Cardiovascular Diseases Final

8/8/2019 Cardiovascular Diseases Final

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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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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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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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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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Mitral Stenosis

-- PathologicnarrowingPathologicnarrowing

oftheorificeoftheoftheorificeofthe

mitralvalvemitralvalve


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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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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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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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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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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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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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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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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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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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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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--IrreversibleIrreversible

myocardialinjurymyocardialinjury

duetoprolongedduetoprolongedischemiaischemia

--Frequently affectsFrequently affects

theleftventricleduetheleftventricledue

toincreased worktoincreased workloadload

M di l I f ti


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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.



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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



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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



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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



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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



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Nsg care


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


Blood pressure is reduced to an acceptable level Understands and adheres to medical regimen

Verbalizes the need for stress reduction

Cardiovascular Diseases Final

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