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Major disorders of Circulatory
System
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general Nursing diagnosis
for clients with circulatory system disorders
A. Decreased cardiac output
1) Excessive cardiac workload
2) Decreased tissue perfusion
3) Blood loss
4) Decrease venous return
B. Altered tissue perfusion rel to
1) Decreased cardiac output
2) Peripheral vasoconstriction or obstruction
3) Inadequate, excessive, or ,inappropriate nutrition
4) Venous stasis
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general Nursing diagnosis
for clients with circulatory system disorders
C. high risk for activity intolerance rel to
1. Decrease cardiac output
2. Dec tissue perfusion
3. Decreased oxygen-carrying capacity of blood
4. PainD. In effective individual coping rel to type A personality
E. Fear rel to questionable prognosis and potential disability
F. Personal identity disturbance related to sick role
G. Pain related to
1. impaired tissue perfusion
2. Operative trauma
H. Sexual dysfunction related to fear, medication, and disease process
I. Fluid volume Excess related to dec cardiac output
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general Nursing diagnosis
for clients with circulatory system disorders
J. ineffective denial related to prognosis and dse.process
K. Noncompliance related to denial of prognosis
L. High risk of injury related to diagnostics andtherapeutics
M. self care deficit related to imposedrestrictions
N. Fatigue related to decreased cardiac outputand decreased oxygen-carrying capacity of theblood
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general Nursing diagnosis
for clients with circulatory system disorders
O. High risk infection related to dse process treatment modalities
P. Ineffective breathing pattern related to trauma of chest surgery
Q. High risk for impaired skin integrity related to altered peripheral
perfusionR. Fluid volume deficit related to blood loss
S.Altered thought process related to decreased cerebral perfusion
T.Altered nutrition, less than body requirements related to
inadequate dietary intake
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ncm102
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Congenital heart disease (CHD)
malformation of the heart or the large bloodvessels near the heart. "Congenital"speaks only to time, not to causation. Itmeans "born with" or "present at birth."
Alternative names forCHD include:congenital heart defect, congenital heartmalformation, congenital cardiovascular
disease, congenital cardiovascular defect,and congenital cardiovascularmalformation.
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Incidence:the most frequent form of major birth defects innewborns affecting close to 1% of newborn babies(8 per 1,000). This figure is an underestimate sinceit does not include some common problems,namely: Patent ductus arteriosus in preterm babies (a temporary
condition)
Bicuspid (two cusps) aortic valve (the aortic valve usuallyhas three cusps or flaps)
Mitral Valve prolapse (drooping of a heart valve) Peripheral pulmonary stenosis (narrowing of the lung
vessels well away from the heart)
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CONGENITALHEART DISEASE
CHD
EARLY CYANOSIS LATE CYANOSIS
1. Transpositionof 1. Ventricular Septal Defect
Great Vessels 2. Atrial Septal Defect
2. Truncus Arteriosus 3. Patent Ductus Arteriosus
3. TetralogyofFallot 4. Arterio-venous Malformation
a. VSD
b. Overridingofthe Aortac. Pulmonic Stenosis
d. Rightventricularhypertrophy
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Conditions
Defects associated with dec pulmonary bld
flow
D
efects associated with inc pulmonary bldflow
Defects causing obstruction to cardiac
chamber outflow
Defects associated with mixing of saturated
and desaturated blood
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Defects associated with dec
pulmonary bld flow
Right to left shunting of blood due to presence of a defect and
obstruction of pulmonary blood flow
Obstructed pulmonary flow leads to higher right side heart pressure
Some or most does not enter the pulmonary circulation anddoes not pick up oxygen in the lungs; instead blood is shunted
to the left side of the heart
Deoxygenated as well as oxygenated blood circulated to the
body
Cyanosis and hypoxemia present
TOF
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Defects associated with inc pulmonary
bld flow
Left to right shunting of blood across a septal
defect or blood vessel
Pulmonary overcirculation and increased workof ventricles
Risk for heart failure
A
cyanotic ASD, VSD, PDA
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Defects causing obstruction to cardiac
chamber outflow
Narrowing of outflow tract from heart to
blood vessels
Increased work of heart as it strains to pushblood out
Risk for heart failure and poor cardiac output
COA, PS, AS
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Defects associated with mixing of
saturated and desaturated blood
Oxygenated and deoxygenated blood mixes in
heart chambers
Increased pulmonary blood flow due to defect Hypoxemia and cyanosis present, often severe
Risk for poor cardiac output and risk for heart
failure (HF) TGA, Truncus arteriosus
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TGA
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Early Cyanotic Disease
Tetralogy of Fallot
AffectedpatientsusuallyhavecyanosisofAffectedpatientsusuallyhavecyanosisof
thelips andskin whenfeedingorcryingthelips andskin whenfeedingorcrying
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Early Cyanotic Disease-
Tetralogy of Fallot
COMPONENTS:COMPONENTS:
1.1. VSDVSD
(Ventriculoseptal(Ventriculoseptal
defect)defect)
2.2. Overriding of theOverriding of the
AortaAorta
3.3. Pulmonic stenosisPulmonic stenosis
4.4. RVH (RightRVH (Right
ventricularventricular
hypertrophy)hypertrophy)
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Late Cyanotic Disease-
Atrial/ Ventricular Septal Defect
ASDASD -- due to incompletedue to incomplete
separation of the atriaseparation of the atria
VSDVSD abnormal opening of theabnormal opening of the
membranous or muscular portion ofmembranous or muscular portion of
the ventricular septumthe ventricular septum
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Late Cyanotic Disease-
Patent DuctusArteriosus
-- FailureoftheductusFailureoftheductusarteriosustoclosearteriosustoclose
after birth,thusthereafter birth,thusthere
is a connectionis a connection
betweenthe aorta andbetweenthe aorta and
the mainorleftthe mainorleftpulmonary arterypulmonary artery
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COARCTATION OF THEAORTA
Narrowing of thearch of the aortabeyond the originof the leftsubclavian artery.
