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Cardiovascular Disorders Gail C Hoyer Nur2310 Fall 2010

Cardiovascular disorders

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Page 1: Cardiovascular disorders

Cardiovascular Disorders

Gail C HoyerNur2310Fall 2010

Page 2: Cardiovascular disorders

Heart Defects that Increase Pulmonary Blood Flow

• PDA- Patent Ductus Arteriosus

• ASD-Atrial Septal Defect• VSD- Ventricular Septal

Defect

Page 3: Cardiovascular disorders

PDA: Pathophysiology, Manifestations, and Clinical Therapy

• Pathophysiology– The Ductus Arteriosus Usually

closes within the first hours of life

– Common in preterm infants• Manifestations

– Continuous “machine” like murmur

– Dyspnea– Tachycardia– Tachypnea– Thrill in pulmonic area– May be asymptomatic

• Therapy– EKG shows left ventricular

hypertrophy– PDA visualized on echo– Surgical Ligation– Intravenous indomethicin

stimulates closure in premature infants but can not be used if CHF is present

• Shunt– Left-to-right can be visualized

on echocardiogram– Increase in pulmonary blood

flow

Page 4: Cardiovascular disorders

PDA: Anatomy

Page 5: Cardiovascular disorders

ASD: Pathophysiology, Manifestations, and Clinical Therapy

• Pathophysiology– Opening in the atrial septum– May occur alone or in

conjunction with a congenital defect

• Manifestations– Usually no symptoms in

infants and young children– With a large ASD, easy tiring,

and poor growth occur

• Therapy– Dilated right ventricle on

echo secondary to blood overload and shunt size

– Spontaneous closure occurs within the first 4 years of life

– Surgery or patch when closure does not occur or when increased pulmonary blood flow results in CHF

• Shunt– Left-to-right resulting in

increased pulmonary blood flow

Page 6: Cardiovascular disorders

ASD: Anatomy

Page 7: Cardiovascular disorders

VSD: Pathophysiology, Manifestations and Clinical Therapy

• Pathophysiology– Opening in ventricular

septum• Manifestations

– Only 15% are large enough to cause CHF or pulmonary hypertension, or pulmonary infections

– Systolic murmur at third or fourth left intercostal space

• Therapy– If small x-ray and ekg reveal

little– Echo establishes diagnosis if

shunting is present– Most close within first 6

months of life– Surgical patching if poor

growth is evident; otherwise treatment is conservative

• Shunt– Left-to-right directly across

septum into pulmonary artery

– Increased pulmonary blood flow

Page 8: Cardiovascular disorders

Heart Defects with Decreased Pulmonary Blood Flow

• Pulmonary Stenosis• TOF-Tetralogy of Fallot

Page 9: Cardiovascular disorders

TOF: Pathophysiology, Manifestations, • Pathophysiology

– Four defects• Pulmonic Stenosis page 1371 • Right Ventricular Hypertrophy• VSD• Overriding Aorta• Some kids have a fifth defect: ASD

• Manifestations– Infant becomes hypoxic and cyanotic as the ductus arteriosus closes– The degree of the pulmonary stenosis determines the severity of the

symptoms– Systolic murmur in the pulmonic area and transmitted to suprasternal notch– Polycythemia, hypercyanotic spell(tet spells), metabolic acidosis, poor

growth, clubbing, and exercise intolerance– Knee chest squat of toddlers to decrease the return of systemic venous

blood to the heart

Page 10: Cardiovascular disorders

TOF: Pathophysiology, Manifestations, and Clinical Therapy

• Therapy– Diagnostic Tests

• X-ray shows “boot shaped” heart due to large right ventricle, prominent aorta

– Treatment• Calm, give oxygen, and

morphine and propanolol to decrease pulmonary vascular resistance

• Modified BT shunt to delay total correction surgery

• Shunt– Right-to-left secondary to elevated

pressures on the right side of the heart

Page 11: Cardiovascular disorders

TOF: Anatomy

Page 12: Cardiovascular disorders

Mixed defects

• TGA- Transposition of the Great Arteries

Page 13: Cardiovascular disorders

TGA: Pathophysiology, Manifestations• Pathophysiology- Parallel circulation – Pulmonary Artery is the outflow tract for the left ventricle– The Aorta is the outflow tract for the right ventricle– Life threatening at birth, survival initially depends on an open ductus

arteriosus and foramen ovale

• Manifestations– Cyanosis apparent soon after birth

• which does not improve with oxygen administration• May be less apparent if VSD is present

