Lewis et al: Medical-Surgical Nursing: Assessment and Management of

Clinical Problems, 7
th
edition
Key Points
Chapter 32: Nursing Assessment: Cardiovascular System
ST!CT!"S AN# $!NCT%&NS
The heart is a four-chamered organ that lies in the mediastinal space in the
thora!"
The heart is divided y the septum# forming the right and left atrium and the right
and left ventricle"
$alves separate the chamers of the heart:
o %itral valve separates the left atrium and the left ventricle"
o Aortic valve separates the left ventricle and the aorta"
o Tricuspid valve separates the right atrium and the right ventricle"
o Pulmonic valve separates the right ventricle and the pulmonary artery"
The heart is:
o Composed of three layers: endocardium# myocardium# and epicardium"
o Surrounded y a firoserous sac called the pericardium"
The right side of the heart receives lood from the ody &via the vena cava' and
pumps it to the lungs (here it is o!ygenated" )lood returns to the left side of the
heart &via the pulmonary arteries' and is pumped to the ody via the aorta"
The coronary circulation provides lood to the myocardium" The right and left
coronary arteries are the first ranches of the aorta"
The conduction system consists of speciali*ed cells that create and transport
electrical impulses" These electrical impulses initiate depolari*ation &contraction'
of the myocardium and ultimately a cardiac contraction"
+ach electrical impulse starts at the SA node &located in the right atrium'# travels
to the A$ node &located at the atrioventricular ,unction'# through the undle of
-is# do(n the right and left undle ranches &located in the ventricular septum'#
terminating in the Pur.in,e fiers"
The electrical activity of the heart is recorded on the electrocardiogram &+C/'"
S'stole, contraction of the myocardium# results in e,ection of lood from the
ventricles" 0ela!ation of the myocardium# or diastole, allo(s for filling of the
ventricles"
Cardiac out(ut &C1' is the amount of lood pumped y each ventricle in 2
minute" 3t is calculated y multiplying the amount of lood e,ected from the
ventricle (ith each hearteat# the stro.e volume &S$'# y the heart rate &-0' per
minute: C1 4 S$ -0"
5actors affecting S$ are preload# afterload# and contractility" Preload is the
volume of lood in the ventricles at the end of diastole# and afterload represents
the peripheral resistance against (hich the left ventricle must pump"
Cardiac reser)e refers to the heart6s aility to alter the C1 in response to an
increase in demand &e"g"# e!ercise# hypovolemia'"
Stimulation of the sympathetic nervous system increases -0# speed of conduction
through the A$ node# and force of atrial and ventricular contractions# (hereas
stimulation of the parasympathetic nervous system decreases -0"
)aroreceptors# located in the aortic arch and carotid sinus# respond to stretch or
pressure (ithin the arterial system" Stimulation of these receptors results in
temporary inhiition of the sympathetic nervous system and an increase in
parasympathetic influence"

Chemoreceptors# located in the aortic arch and carotid ody# can initiate changes
in -0 and arterial pressure in response to decreased arterial 12 pressure# increased
arterial C12 pressure# and decreased plasma p-"
Arterial blood (ressure &)P' measures the pressure e!erted y lood against the
(alls of the arterial system"
The s'stolic blood (ressure &S)P' is the pea. pressure e!erted against the
arteries (hen the heart contracts" The diastolic blood (ressure &7)P' is the
residual pressure of the arterial system during ventricular rela!ation &or filling'"
Normal lood pressure is systolic )P less than 228 mm -g and diastolic )P less
than 98 mm -g"
The t(o main factors influencing )P are cardiac output &C1' and systemic
vascular resistance &S$0'# (hich is the force opposing the movement of lood"
)P can e measured y invasive &catheter inserted in an artery' and noninvasive
techni:ues &using a sphygmomanometer and a stethoscope'"
Pulse (ressure is the difference et(een the S)P and 7)P and it is normally
aout one third of the S)P"
Mean arterial (ressure *MAP+ is the perfusion pressure felt y organs in the
ody# and a %AP of greater than ;8 is necessary to sustain the vital organs of an
average person under most conditions"
ASS"SSM"NT
,ealth ,istor'
<hen conducting a health assessment of the cardiovascular system# a thorough history
should include the follo(ing:
Any past history of chest pain# shortness of reath# alcoholism and=or toacco use#
anemia# rheumatic fever# streptococcal sore throat# congenital heart disease#
stro.e# syncope# hypertension# thromophleitis# intermittent claudication#
varicosities# and edema
Current and past use of medications
3nformation aout specific treatments# past surgeries# or hospital admissions
related to cardiovascular prolems
3nformation aout cardiovascular ris. factors &i"e"# elevated serum lipids#
hypertension'
5amily history (ith cardiovascular illnesses of lood relatives
The patient6s current (eight and (eight history
A typical day6s diet
Prolems (ith urinary &e"g"# nocturia' or o(el elimination &e"g"# constipation'
The types of e!ercise performed and the occurrence of any un(anted effects
3dentification of paro!ysmal nocturnal dyspnea# sleep apnea# and the numer of
pillo(s needed for comfort
3nformation aout the patient6s gender# race# and age
Any prolems in se!ual performance
3nformation aout stressful situations should e e!plored &e"g"# marital
relationships'
3nformation aout a patient6s values and eliefs
Ph'sical "-amination
<hen conducting a health assessment of the cardiovascular system# a thorough physical
e!amination should include the follo(ing:
/eneral appearance# vital signs# including orthostatic &postural' )Ps and -0s
3nspection of the s.in# e!tremities# and the large veins of the nec.
)ilateral and simultaneous palpation of the upper and lo(er e!tremities
)ilateral and simultaneous palpation of the pulses in the e!tremities

Capillary refill
Auscultation of carotid arteries# adominal aorta# and femoral arteries
3nspection and palpation of the thora!# epigastric area# and mitral valve area
Auscultation of the heart (ith the ell and diaphragm of the stethoscope
Auscultation for e!tra heart sounds &S3 or S>' (ith the ell of the stethoscope
#%A.N&ST%C ST!#%"S
The most common procedures used to diagnose cardiovascular disease include the
follo(ing:
)lood studies
o Creatine .inase &CK'-%): levels increase (ith myocardial infarction &%3'
o Cardiac-specific troponin: levels rise (ith myocardial in,ury
o %yogloin: sensitive indicator of early myocardial in,ury
o Serum lipoproteins: including triglycerides# cholesterol# and phospholipids
o C-reactive protein &C0P': emerging as an independent ris. factor for CA7
and a predictor of cardiac events
o -omocysteine &-cy': elevated levels have een lin.ed to an increased ris.
of a first cardiac event and should e measured in patients (ith a familial
predisposition for early cardiovascular disease
o Cardiac natriuretic peptide mar.ers: emerged as the mar.er of choice for
distinguishing a cardiac or respiratory cause of dyspnea
Chest !-ray
+lectrocardiogram
o 7eviations from the normal sinus rhythm can indicate anormalities in
heart function"
o Continuous amulatory +C/ &-olter monitoring': recorder is (orn for 2>
to >9 hours# and the resulting +C/ information is then stored until it is
played ac. for printing and evaluation"
o Transtelephonic event recorders: portale monitor uses electrodes to
transmit a limited +C/ over the phone to a receiving device"
+!ercise or stress testing
o ?sed to evaluate the cardiovascular response to physical stress
;-%inute (al. test
o ?sed for patients (ith heart or peripheral arterial disease to measure
response to medical interventions and determine functional capacity for
daily physical activities
+chocardiogram
o ?ses ultrasound (aves to record the movement of the structures of the
heart"
o Provides information aout &2' valvular structure and motion# &2' cardiac
chamer si*e and contents# &3' ventricular muscle and septal motion and
thic.ness# &>' pericardial sac# &@' ascending aorta# and &;' e/ection
fraction &+5' &percentage of end-diastolic lood volume that is e,ected
during systole'"
Nuclear cardiology
o %ultigated ac:uisition &%?/A' or cardiac lood pool scan
Provides information on (all motion during systole and diastole#
cardiac valves# and +5"
o Single-photon emission computed tomography &SP+CT'
?sed to evaluate the myocardium at ris. of infarction and to
determine infarction si*e"
o Positron emission tomography &P+T' scanning
?ses t(o isotopes to distinguish viale and nonviale myocardial
tissue"
o Perfusion imaging (ith e!ercise testing
7etermines (hether the coronary lood flo( changes (ith
increased activity"
?sed to diagnose CA7# determine the prognosis in already
diagnosed CA7# assess the physiologic significance of a .no(n
coronary lesion# and assess the effectiveness of various therapeutic
modalities such as coronary artery ypass surgery# percutaneous
coronary intervention# or thromolytic therapy"
o %agnetic resonance imaging &%03'
Allo(s detection and locali*ation of areas of %3 in a 3-7 vie(" 3t
is sensitive enough to detect small %3s not apparent (ith SP+CT
imaging and can assist in the final diagnosis of %3"
o %agnetic resonance angiography &%0A'
?sed for imaging vascular occlusive disease and adominal aortic
aneurysms"
Computed tomography &CT' (ith spiral technology
o A noninvasive scan used to :uantify calcium deposits in coronary arteries"
+lectron eam computed tomography &+)CT'# also .no(n as ultrafast CT#
uses a scanning electron eam to :uantify the calcification in the coronary
arteries and the heart valves"
Cardiac catheteri*ation and coronary angiography
o Contrast media &introduced via a catheter inserted in a large peripheral
artery' and fluoroscopy are used to otain information aout the coronary
arteries# heart chamers and valves# ventricular function# intracardiac
pressures# 12 levels in various parts of the heart# C1# and +5"
3ntracoronary ultrasound &3C?S' or intravascular ultrasound &3$?S'
o Performed during coronary angiography" 1tains 2-7 or 3-7 ultrasound
images to provide a cross-sectional vie( of the arterial (alls of the
coronary arteries"
+lectrophysiology study &+PS'
o Studies and manipulates the electrical activity of the heart using electrodes
placed inside the cardiac chamers" Provides information on SA node
function# A$ node conduction# ventricular conduction# and source
treatment dysrhythmias"
7uple! imaging
o ?ses contrast media# in,ected into arteries or veins &arteriography and
venography' to diagnose occlusive disease in the peripheral lood vessels
and thromophleitis"
-emodynamic monitoring
?ses intraarterial and pulmonary artery catheters to monitor arterial )P# intracardiac
pressures# C1# and central venous pressure &C$P
Lewis et al: Medical-Surgical Nursing: Assessment and Management of
Clinical Problems, 7
th
edition
Key Points
Chapter 33: Nursing %anagement: -ypertension
,'(ertension, or high blood (ressure &)P'# is defined as a persistent systolic
lood pressure &S)P' greater than or e:ual to 2>8 mm -g# diastolic lood
pressure &7)P' greater than or e:ual to A8 mm -g# or current use of
antihypertensive medication" There is a direct relationship et(een hypertension
and cardiovascular disease &C$7'"
Contriuting factors to the development of hypertension include cardiovascular
ris. factors comined (ith socioeconomic conditions and ethnic differences"
-ypertension is generally an asymptomatic condition" 3ndividuals (ho remain
undiagnosed and untreated for hypertension present the greatest challenge and
opportunity for health care providers"
".!LAT%&N &$ 0L&&# P"SS!"
)P is the force e!erted y the lood against the (alls of the lood vessel" 3t must
e ade:uate to maintain tissue perfusion during activity and rest"
0egulation of )P involves nervous# cardiovascular# endothelial# renal# and
endocrine functions"
o Sympathetic nervous system &SNS' activation increases heart rate &-0'
and cardiac contractility# produces (idespread vasoconstriction in the
peripheral arterioles# and promotes the release of renin from the .idneys"
o )aroreceptors# located in the carotid artery and the arch of the aorta# sense
changes in )P" <hen )P is increased# these receptors send inhiitory
impulses to the sympathetic vasomotor center in the rainstem resulting in
decreased -0# decreased force of contraction# and vasodilation in
peripheral arterioles"
o A decrease in )P leads to activation of the SNS resulting in constriction of
the peripheral arterioles# increased -0# and increased contractility of the
heart"
o 3n the presence of long-standing hypertension# the aroreceptors ecome
ad,usted to elevated levels of )P and recogni*e this level as Bnormal"C
o Norepinephrine &N+'# released from SNS nerve endings# activates
receptors located in the sinoatrial node# myocardium# and vascular smooth
muscle"
o $ascular endothelium produces vasoactive sustances and gro(th factors"
Nitric o!ide# an endothelium-derived rela!ing factor &+705'#
helps maintain lo( arterial tone at rest# inhiits gro(th of the
smooth muscle layer# and inhiits platelet aggregation"
+ndothelin &+T'# produced y the endothelial cells# is an e!tremely
potent vasoconstrictor"
o Kidneys contriute to )P regulation y controlling sodium e!cretion and
e!tracellular fluid &+C5' volume"
Sodium retention results in (ater retention# (hich causes an
increased +C5 volume" This increases the venous return to the
heart# increasing the stro.e volume# (hich elevates the )P through
an increase in C1"
o +ndocrine system:
The adrenal medulla releases epinephrine in response to SNS
stimulation" +pinephrine activates 2-adrenergic receptors causing
vasodilation" 3n peripheral arterioles (ith only 2-adrenergic
receptors &s.in and .idneys'# epinephrine causes vasoconstriction"
The adrenal corte! is stimulated y A-33 to release aldosterone"
Aldosterone stimulates the .idneys to retain sodium and (ater"
This increases )P y increasing C1"
A7- is released from the posterior pituitary gland in response to
an increased lood sodium and osmolarity level" A7- increases
the +C5 volume y promoting the reasorption of (ater in the
distal and collecting tuules of the .idneys resulting in an increase
in lood volume and )P"
CLASS%$%CAT%&N &$ ,1P"T"NS%&N
-ypertension is classified as follo(s:
o Preh'(ertension: )P 228 to 23A = 98 to 9A mm -g
o -ypertension# Stage 2: )P 2>8 to 2@A = A8 to AA mm -g
o -ypertension# Stage 2: systolic )P greater than or e:ual to 2;8 or diastolic
)P greater than or e:ual to 288 mm -g"
Sutypes of hypertension:
o 3solated systolic hypertension &3S-': average S)P greater than or e:ual to
2>8 mm -g coupled (ith an average 7)P less than A8 mm -g" 3S- is
more common in older adults" Control of 3S- decreases the incidence of
stro.e# heart failure# cardiovascular mortality# and total mortality"
o Pseudohypertension &false hypertension' occurs (ith advanced
arteriosclerosis" Pseudohypertension is suspected if arteries feel rigid or
(hen fe( retinal or cardiac signs are found relative to the pressures
otained y cuff"
"T%&L&.1 &$ ,1P"T"NS%&N
Primar' *essential or idio(athic+ h'(ertension: elevated )P (ithout an
identified causeD accounts for A8E to A@E of all cases of hypertension"

Secondar' h'(ertension: elevated )P (ith a specific causeD accounts for @E to
28E of hypertension in adults"
PAT,&P,1S%&L&.1 &$ P%MA1 ,1P"T"NS%&N
The hemodynamic hallmar. of hypertension is persistently increased S$0"
<ater and sodium retention:
o A high-sodium inta.e may activate a numer of pressor mechanisms and
cause (ater retention"
Altered renin-angiotensin mechanism:
o -igh plasma renin activity &P0A' results in the increased conversion of
angiotensinogen to angiotensin 3 causing arteriolar constriction# vascular
hypertrophy# and aldosterone secretion"
Stress and increased SNS activity:
o Arterial pressure is influenced y factors such as anger# fear# and pain"
o Physiologic responses to stress# (hich are normally protective# may persist
to a pathologic degree# resulting in prolonged increase in SNS activity"
o 3ncreased SNS stimulation produces increased vasoconstriction# increased
-0# and increased renin release"
3nsulin resistance and hyperinsulinemia:
o Anormalities of glucose# insulin# and lipoprotein metaolism are
common in primary hypertension"
o -igh insulin concentration in the lood stimulates SNS activity and
impairs nitric o!ideFmediated vasodilation"
o Additional pressor effects of insulin include vascular hypertrophy and
increased renal sodium reasorption"
+ndothelial cell dysfunction:
o Some hypertensive people have a reduced vasodilator response to nitric
o!ide"
o +ndothelin produces pronounced and prolonged vasoconstriction"
CL%N%CAL MAN%$"STAT%&NS &$ ,1P"T"NS%&N
1ften called the Bsilent .illerC ecause it is fre:uently asymptomatic until it
ecomes severe and target organ disease occurs"
Target organ diseases occur in the heart &hypertensive heart disease'# rain
&cererovascular disease'# peripheral vasculature &peripheral vascular disease'#
.idney &nephrosclerosis'# and eyes &retinal damage'"
-ypertension is a ma,or ris. factor for coronary artery disease &CA7'"
Sustained high )P increases the cardiac (or.load and produces left ventricular
hypertrophy &G$-'" Progressive G$-# especially in association (ith CA7# is
associated (ith the development of heart failure"
-ypertension is a ma,or ris. factor for cereral atherosclerosis and stro.e"
-ypertension speeds up the process of atherosclerosis in the peripheral lood
vessels# leading to the development of peripheral vascular disease# aortic
aneurysm# and aortic dissection"
3ntermittent claudication &ischemic muscle pain precipitated y activity and
relieved (ith rest' is a classic symptom of peripheral vascular disease involving
the arteries"
-ypertension is one of the leading causes of end-stage renal disease# especially
among African Americans" The earliest manifestation of renal dysfunction is
usually nocturia"
The retina provides important information aout the severity and duration of
hypertension" 7amage to retinal vessels provides an indication of concurrent
vessel damage in the heart# rain# and .idney" %anifestations of severe retinal
damage include lurring of vision# retinal hemorrhage# and loss of vision"
#%A.N&ST%C ST!#%"S
)asic laoratory studies are performed to &2' identify or rule out causes of
secondary hypertension# &2' evaluate target organ disease# &3' determine overall
cardiovascular ris.# or &>' estalish aseline levels efore initiating therapy"
0outine urinalysis# )?N# serum creatinine# and creatinine clearance levels are
used to screen for renal involvement and to provide aseline information aout
.idney function"
%easurement of serum electrolytes# especially potassium levels# is done to detect
hyperaldosteronism# a cause of secondary hypertension"
)lood glucose levels assist in the diagnosis of diaetes mellitus"
Gipid profile provides information aout additional ris. factors that predispose to
atherosclerosis and cardiovascular disease"
?ric acid levels are determined to estalish a aseline# ecause the levels often
rise (ith diuretic therapy"
+C/ and echocardiography provide information aout the cardiac status"
Amulatory lood pressure monitoring &A)P%' is a noninvasive# fully automated
system that measures )P at preset intervals over a 2>-hour period"
o Some patients (ith hypertension do not sho( a normal# nocturnal dip in
)P and are referred to as Bnondippers"C
o The asence of diurnal variaility has een associated (ith more target
organ damage and an increased ris. for cardiovascular events" The
presence or asence of diurnal variaility can e determined y A)P%"
N!S%N. AN# C&LLA0&AT%2" MANA."M"NT
Treatment goals are to lo(er )P to less than 2>8 mm -g systolic and less than A8
mm -g diastolic for most persons (ith hypertension &less than 238 mm -g
systolic and less than 98 mm -g diastolic for those (ith diaetes mellitus and
chronic .idney disease'"
Gifestyle modifications are indicated for all patients (ith prehypertension and
hypertension and include the follo(ing:
o <eight reduction" A (eight loss of 28 .g &22 l' may decrease S)P y
appro!imately @ to 28 mm -g"
o 7ietary Approaches to Stop -ypertension &7AS-' eating plan" 3nvolves
eating several servings of fish each (ee.# eating plenty of fruits and
vegetales# increasing fier inta.e# and drin.ing a lot of (ater" The 7AS-
diet significantly lo(ers )P"
o 0estriction of dietary sodium to less than ; g of salt &NaCl' or less than 2">
g of sodium per day"
o This involves avoiding foods .no(n to e high in sodium &e"g"# canned
soups' and not adding salt in the preparation of foods or at meals"
o There is evidence that greater levels of dietary potassium# calcium#
vitamin 7# and omega-3 fatty acids are associated (ith lo(er )P in those
(ith hypertension"
o 0estriction of alcohol to no more than t(o drin.s per day for men and no
more than one drin. per day for (omen
o 0egular aeroic physical activity &e"g"# ris. (al.ing' at least 38 minutes a
day most days of the (ee." %oderately intense activity such as ris.