BP readings arehigher in the upperextremitiescompared to thelower.
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ValvularHeart Disease:
Aortic Stenosis
--PathologicPathologic
narrowing of thenarrowing of theaortic orificeaortic orifice
--May lead to leftMay lead to left
ventricularventricularhypertrophyhypertrophy
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ValvularHeart Disease:
Mitral Stenosis
-- PathologicnarrowingPathologicnarrowing
oftheorificeoftheoftheorificeofthe
mitralvalvemitralvalve
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ValvularHeart Disease:
Mitral Valve Prolapse
--AKA Floppy mitral valve,AKA Floppy mitral valve,
clickclick--murmur syndrome,murmur syndrome,
Barlow syndromeBarlow syndrome
--Prolapse of one or bothProlapse of one or both
cusps of the mitral valve intocusps of the mitral valve into
the left atrium leading tothe left atrium leading to
regurgitationregurgitation
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Nursing care for Infants with Cardiac
malformation
Assessment:
color: cyanosis pallor
Apical pulse, peripheral pulses, presence of
murmurs
Respirations, dyspnea, frequency of colds
Blood pressure
Chest abnormalities
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Nursing care for Infants with Cardiac
malformation
Analysis/ Nursing diagnoses
1. activity intolerance related to imbalance between oxygen supplyand demand
2. Decrease cardiac output related to structural defect
3. Altered growth and development related to inadequate oxygenand nutrients to tissues and limited socialization with peers
4. High risk for infection due to debilitated physical status
5. Altered family processes related to having child with heartcondition
6. High risk for injury complications) related to cardiac conditionsand therapies
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Nursing care for Infants with Cardiac
malformation
Analysis and Diagnosis
7. Body image disturbance related to having physical
defect
8. Social isolation related to inability to participate
in active play
9. High risk for caregiver role strain related to caring
for ill child
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Nursing care for Infants with Cardiac
malformation
Planning/Implementation
Correctly calculate dosage ofDigoxin; usually prescribed in
micrograms (1000 ug = 1mg)
Take the apical pulse prior to administering ofDigoxin or drug
Observe for sign of digitalis toxicity
Teach parent the proper home administration ofDigoxin
Help patient cope with symptoms of the disease
Foster growth promoting family relationships
Preoperative assessment areas necessary for planningpostoperative care
Prepare child emotionally and physically for the surgery
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Cardiac Surgery
Surgical correction of
congenital defects
within the heart or
surgery of the greatvessels in the
immediate area
surrounding theheart
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Open-heart surgery- uses
cardiopulmonary bypass;provides a relatively blood free
operative site; heart-lung
machine maintains gas exchange
during surgery
Closed-heart surgery does notuse cardiopulmonary bypass
machine; indicated for ligation
of a patent ductus arteriosus or
COA
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Nursing Interventions
Determine the childs level of understanding;
drawing a picture or tell a story
Correct misunderstandings/teach the child about
the surgery using a diagrams and play therapy
Accompany the child to the OR and RR
Have child practice post-op procedures
Include parents in teaching sessions
Establish pre-op baseline data for VS
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Post-op
Prevent injury/complicationsVS, ECG, neurosurgical site
Promote gas exchange
I & O
Provide nutrition
Psychologic support of the child/family
Allow activity
Provide client teaching and discharge planning
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Blood dyscrasias
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Sickle CellAnemia (SCA)
AR disorder
genetically recessive, meaning
that one must have inherited a
defective copy of the gene from
both parents to develop thedisorder.
form of iron deficiency caused
by an abnormality in the way
hemoglobin proteins form.
Instead of the saucer-likeshape of normal red blood
cells, these cells are crescent-
or sickle-shaped.
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SCA-
Classification & Pathophysiology
Sickle-shaped red blood cells are unable tocarry oxygen as well as normal cells, leadingto a condition that causes many of thesymptoms of acquired iron deficiencyanemia. However, this disease carries theadded risk of blood clots since the abnormallyshaped cells are more likely to stick to eachother and the walls of the blood vessels.
