A person’s physical size affects his or her heart rate.
cates worsening. Substances that improve ventricu- The larger a person’s size, the slower the heart rate;
lar function include calcium and catecholamines, for example, infants have higher rates than adults in
which will shift the curve to the left. Factors that part due to size differences. Age affects heart rate,
negatively affect the ventricles are hypoxia and its too; heart rates are higher in young people because
subsequent acidosis. These conditions will shift the of their increased metabolism. Gender differences
curve to the right. also affect heart rates. Men, in general, have slower
Afterloud. Afterload is the amount of tension heart rates than women because of size differences.
the ventricles must develop to eject the blood Hypotension increases heart rate and hyperten-
through the semilunar valves. In other words, after- sion decreases it because of the aortic reflex. This
load is the resistance against which the heart must reflex is a response to changes in blood pressure that
pump the blood to all parts of the body. Some resis- stimulates baroreceptors (pressoreceptors) in the aor-
tance is always present. Examples of factors causing tic arch and carotid sinuses. These baroreceptors
higher than normal resistance include the systemic stimulate the cardioregulatory center in the medulla,
and pulmonary arterioles, increased blood viscosity, causing a reflex slowing or quickening of the heart.
aortic and pulmonary valve stenosis, and arterial Hormones, especially epinephrine and thyroxine,
hypertension. increase heart rate. Increased temperature greatly
Many things can affect resistance. According increases the heart rate, and decreased temperature
to La Place’s law, ventricular wall tension is a decreases the rate. It is believed that heat causes an
function of intraventricular systolic pressure, divid- increased permeability of muscles to ions, which
ed by ventricular wall thickness, and multiplied by results in acceleration of the excitation process.
intraventricular radius.42 For example, an increase The autonomic nervous system influences heart
in arterial pressure necessitates increased tension in rate via the sympathetic and parasympathetic
ventricular walls to eject the blood, thus raising branches. The sympathetic branch supplies all areas
resistance. Similarly, an increase in chamber size of the heart. The sympathetic branch increases heart
(increased radius) necessitates more tension to eject rate (ie, chronotropic effect), induces the heart to
the blood and raises resistance. These two factors contract more forcefully (ie, inotropic effect), and
(pressure and size) are offset by the thickness of increases its speed of conduction (ie, dromotropic
the ventricular wall. The thicker the ventricular effect). These effects are the result of cate-
wall is, the less tension is needed to eject the blood cholamines binding to receptor sites on the cardiac
and resistance is lowered. cell membrane and activating channels that allow

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the entry of the sodium and calcium necessary for produces hypotension, which results in decreased
contraction. cardiac
The parasympathetic branch releases acetyl- Celiac reflex. The celiac reflex results from trac-
choline, which binds to other receptor sites on the tion on the mesentery or gallbladder or from vagal
cell membrane. Acetylcholine increases the perme- stimulation. It results in bradycardia and hypotension,
ability of the cell membrane to potassium, allowing which leads to decreased cardiac
it to leak from the cell. This results in hyperpolariza- Diving reflex. The diving reflex occurs during
tion, which makes it more difficult for the impulse to immersion of the face in water and is a protective
reach threshold and inhibits an action potential, mechanism that guards against asphyxia. It results in
slowing the heart rate. The parasympathetic branch apnea, intense vagal slowing of the heart rate, and
affects primarily the S h and AV nodes. vasoconstriction of all blood vessels except the coro-
nary and cerebral vessels. It occurs in humans when
REFLEXES THAT AFFECT CARDIAC OUTPUT diving or on application of cold or iced water to the
The aortic reflex. As previously mentioned, face. It occurs most often in birds and submerged
this reflex is a response to a rise in blood pressure vertebrates, enabling them to remain under water for
that stimulates baroreceptors or pressoreceptors in long periods. Clinically, the diving reflex can be
the aortic arch and carotid sinuses. These barore- used to terminate supraventricular paroxysmal tachy-
ceptors stimulate the cardioregulatory center in the cardia. The reflex is very potent in the neonate and is
medulla, causing a reflex slowing of the heart. If considered a survival mechanism during the birth
the blood pressure decreases, the baroreceptors are process. It is also believed to aid in the survival of
less stimulated and there is an increase in heart children who are accidentally submerged in cold
rate.43 water for long periods?* The central hypervolemia
The Bainbridge reflex. This reflex is triggered that results from vasoconstriction increases cardiac
by high venous blood pressure that stimulates output by improving stroke volume through
venous pressoreceptors in the venae cavae and right enhanced preload.49
atrium. This results in stimulation of the cardioaccel-
eratory center in the medulla and depression of the THE EFFECTS OF MEDICATIONS ON THE HEART
cardioinhibitory center and results in an increase in Medications are used to affect the heart in vari-
heart rate. An increase in heart rate reduces the time ous ways. Some of the more common medications
spent in diastole. This contributes to decreased fill- are discussed here. .e