(al.ing# ,ogging# and s(imming can lo(er )P# promote rela!ation# and
decrease or control ody (eight"
o 3t is strongly recommended that toacco use e avoided"
o Stress can raise )P on a short-term asis and has een implicated in the
development of hypertension" 0ela!ation therapy# guided imagery# and
iofeedac. may e useful in helping patients manage stress# thus
decreasing )P"
#rug Thera('
7rug therapy is not recommended for those persons (ith prehypertension unless
it is re:uired y another condition# such as diaetes mellitus or chronic .idney
disease"
The overall goals for the patient (ith hypertension include &2' achievement and
maintenance of the goal )PD &2' acceptance and implementation of the therapeutic
planD &3' minimal or no unpleasant side effects of therapyD and &>' aility to
manage and cope (ith illness"
7rugs currently availale for treating hypertension (or. y &2' decreasing the
volume of circulating lood# and=or &2' reducing S$0"
o 7iuretics promote sodium and (ater e!cretion# reduce plasma volume#
decrease sodium in the arteriolar (alls# and reduce the vascular response
to catecholamines"
o Adrenergic-inhiiting agents act y diminishing the SNS effects that
increase )P" Adrenergic inhiitors include drugs that act centrally on the
vasomotor center and peripherally to inhiit norepinephrine release or to
loc. the adrenergic receptors on lood vessels"
o 7irect vasodilators decrease the )P y rela!ing vascular smooth muscle
and reducing S$0"
o Calcium channel loc.ers increase sodium e!cretion and cause arteriolar
vasodilation y preventing the movement of e!tracellular calcium into
cells"
o Angiotensin-converting en*yme &AC+' inhiitors prevent the conversion
of angiotensin 3 to angiotensin 33 and reduce angiotensin 33 &A-33'F
mediated vasoconstriction and sodium and (ater retention"
o A-33 receptor loc.ers &A0)s' prevent angiotensin 33 from inding to its
receptors in the (alls of the lood vessels"
o Thia*ide-type diuretics are used as initial therapy for most patients (ith
hypertension# either alone or in comination (ith one of the other classes"
o <hen )P is more than 28=28 mm -g aove S)P and 7)P goals# a second
drug should e considered" %ost patients (ho are hypertensive (ill
re:uire t(o or more antihypertensive medications to achieve their )P
goals"
o Side effects and adverse effects of antihypertensive drugs may e so
severe or undesirale that the patient does not comply (ith therapy"
-yperuricemia# hyperglycemia# and hypo.alemia are common side
effects (ith oth thia*ide and loop diuretics"
AC+ inhiitors lead to high levels of rady.inin# (hich can cause
coughing" An individual (ho develops a cough (ith the use of
AC+ inhiitors may e s(itched to an A0)"
-yper.alemia can e a serious side effect of the potassium-sparing
diuretics and AC+ inhiitors"
Se!ual dysfunction may occur (ith some of the diuretics"
1rthostatic hypotension and se!ual dysfunction are t(o
undesirale effects of adrenergic-inhiiting agents"
Tachycardia and orthostatic hypotension are potential adverse
effects of oth vasodilators and angiotensin inhiitors"
Patient and family teaching related to drug therapy is needed to
identify and minimi*e side effects and to cope (ith therapeutic
effects" Side effects may e an initial response to a drug and may
decrease (ith continued use of the drug"
0esistant hypertension is the failure to reach goal )P in patients (ho are adhering
to full doses of an appropriate three-drug therapy regimen that includes a diuretic"
0lood Pressure Monitoring
The ma,ority of cases of hypertension are identified through routine screening
procedures such as insurance# preemployment# and military physical
e!aminations"
The auscultatory method of )P measurement is recommended" 3nitially# the )P is
ta.en at least t(ice# at least 2 minute apart# (ith the average pressure recorded as
the value for that visit" Si*e and placement of )P cuff are important for accurate
measurement" The forearm is supported at heart level and Korot.off sounds are
auscultated over the radial artery"
)P measurements of oth arms should e performed initially to detect any
differences et(een arms" The arm (ith the higher reading should e used for all
suse:uent )P measurements"
1rthostatic &or postural' changes in )P and pulse should e measured in older
adults# in people ta.ing antihypertensive drugs# and in patients (ho report
symptoms consistent (ith reduced )P upon standing &e"g"# light-headedness#
di**iness# syncope'"
&rthostatic h'(otension is defined as a decrease of 28 mm -g or more in S)P# a
decrease of 28 mm -g or more in 7)P# and=or an increase of 28 eats=minute or
more in pulse from supine to standing"
)P monitoring should focus on controlling )P in the person already identified as
having hypertensionD identifying and controlling )P in at-ris. groups such as
African Americans# oese people# and lood relatives of people (ith
hypertensionD and screening those (ith limited access to the health care system"
N!S%N. MANA."M"NT
The primary nursing responsiilities for long-term management of hypertension
are to assist the patient in reducing )P and complying (ith the treatment plan"
Nursing actions include patient and family teaching# detection and reporting of
adverse treatment effects# compliance assessment and enhancement# and
evaluation of therapeutic effectiveness"
Patient and family teaching includes the follo(ing: &2' nutritional therapy# &2'
drug therapy# &3' physical activity# &>' home monitoring of )P &if appropriate'#
and &@' toacco cessation &if applicale'"
o -ome monitoring of )P should include daily )P readings (hen treatment
is initiated or medications are ad,usted and (ee.ly once the )P has
staili*ed" A log of the )P measurements should e maintained y the
patient" 7evices that have memory or printouts of the readings are
recommended to facilitate accurate reporting"
o A ma,or prolem in the long-term management of the patient (ith
hypertension is poor compliance (ith the prescried treatment plan" The
reasons include inade:uate patient teaching# unpleasant side effects of
drugs# return of )P to normal range (hile on medication# lac. of
motivation# high cost of drugs# lac. of insurance# and lac. of a trusting
relationship et(een the patient and the health care provider"
."&NT&L&.%C C&NS%#"AT%&NS
The prevalence of hypertension increases (ith age" The lifetime ris. of
developing hypertension is appro!imately A8E for middle-aged &age @@ to ;@'
and older &age H;@' normotensive men and (omen"
A numer of age-related physical changes contriute to the pathophysiology of
hypertension in the older adult"
3n some older people# there is a (ide gap et(een the first Korot.off sound and
suse:uent eats &auscultatory gap'" 5ailure to inflate the cuff high enough may
result in underestimating the S)P"
1lder adults are sensitive to )P changes" 0educing S)P to less than 228 mm -g
in a person (ith long-standing hypertension could lead to inade:uate cereral
lood flo("
1lder adults produce less renin and are more resistant to the effects of AC+
inhiitors and angiotensin 33 receptor loc.ers"
1rthostatic hypotension occurs often in older adults ecause of impaired
aroreceptor refle! mechanisms"
1rthostatic hypotension in older adults is often associated (ith volume depletion
or chronic disease states# such as decreased renal and hepatic function or
electrolyte imalance"
To reduce the li.elihood of orthostatic hypotension# antihypertensive drugs should
e started at lo( doses and increased cautiously"
,1P"T"NS%2" C%S%S
,'(ertensi)e crisis is a severe and arupt elevation in )P# aritrarily defined as a
7)P more than 2>8 mm -g"
o -ypertensive crisis occurs most often in patients (ith a history of
hypertension (ho have failed to comply (ith their prescried medications
or (ho have een undermedicated"
o -ypertensive crisis related to cocaine or crac. use is ecoming a more
fre:uent prolem" 1ther drugs such as amphetamines# phencyclidine
&PCP'# and lysergic acid diethylamide &GS7' may also precipitate
hypertensive crisis that may e complicated y drug-induced sei*ures#
stro.e# %3# or encephalopathy"
-ypertensive emergency develops over hours to days and is defined as )P that is
severely elevated &more than 298=228 mm -g' (ith evidence of acute target organ
damage"
o -ypertensive emergencies can precipitate encephalopathy# intracranial or
suarachnoid hemorrhage# acute left ventricular failure (ith pulmonary
edema# %3# renal failure# dissecting aortic aneurysm# and retinopathy"
o -ypertensive emergencies re:uire hospitali*ation# intravenous &3$'
administration of antihypertensive drugs# and intensive care monitoring"
Antihypertensive drugs include vasodilators# adrenergic inhiitors# and the AC+
inhiitor enalaprilat" Sodium nitroprusside is the most effective 3$ drug for the
treatment of hypertensive emergencies"
%ean arterial pressure &%AP' is generally used instead of systolic and diastolic
readings to guide therapy" %AP is calculated as follo(s: %AP 4 &S)P I 2 7)P'
3"
The use of an intraarterial line or an automated# noninvasive )P machine to
monitor the %AP and )P is re:uired" The rate of drug administration is titrated
according to the level of %AP or )P"
The initial treatment goal is to decrease %AP y no more than 2@E (ithin
minutes to 2 hour" 3f the patient is stale# the target goal for )P is 2;8=288 to 228
mm -g over the ne!t 2 to ; hours"
Go(ering )P e!cessively may decrease cereral# coronary# or renal perfusion and
could precipitate a stro.e# acute %3# or renal failure"
Additional gradual reductions to(ard a normal )P should e implemented over
the ne!t 2> to >9 hours if the patient is clinically stale"
0egular# ongoing assessment &e"g"# +C/ monitoring# vital signs# urinary output#
level of consciousness# visual changes' is essential to evaluate the patient (ith
severe hypertension"
-ypertensive urgency develops over days to (ee.s and is defined as a )P that is
severely elevated ut (ith no clinical evidence of target organ damage"
o -ypertensive urgencies usually do not re:uire 3$ medications ut can e
managed (ith oral agents"
o 3f a patient (ith hypertensive urgency is not hospitali*ed# outpatient
follo(-up should e arranged (ithin 2> hours"
Lewis et al: Medical-Surgical Nursing: Assessment and Management of
Clinical Problems, 7
th
edition
Key Points
Chapter 3>: Nursing %anagement: Coronary Artery 7isease and Acute
Coronary Syndrome
Coronar' arter' disease &CA7' is a type of lood vessel disorder included in the
general category of atherosclerosis"
Atherosclerosis is characteri*ed y a focal deposit of cholesterol and lipids
(ithin the intimal (all of the artery" 3nflammation and endothelial in,ury play a
central role in the development of atherosclerosis"
CA7 is a progressive disease that develops in stages and (hen it ecomes
symptomatic# the disease process is usually (ell advanced"
Normally some arterial anastomoses or connections# termed collateral
circulation, e!ist (ithin the coronary circulation" The gro(th and e!tent of
collateral circulation are attriuted to t(o factors: &2' the inherited predisposition
to develop ne( lood vessels &angiogenesis'# and &2' the presence of chronic
ischemia"
%any ris. factors have een associated (ith CA7"
o Nonmodifiale ris. factors are age# gender# ethnicity# family history# and
genetic inheritance"
o %odifiale ris. factors include elevated serum lipids# hypertension#
toacco use# physical inactivity# oesity# diaetes# metaolic syndrome#
psychologic states# and homocysteine level"
+levated serum lipid levels are one of the four most firmly
estalished ris. factors for CA7"
Gipids comine (ith proteins to form lipoproteins and are vehicles
for fat moili*ation and transport" The different types of
lipoproteins are classified as high-density lipoproteins &-7Gs'#
lo(-density lipoproteins &G7Gs'# and very-lo(-density
lipoproteins &$G7Gs'"
-7Gs carry lipids a(ay from arteries and to the liver for
metaolism" -igh serum -7G levels are desirale"
-7G levels are increased y physical activity# moderate
alcohol consumption# and estrogen administration"
+levated G7G levels correlate most closely (ith an
increased incidence of atherosclerosis and CA7"
-ypertension# defined as a )P greater than or e:ual to 2>8=A8 mm
-g# is a ma,or ris. factor in CA7"
Toacco use is also a ma,or ris. factor in CA7" The ris. of
developing CA7 is t(o to si! times higher in those (ho smo.e
toacco than in those (ho do not"
1esity is defined as a ody mass inde! &)%3' of less than 38
.g=m
2
" The increased ris. for CA7 is proportional to the degree of
oesity"
o 7iaetes# metaolic syndrome# and certain ehavioral states &i"e"# stress'
have also een found to e contriuting ris. factors for CA7"
C&&NA1 AT"1 #%S"AS"
Prevention and early treatment of CA7 must involve a multifactorial approach
and needs to e ongoing throughout the lifespan
A complete lipid profile is recommended every @ years eginning at age 28"
Persons (ith a serum cholesterol level greater than 288 mg=dl are at high ris. for
CA7"
%anagement of high-ris. persons starts (ith controlling or changing the additive
effects of modifiale ris. factors"
o A regular physical activity program should e implemented"
o Therapeutic lifestyle changes to reduce the ris. of CA7 include lo(ering
G7G cholesterol y adopting a diet that limits saturated fats and
cholesterol and emphasi*es comple! carohydrates &e"g"# (hole grains#
fruit# vegetales'"
o Go(-dose aspirin is recommended for people at ris. for CA7" Aspirin
therapy is not recommended for (omen (ith lo( ris. for CA7 efore age
;@" Common side effects of aspirin therapy include /3 upset and leeding"
5or people (ho are aspirin intolerant# clopidogrel &Plavi!' can e
considered"
3f levels remain elevated despite modifiale changes# drug therapy is considered"
o Statin drugs (or. y inhiiting the synthesis of cholesterol in the liver"
Giver en*ymes must e regularly monitored"
o Niacin# a (ater-solule ) vitamin# is highly effective in lo(ering G7G and
triglyceride levels y interfering (ith their synthesis" Niacin also increases
-7G levels etter than many other lipid-lo(ering drugs"
o 5iric acid derivatives (or. y accelerating the elimination of $G7Gs and
increasing the production of apoproteins A-3 and A-33"
o )ile-acid se:uestrants increase conversion of cholesterol to ile acids and
decrease hepatic cholesterol content" The primary effect is a decrease in
total cholesterol and G7Gs"
o Certain drugs selectively inhiit the asorption of dietary and iliary
cholesterol across the intestinal (all"
The incidence of cardiac disease is greatly increased in the elderly and is the
leading cause of death in older persons" Strategies to reduce CA7 ris. are
effective in this age group ut are often underprescried"
Aggressive treatment of hypertension and hyperlipidemia (ill staili*e pla:ues in
the coronary arteries of older adults# and cessation of toacco use helps decrease
the ris. for CA7 at any age"
C,&N%C STA0L" AN.%NA
Chronic stable angina refers to chest pain that occurs intermittently over a
long period (ith the same pattern of onset# duration# and intensity of
symptoms"
o Angina is rarely sharp or staing# and it usually does not change (ith
position or reathing" %any people (ith angina complain of
indigestion or a urning sensation in the epigastric region"
o Anginal pain usually lasts for only a fe( minutes &3 to @ minutes' and
commonly susides (hen the precipitating factor is relieved" Pain at
rest is unusual"
The treatment of chronic stale angina is aimed at decreasing o!ygen demand
and=or increasing o!ygen supply and reducing CA7 ris. factors"
o 3n addition to antiplatelet and cholesterol-lo(ering drug therapy# the
most common drugs used to manage chronic stale angina are nitrates"
Short-acting nitrates are first-line therapy for the treatment of
angina" Nitrates produce their principal effects y dilating
peripheral lood vessels# coronary arteries# and collateral
vessels"
Gong acting nitrates are also used to reduce the incidence of
anginal attac.s"
-Adrenergic loc.ers are the preferred drugs for the
management of chronic stale angina"
Calcium channel loc.ers are used if -adrenergic loc.ers are
contraindicated# are poorly tolerated# or do not control anginal
symptoms" The primary effects of calcium channel loc.ers are
&2' systemic vasodilation (ith decreased S$0# &2' decreased
myocardial contractility# and &3' coronary vasodilation"
Certain high-ris. patients &e"g"# patients (ith diaetes' (ith
chronic stale angina may enefit from the addition of an
angiotensin-converting en*yme &AC+' inhiitor"
Common diagnostic tests for a patient (ith a history of CA7 or CA7 include
a chest !-ray# a 22-lead +C/# laoratory tests &e"g"# lipid profile'D nuclear
imagingD e!ercise stress testing# and coronary angiography"
AC!T" C&&NA1 S1N#&M"
Acute coronar' s'ndrome &ACS' develops (hen ischemia is prolonged and