– CHF may develop immediately, over days or weeks– Tachypnea without retractions or other signs of dyspnea– Long time to feed and need frequent rest periods b/c of rapid respiratory

rate and fatigue; growth failure may be seen as early as 2wks if not corrected

– Systolic murmur if VSD present; otherwise none; S2 is loud

Page 14: Cardiovascular disorders

TGA: Clinical Therapy

• Therapy– Diagnosis

• X-ray may reveal classis “egg-shaped heart” on a string with enlarged ventricles

• Echo shows abnormal positioning of the great arteries

– Treatment• Prostaglandin E1 is ordered to maintain a patent ductus

arteriosus until a palliative surgery can be performed• Arterial switch performed before 1 week of life• Balloon atrial septostomy can be performed to allow mixing

until surgery can be performed

Page 15: Cardiovascular disorders

TGA: Anatomy

Page 16: Cardiovascular disorders

BT shunt

Page 17: Cardiovascular disorders

Defects that Obstruct Systemic blood flow

• Coarctation of the Aorta• CHF

Page 18: Cardiovascular disorders

Coarctation of the Aorta: Pathophysiology, Manifestations

• Pathophysiology– Narrowing or constriction of the descending aorta often near the

ductus arteriosus or subclavian artery which obstructs systemic flow

• Manifestations– Many children are asymptomatic– Severe constriction infants have cyanosis in the lower extremities– Blood pressure lower in legs than arms– Brachial and radial pulses are typically bounding and femoral weak or

absent– Older children may complain of leg pain after exercising– S2 is loud and single on auscultation

Page 19: Cardiovascular disorders

Coarctation of the Aorta: clinical Therapy

• Therapy– Diagnosis

• X-ray may show cardiomegaly• Echo confirms narrowing and location

– Treatment• In symptomatic newborns, PGE1 is given to reopen the

ductus arteriosus and promote blood flow to the lower extremities

• Treatment to prevent CHF may include diuretics, inotropic medications and oxygen

• Surgical correction is preferred

Page 20: Cardiovascular disorders

Coarctation of the Aorta: Anatomy

Page 21: Cardiovascular disorders

Congestive Heart Failure (CHF)• Disorder in which circulation is inadequate to support the body’s

circulatory and metabolic needs.• Etiology– Most common cause

• May be caused by congenital heart defects that obstruct systemic blood outflow tract or cause increased pulmonary blood flow

• children with uncorrected defects develop CHF with 6 to 12 months of life– Other causes

• Problems with heart contractility• Pathologic conditions that require high cardiac output(severe anemia,

acidosis, or respiratory disease)• Acquired heart disease(cardiomyopathy, rheumatic heart disease, and

Kawasaki disease)• Disorders such as Duchenne muscular dystrophy

Page 22: Cardiovascular disorders

CHF: Pathophysiology

• Pathophysiology– Left-to-right shunts

result in increased blood to the pulmonary system and can result in pulmonary hypertension

– Obstructive defects restrict the flow of blood so the heart muscle hypertrophies to work harder to force blood through the structures

Page 23: Cardiovascular disorders

CHF: Manifestations in Infants

• Initial Manifestations– Tiring easily, especially

during feedings– Weight loss or lack of

normal weight gain– Diaphoresis– Irritability– Frequent Respiratory

infections

• Later Manifestations– Tachypnea– Tachycardia– Pallor– Cyanosis– Nasal Flaring– Grunting– Retractions– Cough or crackles– Third heart sound