Types Homozygous SCA
Heterozygous SCA
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SCA-
clinical findings
Vaso-occlusive Crisis
Most common and only painful type
Results from sickled cells obstructing BV leading
to occlusion, ischemia, and potential necrosis
Blockage causes the blood viscosity to increase,
producing sludging and resulting in further
hypoxia and increased sickling
S/S: fever, acute abdominal pain, hypoxia, Hand-
foot syndrome, arthralgia without an exacerbation
of anemia
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SCA-
clinical findings
Splenic sequestration crisis
Results from the spleen pooling largequantities of blood in spleen, which causes a
precipitous drop in BP and ultimately to shockACUTE episodes:
Most common in 8mos to 5 y/o
Can result to death due to anemia and CVS
collapse CHRONIC states
functional ASPLENIA
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SCA-
clinical findings
Aplastic Crisis- diminished RBC production
Maybe triggered by viral or other infection
Profound anemia results from rapid destruction of
RBC combined with decreased production
Hyper-hemolytic Crisis
S/S: anemia jaundice and reticulocytosis ARare cases and suggests a coexisting abn.
such as G6PD
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SCA-
therapeutics
Unfortunately, simply increasing the dietary iron intake will
not help individuals with this disease.
There is currently no cure, but there is hope that through
persistent research, a cure can be found.
Currently, people with sickle-cell disease can be treated
with a host of drugs that alleviate symptoms and prevent
opportunistic infections that arise as a result of a weakened
immune system.
A 1999 report in the Journal of theAmerican MedicalAssociation (JAMA) described in vitro fertilization
techniques can prevent the disease from being handed
down to offspring.
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SCA-
therapeutics
1. prevention of sickling phenomenon Adequate oxygenation
Adequate hydration
2.treatment of crisis Rest
Hydration/ electrolyte replacement
Pain mngt
Antibiotic therapy
Blood products: transfusion therapy RBC
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SCA
NSG care
1.mngt of pain Use of analgesia
Joint swelling: elevation of body part
Relaxation/breathing techniques/distraction Physical therapy, whirlpool baths, transcutaneousnerve stimulation (TENS)
2.mngt of infection Nsg care focus : ID of s/s of infection
Home medications: advise pt for compliance ofthe whole therapy
3. Promote coping skills
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SCA
NSG care
Monitoring and managing Complications
1. Leg ulcers: Wound ostomy-continencenurse
2. Priapism leading to impotence` Advise pt to empty his bladder at the onset of the
attack, exercise and take a warm bath
` Persistence of symptoms needs immediate
medical attention-IV hydartion, analgesia.Possible intracavernosal aspiration
3. Chronic pain and substance abuse
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Hemophilia
Blood clotting disorder; Genetic : X-linked
Recessive transmission; males
Types: Hemophilia typeA : Factor VIII deficiency;
Classic Hemophilia ;More common
Hemophilia type B: Factor IX def.; Christmas Hemophilia
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Hemophilia-
clinical findings
Prolonged bleeding from any wound
Hemarthrosis: bleeding into the joints; resulting in pain;deformity and retarded growth
Intracranial hemorrhage
Anemia
Severity of bleeding
severity F8 activity Remarks
Mild 5-50% Bleeding with sever trauma
or SxModerate 1-5% Bleeding with trauma
Severe
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Hemophilia-
therapeutics
1. Control of bleeding
2. Prevention of bleeding with the use of
factor replacementa. Drugs that replace deficient coagulationfactors
a) Factor 8 concentrate
Obatained from human sources and provides good sourceof concentarted F8
b) Factor 9 complex: contains F2, F7, F9, F10conc
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Hemophilia-
therapeutics
a. Adjunctive measures
a) Aminocaproic acid (Amicar): inhibits the enzyme
that destroys fromed fibrin and inc fibrinogen
activity in clot formationb) Fibrinogen: maintains plasma fibrinogen levels
required for clotting materials
c) Thrombin: supplies physiologic levels of natural
material at superficial bleeding sites to control
beeding
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Hemophilia-
NSG Care
1. ASSESSMENT:
a. Parent/child knowledge of disease process and injuryprevention
b. Joint bleeding
c. Mobility of joints2. ANALYSIS/NSG DX
a. High risk for injury (hemorrhage) related to deficient bloodclotting
b. Pain related to bleeding into joints/tissues
c. Impaired mobility rel to effects of hemorrhages into joints andtissues
d. Altered family processes rel to situational crisis
(child with chronic disease)
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Hemophilia-
NSG Care
2. ANALYSIS/NSG DX
e. Knowledge deficit rel to
1) Disease process, home mngt., activity limitations
f. Body image disturbance related to
1) Perception of self as a different
2) Inability to participate
g. Body image disturbance rel to1) Perception of self as different
2) Inability to participate in selected activities
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Hemophilia-
Planning /implementation
1. Instruct the child and parents in the tx of thebleeding, esp the joints
1. Immobilization of the area
2. Compression of the area
3. Elevation of the body part
2. Provide appropriate activity that lessens thechance of trauma, which is often difficultbcoz boys are physically active
3. Select safe toys; inform parents to safe-proof house to minimize injuries
4. Avoid use of aspirin or ibuprofen
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Hemophilia-
Planning /implementation
Control joint pain so the child to prevent
muscle atrophy
Provide counseling about geneticpredisposition
Encourage parents to treat the child as
normally as possible, avoiding
overprotection and over permissiveness