not immediately reversile" ACS encompasses the spectrum of unstale
angina# nonFST-segment-elevation myocardial infarction &NST+%3'# and ST-
segment-elevation myocardial infarction &ST+%3'"
ACS is associated (ith deterioration of a once stale atherosclerotic pla:ue"
This unstale lesion may e partially occluded y a thromus &manifesting as
?A or NST+%3' or totally occluded y a thromus &manifesting as ST+%3'"
!nstable angina &?A' is chest pain that is ne( in onset# occurs at rest# or has
a (orsening pattern" ?A is unpredictale and represents an emergency"
M'ocardial infarction *M%+ occurs as a result of sustained ischemia# causing
irreversile myocardial cell death" +ighty percent to A8E of all %3s are due to
the development of a thromus that halts perfusion to the myocardium distal
to the occlusion" Contractile function of the heart stops in the infracted area&s'"
o Cardiac cells can (ithstand ischemic conditions for appro!imately 28
minutes" 3t ta.es appro!imately > to ; hours for the entire thic.ness of
the heart muscle to infarct"
o 3nfarctions are descried ased on the location of damage &e"g"#
anterior# inferior# lateral# or posterior (all infarction'"
o Severe# immoili*ing chest pain not relieved y rest# position change#
or nitrate administration is the hallmar. of an %3" The pain is usually
descried as a heaviness# pressure# tightness# urning# constriction# or
crushing"
o Complications after %3
The most common complication after an %3 is dysrhythmias#
and dysrhythmias are the most common cause of death in
patients in the prehospital period"
-5 is a complication that occurs (hen the pumping po(er of
the heart has diminished"
Cardiogenic shoc. occurs (hen inade:uate o!ygen and
nutrients are supplied to the tissues ecause of severe left
ventricular failure" <hen it occurs# it has a high mortality rate"
Papillary muscle dysfunction may occur if the infarcted area
includes or is ad,acent to the papillary muscle that attaches to
the mitral valve" Papillary muscle dysfunction causes mitral
valve regurgitation and is detected y a systolic murmur at the
cardiac ape! radiating to(ard the a!illa"
Papillary muscle rupture is a rare ut life-threatening
complication that causes massive mitral valve regurgitation#
resulting in dyspnea# pulmonary edema# and decreased C1"
$entricular aneurysm results (hen the infarcted myocardial
(all ecomes thinned and ulges out during contraction"
Pericarditis may occur 2 to 3 days after an acute %3 as a
common complication of the infarction"
Primary diagnostic studies used to determine (hether a person has ?A or an
%3 include an +C/ and serum cardiac mar.ers"
#rug Thera('
3nitial management of the patient (ith chest pain includes aspirin# sulingual
nitroglycerin# morphine sulfate for pain unrelieved y nitroglycerin# and
o!ygen"
3$ nitroglycerin# aspirin# -adrenergic loc.ers# and systemic anticoagulation
(ith either lo( molecular (eight heparin given sucutaneously or 3$
unfractionated heparin &?-' are the initial drug treatments of choice for ACS"
3$ antiplatelet agents &e"g"# glycoprotein 33=333a inhiitor' may also e used if
percutaneous coronary intervention &PC3' is anticipated"
AC+ inhiitors help prevent ventricular remodeling and prevent or slo( the
progression of -5" They are recommended follo(ing anterior (all %3s or %3s
that result in decreased left ventricular function &e,ection fraction J+5K less
than >8E' or pulmonary congestion and should e continued indefinitely" 5or
patients (ho cannot tolerate AC+ inhiitors# angiotensin receptor loc.ers
should e considered"
Calcium channel loc.ers or long-acting nitrates can e added if the patient is
already on ade:uate doses of -adrenergic loc.ers or cannot tolerate -
adrenergic loc.ers# or has Prin*metal6s angina"
Stool softeners are given to facilitate and promote the comfort of o(el
evacuation" This prevents straining and the resultant vagal stimulation from
the $alsalva maneuver" $agal stimulation produces radycardia and can
provo.e dysrhythmias"
3nitially# patients may e NP1 &nothing y mouth' e!cept for sips of (ater
until stale &e"g"# pain free# nausea resolved'" 7iet is advanced as tolerated to a
lo(-salt# lo(-saturated-fat# and lo(-cholesterol diet"
Surgical Thera('
Coronar' re)asculari3ation (ith coronary artery ypass graft &CA)/'
surgery is recommended for patients (ho &2' fail medical management# &2'
have left main coronary artery or three-vessel disease# &3' are not candidates
for PC3 &e"g"# lesions are long or difficult to access'# or &>' have failed PC3
(ith ongoing chest pain"
%inimally invasive direct coronary artery ypass &%37CA)' surgery can e
used for patients (ith single-vessel disease"
The off-pump coronary artery ypass &1PCA)' procedure uses full or partial
sternotomy to enale access to all coronary vessels" 1PCA) is also performed
on a eating heart using mechanical staili*ers and (ithout cardiopulmonary
ypass &CP)'"
Transmyocardial laser revasculari*ation &T%0' is an indirect
revasculari*ation procedure used for patients (ith advanced CA7 (ho are not
candidates for traditional ypass surgery and (ho have persistent angina after
ma!imum medical therapy"
Nursing Management: Chronic Stable Angina and Acute Coronar' S'ndrome
The follo(ing nursing measures should e instituted for a patient e!periencing
angina: &2' administration of supplemental o!ygen# &2' determination of vital
signs# &3' 22-lead +C/# &>' prompt pain relief first (ith a nitrate follo(ed y
an opioid analgesic if needed# &@' auscultation of heart sounds# and &;'
comfortale positioning of the patient"
3nitial treatment of a patient (ith ACS includes pain assessment and relief#
physiologic monitoring# promotion of rest and comfort# alleviation of stress
and an!iety# and understanding of the patient6s emotional and ehavioral
reactions"
o Nitroglycerin# morphine sulfate# and supplemental o!ygen should e
provided as needed to eliminate or reduce chest pain"
o Continuous +C/ monitoring is initiated and maintained throughout the
hospitali*ation"
o 5re:uent vital signs# inta.e and output &at least once a shift'# and
physical assessment should e done to detect deviations from the
patient6s aseline parameters" 3ncluded is an assessment of lung sounds
and heart sounds and inspection for evidence of early -5 &e"g"#
dyspnea# tachycardia# pulmonary congestion# distended nec. veins'"
)ed rest may e ordered for the first fe( days after an %3 involving a large
portion of the ventricle" A patient (ith an uncomplicated %3 &e"g"# angina
resolved# no signs of complications' may rest in a chair (ithin 9 to 22 hours
after the event" The use of a commode or edpan is ased on patient
preference"
3t is important to plan nursing and therapeutic actions to ensure ade:uate rest
periods free from interruption" Comfort measures that can promote rest
include fre:uent oral care# ade:uate (armth# a :uiet atmosphere# use of
rela!ation therapy &e"g"# guided imagery'# and assurance that personnel are
neary and responsive to the patient6s needs"
Cardiac (or.load is gradually increased through more demanding physical
tas.s so that the patient can achieve a discharge activity level ade:uate for
home care"
An!iety is present in all patients (ith ACS to various degrees" The nurse6s
role is to identify the source of an!iety and assist the patient in reducing it"
The emotional and ehavioral reactions of a patient are varied and fre:uently
follo( a predictale response pattern" The role of the nurse is to understand
(hat the patient is currently e!periencing# to assist the patient in testing
reality# and to support the use of constructive coping styles" 7enial may e a
positive coping style in the early phase of recovery from ACS"
The ma,or nursing responsiilities for the care of the patient follo(ing PC3
involves monitoring for signs of recurrent anginaD fre:uent assessment of vital
signs# including -0 and rhythmD evaluation of the groin site for signs of
leedingD and maintenance of ed rest per institution policy"
5or patients having CA)/ surgery# care is provided in the intensive care unit
for the first 2> to 3; hours# (here ongoing monitoring of the patient6s +C/
and hemodynamic status is critical"
Cardiac rehailitation restores a person to an optimal state of function in si!
areas: physiologic# psychologic# mental# spiritual# economic# and vocational"
Patient teaching egins (ith the +7 nurse and progresses through the staff
nurse to the community health nurse" Careful assessment of the patient6s
learning needs helps the nurse set goals and o,ectives that are realistic"
Physical activity is necessary for optimal physiologic functioning and
psychologic (ell-eing" A regular schedule of physical activity# even after
many years of sedentary living# is eneficial"
o Activity level is gradually increased so that y the time of discharge
the patient can tolerate moderate-energy activities of 3 to ; %+Ts"
o Patients (ith ?A that has resolved or an uncomplicated %3 are in the
hospital for appro!imately 3 to > days and y day 2 can amulate in
the hall(ay and egin limited stair climing &e"g"# three to four steps'"
o )ecause of the short hospital stay# it is critical to give the patient
specific guidelines for physical activity so that overe!ertion (ill not
occur" Patients should Blisten to (hat the ody is saying"C
o Patients should e taught to chec. their pulse rate and the parameters
(ithin (hich to e!ercise" The more important factor is the patient6s
response to physical activity in terms of symptoms rather than asolute
-0# especially since many patients are on -adrenergic loc.ers and
may not e ale to reach a target -0"
%any patients (ill e referred to an outpatient or home-ased cardiac
rehailitation program" %aintaining contact (ith the patient appears to e the
.ey to the success of these programs"
1ne factor that has een lin.ed to poor adherence to a physical activity
program after %3 is depression" )oth men and (omen e!perience mild to
moderate depression post-%3 that should resolve in 2 to > months"
Se!ual counseling for cardiac patients and their partners should e provided"
The patient6s concern aout resumption of se!ual activity after hospitali*ation
for ACS often produces more stress than the physiologic act itself"
o )efore the nurse provides guidelines on resumption of se!ual activity#
it is important to .no( the physiologic status of the patient# the
physiologic effects of se!ual activity# and the psychologic effects of
having a heart attac." Se!ual activity for middle-aged men and (omen
(ith their usual partners is no more strenuous than climing t(o
flights of stairs"
o The inaility to perform se!ually after %3 is common and se!ual
dysfunction usually disappears after several attempts"
o Patients should .no( that drugs used for erectile dysfunction should
not e used (ith nitrates as severe hypotension and even death have
een reported"
o Typically# it is safe to resume se!ual activity L to 28 days after an
uncomplicated %3"
S!##"N CA#%AC #"AT,
Sudden cardiac death &SC7' is une!pected death from cardiac causes"
CA7 is the most common cause of SC7 and accounts for 98E of all SC7s"
SC7 involves an arupt disruption in cardiac function# producing an arupt
loss of cardiac output and cereral lood flo(" 7eath usually occurs (ithin 2
hour of the onset of acute symptoms &e"g"# angina# palpitations'"
The ma,ority of cases of SC7 are caused y acute ventricular dysrhythmias
&e"g"# ventricular tachycardia# ventricular firillation'"
Persons (ho e!perience SC7 as a result of CA7 fall into t(o groups: &2'
those (ho had an acute %3 and &2' those (ho did not have an acute %3" The
latter group accounts for the ma,ority of cases of SC7" 3n this instance#
victims usually have no (arning signs or symptoms"
Patients (ho survive are at ris. for recurrent SC7 due to the continued
electrical instaility of the myocardium that caused the initial event to occur"
0is. factors for SC7 include left ventricular dysfunction &+5 less than 38E'#
ventricular dysrhythmias follo(ing %3# male gender &especially African
American men'# family history of premature atherosclerosis# toacco use#
diaetes mellitus# hypercholesterolemia# hypertension# and cardiomyopathy"
%ost SC7 patients have a lethal ventricular dysrhythmia and re:uire 2>-hour
-olter monitoring or other type of event recorder# e!ercise stress testing#
signal-averaged +C/# and electrophysiologic study &+PS'"
The most common approach to preventing a recurrence and improving
survival is the use of an implantale cardioverter-defirillator &3C7'"
7rug therapy may e used in con,unction (ith an 3C7 to decrease episodes of
ventricular dysrhythmias"
Survivors of SC7 develop a Btime omC mentality# fearing the recurrence of
cardiopulmonary arrest" They and their families may ecome an!ious# angry#
and depressed"
Patients and families also may need to deal (ith additional issues such as
possile driving restrictions and change in occupation" The grief response
varies among SC7 survivors and their families"
Lewis et al: Medical-Surgical Nursing: Assessment and Management of
Clinical Problems, 7
th
edition
Key Points
Chapter 3@: Nursing %anagement: -eart 5ailure
"T%&L&.1 AN# PAT,&P,1S%&L&.1
,eart failure &-5' is an anormal clinical condition involving impaired cardiac
pumping that results in the characteristic pathophysiologic changes of
vasoconstriction and fluid retention"
-5 is characteri*ed y ventricular dysfunction# reduced e!ercise tolerance#
diminished :uality of life# and shortened life e!pectancy"
0is. factors include coronary artery disease &CA7' and advancing age"
-ypertension# diaetes# cigarette smo.ing# oesity# and high serum cholesterol also
contriute to the development of -5"
CLASS%$%CAT%&N
-eart failure is classified as systolic or diastolic failure"
o S'stolic failure, the most common cause of -5# results from an inaility of
the heart to pump lood"
o #iastolic failure is an impaired aility of the ventricles to rela! and fill
during diastole" 7ecreased filling of the ventricles (ill result in decreased
stro.e volume and cardiac output &C1'"
CL%N%CAL MAN%$"STAT%&NS
-5 can have an arupt onset or it can e an insidious process resulting from slo(#
progressive changes" Compensatory mechanisms are activated to maintain
ade:uate C1"
To maintain alance in -5# several counter regulatory processes are activated#
including the production of hormones from the heart muscle to promote
vasodilation"
Cardiac compensation occurs (hen compensatory mechanisms succeed in
maintaining an ade:uate C1 that is needed for tissue perfusion"
Cardiac decompensation occurs (hen these mechanisms can no longer maintain
ade:uate C1 and inade:uate tissue perfusion results"
The most common form of -5 is left-sided failure from left ventricular
dysfunction" )lood ac.s up into the left atrium and into the pulmonary veins
causing pulmonary congestion and edema" -5 is usually manifested y
iventricular failure"
Acute decompensated heart failure &A7-5' typically manifests as (ulmonar'
edema, an acute# life-threatening situation"
Clinical manifestations of chronic -5 depend on the patient6s age and the
underlying type and e!tent of heart disease" Common symptoms include fatigue#
dyspnea# tachycardia# edema# and unusual ehavior"
Pleural effusion# atrial firillation# thromus formation# renal insufficiency# and
hepatomegaly are all complications of -5"
#%A.N&ST%C ST!#%"S
The primary goal in diagnosis of -5 is to determine the underlying etiology of -5"
o A thorough history# physical e!amination# chest !-ray# electrocardiogram
&+C/'# laoratory data &cardiac en*ymes# -type natriuretic protein &)NP'#
serum chemistries# liver function studies# thyroid function studies# and
complete lood count'# hemodynamic assessment# echocardiogram# stress
testing# and cardiac catheteri*ation are performed"
NURSING AND COLLABORATIVE MANAGEMENT: ADHF AND
PULMONARY EDEMA
The goals of therapy for oth A7-5 and chronic -5 are to decrease patient
symptoms# reverse ventricular remodeling# improve :uality of life# and decrease
mortality and moridity"
Treatment strategies should include the follo(ing:
o 7ecreasing intravascular volume (ith the use of diuretics to reduce
venous return and preload"
o 7ecreasing venous return &preload' to reduce the amount of volume
returned to the G$ during diastole"
o 7ecreasing afterload &the resistance against (hich the G$ must pump'
improves C1 and decreases pulmonary congestion"
o /as e!change is improved y the administration of 3$ morphine sulfate
and supplemental o!ygen"
o 3notropic therapy and hemodynamic monitoring may e needed in patients
(ho do not respond to conventional pharmacotherapy &e"g"# diuretics#
vasodilators# morphine sulfate'"
o 0eduction of an!iety is an important nursing function# since an!iety may
increase the SNS response and further increase myocardial (or.load"
C&LLA0&AT%2" CA": C,&N%C ,"AT $A%L!"