Page 24: Cardiovascular disorders

CHF: Manifestations in Older Children

• Initial Manifestations– Exercise Intolerance– Dyspnea– Abdominal pain or

distention– Peripheral edema

• Later Manifestations– Generalized fluid volume

overload– Jugular vein distention

Page 25: Cardiovascular disorders

CHF: Nursing Management• Assessment

– Physiologic assessment– Developmental assessment

• Planning and Implementation– Administer and monitor

prescribed medications• Lasix and digoxin see page 1388

– Maintain oxygen and myocardial function

– Promote rest– Foster development– Provide adequate nutrition– Provide emotional support– Discharge planning and home

care teaching

• Evaluation

Page 26: Cardiovascular disorders

Acquired heart Diseases

• Rheumatic Fever• Kawasaki Disease

Page 27: Cardiovascular disorders

Kawasaki Disease

• Acute febrile, systemic vascular inflammatory disorder that affects the small and midsize arteries, including the coronary arteries

• Leading cause of acquired heart disease in children in the US

• Etiology unknown, thought to be caused by an unidentified infectious agent

Page 28: Cardiovascular disorders

Kawasaki Disease: Manifestations and Clinical Therapy

• Manifestations– Acute 1-2 weeks

• Irritability, high fever that persists more than 5 days, hyperemic conjunctivae, red throat, swollen, hands and feet, rash on trunk and perineal area, cervical lymph node enlargement(unilateral)

– Subacute 2-4 weeks• Cracking lips and fissures, desquamation of the skin on the tips of toes

and fingers and toes, joint pain, cardiac disease, and thrombocytosis

– Convalescent stage 6-8 weeks• Child appears normal but lingering signs of inflammation may be present

• Clinical Therapy– Intravenous Immunoglobulin– High does of aspirin for fever– Hospitalization

Page 29: Cardiovascular disorders

Kawasaki Disease: nursing management

• Assessment– Temperature, skin, eyes, I&O,

weight, cardiac

• Medication– Aspiring administration

• Monitor for side effects(bleeding, GI upset)

– Immune Globulin• Treat and administer like

a blood product

• Comfort– Skin clean and dry– Cool compresses, tepid baths– Small frequent feeding

• Exercise– Passive ROM

• Discharge planning– Teaching on aspiring therapy– Postpone live virus vaccines

(measles and varicella) for 11 months after immune globulin administration, others may be given on schedule

Page 30: Cardiovascular disorders

Rheumatic Heart Disease

• Inflammatory disorder of the connective tissue that results from an autoimmune response to some strains of A beta-hemolytic streptococci

• Affects joints, brain, and skin tissue• Children between 5 and early adolescent are

more commonly infected• Rheumatic heart disease develops in 10% of

individuals with rheumatic fever

Page 31: Cardiovascular disorders

Rheumatic Heart Disease: Manifestations and Clinical Therapy

• Hallmark signs– Occur three weeks after an untreated streptococcal infection

• Carditis involving the mitral or aortic valve is detected by presence of a new murmur

• Chest pain• Two or more large joints become inflamed with pain, welling,

tenderness, erythema, and heat• Non pruritic skin rash with pink macules and blanching in the

middle of the lesions on the trunk

• Clinical Therapy– Antibiotics (penicillin, to eradicate strep infection)– Corticosteroids (to reduce inflammation)

Page 32: Cardiovascular disorders

Rheumatic Heart Disease: Nursing Management

• Prevention– Children with possible throat

infections would be cultured for strep

• Hospitalization– Children with rheumatic fever

should be hospitalized– Bed rest for monitoring

carditis – 4weeks bed rest if carditis

develops

• Medications– Antibiotics and aspirin

• Discharge Planning– Recovery phase occurs at

home• Activity limitations• Antibiotic prescribed

– Teaching• Reoccurrence of sore

throat need for culture• Follow up care to monitor

heart function