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Kawasaki DSE
Aka: MUCOCUTANEOUS LYMPH NODESYNDROME
Acute febrile illness of unknown cause; the
principal area of involvement iscardiovascular system with extensiveperivasculitis of arterioles, venules, andcapillaries, incl the coronary arteries,panvasculitis of arterioles
Classification; common among japanese,then blacks, then caucasians
Geograhic and seasonal outbreaks
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Kawasaki Disease-
clinical findings
Fever for more than 5 days
Bilateral congestion of ocular conjunctiva without exudation
Changes is mucous membranes of the oral cavity such as
erythema, dryness, and fissuring of the lips, orpharyngeal
reddening orstrawberry tongue
Changes in extremities, such as peripheral edema,
erythema and desquamation of palms and soles,
particularly the periungal peeling
Polymorphous rash, primarily the trunk Cervical LAD
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Kawasaki Disease-
therapeutics
Primarily supportive and directed toward
controlling fever, preventing dehydration
and minimizing possible cardiac
complications
Large doses of aspirin
IV gamma globulin
Monitoring cardiac status
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Kawasaki Dse-
planning and implementation
to control fever:Administer aspirin
To control joint pains
Observe for allergic reaction to and side
effects of IV gamma globulin Monitor for signs of heart disease, especially
arrhythmias
See general Nursing Care of preschoolers
with health problems See meeting the needs of the family of thechild with disability
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Kawasaki Disease-
Evaluation and outcome
Parents and child can discuss concerns
about illness
Child exhibits no sign of impaired skin
Child does not report the presence of pain
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Rheumatic Fever
Collagen disease: characterized by damaged connectivetissue and usually blood vessels
Classification: Autoimmune reaction to GABHS pharyngitis Self-limited involves joint: involves joints, skin brain
Clinical Findings Heart: Mitral and aortic stenosis occur Joints: edema, inflammation and effusion esp. in the knees,
elbows, joints hips, shoulder and wrist Skin: erythema, macular with clear center and wavy
demarcated border usually on the trunk and proximalextremeties
Neorologic: chorea Low-grade fever, epistaxis, abdominal pain, arthralgia,
weakness, fatigue, pallor, anorexia and weight loss
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Assessment Findings
Major symptoms (J
ones Criteria) Carditis cardiomegaly, Aschoff nodules (areas of
inflammation and degeneration around heart valves,
pericardium, and myocardium), valvular insufficiency of
mitral and aortic valves; SOB, hepatomegaly, edema
Polyarthritis migratory, large joints become red, swollen
and painful
Chorea (Sydenhams chorea, St Vitus dance) CNS
disorder char by abrupt, purposeless, involuntary muscular
movements
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Subcutaneous nodules
usually a sign of severedisease; occurs with active
carditis; firm, nontender, no
lesion bony prominences of
joints
Erythema marginatum
transient nonpruritic rash
starting with central red
patches that expand
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Minor symptoms
Reliable history of RF,
Fever
Arthralgias
Recent history of strep infection Diagnostic tests: antistreptolysin O (ASO) titer
increased
Elevated Sedimentation Rate (ESR)
Elevated C- reactive protein
Prolonged PR Interval on Electrocardiogram
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Diagnostic criteria
Two Major Criteria or
One Major and 2 Minor Criteria
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Rheumatic Fever
Therapeutics
Antibiotic therapy to eradicate the organismand preventing recurrence Penicillin used prophylactically to prevent future
attacks of strep and further damage to the heart
To be taken until age 20 or for 5 years after attack,whichever is longer
Arhtritis - aspirin
Chorea decrease stimulation; provide a
safe environment Prevention of permanent cardiac damage
Palliation of other symptoms
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Rheumatic Fever
NSG Care
Assessment Child/parent compliance with drug regimen
Symptoms development
Nutritional intake
Activity level
Analysis and Diagnosis High risk for injury rel to autoimmune system
Decrease cardiac output rel to disease process
Altered nutrition: less than the body requirements Rel to anorexia/ fatigue
High risk for impaired skin integrity rel to disease process
Impaired physical mobility Pain related to inflammation of the joints
Fatigue related decreased cardiac output
Activity tolerance
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Rheumatic Fever
NSG Care
Planning and implementation1. Encourage bed rest and reduce work load of the heart
2. Encourage child to do schoolwork and keep with the class
3. Stimulate the development of quiet hobbies and collections
4. Gradually increase activities over a period of weeks to
months
5. Handle painful joins carefully
6. Maintain proper body alignment to prevent deformities
7. Monitor for pain medication and administer when necessary8. Encourage an increase intake of Nutritious food
9. Provide small frequent. nutrional
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YoungAdult
Cardiac Diseases Hodgkins Disease
Infectious Mononucleosis
Pericarditis
Myocarditits
Endocarditis
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Hodgkins Disease
Etio: unknown
Higher incidence among male and youngadults
Proliferation of malignant cells (ReedSternberg cells ) within the Lymph nodes
All tissues may eventually be involved butchiefly lymph node, spleen, liver, tonsils andbone marrow
Classification by staging and the presence orabsence of systemic symptoms
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Hodgkins Disease-
clinical Findings
Dyspnea and dysphagia caused by pressure from theenlarge nodes
Pruritus