The main goal in the treatment of chronic -5 is to treat the underlying cause and
contriuting factors# ma!imi*e C1# provide treatment to alleviate symptoms#
improve ventricular function# improve :uality of life# preserve target organ
function# and improve mortality and moridity"
Administration of o!ygen improves saturation and assists greatly in meeting
tissue o!ygen needs and helps relieve dyspnea and fatigue"
Physical and emotional rest allo(s the patient to conserve energy and decreases
the need for additional o!ygen" The degree of rest recommended depends on the
severity of -5"
Nonpharmacologic therapies used in the management of -5 patients (ho are
receiving ma!imum medical therapy# continue to have NM-A 5unctional Class
333 or 3$ symptoms# and have a (idened N0S interval include the follo(ing:
o Cardiac resynchroni*ation therapy &C0T' or iventricular pacing" 3nvolves
pacing oth the right and left ventricles to achieve coordination of right
and left ventricle contractility"
o Cardiac transplantation" Strict criteria are used to select the fe( patients
(ith advanced -5 (ho can even hope to receive a transplanted heart"
o 3ntraaortic alloon pump &3A)P' therapy" The 3A)P can e useful in the
hemodynamically unstale -5 patient ecause it decreases S$0# PA<P#
and PAP as much as 2@E# leading to improved C1" -o(ever# the
limitations of ed rest# infection# and vascular complications preclude
long-term use"
o $entricular assist devices &$A7s'" $A7s provide highly effective long-
term support for up to 2 years and have ecome standard care in many
heart transplant centers" $A7s are used as a ridge to transplantation"
o 7estination therapy" The use of a permanent# implantale $A7# .no(n as
destination therapy# is an option for patients (ith advanced NM-A
5unctional Class 3$ -5 (ho are not candidates for heart transplantation"
/eneral therapeutic o,ectives for drug management of chronic -5 include: &2'
identification of the type of -5 and underlying causes# &2' correction of sodium
and (ater retention and volume overload# &3' reduction of cardiac (or.load# &>'
improvement of myocardial contractility# and &@' control of precipitating and
complicating factors"
o 7iuretics are used in -5 to moili*e edematous fluid# reduce pulmonary
venous pressure# and reduce preload"
Thia*ide diuretics may e the first choice in chronic -5 ecause of
their convenience# safety# lo( cost# and effectiveness" They are
particularly useful in treating edema secondary to -5 and in
controlling hypertension"
Goop diuretics are potent diuretics" These drugs act on the
ascending loop of -enle to promote sodium# chloride# and (ater
e!cretion" Prolems in using loop diuretics include reduction in
serum potassium levels# ototo!icity# and possile allergic reaction
in the patient (ho is sensitive to sulfa-type drugs"
Spironolactone &Aldactone' is an ine!pensive# potassium-sparing
diuretic that promotes sodium and (ater e!cretion ut loc.s
potassium e!cretion" This aldosterone receptor antagonist also
loc.s the harmful neurohormonal effects of aldosterone on the
heart lood vessels"
Spironolactone adds to the enefits of angiotensin-
converting en*yme &AC+' inhiitors# and is appropriate to
use (hile renal function is ade:uate"
Spironolactone may also e used in con,unction (ith other
diuretics# such as furosemide"
$asodilator drugs have een sho(n to improve survival in -5" The
goals of vasodilator therapy in the treatment of -5 include &2'
increasing venous capacity# &2' improving +5 through improved
ventricular contraction# &3' slo(ing the process of ventricular
dysfunction# &>' decreasing heart si*e# &@' avoiding stimulation of
the neurohormonal responses initiated y the compensatory
mechanisms of -5# and &;' enhancing neurohormonal loc.ade"
AC+ inhiitors &e"g"# captopril JCapotenK# ena*epril
JGotensinK# enalapril J$asotecK' are useful in oth systolic
and diastolic -5# and they are the first-line therapy in the
treatment of chronic -5"
Angiotensin 33 receptor loc.ers &e"g"# losartan JCo*aarK#
valsartan J7iovanK' may e used in patients (ho are AC+
inhiitor intolerant"
Nitrates are used to treat -5 y acting directly on the
smooth muscle of the vessel (all" %a,or effects include a
decrease in preload and vasodilation of coronary arteries"
Nesiritide# a synthetic form of human )NP# eing studied
for its use in the ongoing treatment of patients (ith chronic
-5"
-Adrenegic loc.ers# specifically carvedilol &Coreg' and
metoprolol &Toprol-OG'# have improved survival of
patients (ith -5"
Positive inotropic agents improve cardiac contractility and C1#
decrease G$ diastolic pressure# and decrease S$0"
7igitalis glycosides Je"g"# digo!in &Gano!in'K remain the
mainstay in the treatment of -5# ho(ever# they have not
een sho(n to prolong life"
Calcium sensiti*ers are novel positive inotropic agents in
the treatment of -5" They improve cardiac performance y
interacting directly (ith contractile proteins (ithout
affecting intracellular calcium concentrations or increasing
myocardial o!ygen demand"
)i7il# a comination drug containing isosoride dinitrate
and hydrala*ine# approved only for the treatment of -5 in
African Americans (ho are already eing treated (ith
standard therapy"
o 7iet education and (eight management are critical to the patient6s control
of chronic -5"
7iet and (eight management recommendations must e
individuali*ed and culturally sensitive if the necessary changes are
to e reali*ed"
A detailed diet history should e otained and should include the
sociocultural value of food to the patient"
The 7ietary Approaches to Stop -ypertension &7AS-' diet is
effective as a first-line therapy for many individuals (ith
hypertension# and this diet is (idely used for the patient (ith -5"
The edema of chronic -5 is often treated y dietary restriction of
sodium"
5luid restrictions are not commonly prescried for the patient (ith
mild to moderate -5" -o(ever# in moderate to severe -5 and renal
insufficiency# fluid restrictions are usually implemented"
Patients should (eigh themselves daily to monitor fluid retention#
as (ell as (eight reduction" 3f a patient e!periences a (eight gain
of 3 l &2"> .g' over 2 days or a 3- to @-l &2"3 .g' gain over a
(ee.# the primary care provider should e called"
N!S%N. MANA."M"NT: C,&N%C ,"AT $A%L!"
The overall goals for the patient (ith -5 include &2' a decrease in symptoms
&e"g"# shortness of reath# fatigue'# &2' a decrease in peripheral edema# &3' an
increase in e!ercise tolerance# &>' compliance (ith the medical regimen# and &@'
no complications related to -5"
Treatment or control of underlying heart disease is .ey to preventing -5 and
episodes of A7-5"
o 5or e!ample# valve replacement should e planned efore lung congestion
develops# and early and continued treatment of CA7 and hypertension is
critical"
o The use of antidysrhythmic agents or pacema.ers is indicated for people
(ith serious dysrhythmias or conduction disturances"
Patients (ith -5 should e counseled to otain vaccinations against the flu and
pneumonia"
Preventive care should focus on slo(ing the progression of the disease"
o Patient teaching must include information on medications# diet# and
e!ercise regimens" +!ercise training &e"g"# cardiac rehailitation' does
improve symptoms of chronic -5 ut is often underprescried"
o -ome nursing care for follo(-up care and to monitor the patient6s
response to treatment may e re:uired"
Successful -5 management is dependent on the follo(ing principles: &2' -5 is a
progressive disease# and treatment plans are estalished (ith :uality-of-life goalsD
&2' symptom management is controlled y the patient (ith self-management tools
&e"g"# daily (eights# drug regimens# diet and e!ercise plans'D &3' salt and (ater
must e restrictedD &>' energy must e conservedD and &@' support systems are
essential to the success of the entire treatment plan"
3mportant nursing responsiilities in the care of a patient (ith -5 include &2'
teaching the patient aout the physiologic changes that have occurred# &2'
assisting the patient to adapt to oth the physiologic and psychologic changes# and
&3' integrating the patient and the patient6s family or support system in the overall
care plan"
o %any patients (ith -5 are at high ris. for an!iety and depression# and
ma,or depression is more prevalent in female patients and patients less
than ;8 years of age"
o Patients (ith -5 can live productive lives (ith chronic -5"
o +ffective home health care can prevent or limit future hospitali*ation"
%anaging -5 patients out of the hospital is a priority of care"
o Patients (ith -5 (ill ta.e medication for the rest of their lives" This can
ecome difficult ecause a patient may e asymptomatic (hen -5 is
under control"
o Patients should e taught to evaluate the action of the prescried drugs and
to recogni*e the manifestations of drug to!icity"
Patients should e taught ho( to ta.e their pulse rate and to .no(
under (hat circumstances drugs# especially digitalis and -
adrenergic loc.ers# should e (ithheld and a health care provider
consulted"
3t may e appropriate to instruct patients in home )P monitoring#
especially for those -5 patients (ith hypertension"
Patients should e taught the symptoms of hypo- and hyper.alemia
if diuretics that deplete or spare potassium are eing ta.en"
5re:uently the patient (ho is ta.ing thia*ide or loop diuretics is
given supplemental potassium"
o The nurse# physical therapist# or occupational therapist should instruct the
patient in energy-conserving and energy-efficient ehaviors after an
evaluation of daily activities has een done"
Patients may need a prescription for rest after an activity" %any
hard-driving persons need the BpermissionC to not feel Bla*y"C
Sometimes an activity that the patient en,oys may need to e
eliminated" 3n such situations the patient should e helped to
e!plore alternative activities that cause less physical and cardiac
stress"
The physical environment may re:uire modification in situations in
(hich there is an increased cardiac (or.load demand &e"g"#
fre:uent climing of stairs'" The nurse can help the patient identify
areas (here outside assistance can e otained"
o -ome health nursing is an essential component in the care of the -5
patient and family"
-ome health nurses conduct fre:uent physical assessments#
including vital signs and (eight"
Protocols enale the nurse and patient to identify prolems# such as
evidence of (orsening -5# and institute interventions to prevent
hospitali*ation" This may include altering medications and
initiating fluid restrictions"
CA#%AC TANSPLANTAT%&N
Cardiac trans(lantation has ecome the treatment of choice for patients (ith
refractory end-stage -5# cardiomyopathy# and inoperale CA7"
1nce a patient meets the criteria for cardiac transplantation# the goal of the
evaluation process is to identify patients (ho (ould most enefit from a ne(
heart"
o After a complete physical e!amination and diagnostic (or.up# the patient
and family then undergo a comprehensive psychologic profile"
o The comple!ity of the transplant process may e over(helming to a
patient (ith inade:uate support systems and a poor understanding of the
lifestyle changes re:uired after transplant"
1nce a patient is accepted as a transplant candidate &this may happen rapidly
during an acute illness or over a longer period'# he or she is placed on a transplant
list"
o Stale patients (ait at home and receive ongoing medical care"
o ?nstale patients may re:uire hospitali*ation for more intensive therapy"
o The overall (aiting period for a transplant is long# and many patients die
(hile (aiting for a transplant"
%ost donor hearts are otained at sites distant from the institution performing the
transplant" The ma!imum acceptale time from harvesting the donor heart to
transplantation is > to ; hours"
The heart recipient is prepared for surgery# and cardiopulmonary ypass is used"
o The surgical procedure involves removing the recipient6s heart# e!cept for
the posterior right and left atrial (alls and their venous connections"
o The recipient6s heart is then replaced (ith the donor heart" Care is ta.en to
preserve the integrity of the donor sinoatrial &SA' node so that a sinus
rhythm may e achieved postoperatively"
o 3mmunosuppressive therapy usually egins in the operating room"

+ndomyocardial iopsies are typically otained from the right ventricle &via the
right internal ,ugular vein' on a (ee.ly asis for the first month# monthly for the
follo(ing ; months# and yearly thereafter to detect re,ection"
o The -eartsreath test is used along (ith endomyocardial iopsy to assess
organ re,ection in heart transplant patients"
The test (or.s y measuring the amount of methylated al.anes
&natural chemicals found in the reath and air' in a patientPs reath"
The value is compared (ith the results of a iopsy performed
during the previous month to measure the proaility of the
transplanted heart eing re,ected"
The -eartsreath test is used in the first year follo(ing heart
transplantation and along (ith the results of a heart iopsy to help
guide short-term and long-term medical care of heart transplant
patients"
The test helps to separate less severe organ re,ection &grades 8# 2#
and 2' from more severe re,ection &grade 3'"
o Peripheral lood T lymphocyte monitoring is also done to assess the
recipient6s immune status"
Nursing management throughout the posttransplant period focuses on promoting
patient adaptation to the transplant process# monitoring cardiac function#
managing lifestyle changes# and providing ongoing teaching of the patient and
family"
Several devices are availale as a ridge to transplantation
o The A)@888 Circulatory Support System and the )$S @888
)iventricular Support System provide temporary support for one or oth
sides of the heart in circumstances in (hich the heart has failed ut has the
potential to recover &e"g"# reversile -5# myocarditis# and acute %3'"
o The Thoratec $entricular Assist 7evice &$A7' system can support one or
oth ventricles# and it has een approved as a ridging device for
transplantation and for recovery of the heart after cardiac surgery"
AT%$%C%AL ,"AT
The lac. of availale transplant hearts and the increasing numer of patients in
need have triggered the movement to develop artificial hearts"
o T(o implantale artificial hearts# the Cardio<est Total Artificial -eart and
the AioCor 3mplantale 0eplacement -eart# have een developed"
o )oth are designed (ith materials that minimi*e coagulation and contain
motor-driven pumping systems &artificial ventricles' that operate on oth
internal and e!ternal atteries"
An electronic pac.age in the adomen monitors the system#
including ad,usting the heart rate ased on the patient6s activity"
An e!ternal attery pac. allo(s for periods of independence from
the console"
The total artificial heart re:uires no immunosuppression and may
hold promise for short-term survival in patients (ith end-stage -5"
Lewis et al: Medical-Surgical Nursing: Assessment and Management of
Clinical Problems, 7
th
edition
Key Points
Chapter 3;: Nursing %anagement: 7ysrhythmias
The aility to recogni*e normal and anormal cardiac rhythms# called
d'srh'thmias, is an essential s.ill for the nurse"
5our properties of cardiac cells &automaticity# e!citaility# conductivity# and
contractility' enale the conduction system to initiate an electrical impulse#
transmit it through the cardiac tissue# and stimulate the myocardial tissue to
contract"
o A normal cardiac impulse egins in the sinoatrial &SA' node in the upper
right atrium"
o The signal is transmitted over the atrial myocardium via )achmann6s
undle and internodal path(ays# causing atrial contraction"
o The impulse then travels to the atrioventricular &A$' node through the
undle of -is and do(n the left and right undle ranches# ending in the
Pur.in,e fiers# (hich transmit the impulse to the ventricles# resulting in
ventricular contraction"
The autonomic nervous system plays an important role in the rate of impulse
formation# the speed of conduction# and the strength of cardiac contraction"
o Components of the autonomic nervous system that affect the heart are the
right and left vagus nerve fiers of the parasympathetic nervous system
and fiers of the sympathetic nervous system"
"C. M&N%T&%N.