ing and decreased stroke volume, which results in Digitalis. Digitalis increases the force of con-
decreased cardiac traction (positive inotropy) by inhibiting the sodi-
The Valsalva maneuver. The Valsalva maneu- um/potassium pump, thus increasing intracellular
ver consists of forced expiration against a closed sodium. Sodium is then exchanged for calcium,
glottis. This maneuver increases intrathoracic pres- which results in a buildup of intracellular calcium.
sure, which affects the baroreceptors in the aortic Increased calcium results in more excitation-contrac-
arch and carotid bodies. Afferent impulses traveling tion coupling and heightened contractility. Digitalis
in the glossopharyngeal nerve (ie, Hemng’s nerve) also prolongs the heart’s refractory period and slows
from the carotid sinus or from the vagus (via the aor- conduction at the AV node.50
tic arch) travel to the vasomotor center in the medul- Antiarrhythmics. The effects of these medica-
la, where they stimulate parasympathetic fibers that tions vary depending on the class of medication
decrease heart rate, blood pressure, and cardiac out- used. Class I medications (eg, quinidine) have local
put. The increased intrathoracic pressure resulting anesthetic properties and will depress the fast-inward
from the Valsalva maneuver decreases venous return sodium current, reducing the rate of depolarization
and cardiac output.45 and increasing the threshold of excitability by mak-
Oculocardiac reflex. The oculocardiac reflex ing the resting membrane potential more negative.
occurs when there is traction on orbital structures, Conduction velocity is slowed and the refractory
the conjunctiva, or the extraocular muscles; trauma period is prolonged. Class I1 medications, the beta-
to the eye; presence of a retrobulbar block (ie, anes- adrenergic blockers (eg, propranalol), reduce sympa-
thesia of multiple cranial nerves); and pressure on thetic stimulation and depress the slope of sponta-
remaining orbital tissue after enucleation. This reflex neous depolarization of slow-response cells. Class