Anorexia
Enlarged LN (generally cervical LN are involved first Diagnosis confirmed by histologic examination of a lymphnode
Progressive anemia
Elevated temperature
Enlarged spleen and liver may occur Pressure from the enlarged LN may lead to edema andobstructive jaundice
thrombocytopenia
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Hodgkins Disease-
therapeutics
Staging procedures include: CBC, liver fxnstudies ; CT thorax and abdomen; bonemarrow and lymph node biopsies;lymphangiography
Radiotherapy Vital organs must be shielded
Potential side effects: nausea, skin rashes; drymouth, dysphagia
Surgical intervention includes excision ofmasses to relieve pressure on the otherorgans
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Hodgkins Disease-
therapeutics
Chemotherapy Nitrogen mustard Thiophosphoramide Chlorambucil
Vincristine Doxorubicine Prednisone Procarbazine hydrochloride Bleomycin
Vinblastine Dacarbazine MOPP andABVD protocols
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Hodgkins Disease-
NSG care
Assessment
LN to determine enlargement
Temperature for baseline data
Liver and spleen to determine enlargenment
Analysis and Diagnosis
Refer to the general Nursing diagnosis for
clients with circulatory system disorders
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Hodgkins Disease-
NSG care
Planning and implementation Provide emotional support for the client and
family
Protect from infection
Monitor infection Monitor temperature
Observe for signs of anemia; provide adequaterest
Examine sclera and skins for signs of jaundice Encourage high nutrient density foods; observe
for anorexia and nausea
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Hodgkins Disease-
NSG care
Evaluation and outcomes
Remains afebrile
Conserves energy
Verbalizes feelings related to therapy and
prognosis
Continues supervision
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Infectious Mononucleosis
Acute infectious disease of the lymphaticsystem
caused by Epstein barr Virus
MOT: respiratory droplets Incubation period: uncertain; probably 28-
42D
Incidence: high among 15-35 years old
Complication: hepatitis, ruptured spleen,pericarditis and meningoencephalitis
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Infectious Mononucleosis
clinical manifestation
Sore throat, malaise, stiff neck, nausea
Elevated temp, enlarged tenderLN (esp those atthe cervical nodes involved first)
Splenomegaly in approximately 50% of the clients Elevated lymphocytes and monocytes counts
Positive heterophile antibody agglutination test
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Diagnosis of infectious mononucleosis
requires the evaluation of clinical symptoms andhematologic and serologic laboratory testresults.
Hematologic studies reveal a normal to
increased white blood cell count, decreasedsegmented neutrophils, and markedlyincreasedreactive lymphocytes.
Serologic tests include assays for heterophileantibodies and assays for antibodies specific for
EBV. In about 85% of IM cases, patients produce IgM
heterophile antibodies.
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A heterophile antibody is an antibody that willreact with an antigen other than the antigen forwhich it was produced.
In the case of infectious mononucleosis, the
patient produces heterophile antibodies whichmay react with the erythrocytes of sheep, beef,oxen, or horses.
Heterophile antibodies are detectable about oneweek after infection, peak at 2 to 4 weeks, anddecrease to undetectable levels at about 12weeks.
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Infectious mononucleosis
Nursing Care
Assessment: Temperature for baseline data
History of lethargy and fatigue
Cervical Lymphadenopathy Hepatosplenomegaly
Inflammation of the throat-swelling, grayish whiteexudate in the tonsils
Analysis/Nursing Refer to General Nursing diagnosis for clients
with circulatory Disorder: N, O
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Infectious mononucleosis
Nursing Care
Planning and Implementation Provide rest Administer aspirin as ordered Assess for signs of complications; spleen should
not be palpated once the diagnosis is made Increase fluid intake Support natural defense mechanism; encourage
intake of foods rich in immune stimulatingnutrients, esp. VitaminA,C E, minerals: seleniumand zinc
Evaluation: Fatigue is reduced Afebrile state is maintained
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Inflammatory diseases of the heart
Pericarditis
Myocarditis
Infective Subacute endocarditis
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Pericarditis
Etio: bacterial (streptococcus,staphylococcus, gonococcus,meningococcus, Viral (coxakie, influenza),
Mycotic(Fungal), rickettsial, parasitic, trauma,collagen disease, rhematic fever, neoplasticdisease
Sequelae
Loss of pericardial elasticity or accumulation offluid within the sac
Heart failure or cardiac tamponade
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Pericarditis, acute
Central chest pain aggravated by coughing,inspiration and recumbency
Pericardial friction rub on ausculation
Characteristic ECG changes Treatment: Treat underlying cause
NSAIDs
Steriods are used for unresponsive to NSAIDs
Cochicine for recurrenct episodes
Pericardiectomy in rare cases
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Pericarditis, constrictive
Constrictivepericarditis: scarring and
calcificationofthepericardium as a
lateconsequenceofinflammation
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Pericarditis, Constrictive
Markedly elevated jugular venous pressure
With accentuated x and y descents andKaussmul sign
Pericardial knock on auscultation MRI, CT or ECHo imaging shows thickened
pericardium
Treatment Surgical Pericardiectomy
A low cardiac output state may occur after surgerybcoz myocardial atrophy from long termcompression and may require prolonged pressortherapy
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PERICARDITIS WITH EFFUSION Inflammation of the pericardium accompanied by fluid
accumulation in the pericardial sac.