The electrocardiogram &+C/' is a graphic tracing of the electrical impulses
produced in the heart"
+C/ (aveforms are produced y the movement of charged ions across the
semipermeale memranes of myocardial cells"
There are 22 recording leads in the standard +C/"
o Si! of the 22 +C/ leads measure electrical forces in the frontal plane
&leads 3# 33# 333# a$0# a$G# and a$5'"
o The remaining si! leads &$2 through $;' measure the electrical forces in
the hori*ontal plane &precordial leads'"
o The 22-lead +C/ may sho( changes that are indicative of structural
changes# damage such as ischemia or infarction# electrolyte imalance#
dysrhythmias# or drug to!icity"
Continuous +C/ monitoring is done using leads 33# $2# and %CG2"
o %CG2 is a modified chest lead that is similar to $2 and is used (hen only
three leads are availale for monitoring"
o %onitoring leads should e selected ased on the patient6s clinical
situation"
The +C/ can e visuali*ed continuously on a monitor oscilloscope# and a
recording of the +C/ &i"e"# rhythm strip' can e otained on +C/ paper attached
to the monitor"
+C/ leads are attached to the patient6s chest (all via an electrode pad fi!ed (ith
electrical conductive paste"
Telemetr' monitoring involves the oservation of a patient6s -0 and rhythm to
rapidly diagnose dysrhythmias# ischemia# or infarction"
Normal sinus rhythm refers to a rhythm that originates in the SA node and follo(s
the normal conduction pattern of the cardiac cycle"
o The P (ave represents the depolari*ation of the atria &passage of an
electrical impulse through the atria'# causing atrial contraction"
o The P0 interval represents the time period for the impulse to spread
through the atria# A$ node# undle of -is# and Pur.in,e fiers"
o The N0S comple! represents depolari*ation of the ventricles &ventricular
contraction'# and the N0S interval represents the time it ta.es for
depolari*ation"
o The ST segment represents the time et(een ventricular depolari*ation
and repolari*ation" This segment should e flat or isoelectric and
represents the asence of any electrical activity et(een these t(o events"
o The T (ave represents repolari*ation of the ventricles"
o The NT interval represents the total time for depolari*ation and
repolari*ation of the ventricles"
M"C,AN%SMS &$ #1S,1T,M%AS
Normally the main pacema.er of the heart is the SA node# (hich spontaneously
discharges ;8 to 288 times per minute" 7isorders of impulse formation can cause
dysrhythmias"
A pacema.er from another site can lead to dysrhythmias and may e discharged in
a numer of (ays"
o Secondary pacema.ers may originate from the A$ node or -is-Pur.in,e
system"
o Secondary pacema.ers can originate (hen they discharge more rapidly
than the normal pacema.er of the SA node"
o Triggered eats &early or late' may come from an ectopic focus &area
outside the normal conduction path(ay' in the atria# A$ node# or
ventricles"
"2AL!AT%&N &$ #1S,1T,M%AS
7ysrhythmias result from various anormalities and disease states# and the cause
of a dysrhythmia influences the treatment"
Several diagnostic tests are used to evaluate cardiac dysrhythmias and the
effectiveness of antidysrhythmia drug therapy"
o -olter monitoring records the +C/ (hile the patient is amulatory and
performing daily activities"
o +vent monitors have improved the evaluation of outpatient dysrhythmias"
o Signal-averaged +C/ &SA+C/' is a high-resolution +C/ used to identify
the patient at ris. for developing comple! ventricular dysrhythmias"
o +!ercise treadmill testing is used for evaluation of cardiac rhythm
response to e!ercise"
o An electrophysiologic study &+PS' identifies different mechanisms of
tachydysrhythmias# heart loc.s# radydysrhythmias# and causes of
syncope"
T1P"S &$ #1S,1T,M%AS
Sinus bradycardia has a normal sinus rhythm# ut the SA node fires at a rate less
than ;8 eats=minute and is referred to as asolute radycardia"
o Clinical associations" Sinus radycardia may e a normal sinus rhythm
&e"g"# in aeroically trained athletes'# and it may occur in response to
carotid sinus massage# $alsalva maneuver# hypothermia# and
administration of parasympathomimetic drugs"
o 7isease states associated (ith sinus radycardia are hypothyroidism#
increased intracranial pressure# ostructive ,aundice# and inferior (all
myocardial infarction &%3'"
o Treatment consists of administration of atropine &an anticholinergic drug'
for the patient (ith symptoms" Pacema.er therapy may e re:uired"
Sinus tachycardia has a normal sinus rhythm# ut the SA node fires at a rate
greater than 288 eats=minute as a result of vagal inhiition or sympathetic
stimulation"
o Clinical associations" Sinus tachycardia is associated (ith physiologic and
psychologic stressors such as e!ercise# fever# pain# hypotension#
hypovolemia# anemia# hypo!ia# hypoglycemia# myocardial ischemia# heart
failure &-5'# hyperthyroidism# an!iety# and fear" 3t can also e an effect of
certain drugs"
o Angina may result from sinus tachycardia due to the increased myocardial
o!ygen consumption that is associated (ith an increased -0"
o Treatment is ased on the underlying cause" 5or e!ample# if a patient is
e!periencing tachycardia from pain# tachycardia should resolve (ith
effective pain management"
Premature atrial contraction &PAC' is a contraction originating from an ectopic
focus in the atrium in a location other than the sinus node" A PAC may e stopped
&nonconducted PAC'# delayed &lengthened P0 interval'# or conducted normally
through the A$ node"
o Clinical associations" PACs can result from emotional stress or physical
fatigueD from the use of caffeine# toacco# or alcoholD from hypo!ia or
electrolyte imalancesD and from disease states such as hyperthyroidism#
chronic ostructive pulmonary disease &C1P7'# and heart disease
including coronary artery disease &CA7' and valvular disease"
o 3n healthy persons# isolated PACs are not significant" 3n persons (ith heart
disease# fre:uent PACs may indicate enhanced automaticit' of the atria or
a reentry mechanism and may (arn of or initiate more serious
dysrhythmias"
o Treatment depends on the patient6s symptoms" 5or e!ample# (ithdra(al of
sources of stimulation such as caffeine or sympathomimetic drugs may e
(arranted"
Paroxysmal supraventricular tachycardia &PS$T' is a dysrhythmia originating in
an ectopic focus any(here aove the ifurcation of the undle of -is"
o PS$T occurs ecause of a reentrant phenomenon &ree!citation of the atria
(hen there is a one-(ay loc.' and is usually triggered y a PAC"
o 3n the normal heart# PS$T is associated (ith overe!ertion# emotional
stress# deep inspiration# and stimulants such as caffeine and toacco" 3t is
also associated (ith rheumatic heart disease# digitalis to!icity# CA7# and
cor pulmonale"
o Prolonged PS$T (ith -0 greater than 298 eats=minute may precipitate a
decreased C1# resulting in hypotension# dyspnea# and angina"
o Treatment for PS$T includes vagal stimulation and drug therapy &i"e"# 3$
adenosine'"
Atrial flutter is an atrial tachydysrhythmia identified y recurring# regular#
sa(tooth-shaped flutter (aves that originate from a single ectopic focus in the
right atrium"
o Atrial flutter is associated (ith CA7# hypertension# mitral valve disorders#
pulmonary emolus# chronic lung disease# cor pulmonale#
cardiomyopathy# hyperthyroidism# and the use of drugs such as digo!in#
:uinidine# and epinephrine"
o -igh ventricular rates &over 288=minute' and the loss of the atrial B.ic.C
&atrial contraction reflected y a sinus P (ave' can decrease C1 and cause
serious conse:uences such as chest pain and -5"
o Patients (ith atrial flutter are at increased ris. of stro.e ecause of the ris.
of thromus formation in the atria from the stasis of lood"
o The primary goal in treatment of atrial flutter is to slo( the ventricular
response y increasing A$ loc."
Atrial fibrillation is characteri*ed y a total disorgani*ation of atrial electrical
activity due to multiple ectopic foci resulting in loss of effective atrial contraction"
o Atrial firillation usually occurs in the patient (ith underlying heart
disease# such as CA7# rheumatic heart disease# cardiomyopathy#
hypertensive heart disease# -5# and pericarditis" 3t can e caused y
thyroto!icosis# alcohol into!ication# caffeine use# electrolyte disturances#
stress# and cardiac surgery"
o Atrial firillation can often result in a decrease in C1# and thromi may
form in the atria as a result of lood stasis" An emoli*ed clot may develop
and pass to the rain# causing a stro.e"
o The goals of treatment include a decrease in ventricular response and
prevention of cereral emolic events"

Junctional dysrhythmias refer to dysrhythmias that originate in the area of the
A$ node# primarily ecause the SA node has failed to fire or the signal has een
loc.ed" 3n this situation# the A$ node ecomes the pacema.er of the heart"
o Qunctional premature eats are treated in a manner similar to that for
PACs"
o 1ther ,unctional dysrhythmias include ,unctional escape rhythm#
accelerated ,unctional rhythm# and ,unctional tachycardia" These
dysrhythmias are treated according to the patient6s tolerance of the rhythm
and the patient6s clinical condition"
o Qunctional dysrhythmias are often associated (ith CA7# -5#
cardiomyopathy# electrolyte imalances# inferior %3# and rheumatic heart
disease" Certain drugs &e"g"# digo!in# amphetamines# caffeine# nicotine'
can also cause ,unctional dysrhythmias"
o Treatment varies according to the type of ,unctional dysrhythmia"
First-degree AV block is a type of A$ loc. in (hich every impulse is conducted
to the ventricles ut the duration of A$ conduction is prolonged"
o 5irst-degree A$ loc. is associated (ith %3# CA7# rheumatic fever#
hyperthyroidism# vagal stimulation# and drugs such as digo!in# -
adrenergic loc.ers# calcium channel loc.ers# and flecainide"
o 5irst-degree A$ loc. is usually not serious ut can e a precursor of
higher degrees of A$ loc." Patients (ith first-degree A$ loc. are
asymptomatic"
o There is no treatment for first-degree A$ loc." Patients should continue
to e monitored for any ne( changes in heart rhythm"
Second-degree AV block# Type 3 &%oit* 3 or <enc.each heart loc.' is a
gradual lengthening of the P0 interval" 3t occurs ecause of a prolonged A$
conduction time until an atrial impulse is nonconducted and a N0S comple! is
loc.ed &missing'"
o Type 3 A$ loc. may result from use of drugs such as digo!in or -
adrenergic loc.ers" 3t may also e associated (ith CA7 and other
diseases that can slo( A$ conduction"
o Type 3 A$ loc. is usually a result of myocardial ischemia or infarction" 3t
is almost al(ays transient and is usually (ell tolerated" -o(ever# it may
e a (arning signal of a more serious A$ conduction disturance"
o 3f the patient is symptomatic# atropine is used to increase -0# or a
temporary pacema.er may e needed"
Second-degree AV block# Type 33 &%oit* 33 heart loc.'# involves a P (ave that
is nonconducted (ithout progressive antecedent P0 lengthening" This almost
al(ays occurs (hen a loc. in one of the undle ranches is present"
o Type 33 second-degree A$ loc. is a more serious type of loc. in (hich a
certain numer of impulses from the SA node are not conducted to the
ventricles"
o Type 33 A$ loc. is associated (ith rheumatic heart disease# CA7#
anterior %3# and digitalis to!icity"
o Type 33 A$ loc. often progresses to third-degree A$ loc. and is
associated (ith a poor prognosis" The reduced -0 often results in
decreased C1 (ith suse:uent hypotension and myocardial ischemia"
o Temporary treatment efore the insertion of a permanent pacema.er may
e necessary if the patient ecomes symptomatic &e"g"# hypotension#
angina' and involves the use of a temporary transvenous or transcutaneous
pacema.er"
Third-degree AV block or complete heart loc.# constitutes one form of A$
dissociation in (hich no impulses from the atria are conducted to the ventricles"
o Third-degree A$ loc. is associated (ith severe heart disease# including
CA7# %3# myocarditis# cardiomyopathy# and some systemic diseases such
as amyloidosis and progressive systemic sclerosis &scleroderma'"
o Third-degree A$ loc. almost al(ays results in reduced C1 (ith
suse:uent ischemia# -5# and shoc." Syncope from third-degree A$ loc.
may result from severe radycardia or even periods of asystole"
o Treatment" 5or symptomatic patients# a transcutaneous pacema.er is used
until a temporary transvenous pacema.er can e inserted"
Premature ventricular contraction &P$C' is a contraction originating in an
ectopic focus in the ventricles" 3t is the premature occurrence of a N0S comple!#
(hich is (ide and distorted in shape compared (ith a N0S comple! initiated
from the normal conduction path(ay"
o P$Cs are associated (ith stimulants such as caffeine# alcohol# nicotine#
aminophylline# epinephrine# isoproterenol# and digo!in" They are also
associated (ith electrolyte imalances# hypo!ia# fever# e!ercise# and
emotional stress" 7isease states associated (ith P$Cs include %3# mitral
valve prolapse# -5# and CA7"
o P$Cs are usually a enign finding in the patient (ith a normal heart" 3n
heart disease# depending on fre:uency# P$Cs may reduce the C1 and
precipitate angina and -5"
o Treatment is often ased on the cause of the P$Cs &e"g"# o!ygen therapy
for hypo!ia# electrolyte replacement'" 7rugs that can e considered
include -adrenergic loc.ers# procainamide# amiodarone# or lidocaine
&Oylocaine'"

Ventricular tachycardia &$T' is a run of three or more P$Cs" 3t occurs (hen an
ectopic focus or foci fire repetitively and the ventricle ta.es control as the
pacema.er"
o $T is a life-threatening dysrhythmia ecause of decreased C1 and the
possiility of deterioration to ventricular firillation# (hich is a lethal
dysrhythmia"
o $T is associated (ith %3# CA7# significant electrolyte imalances#
cardiomyopathy# mitral valve prolapse# long NT syndrome# digitalis
to!icity# and central nervous system disorders"
o $T can e stale &patient has a pulse' or unstale &patient is pulseless'"
o Treatment" Precipitating causes must e identified and treated &e"g"#
electrolyte imalances# ischemia'"
Ventricular fibrillation &$5' is a severe derangement of the heart rhythm
characteri*ed on +C/ y irregular undulations of varying shapes and amplitude"
%echanically the ventricle is simply B:uivering#C and no effective contraction#
and conse:uently no C1# occurs"
o $5 occurs in acute %3 and myocardial ischemia and in chronic diseases
such as CA7 and cardiomyopathy"
o $5 results in an unresponsive# pulseless# and apneic state" 3f not rapidly
treated# the patient (ill die"
o Treatment consists of immediate initiation of CP0 and advanced cardiac
life support &ACGS' measures (ith the use of defirillation and definitive
drug therapy"
Asystole represents the total asence of ventricular electrical activity" No
ventricular contraction occurs ecause depolari*ation does not occur"
o Asystole is usually a result of advanced cardiac disease# a severe cardiac
conduction system disturance# or end-stage -5"
o Patients are unresponsive# pulseless# and apneic"
o Asystole is a lethal dysrhythmia that re:uires immediate treatment
consisting of CP0 (ith initiation of ACGS measures &e"g"# intuation#
transcutaneous pacing# and 3$ therapy (ith epinephrine and atropine'"
Pulseless electrical activity &P+A' descries a situation in (hich electrical
activity can e oserved on the +C/# ut there is no mechanical activity of the
ventricles and the patient has no pulse"
o Prognosis is poor unless the underlying cause can e identified and
:uic.ly corrected"
o Treatment egins (ith CP0 follo(ed y intuation and 3$ therapy (ith
epinephrine"
S!##"N CA#%AC #"AT,
Sudden cardiac death &SC7' refers to death from a cardiac cause"
The ma,ority of SC7s result from ventricular dysrhythmias# specifically ventricular
tachycardia or firillation"
P&#1S,1T,M%A
Antidysrhythmia drugs may cause life-threatening dysrhythmias similar to those for
(hich they are administered" This concept is termed prodysrhythmia"
o The patient (ho has severe left ventricular dysfunction is the most susceptile
to prodysrhythmias"
o 7igo!in and some antidysrhythmia drugs can cause a prodysrhythmic
response"
#"$%0%LLAT%&N
7efirillation is the most effective method of terminating $5 and pulseless $T"
7efirillation is accomplished y the passage of a 7C electrical shoc. through the
heart to depolari*e the cells of the myocardium" The intent is that suse:uent
repolari*ation of myocardial cells (ill allo( the SA node to resume the role of
pacema.er"
0apid defirillation can e performed using a manual or automatic device"
o %anual defirillators re:uire health care providers to interpret cardiac
rhythms# determine the need for a shoc.# and deliver a shoc."