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G u ~ ~ l l ~ ‘l ~ u l l

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

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


I . M H Swartz. ?e.vthook of P t i w 1992)34 1. 6. C M Poith. Putlri~p~r~.siolo,s~:
i d Diugriosis: tli.stor:v und E.~-unii- 4. J M Black. E M Jacobs, L u c ~ - Coticqits of‘Altc~retlIleulth Srarcs,
ntrtion. second ed (Philadelphia: W B i n n m irnd Sorvnson ’ .Y Mrrliccil Sui;qi- fourth ed (Philadelphia: J B 1.ippin-
Saunders Co, 1994)223. m l Nirrsirig:A Ps~c~Iiopliq.siolo~ic~uIcott Co. 1994) 404.
2. J R Turner, Cor.dio~~o.sculu~~ Approach, fouith cd (Philadelphia: 7. K L McCancc. S E Huether.
Reurtiviry orirl Stress: Patterxs of 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
Phvsiologii~olResponse (New York: 5 . T J Nvwak. A Ci Handford. f i n . Di.rc~i.ve in Adirlis und Chilil~-c~n,
Plenum Press, 1994)22. Es.seniir11.c of Prrilio~~h~.siolo~~y:
Coil- second ed (St Louis: Mosby-Year
3. L 0 Burrell, Adult Nursing in ccpts und Ap/~lic~rrtiorisfi~i.Heulth Book, Inc. 1994) 1033.
Ilo.spitol or id Conim~iniiySettings 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, physiology: The Biologic Basisfor the surgical cardiac patient,” in The
second ed, 224. Disease in Adults and Children, sec- Cardiac Patient: A Comprehensive
9. Porth, Pathophysiology: Con- ond ed, 952. Approach. Saunders Monographs in
cepts qf Altered Health States, 21. 12. Naglehout, Zaglaniczny, Nurse Clinical NursinAL2, ed R G Sander-
10. A Farb, A P Burke, R Vir- Anesthesia, 132. son (Philadelphia: W B Saunders Co,
manl, “Anatomy and pathology of 23. R M Beme, M N Levy, Physi- 1972) 474.
the right ventricle (including ology, third ed (St Louis: Mosby- 42. Schlant, Alexander, Hurst’s
acquired tricuspid and pulmonic YearBook, Inc, 1993) 514. The Heart, 527.
valve disease ),” Cardiology Clinics 24. A C Guyton, Textbook of Med- 43. Price, Wilson, Pathophysiolo-
10 (February 1992) 1-21. B F ical Physiology, eighth ed (Philadel- gy: Clinical Concepts of Disease
Walker, R C Schlant, “Anatomy of phia: W B Saunders Co, 1991) 239. Process, 389.
the heart,” in Hurst’s The Heart, 25. Ibid, 239. 44. Nagelhout, Zaglaniczny,
eighth ed, R C Schlant, R W 26. Guyton, Human Physiology and Nurse Anesthesia, 139, 140.
Alexander, eds (New York: Mechanisms ofDisease, fifth ed, 80. 45. Ibid.
McGraw-Hill, Inc, 1994) 64. 17. Ganong, Review of Medical 46. Ibid.
11. McCance, Huether, Patho- Physiology, 498; Schlant, Alexander, 47. h i d .
physiology: The Biologic Basis,for Hurst’s The Heart, eighth ed, 96. 48. Ibid.
Disease in Adults and Children, sec- 18.L H Opie. “Mechanisms of 49. Porth, Pathophysiology: Con-
ond ed, 950. cardiac contraction and relaxation,” cepts of Altered Health States, 416.
12. F A Lee, “Hemodynamics of in Heart Disease: A Te.rtbook of SO. D K Moser, “Maximizing ther-
the right ventricle in normal and dis- Cardiovascular Medicine, fifth ed, apy in the advanced heart failure
ease states,” Cardiobgy Clinics 10 E Braunwald, ed (Philadelphia: W B patient,” The Journal of Cardiovascu-
(February 1992) 59-67. Saunders Co, 1997) 377. lar Nursing I0 (January 1996) 29-46.
13. J J Naglehout, K L Zaglan- 29. Guzzetta, Dossey, Cardiovas- 5 1. W.G Clark, D C Brater, A R
iczny, Nurse Anesthesia (Philadel- cular Nursing: Holistic Practice, 61, Johnson, Goth’s Medical Plzarmacol-
phia: W B Saunders Co, 1997) 129. 65. ogy, 13th ed (St Louis: Mosby-Year
14. C E Guzzetta, B M Dossey, 30. Ibid. Book, Inc, 1992) 423-424.
CardiovascularNursing: Holistic 31. Ibid. 52. H Taegtmeyer, R Russell,
Nursing (St Louis: Mosby-Year 32. Guyton, Textbook of Medical “Biochemistry of the heart,’’in Cur-
Book, Inc: 1992) 320,359. Physiology, eighth ed, 103. rent Concepts in Cardioiiascular
15. Ibid, 359. 33. Guzzetta, Dossey, Cardiovas- Physiology, ed 0 B Garfin (San
16. A C Guyton, Human Physiolo- cular Nursing: Holistic Nursing, 61, Diego: Academic Press, 1990) 3.
g y and Mechanisms of Disease, fifth 65. 53. A Margherita, “Effects of exer-
ed (Philadelphia: W B Saunders Co, 34. Guyton, Textbook of Medical cise and training in cardiovascular
1992) 83. Physiology, eighth ed, 101. function,” Physical Medicine and
17. Guzzetta, Dossey, Cardiovascu- 35. Guzzetta, Dossey, Cardiovas- Rehabilitation Clinics of North
lar Nursing: Holistic Nursing, 65,68. cular Nursing: Holistic Nursing, 66. America6 (May 1995) 225-241.
18. Black, Jacobs, Luckman and 36. Ibid, 61.65. 54. M Kohno et al, “Brain natriuret-
Sorensen’s Medical Surgical Nurs- 37. Ibid, 61,65-66. ic peptide as a marker for hypertensive
ing: A Psychophysiological 38. Ibid, 65-66. left ventricular hypertrophy: Changes
Approach, fourth ed, 1100. 39. Ibid, 65; Swartz, Textbook of during 1-year antihypertensivetherapy
19. Burrell, Adult Nursing in Hos- Physical Diagnosis: History and with angiotensin-convertingenzyme
pital and Community Settings, 355. Examination, second ed, 230. inhibitor,” American Journal of Medi-
20. S A Price, L M Wilson, Patho- 40. Nowack, Handford, Essentials cine 93 (March 1995)257-262; M
physiology: Clinical Concepts of Dis- of Pathophysiology: Concepts and Mukoyama et al, “Human brain natri-
ease Processes (St Louis: Mosby- Applicationsfor Health Care Profes- uretic peptide: A novel cardiac hor-
Year Book, Inc, 1992) 376. sionals, 226. mone,” [letter] Lancet 335 (March 31,
21. McCance, Huether, Patho- 41. S A Sedlock “Nursing care of 1990) 801-802.

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