Dyspnea, orthopnea
Palpitations, cough
Dysphagia
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Myocarditis
Inflammationofthe myocardiumInflammationofthe myocardium
Etiology:Etiology:
viruses (Coxsackie B), bacteria,viruses (Coxsackie B), bacteria,
chemicals, radiationetc.chemicals, radiationetc.
RheumaticfeverRheumaticfever
EndocarditicdseEndocarditicdse
SequelaeSequelae
ImpairedcontractilityoftheheartImpairedcontractilityoftheheart
caused byinflammatoryprocesscaused byinflammatoryprocess
Myocardialischemia andMyocardialischemia and
necrosisnecrosis
Endocarditis
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Endocarditis
Subacute Bacterial Endocarditis
ENDOCARDITISENDOCARDITIS
inflammation of theinflammation of the
endocardium usually involvingendocardium usually involving
the valvesthe valves
SUBACUTE BACTERIALSUBACUTE BACTERIAL
ENDOCARDITISENDOCARDITIS
-- occurs in an abnormal valveoccurs in an abnormal valve
-- Underlying cause could beUnderlying cause could bedue rheumatic heart disease,due rheumatic heart disease,
congenital heart disease,congenital heart disease,
MVP or previous valveMVP or previous valve
surgerysurgery
I fl t Di Of Th H t
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Inflammatory Diseases Of The Heart
Therapeutic interventions
Oxygen therapy, Bed rest,
antibiotic to relive underlying infection
Corticosteroids, anti-dysrhythmias Pericardiectomy
Salicylates to suppress rheumatic activity
Cardiac monitoring
I fl t Di Of Th H t
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Inflammatory Diseases Of The Heart
NSG care
Assessment
Signs of shock, heart failure and dysrhythmias
Temperature for baseline data
Distention of neck veins, friction rub andmurmur
Overt and covert indicators of pain
Analysis/Nursing diagnosis
Refer to General Nursing diagnosis for clientswith circulatory Disorder:A1 B1 C E N O
I fl t Di Of Th H t
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Inflammatory Diseases Of The Heart
NSG care
Planning and implementation Maintain tranquil environment and help the client
achieve the maximum rest
Medicate for discomfort as needed
Allow expression of concerns Explain post-hospitalization therapy to improve
compliance
Administer antibiotics as ordered
Monitor temperature and blood cultures todetermine the effect of antibiotic therapy
If Sx is undertaken, care for chest tubes andfollow post operative chest surgery routine
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ADULT CARDIACDISEASES
Atherosclerosis
Coronary Heart Disease
Angina Pectoris
Myocardial Infarction
Hypertension Peripheral Vascular diseases
Across the life span
Anemia
Leukemia
DIC
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Arteriosclerosis; Hardening of the arteries;Plaque buildup arteries
Definition Atherosclerosis is a condition in which fatty
material collects along the walls of arteries. Thisfatty material thickens, hardens, and mayeventually block the arteries.
Atherosclerosis is a type of arteriosclerosis. Thetwo terms are often used to mean the same thing.
Atherosclerosis
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Atherosclerosis
Causes and incidence,
Atherosclerosis is a common disorder of the arteries. It occurs whenfat, cholesterol, and other substances build up in the walls of arteriesand form hard substances called plaque.
Eventually, the plaque deposits can make the artery narrow and lessflexible. This makes it harder for blood to flow. If the coronary
arteries become narrow, blood flow to the heart can slow down orstop, causing chest pain (stable angina), shortness of breath, heartattack, and other symptoms.
Pieces of plaque can break apart and move through thebloodstream. This is a common cause of heart attack and stroke.Blood clots can also form around the plaque deposits. Clots block
blood flow. If the clot moves into the heart, lungs, or brain, it cancause a stroke, heart attack, or pulmonary embolism.
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risk factors
Risk factors for atherosclerosis include: Diabetes
High blood pressure
High cholesterol
High-fat diet
Obesity Personal or family history of heart disease
Smoking
The following conditions have also been linked toatherosclerosis:
Cerebrovascular disease Kidney disease involving dialysis
Peripheral vascular disease
Atherosclerosis
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Atherosclerosis
clinical Manifestation
More common symptoms of coronary heart disease include thefollowing. No one person usually has all of these symptoms.
Chest pain on exertion (angina pectoris), which may be relieved byrest
Shortness of breath on exertion
Jaw pain, back pain, or arm pain, especially on left side, eitherduring exertion or at rest
Palpitations (a sensation of rapid or very strong heart beats in yourchest)
Dizziness, light-headedness, or fainting
IrregularHeartbeat
Weakness on exertion or at rest Silent ischemia is a condition in which no symptoms occur eventhough an electrocardiogram (ECG, or heart tracing) and/or othertests show evidence of ischemia.Arteries may be blocked 50% ormore without causing any symptoms.