o Automatic e-ternal defibrillators &A+7s' are defirillators that have rhythm
detection capaility and the aility to advise the operator to deliver a shoc.
using hands-free defirillator pads"
S1NC,&N%4"# CA#%&2"S%&N
Synchroni*ed cardioversion is the therapy of choice for the patient (ith
hemodynamically unstale ventricular or supraventricular tachydysrhythmias"
o A synchroni*ed circuit in the defirillator is used to deliver a countershoc.
that is programmed to occur on the 0 (ave of the N0S comple! of the +C/"
o The synchroni*er s(itch must e turned on (hen cardioversion is planned"
The procedure for synchroni*ed cardioversion is the same as for defirillation# (ith
some e!ceptions"
%MPLANTA0L" CA#%&2"T"-#"$%0%LLAT& *%C#+
The 3C7 is used for patients (ho &2' have survived SC7# &2' have spontaneous
sustained $T# &3' have syncope (ith inducile ventricular tachycardia=firillation
during +PS# and &>' are at high ris. for future life-threatening dysrhythmias &e"g"#
have cardiomyopathy'"
The 3C7 consists of a lead system placed via a suclavian vein to the endocardium"
A attery-po(ered pulse generator is implanted sucutaneously# usually over the
pectoral muscle on the patient6s nondominant side"
o The 3C7 sensing system monitors the -0 and rhythm and identifies $T or
$5"
Appro!imately 2@ seconds after the sensing system detects a lethal
dysrhythmia# the defirillating mechanism delivers a shoc. to the
patient6s heart"
3f the first shoc. is unsuccessful# the generator recycles and can
continue to deliver shoc.s"
3n addition to defirillation capailities# 3C7s are e:uipped (ith antitachycardia and
antiradycardia pacema.ers"
+ducation of the patient (ho is receiving an 3C7 is of e!treme importance"
PAC"MA5"S
The artificial cardiac (acema6er is an electronic device used to pace the heart
(hen the normal conduction path(ay is damaged or diseased"
Pacema.ers (ere initially indicated for symptomatic radydysrhythmias" They
no( provide antitachycardia and overdrive pacing"
A permanent pacema.er is one that is implanted totally (ithin the ody"
A speciali*ed type of cardiac pacing has een developed for the management of
-5"
o Cardiac resynchroni*ation therapy &C0T' is a pacing techni:ue that
resynchroni*es the cardiac cycle y pacing oth ventricles# thus promoting
improvement in ventricular function"
o Several devices are availale that have comined C0T (ith an 3C7 for
ma!imum therapy"
A temporary pacema.er is one that has the po(er source outside the ody" There
are three types of temporary pacema.ers: transvenous# epicardial# and
transcutaneous pacema.ers"
Patients (ith temporary or permanent pacema.ers (ill e +C/ monitored to
evaluate the status of the pacema.er"
Complications of invasive temporary &i"e"# transvenous' or permanent pacema.er
insertion include infection and hematoma formation at the site of insertion of the
pacema.er po(er source or leads# pneumothora!# failure to sense or capture (ith
possile symptomatic radycardia# perforation of the atrial or ventricular septum
y the pacing lead# and appearance of Bend-of-lifeC attery parameters on testing
the pacema.er"
A#%&$"7!"NC1 CAT,"T" A0LAT%&N T,"AP1
0adiofre:uency catheter alation therapy is a relatively ne( development in the
area of antidysrhythmia therapy" Alation therapy is done after +PS has identified
the source of the dysrhythmia"
An electrode-tipped alation catheter is used to BurnC or alate accessory
path(ays or ectopic sites in the atria# A$ node# and ventricles"
Catheter alation is considered the nonpharmacologic treatment of choice for A$
nodal reentrant tachycardia or for reentrant tachycardia related to accessory
ypass tracts# and to control the ventricular response of certain
tachydysrhythmias"
The alation procedure is a successful therapy (ith a lo( complication rate" Care
of the patient follo(ing alation therapy is similar to that of a patient undergoing
cardiac catheteri*ation"
"C. C,AN."S ASS&C%AT"# 8%T, AC!T" C&&NA1 S1N#&M"
The 22-lead +C/ is the primary diagnostic tool used to evaluate patients
presenting (ith ACS"
There are definitive +C/ changes that occur in response to ischemia# in,ury# or
infarction of myocardial cells and (ill e seen in the leads that face the area of
involvement"
Typical +C/ changes seen in myocardial ischemia include ST-segment
depression and=or T (ave inversion"
The typical +C/ change seen during myocardial in,ury is ST-segment elevation"
An ST-segment elevation and a pathologic N (ave may e seen on the +C/ (ith
myocardial infarction"
Patient monitoring guidelines for patients (ith suspected ACS include continuous#
multilead +C/ and ST-segment monitoring" The leads selected for monitoring
should minimally include the leads that reflect the area of ischemia# in,ury# or
infarction"
S1NC&P"
Syncope# a rief lapse in consciousness accompanied y a loss in postural tone
&fainting'# is a common diagnosis of patients coming into the emergency
department"
The causes of syncope can e categori*ed as cardiovascular or noncardiovascular"
o Common cardiovascular causes of syncope include &2' neurocardiogenic
syncope or BvasovagalC syncope &e"g"# carotid sinus sensitivity' and &2'
primary cardiac dysrhythmias &e"g"# tachycardias# radycardias'"
o Noncardiovascular causes can include hypoglycemia# hysteria#
un(itnessed sei*ure# and verteroasilar transient ischemic attac."
The diagnostic (or.up for a patient (ith syncope from a suspected cardiac cause
egins (ith ruling out structural and=or ischemic heart disease"
o +chocardiography and stress testing are performed"
o 3n the older patient# (ho is more li.ely to have ischemic and structural heart
disease# +PS is used to diagnose atrial and ventricular tachydysrhythmias# as
(ell as conduction system disease causing radydysrhythmias"
o 3n patients (ithout structural heart disease or in (hom +PS testing is not
diagnostic# head-upright tilt tale testing may e performed"
o 1ther diagnostic tests for syncope include various recording devices"
-olter monitors and event monitors can e used"
A sucutaneously implanted loop recording device can also e used to
record the +C/ during presyncopal and syncopal events"
Lewis et al: Medical-Surgical Nursing: Assessment and Management of
Clinical Problems, 7
th
edition
Key Points
Chapter 3L: Nursing %anagement: 3nflammatory and Structural -eart
7isorders
%N$"CT%2" "N#&CA#%T%S
%nfecti)e endocarditis &3+' is an infection of the endocardial surface of the heart
that affects the cardiac valves" 3t is treated (ith penicillin"
T(o forms of 3+ include the suacute form &typically affecting those (ith
pree!isting valve disease' and the acute form &typically affecting those (ith
healthy valves'"
The most common causative organisms of 3+ are Staphylococcus aureus and
Streptococcus viridans.
The principal ris. factors for 3+ are prior endocarditis# prosthetic valves# ac:uired
valvular disease# and cardiac lesions"
$egetations# the primary lesions of 3+# adhere to the valve surface or endocardium
and can emoli*e to various organs &particularly the lungs# rain# .idneys# and
spleen' and to the e!tremities# causing lim infarction"
The infection may spread locally to cause damage to the valves or to their
supporting structures resulting in dysrhythmias# valvular incompetence# and
eventual invasion of the myocardium# leading to heart failure &-5'# sepsis# and
heart loc."
Clinical findings in 3+ are nonspecific and can include the follo(ing:
o Go(-grade fever# chills# (ea.ness# malaise# fatigue# and anore!ia
o Arthralgias# myalgias# ac. pain# adominal discomfort# (eight loss#
headache# and cluing of fingers
o Splinter hemorrhages &lac. longitudinal strea.s' in the nail eds
o Petechiae &a result of fragmentation and microemoli*ation of vegetative
lesions' in the con,unctivae# the lips# the uccal mucosa# and the palate
and over the an.les# the feet# and the antecuital and popliteal areas
o &sler9s nodes &painful# tender# red or purple# pea-si*e lesions' on the
fingertips or toes and :anewa'9s lesions &flat# painless# small# red spots'
on the palms and soles
o -emorrhagic retinal lesions called 0oth6s spots
o A ne( or changing murmur in the aortic or mitral valve
o -5
7efinitive diagnosis of 3+ e!ists if t(o of the follo(ing ma,or criteria are present:
positive lood cultures# ne( or changed cardiac murmur# or intracardiac mass or
vegetation noted on echocardiography"
Collaorative care consists of antiiotic prophyla!is for patients (ith specific
cardiac conditions efore dental# respiratory tract# gastrointestinal &/3'# and
genitourinary &/?' procedures and for high-ris. patients (ho &2' are to undergo
removal or drainage of infected tissue# &2' receive renal dialysis# or &3' have
ventriculoatrial shunts for management of hydrocephalus"
7rug therapy consists of long-term treatment (ith 3$ antiiotic therapy (ith
suse:uent lood cultures to evaluate the effectiveness of antiiotic therapy"
+arly valve replacement follo(ed y prolonged &; (ee.s or longer' drug therapy
is recommended for patients (ith fungal infection and prosthetic valve
endocarditis"
5ever is treated (ith aspirin# acetaminophen &Tylenol'# iuprofen &%otrin'# fluids#
and rest"
Complete ed rest is usually not indicated unless the temperature remains
elevated or there are signs of -5"
1verall goals for the patient (ith 3+ include &2' normal or aseline cardiac
function# &2' performance of activities of daily living &A7Gs' (ithout fatigue# and
&3' .no(ledge of the therapeutic regimen to prevent recurrence of endocarditis"
Patients and families must e taught to recogni*e signs and symptoms of life-
threatening complications of 3+# such as cereral emoli &e"g"# change in mental
status'# pulmonary edema &e"g"# dyspnea'# and -5 &e"g"# chest pain'"
o 5ever &chronic or intermittent' is a common early sign that the drug
therapy is ineffective"
Gaoratory data and lood cultures are monitored to determine the effectiveness
of the antiiotic therapy"
AC!T" P"%CA#%T%S
Pericarditis is caused y inflammation of the pericardial sac &the pericardium'"
Acute pericarditis most often is idiopathic ut can e caused y uremia# viral or
acterial infection# acute myocardial infarction &%3'# tuerculosis# neoplasm# and
trauma"
Pericarditis in the acute %3 patient may e descried as t(o distinct syndromes:
&2' acute pericarditis &occurs (ithin the initial >9 to L2 hours after an %3'# and &2'
7ressler syndrome &late pericarditis (hich appears > to ; (ee.s after an %3'"
Clinical manifestations include the follo(ing:
o Progressive# fre:uently severe chest pain that is sharp and pleuritic in
nature and (orse (ith deep inspiration and (hen lying supine" The pain is
relieved y sitting"
o Pain can e referred to the trape*ius muscle &shoulder# upper ac.'"
o The hallmar. finding in acute pericarditis is the (ericardial friction rub;
Complications include (ericardial effusion and cardiac tam(onade;
Collaorative care includes the follo(ing:
o Antiiotics
o Corticosteroids for pericarditis secondary to systemic lupus
erythematosus# patients already ta.ing corticosteroids for a rheumatologic
or other immune system condition# or patients (ho do not respond to
nonsteroidal antiinflammatory drugs &NSA37s'
o Pain and inflammation are usually treated (ith NSA37s or high-dose
salicylates &e"g"# aspirin'"
o Colchicine# an antiinflammatory agent used for gout# may e considered
for patients (ho have recurrent pericarditis"
o Pericardiocentesis is usually performed for pericardial effusion (ith
acute cardiac tamponade# purulent pericarditis# and a high suspicion of a
neoplasm"
Complications from pericardiocentesis include dysrhythmias#
further cardiac tamponade# pneumomediastinum# pneumothora!#
myocardial laceration# and coronary artery laceration"
The management of the patient6s pain and an!iety during acute pericarditis is a
primary nursing consideration"
+C/ monitoring can aid in distinguishing ischemic pain from pericardial pain as
ischemia involves locali*ed ST-segment changes# as compared to the diffuse ST-
segment changes present in acute pericarditis"
Pain relief measures include maintaining ed rest (ith the head of the ed
elevated to >@ degrees and providing an overed tale for support# and
antiinflammatory medications"
C,&N%C C&NST%CT%2" P"%CA#%T%S
Chronic constricti)e (ericarditis results from scarring (ith conse:uent loss of
elasticity of the pericardial sac and egins (ith an initial episode of acute
pericarditis follo(ed y firous scarring# thic.ening of the pericardium from
calcium deposition# and eventual oliteration of the pericardial space"
The end result is that the firotic# thic.ened# and adherent pericardium impairs the
aility of the atria and ventricles to stretch ade:uately during diastole"
Clinical manifestations mimic -5 and cor pulmonale and include dyspnea on
e!ertion# peripheral edema# ascites# fatigue# anore!ia# and (eight loss"
The most prominent finding is ,ugular venous distention"
Auscultation reveals a pericardial .noc.# (hich is a loud early diastolic sound
often heard along the left sternal order"
Treatment of choice for chronic constrictive pericarditis is a pericardiectomy"
Pericardiectomy involves complete resection of the pericardium through a median
sternotomy (ith the use of cardiopulmonary ypass"
M1&CA#%T%S
M'ocarditis is a focal or diffuse inflammation of the myocardium caused y
viruses# acteria# fungi# radiation therapy# and pharmacologic and chemical
factors"
%yocarditis is fre:uently associated (ith acute pericarditis# particularly (hen it is
caused y co!sac.ievirus ) strains"
%yocarditis results in cardiac dysfunction and has een lin.ed to the development
of dilated cardiomyopathy"
Clinical manifestations include the follo(ing:
o 5ever# fatigue# malaise# myalgias# pharyngitis# dyspnea# lymphadenopathy#
and nausea and vomiting are early systemic manifestations of the viral
illness"
o +arly cardiac manifestations appear L to 28 days after viral infection and
include pleuritic chest pain (ith a pericardial friction ru and effusion"
o Gate cardiac signs relate to the development of -5 and may include an S3
heart sound# crac.les# ,ugular venous distention# syncope# peripheral
edema# and angina"
Collaorative care includes the follo(ing:
o %anaging associated cardiac decompensation (ith:
7igo!in &Gano!in' to treat ventricular failure
7iuretics to reduce fluid volume and decrease preload
Nitroprusside &Nitropress'# inamrinone &3nocor'# and milrinone
&Primacor' to reduce afterload and improve cardiac output
The use of anticoagulation therapy may e considered in patients
(ith a lo( e,ection fraction (ho are at ris. for thromus formation
from lood stasis in the cardiac chamers"
o 3mmunosuppressive therapy to reduce myocardial inflammation and to
prevent irreversile myocardial damage"
o 1!ygen therapy# ed rest# and restricted activity"
o 3ntraaortic alloon pump therapy and ventricular assist devices"
Nursing interventions focus on assessment for the signs and symptoms of -5 and
include assessing the level of an!iety# instituting measures to decrease an!iety#
and .eeping the patient and family informed aout therapeutic measures"
%ost patients (ith myocarditis recover spontaneously# although some may
develop dilated cardiomyopathy" 3f severe -5 occurs# the patient may re:uire
heart transplantation"
,"!MAT%C $"2" AN# ,"AT #%S"AS"
heumatic fe)er is an inflammatory disease of the heart potentially involving all
layers of the heart"
heumatic heart disease is a chronic condition resulting from rheumatic fever
that is characteri*ed y scarring and deformity of the heart valves"
Acute rheumatic fe)er &A05' is a complication that occurs as a delayed se:uela
of a group A streptococcal pharyngitis and affects the heart# ,oints# central nervous
system &CNS'# and s.in"
Aout >8E of A05 episodes are mar.ed y carditis# meaning that all layers of the
heart are involved# and this is referred to as rheumatic pancarditis"
o 0heumatic endocarditis is found primarily in the valves" $egetation forms
and valve leaflets may fuse and ecome thic.ened or even calcified#
resulting in stenosis or regurgitation"
o %yocardial involvement is characteri*ed y Aschoff9s bodies;
o 0heumatic pericarditis affects the pericardium# (hich ecomes thic.ened
and covered (ith a firinous e!udate# and often involves pericardial
effusion"
o The lesions of rheumatic fever are systemic# especially involving the
connective tissue# as (ell as the ,oints# s.in# and CNS"
Clinical manifestations of A05 include the follo(ing:
o The presence of t(o ma,or criteria or one ma,or and t(o minor criteria
plus evidence of a preceding group A streptococcal infection"
%a,or criteria:
Carditis results in three signs: &2' murmurs of mitral or aortic
regurgitation# or mitral stenosisD &2' cardiac enlargement and
-5D &3' pericarditis"
%ono- or polyarthritis causes s(elling# heat# redness#
tenderness# and limitation of motion"
Chorea &Sydenham6s chorea' involves involuntary movements#
especially of the face and lims# muscle (ea.ness# and
disturances of speech and gait"
+rythema marginatum lesions are right pin.# nonpruritic#
mapli.e macular lesions that occur mainly on the trun. and
pro!imal e!tremities"
Sucutaneous nodules are firm# small# hard# painless
s(ellings located over e!tensor surfaces of the ,oints"
%inor criteria:
Clinical findings: fever# polyarthralgia
Gaoratory findings: elevated +S0# elevated <)C#
elevated C0P
Complications of A05 include chronic rheumatic carditis"
S.in should e assessed for sucutaneous nodules and erythema marginatum"
The overall goals for a patient (ith rheumatic fever include &2' normal or aseline
heart function# &2' resumption of daily activities (ithout ,oint pain# and &3'
verali*ation of the aility to manage the disease"
-ealth promotion emphasi*es prevention of rheumatic fever y early detection
and treatment of group A streptococcal pharyngitis (ith antiiotics# specifically
penicillin"
o The success of treatment re:uires strict adherence to the full course of
antiiotic therapy"
o The primary goals of managing a patient (ith A05 are to control and
eradicate the infecting organismD prevent cardiac complicationsD and
relieve ,oint pain# fever# and other symptoms (ith antiioticsD optimal restD
and antipyretics# NSA37s# and corticosteroids"
o Secondary prevention aims at preventing the recurrence of rheumatic fever
(ith monthly in,ections of long-acting penicillin" Additional prophyla!is
is necessary if a patient (ith .no(n rheumatic heart disease has dental or
surgical procedures involving the upper respiratory# /3 &e"g"# endoscopy'#
or /? tract"
The e!pected outcomes for the patient (ith rheumatic fever and heart disease
include &2' aility to perform A7Gs (ith minimal fatigue and pain# &2' adherence
to treatment regimen# and &3' e!pression of confidence in managing disease"
2AL2!LA ,"AT #%S"AS"
$alvular stenosis refers to a constriction or narro(ing of the valve opening"
$alvular regurgitation &also called valvular incompetence or insufficiency'
occurs (ith incomplete closure of the valve leaflets and results in the ac.(ard
flo( of lood"
Mitral 2al)e Stenosis
Adult mitral valve stenosis results from rheumatic heart disease" Gess
commonly# it can occur congenitally# from rheumatoid arthritis and from
systemic lupus erythematosus"
Clinical manifestations of mitral stenosis include e!ertional dyspnea# fatigue#
palpitations from atrial firillation# and a loud first heart sound and a lo(-pitched#
rumling diastolic murmur"
Mitral egurgitation
%itral regurgitation &%0' is caused y %3# chronic rheumatic heart disease# mitral
valve prolapse# ischemic papillary muscle dysfunction# and 3+"
3n chronic %0# the additional volume load results in atrial enlargement#
ventricular dilation# and eventual ventricular hypertrophy"
3n acute %0# there is a sudden increase in pressure and volume that is transmitted
to the pulmonary ed# resulting in pulmonary edema and life-threatening shoc."