Atherosclerosis
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Atherosclerosis
clinical Manifestation
Diaphoresis
BP elevation
Signs of underlying disease maybeevident (cardiomegaly, valvular disease,
dysrythmias)
ECG recordings: varied in different
activities
ECG often reveals previous infarction
Atherosclerosis
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Atherosclerosis
Diagnostics
Tests that may be used to diagnoseatherosclerosis or complications include:
Ankle/brachial index (ABI)
Arteriography Cardiac stress testing
CT scan
Doppler study
Intravascular ultrasound (IVUS)
Magnetic resonance arteriography (MRA
Atherosclerosis
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Atherosclerosis
Therapeutic Intervention
Restricted activity
Pharmacologic mngt. Aspirin: When taken daily or every other day, aspirin reduces
the risk of developing angina or heart attack by reducing thetendency of your blood to clot.
It reduces the chance that a clot will form over a rupturingplaque in the coronary artery, a common underlyingphenomenon in heart attack (myocardial infarction).
Side effects of aspirin include ulcers or bleeding problems.
Talk to your health care provider before starting aspirin.
Beta-blockers - Beta-blockers decrease your heart rate and
blood pressure, thus reducing your hearts demand foroxygen. Clinical trials have shown prevention of future heartattacks and sudden death.
Atherosclerosis
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Atherosclerosis
Therapeutic Intervention
Nitroglycerin: This medication reduces chest painboth by decreasing your hearts oxygen demandand by dilating the coronary arteries, increasingthe oxygen supply.
Sprays or tablets placed under your tongue aredesigned to be taken when you need instant relief fromangina.
Long-acting nitroglycerin tablets or skin patches workslowly over many hours.
Calcium channel blockers - Calcium channel
blockers dilate the coronary arteries to improveblood flow. They also reduce blood pressure, andslow heart rate.
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Atherosclerosis
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Atherosclerosis
NSG care
Assessment Vital signs, activity tolerance
History of precipitating factors
Analysis/Nsg diagnosis Refer to General Nursing diagnosis for clients with circulatory
System disorder A1,C2, E, F
Planning and Implementation Provide physical and mental rest
Relieve pain by administration of vasodilators
Discourage smoking Educate clients regarding diet medication and activity
Provide necessary emotional support to clients regardingalteration in life style
Atherosclerosis
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Atherosclerosis
Evaluation/Outcomes
Describe the use of therapeutic
medications
Alters life style, which contributes to
improvement in the disease process
Episodes of pain are decreased in
frequency, duration, and intensity
Coronary Artery Disease:
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CoronaryArtery Disease:
Angina Pectoris
--EpisodicprecordialorEpisodicprecordialor
substernalchestpainduetosubsternalchestpaindueto
inadequate bloodsupplyforinadequate bloodsupplyfor
myocardialoxygenationmyocardialoxygenation
STABLESTABLE chestpainchestpainprecipitated byexertion,precipitated byexertion,
relieved by restrelieved by rest
VARIANT/PRINZMETALVARIANT/PRINZMETAL
chestpain at rest,duetochestpain at rest,dueto
coronary arteryspasmcoronary arteryspasm
UNSTABLEUNSTABLE longerlonger
duration,severesymptoms,duration,severesymptoms,
must ruleout MYOCARDIALmust ruleout MYOCARDIAL
INFARCTINFARCT
CoronaryArtery Disease:Angina Pectoris
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Patterns of Ischemic Heart Disease (IHD)
Angina pectoris - a symptom complex of IHD characterized by
paroxysmal attacks of chest pain, usually substernal or precordial,caused by myocardial ischemia that falls short of inducinginfarction. There are several patterns:
1. Stable angina (typical) - paroxysms of pain related to exertion andrelieved by rest or vasodilators. subendocardial ischemia with ST-segment depression
2. Variant or Prinzmetal's angina - angina that classically occurs atrest and is caused by reversible spasm in normal to severelyatherosclerotic coronary arteries. ST-segment elevation ordepression maybe seen during attacks.
3. Unstable angina - prolonged pain, pain at rest in a person withstable angina, or worsening of pain in stable angina. ST-segmentdepression (usually) and ST-segment elevation.
4. Sudden cardiac death - Unexpected death from cardiac causesusually within one hour after a cardiac event or without the onset ofsymptoms. Strikes 300,000 - 400,000 persons annually. Usuallyhigh-grade stenosis with acute coronary changes.
Coronary Artery Disease: Angina Pectoris
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CoronaryArtery Disease:Angina Pectoris
NSG care
Assessment
Vital signs
Activity tolerance
History of precipitating factors
Analysis/Nsg diagnosis
Refer to General Nursing diagnosis for clients with circulatory
System disorder
A1 C2 E F
Coronary Artery Disease: Angina Pectoris
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CoronaryArtery Disease:Angina Pectoris
NSG care
Planning and implementation
Provide physical and mental rest
Relieve pain by administration of vasodilators
Discourage smoking educate client regarding diet, medicationand activity
Provide necessary emotional support to the client regardingmodification of life-styles
Evaluation/outcomes Describes he use of therapeutic medication
Alters the life style, which contributes to the improvement ofdisease process
Episodes of pain are decrease in frequency, intensity andduration
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Myocardial Infarction
--IrreversibleIrreversible
myocardialinjurymyocardialinjury
duetoprolongedduetoprolongedischemiaischemia
--Frequently affectsFrequently affects
theleftventricleduetheleftventricledue
toincreased worktoincreased workloadload
M di l I f ti
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Myocardial Infarction
The pathogenesis can include: Occlusive intracoronary thrombus - a thrombus
overlying an ulcerated or fissured stenotic plaquecauses 90% of transmural acute myocardial
infarctions. Vasospasm - with or without coronaryatherosclerosis and possible association withplatelet aggregation.
Emboli - from left sided mural thrombosis,
vegetative endocarditis, or paradoxic emboli fromthe right side of heart through a patent foramenovale.
Myocardial Infarction
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Myocardial Infarction
Signs and Symptoms
Chest pain described as a pressure sensation,fullness, or squeezing in the midportion of thethorax
Radiation of chest pain into the jaw/teeth,shoulder, arm, and/or back
Associated dyspnea or shortness of breath
Associated epigastric discomfort with or withoutnausea and vomiting
Associated diaphoresis or sweating
Syncope or near-syncope without other cause Impairment of cognitive function without other
cause
Myocardial Infarction
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Myocardial Infarction
diagnostics
Laboratory DiagnosisofMyocardialInfarction A number of laboratory tests are available. None is
completely sensitive and specific for myocardial infarction,particularly in the hours following onset of symptoms. Timingis important, as are correlation with patient symptoms,electrocardiograms, and angiographic studies.
The following tests are available as markers for acutemyocardial infarction: Creatine Kinase- Total:
Creatine Kinase- MB Fraction:
CK-MB Isoforms:
Troponins: Myoglobin:
Lactatedehydrogenase:
M di l I f ti C li ti
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Myocardial Infarction Complications
Arrhythmias and conduction defects, with possible "sudden
death"
Extension of infarction, or re-infarction
Congestive heart failure (pulmonary edema)
Cardiogenic shock
Pericarditis
Mural thrombosis, with possible embolization
Myocardial wall rupture, with possible tamponade
Papillary muscle rupture, with possible valvular
insufficiency
Ventricular aneurysm formation
Myocardial Infarction
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Myocardial Infarction
Nsg care
Assessment
Changes in heart rate, rhythm, and conduction of heartfunction evidenced on electrocardiogram
Life-threatening dysrhythmias Ventricular fibrillation andasystole
PVCs close to a T-wave, V-tachycardia,AF
If these occur, administer prescribed medication, document therhythm
Vital signs every minute until stable
Intake and output
Pulmonary congestion and dependent edema
Occurrence of chest pain and restlessness
Cyanosis and dyspnea
Myocardial Infarction
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Myocardial Infarction
Nsg care
Planning/Implementation Respond to dysrhythmias with defibrillation,
cardiac massage, or medications as appropriate Administer drug as ordered Administered oxygen as necessary Recognize that the client is subject to sensory
overload Orient the unit and machinery] Allow pt time to express feelings and fears
Provide gradual increase in activity
Apply anti-embolism stockings Provide emotional support to client and family Reduce anxiety and accept clients fears
Myocardial Infarction
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Myocardial Infarction
Nsg care
Evaluation and outcomes
Pain is reduced
Adequate tissue perfusion is maintained
Verbalizes a reduction in anxiety and fear
Adheres to prescribe regimen (dietary,
pharmacologic and exercise)
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JNC VII (J i t N ti l C itt th
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JNC VII (Joint National Committee on the
Prevention, Detection, Evaluation & Treatment
ofHigh BP)
CATEGORY SYSTOLIC DIASTOLIC
NORMAL /= 100
P th h i l
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Pathophysiology
Major risk factor
Smoking, dyslipedemia (elevated LDL [or Total cholesterol and /
low HDL cholesterol
Diabetes mellitus
Impaired renal function (GFR
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g g g
Disease
Heart disease( left ventricular Hypertrophy,
angina or previous myocardial infarction,
previous coronary revascularization, heart
failure) Stroke (CVA) or TIA
Chronic kidney disease
Peripheral arterial disease
Retinopathy
Medical mngt
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Medical mngt
Lifestyle modification
Pharmacologic:
Thiazides, ACE inhibitors, ARB, BB, CCB, aldosterone antagonist
sedatives
Weight reduction Cessation of smoking
Sodium restricted diet
Establishment of regular exercise program
Biofeedback
Relaxation modalities
Sympathectomy to dilate arteries
Hypertension
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yp
NSG care
Assessment
Vita signs with client in both upright and
recumbent positions
Baseline weight Headache, tinnitus, fatigability, memory loss,
palpitations
A
nalysis/D
iagnoses Refer to General Nursing diagnosis for clients with circulatorySystem disorder: B1, B2, D, J, K
Hypertension
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yp
NSG care
Planning/Implementation Monitor vital signs with client both upright and
recumbent position
Weigh client daily
Pay particular attention to calcium and potassiumintake because HPN has been associated withdeficiencies of these minerals; monitor blood work
Reassure and support any expression of emotions
If epistaxis occurs, place an icepack on the back of theneck, which may alleviate it; packing is sometimesrequired
Hypertension
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NSG care
Educate the client regarding drugs, follow-up care,activity restrictions, and diet; note that many saltsubstitutes contain potassium chloride rather thansodium chloride and may be permitted if client
has no renal impairment
Evaluation and outcomes
Blood pressure is reduced to an acceptable level Understands and adheres to medical regimen
Verbalizes the need for stress reduction