Clinical manifestations of acute %0 include thready# peripheral pulses and cool#
clammy e!tremitiesD and a ne( systolic murmur"
Patients (ith asymptomatic %0 should e monitored carefully# and surgery
considered efore significant left ventricular failure or pulmonary hypertension
develops"
Mitral 2al)e Prola(se
Mitral )al)e (rola(se &%$P' is an anormality of the mitral valve leaflets and
the papillary muscles or chordae that allo(s the leaflets to prolapse# or uc.le#
ac. into the left atrium during systole" The etiology of %$P is un.no(n ut is
related to diverse pathogenic mechanisms of the mitral valve apparatus"
3n many patients %$P found y echocardiography is not accompanied y any
other clinical manifestations of cardiac disease# and the significance of the finding
is unclear"
Clinical manifestations of %$P can include a murmur from regurgitation that gets
more intense through systole# chest pain# dyspnea# palpitations# and syncope"
Aortic 2al)e Stenosis
3n older patients# aortic stenosis is a result of rheumatic fever or senile
firocalcific degeneration that may have an etiology similar to coronary artery
disease"
Aortic stenosis results in left ventricular hypertrophy and increased myocardial
o!ygen consumption# and eventually# reduced cardiac output leading to
pulmonary hypertension and -5"
Clinical manifestations include a systolic# crescendo-decrescendo murmur and the
classic triad of angina# syncope# and e!ertional dyspnea"
Aortic 2al)e egurgitation
Acute aortic regurgitation &A0' is caused y 3+# trauma# or aortic dissection"
Chronic A0 is generally the result of rheumatic heart disease# a congenital
icuspid aortic valve# syphilis# or chronic rheumatic conditions"
Clinical manifestations of acute A0 include severe dyspnea# chest pain# and
hypotension indicating left ventricular failure and shoc. that constitute a medical
emergency"
Clinical manifestations of chronic A0 include e!ertional dyspnea# orthopnea# and
paro!ysmal nocturnal dyspnea after considerale myocardial dysfunction has
occurred"
Tricus(id and Pulmonic 2al)e #isease
7iseases of the tricuspid and pulmonic valves are uncommon# (ith stenosis
occurring more fre:uently than regurgitation"
Tricuspid valve stenosis occurs almost e!clusively in patients (ith rheumatic
mitral stenosis# in 3$ drug ausers# or in patients treated (ith a dopamine agonist"
Pulmonary stenosis is almost al(ays congenital"
Tricuspid and pulmonic stenosis oth result in the ac.(ard flo( of lood to the
right atrium and right ventricle# respectively"
Tricuspid stenosis results in right atrial enlargement and elevated systemic venous
pressures" Pulmonic stenosis results in right ventricular hypertension and
hypertrophy"
Collaborati)e Care of 2al)ular ,eart #isease
Collaorative care of valvular heart disease includes the prevention of recurrent
rheumatic fever and 3+ and the prevention of e!acerations of -5# acute
pulmonary edema# and thromoemolism"
Anticoagulant therapy is used to prevent and treat systemic or pulmonary
emoli*ation and is used prophylactically in patients (ith atrial firillation"
An alternative treatment for valvular heart disease is percutaneous transluminal
alloon valvuloplasty &PT)$' to split open the fused commissures" 3t is used for
mitral# tricuspid# and pulmonic stenosis# and less often for aortic stenosis"
Surgical intervention is ased on the clinical state of the patient and depends on
the valves involved# the valvular pathology# the severity of the disease# and the
patient6s clinical condition"
$alve repair &e"g"# mitral commissurotomy JvalvulotomyK# is typically the surgical
procedure of choice"
1pen surgical valvuloplasty involves repair of the valve y suturing the torn
leaflets# chordae tendineae# or papillary muscles and is used to treat mitral or
tricuspid regurgitation"
Annuloplasty entails reconstruction of the annulus# (ith or (ithout the aid of
prosthetic rings &e"g"# a Carpentier ring'"
Prosthetic mechanical valves are made from manmade materials"
Prosthetic iologic valves are constructed from ovine# porcine# and human
cardiac tissue and usually contain some human-made materials"
%echanical prosthetic valves are more durale and last longer than iologic
valves ut have an increased ris. of thromoemolism# necessitating long-term
anticoagulation therapy"
)iologic valves do not re:uire anticoagulation therapy due to their lo(
thromogenicity" -o(ever# they are less durale due to the tendency for early
calcification# tissue degeneration# and stiffening of the leaflets"
Auscultation of the heart should e performed to monitor the effectiveness of
digo!in# -adrenergic loc.ers# and antidysrhythmic drugs"
Prophylactic antiiotic therapy is necessary to prevent 3+ and# if the valve disease
(as caused y rheumatic fever# ongoing prophyla!is is necessary"
Patients on anticoagulation therapy after valve replacement surgery must have the
international normali*ed ratio &3N0' chec.ed regularly &usually monthly' to
assess the ade:uacy of therapy" Therapeutic values are 2"@ to 3"@"
The nurse must teach the patient to see. medical care if any manifestations of
infection or -5# any signs of leeding# and any planned invasive or dental
procedures are planned"
Patients on anticoagulation therapy should e encouraged to (ear a medical alert
racelet"
CA#%&M1&PAT,1
Cardiom'o(ath' &C%P' constitutes a group of diseases that directly affect the
structural or functional aility of the myocardium"
C%P is classified as primary &refers to those conditions in (hich the etiology of
the heart disease is un.no(n' or secondary &the cause of the myocardial disease is
.no(n and is secondary to another disease process'"
Cardiomyopathies can lead to cardiomegaly and -5# and are the leading cause for
heart transplantation"
#ilated Cardiom'o(ath'
#ilated cardiom'o(ath' is characteri*ed y a diffuse inflammation and rapid
degeneration of myocardial fiers that results in ventricular dilation# impairment
of systolic function# atrial enlargement# and stasis of lood in the left ventricle"
Clinical manifestations develop acutely after an infectious process or insidiously
over a period of time"
o Symptoms include decreased e!ercise capacity# fatigue# dyspnea at rest#
paro!ysmal nocturnal dyspnea# orthopnea# palpitations# adominal
loating# nausea# vomiting# and anore!ia"
o Signs include an irregular heart rate (ith an anormal S3 and=or S>#
tachycardia or radycardia# pulmonary crac.les# edema# (ea. peripheral
pulses# pallor# hepatomegaly# and ,ugular venous distention"
o -eart murmurs and dysrhythmias are common"
3nterventions focus on controlling -5 y enhancing myocardial contractility and
decreasing afterload (ith drug therapy"
Nutritional therapy and cardiac rehailitation may help alleviate symptoms of -5
and improve C1 and :uality of life"
7ilated C%P does not respond (ell to therapy# and patients may enefit from a
ventricular assist device &$A7' to allo( the heart to rest and recover from acute
-5 or as a ridge to heart transplantation"
Cardiac resynchroni*ation therapy and an implantale cardioverter-defirillator
may e considered in appropriate patients" The patient6s family must learn
cardiopulmonary resuscitation &CP0' and ho( to access emergency care"
The goal of therapy is to .eep the patient at an optimal level of function and out
of the hospital"
,'(ertro(hic Cardiom'o(ath'
,'(ertro(hic cardiom'o(ath' &-C%' is asymmetric left ventricular
hypertrophy (ithout ventricular dilation"
The four main characteristics of -C% are: &2' massive ventricular hypertrophyD
&2' rapid# forceful contraction of the left ventricleD &3' impaired rela!ation
&diastole'D and &>' ostruction to aortic outflo( &not present in all patients'" The
end result is impaired ventricular filling as the ventricle ecomes noncompliant
and unale to rela!"
-C% is the most common cause of SC7 in other(ise healthy young people"
Patients (ith -C% may e asymptomatic or may have e!ertional dyspnea#
fatigue# angina# syncope# and dysrhythmias"
/oals of intervention are to improve ventricular filling y reducing ventricular
contractility and relieving left ventricular outflo( ostruction"
7rug therapy for -C% includes -adrenergic loc.ers or calcium channel
loc.ers" 7igitalis preparations are contraindicated unless they are used to treat
atrial firillation# and antidysrhythmics are used as needed"
5or patients at ris. for SC7# the implantation of a cardioverter-defirillator is
recommended"
Atrioventricular pacing can e eneficial for patients (ith -C% and outflo(
ostruction"
Some patients may e candidates for a surgical procedure called
ventriculomyotomy and myectomy# (hich involves incision of the hypertrophied
septal muscle and resection of some of the hypertrophied ventricular muscle"
Nursing interventions for -C% focus on relieving symptoms# oserving for and
preventing complications# and providing emotional and psychologic support"
estricti)e Cardiom'o(ath'
estricti)e cardiom'o(ath', the least common C%P# impairs diastolic filling
and stretch though systolic function remains unaffected"
The specific etiology of restrictive C%P is un.no(n"
Clinical manifestations include fatigue# e!ercise intolerance# and dyspnea ecause
the heart cannot increase C1 y increasing the heart rate (ithout further
compromising ventricular filling"
Currently no specific treatment for restrictive C%P e!ists and interventions are
aimed at improving diastolic filling and the underlying disease process"
o Treatment includes conventional therapy for -5 and dysrhythmias"
o -eart transplant may also e a consideration"
o Nursing care is similar to the care of a patient (ith -5"
Lewis et al: Medical-Surgical Nursing: Assessment and Management of
Clinical Problems, 7
th
edition
Key Points
Chapter 39: Nursing %anagement: $ascular 7isorders
P"%P,"AL AT"%AL #%S"AS"
Peri(heral arterial disease &PA7' is a progressive narro(ing and degeneration
of the arteries of the nec.# adomen# and e!tremities" 3n most cases# it is a result
of atherosclerosis"
PA7 typically appears in the si!th to eighth decades of life" 3t occurs at an earlier
age in persons (ith diaetes mellitus and more fre:uently in African Americans"
The four most significant ris. factors for PA7 are cigarette smo.ing &most
important'# hyperlipidemia# hypertension# and diaetes mellitus"
The most common locations for PA7 are the coronary arteries# carotid arteries#
aortic ifurcation# iliac and common femoral arteries# profunda femoris artery#
superficial femoral artery# and distal popliteal artery"
AN"!1SMS
Aortic aneur'sms are outpouchings or dilations of the arterial (all"
The primary causes of aortic aneurysms can e classified as degenerative#
congenital# mechanical# inflammatory# or infectious"
Aortic aneurysms may involve the aortic arch# thoracic aorta# and=or adominal
aorta# ut most are found in the adominal aorta elo( the level of the renal
arteries"
Thoracic aorta aneurysms are often asymptomatic# ut the most common
manifestations are deep# diffuse chest pain that may e!tend to the interscapular
areaD hoarseness as a result of pressure on the recurrent laryngeal nerveD and
dysphagia from pressure on the esophagus"
Adominal aortic aneurysms &AAAs' are often asymptomatic ut symptoms may
mimic pain associated (ith adominal or ac. disorders"
The most serious complication related to an untreated aneurysm is rupture and
leeding"
7iagnostic tests for AAAs include chest !-ray# electrocardiogram &to rule out
myocardial infarction'# echocardiography# CT scan# and magnetic resonance
imaging scan"
The goal of management is to prevent the aneurysm from rupturing"
Surgical repair of AAA involves &2' incising the diseased segment of the aorta# &2'
removing intraluminal thromus or pla:ue# &3' inserting a synthetic graft# and &>'
suturing the native aortic (all around the graft"
%inimally invasive endovascular grafting is an alternative to conventional
surgical repair of AAA and involves the placement of a sutureless aortic graft into
the adominal aorta inside the aneurysm via a femoral artery cutdo(n"
Preoperatively# the patient is monitored for indications of aneurysm rupture"
Preoperative teaching should include a rief e!planation of the disease process#
the planned surgical procedure&s'# preoperative routines# and (hat to e!pect
immediately after surgery"
The overall goals for a patient undergoing aortic surgery include &2' normal tissue
perfusion# &2' intact motor and sensory function# and &3' no complications related
to surgical repair# such as thromosis or infection"
Postoperatively# the patient (ill have an endotracheal tue for mechanical
ventilation# an arterial line# a central venous pressure or pulmonary artery
catheter# peripheral intravenous lines# an ind(elling urinary catheter# a nasogastric
tue# and continuous +C/ and pulse o!imetry monitoring"
o %onitoring for graft patency and ade:uate renal perfusion are prioritiesD
maintenance of an ade:uate )P is e!tremely important"
o Antiiotics are given to prevent infection"
o Peripheral pulses# s.in temperature and color# capillary refill time# and
sensation and movement of the e!tremities are assessed and recorded per
hospital policy"
o -ourly urine outputs and daily (eights are recorded"

1n discharge# the patient should e instructed to gradually increase activities ut
to avoid heavy lifting for at least > to ; (ee.s"
+!pected outcomes for the patient (ho undergoes aortic surgery include &2'
patent arterial graft (ith ade:uate distal perfusion# &2' ade:uate urine output# &3'
normal ody temperature# and &>' no signs of infection"
A&T%C #%SS"CT%&N
Aortic dissection occurs most commonly in the thoracic aorta and is the result of
a tear in the intimal &innermost' lining of the arterial (all allo(ing lood to
Btrac.C et(een the intima and media and creates a false lumen of lood flo("
The e!act cause of aortic dissection is uncertain# and most people (ith dissection
are older and have chronic hypertension"
Clinical manifestations include a sudden# severe pain in the anterior part of the
chest or intrascapular pain radiating do(n the spine into the adomen or legs that
is descried as BtearingC or Bripping"C
7iagnostic studies used to assess aortic dissection are similar to those performed
for AAA"
The initial goal of therapy for aortic dissection (ithout complications is to lo(er
the )P and myocardial contractility (ith drug therapy"
Surgery is indicated (hen drug therapy is ineffective or (hen complications of
aortic dissection are present"
P"%P,"AL AT"%AL #%S"AS" &$ T," L&8" "<T"M%T%"S
PA7 of the lo(er e!tremities affects the aortoiliac# femoral# popliteal# tiial# or
peroneal arteries"
The classic symptom of PA7 of the lo(er e!tremities is intermittent
claudication, (hich is defined as ischemic muscle ache or pain that is
precipitated y a consistent level of e!ercise# resolves (ithin 28 minutes or less
(ith rest# and is reproducile"
Paresthesia# manifested as numness or tingling in the toes or feet# may result
from nerve tissue ischemia" /radually diminishing perfusion to neurons produces
loss of oth pressure and deep pain sensations"
Physical findings include thin# shiny# and taut s.inD loss of hair on the lo(er legsD
diminished or asent pedal# popliteal# or femoral pulsesD pallor or lanching of the
foot in response to leg elevation &elevation pallor'D and reactive hyperemia
&redness of the foot' (hen the lim is in a dependent position &dependent ruor'"
0est pain most often occurs in the forefoot or toes# is aggravated y lim
elevation# and occurs (hen there is insufficient lood flo( to maintain asic
metaolic re:uirements of the tissues and nerves of the distal e!tremity"
Complications of PA7 include nonhealing ulcers over ony prominences on the
toes# feet# and lo(er leg# and gangrene" Amputation may e re:uired if lood flo(
is not restored"
Tests used to diagnose PA7 include 7oppler ultrasound (ith segmental lood
pressures at the thigh# elo( the .nee# and at an.le level" A falloff in segmental
)P of more than 38 mm -g indicates PA7"
Angiography is used to delineate the location and e!tent of the disease process"

The first treatment goal is to aggressively modify all cardiovascular ris. factors in
all patients (ith PA7# (ith smo.ing cessation a priority"
7rug therapy includes antiplatelet agents and AC+ inhiitors" T(o drugs are
approved to treat intermittent claudication# pento!ifylline &Trental' and cilosta*ol
&Pletal'"
The primary nonpharmacologic treatment for claudication is a formal e!ercise-
training program (ith (al.ing eing the most effective e!ercise"
/in.go iloa has een found to increase (al.ing distance for patients (ith
intermittent claudication"
Critical limb ischemia is a chronic condition characteri*ed y ischemic rest pain#
arterial leg ulcers# and=or gangrene of the leg due to advanced PA7"
3nterventional radiologic procedures for PA7 include percutaneous transluminal
alloon angioplasty" There is a relatively high rate of restenosis after alloon
angioplasty"
The most common surgical procedure for PA7 is a peripheral arterial ypass
operation (ith autogenous vein or synthetic graft material to ypass or carry
lood around the lesion"
The overall goals for the patient (ith lo(er e!tremity PA7 include &2' ade:uate
tissue perfusion# &2' relief of pain# &3' increased e!ercise tolerance# and &>' intact#
healthy s.in on e!tremities"
After surgical or radiologic intervention# the operative e!tremity should e
chec.ed every 2@ minutes initially and then hourly for s.in color and temperature#
capillary refill# presence of peripheral pulses# and sensation and movement of the
e!tremity"
All patients (ith PA7 should e taught the importance of meticulous foot care to
prevent in,ury"
Acute arterial ischemia is a sudden interruption in the arterial lood supply to
tissue# an organ# or an e!tremity that# if left untreated# can result in tissue death"
Signs and symptoms of an acute arterial ischemia usually have an arupt onset
and include the Bsi! Ps:C pain# pallor# pulselessness# paresthesia# paralysis# and
poi.ilothermia &adaptation of the ischemic lim to its environmental temperature#
most often cool'"
Treatment options include anticoagulation# thromolysis# emolectomy# surgical
revasculari*ation# or amputation"
T,&M0&AN.%%T%S &0L%T"ANS *0!"."9S #%S"AS"+
Thromboangiitis obliterans is a some(hat rare nonatherosclerotic# segmental#
recurrent inflammatory vaso-occlusive disorder of the small and medium-si*ed
arteries# veins# and nerves of the upper and lo(er e!tremities"
Patients may have intermittent claudication of the feet# hands# or arms"
As the disease progresses# rest pain and ischemic ulcerations develop"
There are no laoratory or diagnostic tests specific to )uerger6s disease"

Treatment includes complete cessation of toacco use in any form &including
secondhand smo.e'" 1ther therapies can e considered ut have had limited
success"
Surgical options include revasculari*ation and sympathectomy# (ith the most
common eing sympathectomy &transection of a nerve# ganglion# and=or ple!us of
the sympathetic nervous system'"
A1NA!#9S P,"N&M"N&N
a'naud9s (henomenon is an episodic vasospastic disorder of small cutaneous
arteries# most fre:uently involving the fingers and toes" The e!act etiology of
0aynaud6s phenomenon remains un.no(n"
Clinical symptoms include vasospasm-induced color changes of the fingers# toes#
ears# and nose &(hite# lue# and red'" An episode usually lasts only minutes ut in
severe cases may persist for several hours"
Symptoms usually are precipitated y e!posure to cold# emotional upsets#
caffeine# and toacco use"
There is no simple diagnostic test for 0aynaud6s phenomenon# and diagnosis is
ased on persistent symptoms for at least 2 years"
Patient teaching should e directed to(ard prevention of recurrent episodes:
temperature e!tremes and all toacco products should e avoided"
Calcium channel loc.ers are the first-line drug therapy"
2"N&!S T,&M0&S%S
2enous thrombosis is the most common disorder of the veins and involves the
formation of a thromus &clot' in association (ith inflammation of the vein"
Su(erficial thrombo(hlebitis occurs in aout ;@E of all patients receiving 3$
therapy and is of minor significance"
#ee( )ein thrombosis &7$T' involves a thromus in a deep vein# most
commonly the iliac and femoral veins# and can result in emoli*ation of thromi
to the lungs"
Three important factors &called 2irchow9s triad' in the etiology of venous
thromosis are &2' venous stasis# &2' damage of the endothelium# and &3'
hypercoagulaility of the lood"
Superficial thromophleitis presents as a palpale# firm# sucutaneous cordli.e
vein" The area surrounding the vein may e tender to the touch# reddened# and
(arm" A mild systemic temperature elevation and leu.ocytosis may e present"
o Treatment of superficial thromophleitis includes elevating the affected
e!tremity to promote venous return and decrease the edema and applying
(arm# moist heat"
o %ild oral analgesics such as acetaminophen or aspirin are used to relieve
pain"
The patient (ith 7$T may or may not have unilateral leg edema# e!tremity pain#
(arm s.in# erythema# and a systemic temperature greater than 288"> 5 &39 C'"
The most serious complications of 7$T are pulmonary emolism &P+' and
chronic venous insufficiency" Chronic venous insufficiency &C$3' results from
valvular destruction# allo(ing retrograde flo( of venous lood"
3nterventions for patients at ris. for 7$T include early moili*ation of surgical
patients" Patients on ed rest need to e instructed to change position# dorsifle!
their feet# and rotate their an.les every 2 to > hours"
The usual treatment of 7$T in hospitali*ed patients involves ed rest# elevation
of the e!tremity# and anticoagulation"
Patients (ith hyperhomocysteinemia are treated (ith vitamins );# )22# and folic
acid to reduce homocysteine levels"
The goal of anticoagulation therapy for 7$T prophyla!is is to prevent 7$T
formationD the goals in the treatment of 7$T are to prevent propagation of the
clot# development of any ne( thromi# and emoli*ation"
3ndirect thromin inhiitors include unfractionated heparin &?-' and lo(-
molecular-(eight heparin &G%<-'"
o ?- affects oth the intrinsic and common path(ays of lood coagulation
y (ay of the plasma cofactor antithromin"
o G%<- is derived from heparin and also acts via antithromin# ut has an
increased affinity for inhiiting factor Oa"
7irect thromin inhiitors can e classified as hirudin derivatives or synthetic
thromin inhiitors" -irudin inds specifically (ith thromin# therey directly
inhiiting its function (ithout causing plasma protein and platelet interactions"
5actor Oa inhiitors inhiit factor Oa directly or indirectly# producing rapid
anticoagulation"
o 5ondaparinu! &Ari!tra' is administered sucutaneously and is approved
for 7$T prevention in orthopedic patients and treatment of 7$T and P+
in hospitali*ed patients (hen administered in con,unction (ith (arfarin"
o )oth direct thromin inhiitors and factor Oa inhiitors have no antidote"
5or 7$T prophyla!is# lo(-dose ?-# G%<-# fondaparinu!# or (arfarin can e
prescried"
o G%<- has replaced heparin as the anticoagulant of choice to prevent
7$T for most surgical patients"
o 7$T prophyla!is typically lasts the duration of the hospitali*ation"
o Patients undergoing ma,or orthopedic surgery may e prescried
prophyla!is for up to 2 month postdischarge"
$ena cava interruption devices# such as the /reenfield filter# can e inserted
percutaneously through right femoral or right internal ,ugular vein to filter clots
(ithout interrupting lood flo("
Nursing diagnoses and collaorative prolems for the patient (ith venous
thromosis can include the follo(ing:
o Acute pain related to venous congestion# impaired venous return# and
inflammation
o 3neffective health maintenance related to lac. of .no(ledge aout the
disorder and its treatment
o 0is. for impaired s.in integrity related to altered peripheral tissue
perfusion
o Potential complication: leeding related to anticoagulant therapy
o Potential complication: pulmonary emolism related to emoli*ation of
thromus# dehydration# and immoility
The overall goals for the patient (ith venous thromosis include &2' relief of pain#
&2' decreased edema# &3' no s.in ulceration# &>' no complications from
anticoagulant therapy# and &@' no evidence of pulmonary emoli"
o 7epending on the anticoagulant prescried# ACT# aPTT# 3N0# hemogloin#
hematocrit# platelet levels# and=or liver en*ymes are monitored"
o Platelet counts are monitored for patients receiving ?- or G%<- to
assess for -3T"
o ?-# (arfarin# and direct thromin inhiitors are titrated according to the
results of clotting studies"
o The nurse oserves for signs of leeding# including epista!is# gingival
leeding# hematuria# and melena"
7ischarge teaching should focus on elimination of modifiale ris. factors for
7$T# the importance of compression stoc.ings and monitoring of laoratory
values# medication instructions# and guidelines for follo(-up"
o The patient and family should e taught aout signs and symptoms of P+
such as sudden onset of dyspnea# tachypnea# and pleuritic chest pain"
o 3f the patient is on anticoagulant therapy# the patient and family need
information on dosage# actions# and side effects# as (ell as the importance
of routine lood tests and (hat symptoms to report to the health care
provider"
o -ome monitoring devices are no( availale for testing of PT=3N0"
o Patients on G%<- (ill need to learn ho( to self-administer the drug or
have a friend or family memer administer it"
o Patients on (arfarin should e instructed to follo( a consistent diet of
foods containing vitamin K and to avoid any additional supplements that
contain vitamin K"
o Proper hydration is recommended to prevent additional
hypercoagulaility"
o +!ercise programs should e developed (ith an emphasis on (al.ing#
s(imming# and (ading"
The e!pected outcomes for the patient (ith venous thromosis include &2'
minimal to no pain# &2' intact s.in# &3' no signs of hemorrhage or occult leeding#
and &>' no signs of respiratory distress"
2A%C&S" 2"%NS
2aricose )eins, or varicosities# are dilated# tortuous sucutaneous veins most
fre:uently found in the saphenous system"
o Primary varicose veins are more common in (omen and patients (ith a
strong family history and are proaly caused y congenital (ea.ness of
the veins"
o Secondary varicose veins typically result from a previous 7$T"
o Secondary varicose veins also may occur in the esophagus# in the
anorectal area# and as anormal arteriovenous connections"
o 0eticular veins are smaller varicose veins that appear flat# less tortuous#
and lue-green in color"
o Telangiectasias &.no(n as spider veins' are very small visile vessels that
appear luish-lac.# purple# or red"
The etiology of varicose veins is un.no(n and ris. factors include congenital
(ea.ness of the vein structure# female gender# use of hormones &oral
contraceptives or -0T'# increasing age# oesity# pregnancy# venous
ostruction resulting from thromosis or e!trinsic pressure y tumors# or
occupations that re:uire prolonged standing"
The most common symptom of varicose veins is an ache or pain after
prolonged standing# (hich is relieved y (al.ing or y elevating the lim"
Nocturnal leg cramps in the calf may occur"
Treatment usually is not indicated if varicose veins are only a cosmetic
prolem"
Collaorative care involves rest (ith the affected lim elevated# compression
stoc.ings# and e!ercise# such as (al.ing"
An heral therapy used for the treatment of varicose veins is horse chestnut
seed e!tract"
Sclerotherapy involves the in,ection of a sustance that oliterates venous
telangiectasias# reticular veins# and small# superficial varicose veins"
Ne(er# more costly# noninvasive options for the treatment of venous
telangiectasias include laser therapy and high-intensity pulsed-light therapy"
Surgical intervention is indicated for recurrent thromophleitis or (hen
chronic venous insufficiency cannot e controlled (ith conservative therapy"
o Surgical intervention involves ligation of the entire vein &usually the
greater saphenous' and dissection and removal of its incompetent
triutaries"
o An alternative techni:ue is amulatory phleectomy# (hich involves
pulling the varicosity through a BstaC incision# follo(ed y e!cision
of the vein"
o Ne(er# less invasive procedures include endovenous occlusion using
radiofre:uency closure or laser# or transilluminated po(ered
phleectomy"
Prevention is a .ey factor related to varicose veins and the patient should
avoid sitting or standing for long periods of time# maintain ideal ody (eight#
ta.e precautions against in,ury to the e!tremities# avoid (earing constrictive
clothing# and participate in a daily (al.ing program"
C,&N%C 2"N&!S %NS!$$%C%"NC1 AN# L". !LC"S
Chronic )enous insufficienc' &C$3' is a condition in (hich the valves in the
veins are damaged# (hich results in retrograde venous lood flo(# pooling of
lood in the legs# and s(elling"
C$3 often occurs as a result of previous episodes of 7$T and can lead to venous
leg ulcers"
Causes of C$3 include vein incompetence# deep vein ostruction# congenital
venous malformation# A$ fistula# and calf muscle failure"
o 1ver time# the s.in and sucutaneous tissue around the an.le are replaced
y firous tissue# resulting in thic.# hardened# contracted s.in"
o The s.in of the lo(er leg is leathery# (ith a characteristic ro(nish or
Bra(nyC appearance from the hemosiderin deposition"
o +dema and ec*ema# or Bstasis dermatitis#C are often present# and pruritus is
a common complaint"
$enous ulcers classically are located aove the medial malleolus"
o The (ound margins are irregularly shaped# and the tissue is typically a
ruddy color"
o ?lcer drainage may e e!tensive# especially (hen the leg is edematous"
o Pain is present and may e (orse (hen the leg is in a dependent position"
Compression is essential to the management of C$3# venous ulcer healing# and
prevention of ulcer recurrence"
o 1ptions include elastic (raps# custom-fitted compression stoc.ings#
elastic tuular support andages# a $elcro (rap# intermittent compression
devices# a paste andage (ith an elastic (rap# and multilayer &three or
four' andage systems"
o %oist environment dressings are the mainstay of (ound care and include
transparent film dressings# hydrocolloids# hydrogels# foams# calcium
alginates# impregnated gau*e# gau*e moistened (ith saline# and
comination dressings"
o Nutritional status and inta.e should e evaluated in a patient (ith a venous
leg ulcer"
o 0outine prophylactic antiiotic therapy typically is not indicated"
o Clinical signs of infection in a venous ulcer include change in :uantity#
color# or odor of the drainageD presence of pusD erythema of the (ound
edgesD change in sensation around the (oundD (armth around the (oundD
increased local pain# edema# or othD dar.-colored granulation tissueD
induration around the (oundD delayed healingD and cellulitis"
The usual treatment for infection is sharp deridement# (ound
e!cision# and systemic antiiotics"
3f the ulcer fails to respond to conservative therapy# alternative
treatments may include use of a radiant heat andage# vacuum-
assisted closure therapy# and coverage (ith a split-thic.ness s.in
graft# cultured epithelial autograft# allograft# or ioengineered s.in"
o An heral therapy used for the treatment of C$3 is horse chestnut seed
e!tract"
Gong-term management of venous leg ulcers should focus on teaching the patient
aout self-care measures ecause the incidence of recurrence is high"
o Proper foot and leg care is essential to avoid additional trauma to the s.in"
o The patient (ith C$3 (ith or (ithout a venous ulcer is instructed to avoid
standing or sitting (ith the feet dependent for long periods"
o $enous ulcer patients are instructed to elevate their legs aove the level of
the heart to reduce edema"
1nce an ulcer is healed# a daily (al.ing program is encouraged"
Prescription compression stoc.ings should e (orn daily and
replaced every > to ; months to reduce the occurrence of C$3"