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Nursing Care of a Child with a Cardiovascular Disorder

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Holly Williams

on 13 September 2018

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Transcript of Nursing Care of a Child with a Cardiovascular Disorder

CV Disorders in Children
Congenital Defects
Persistent structures of fetal circulation
Structural anomalies

Foramen Ovale
Ductus Ateriosus

Primary Complication: Congestive Heart Failure
Rare in early childhood, but will be seen later if defect not corrected

More common with decreased pulmonary blood flow and obstructive defects
Etiology: autoimmune
Ages: 80% under 5 yrs
Inflammation affecting blood vessels all over the body
triggered by acute infection or bacterial toxin
Cardiac involvement
May lead to coronary aneurysm, thrombus formation

Big Hearts in Little Bodies
Nursing Care of a Child with a Cardiovascular Disorder
Three Classifications:
Increased Pulmonary Blood Flow
Obstruction to Blood Flow
Decreased Pulmonary Blood Flow

Rheumatic Fever
Inflammatory condition of the connective tissue
Most serious complication is rheumatic heart disease
resulting in permanent damage to cardiac valves
Manifests 2-6 weeks after streptococcal infection of the upper respiratory tract.
May or may not produce symptoms of pharyngitis
Foramen Ovale
As a result the blood with the most oxygen gets to the brain.
This hole allows the reddest (oxygenated) blood to go from the right atrium to left atrium.
Ductus Arteriosus
The ductus arteriosus diverts blood away from the lungs and shunts it directly to the descending aorta.
The lungs are not used while a fetus is in the womb because the baby gets oxygen directly from the mother's placenta.
Circulatory Changes at Birth
Placental blood flow ceases
Drop in right atrial pressure
Increased pressure in left atrium
Foramen ovale closes

First breath – lungs expand
Fall in pulmonary vascular resistance
Blood from the right ventricle rushes in to the pulmonary vascular system
Pressure on the right side decreases

Blood returned via the pulmonary veins
Pressure in left side increases

As levels of prostaglandins from the placenta fall, causes the ductus arteriosus to close
Congenital Cardiac Defects
Left to Right Shunting Lesions

3 Defects:
Ventricular Septal Defect (VSD)
Atrial Septal Defect (ASD)
Patent Ductus Arteriosus (PDA)

Blood flow through the fetus is more complicated than after the baby is born (normal heart).

Significance of Fetal Circulation
This is because the placenta (mother) is doing the work that the baby’s lungs will do after birth.
Placenta accepts blood without oxygen from the fetus through 2 umbilical arteries.
When blood goes through the placenta it picks up oxygen then returns to the fetus via the third vessel in the umbilical cord (umbilical vein).

blood that enters the fetus passes through the fetal liver and enters the right side of the heart.
Oxygen and nutrients from the mother's blood are released into the fetus' blood circulatory system.
This blood then enters the umbilical arteries and flows into the placenta to be oxygenated by the mother's circulatory system.
Blood then travels to the left ventricle and out the aorta.
Septal Defect
Abnormal opening between the ventricles
Some children remain asymptomatic for years - may not be diagnosed until adults
Loud, harsh systolic murmur
Palpable thrill
Diastolic murmur & gallop MAY be present
30%-40% close spontaneously
Intervention includes insertion of occluder device
Atrial Septal Defect
Abnormal opening between the atria
Fatigue, dyspnea on exertion, palpitations, atrial dysrhythmias
Recurrent respiratory infections related to increased pulmonary blood flow
Systolic murmur
Diastolic murmur with large shunting
Mitral regurg is possible
Risk for stroke
Heart failure may develop in adulthood if not repaired.
Diuretics with conservative management
Surgical placement of occluder device
Patent Ductus Arteriosus
Failure of the fetal ductus arteriosus to close completely after birth
Normal closure within 24-72 hrs after birth as a response to decreased placental prostaglandin levels
Continuous, "machinery" murmur
Signs of heart failure
Widened pulse pressure (difference between diastolic and systolic readings)
Bounding pulses
Cardiac enlargement
Indomethacin (PG inhibitor) is given
Surgical intervention - coil placed for scar tissue occlusion
Blood Flow Obstructions
C -
A -
P -
Coarctation of aorta
Aortic Stenosis
Pulmonary Stenosis
Results in decreased cardiac output
Coarctation (Constriction) of the Aorta
Results in:
Increased blood supply in upper body
Decreased blood supply in lower body
left sided HF
poor lower extremity perfusion
asymptomatic children may show pulse and blood pressure differences between upper and lower extremities
weakness, tingling, cramps in lower extremities
Therapeutic Management
diuretics & digoxin to improve cardiac output
balloon dilation with stent placement ONLY for recurrences. If used initially, it INCREASES incidence of recurrence.
end-to-end anastomosis using left subclavian artery patch usually performed shortly after diagnosis.
results in postoperative absence of left palpable pulse
Aortic Stenosis
Narrowing of the entrance to the aorta
can be asymptomatic
exercise intolerance
systolic ejection murmur with thrill or click
chest pain, dizziness, syncope
sudden death with strenuous exercise is a possibility
Medical Management:
balloon valvuloplasty
aortic valve replacement
warfarin treatment if mechanical valve is used
Defects with Decreased Pulmonary Blood Flow
Right–to–Left Shunt Cyanotic Defects

5 T'S
Tetralogy of Fallot
Truncus arteriosus
Transposition of the great arteries
Tricuspid atresia
Total anomalous pulmonary venous return

Tetralogy of Fallot
extreme fatigue
hypercyanotic episodes
chronic hypoxemia
harsh systolic murmur with palpable thrill
Medical Management
Prostaglandin E1 infusion to maintain PDA (blood flow to the lungs) until surgical repair
surgery requires primary repair of defects in multiple stages
high rate of complications (see notes)
4 defects:
right ventricular hypertrophy
overriding of the aorta
pulmonary stenosis
Characteristics of defects with decreased pulmonary blood flow
R–to-L shunting of blood
“Blue Babies”
Surgery in several stages (technically complex)
Guarded prognosis
Transposition of the Great Arteries
Abnormal separation and rotation of fetal truncal vessels - aorta arises from right ventricle and pulmonary artery arises from the left ventricle
developing HF
progressive desaturation and acidosis
Hypoxemia despite oxygen administration
Cyanosis at birth
Medical Management:
Emergency PGE1 infusion
arterial switch procedure
Diagnostic Tests
Electrocardiogram (ECG or EKG)
records heart's electrical activity from outside surface
Holter Monitor
continuously records heart rate and rhythm for 24 hrs
Echocardiography (ECHO)
uses ultrasound to generate an image of the heart and associated structures.
sedation may be necessary since child MUST be able to lie still for up to 1 hr
child or parent records times of activities and symptoms or other events in a diary to be returned with the device
skin should be free of lotions and oils
best done when the child is quiet and cooperative
detects chamber enlargement and deviations that may be caused from defects
Serum Potassium (K+)
Normal level is essential
3.5 - 5.0 is normal range - varies slightly with age of child and with each lab.
A level significantly higher or lower can be life threatening
Cardiac Catheterization
Catheter inserted in femoral artery and threaded to heart
Records hemodynamics
Contrast dye injected to see cardiac anatomy

Nursing Care
Obtain Baseline VS and Mark Pedal Pulses
Prepare child/family for procedure
Explanation - careful terminology
Visit cath lab or show photos of what child will see
Must lie still
Not generally painful, may be uncomfortable
Nursing Care
Post- Procedure:
Pressure Dressing
Keep flat 2-3 hours
Do not bend extremity at insertion site
VS q 15 min. x 1st hr, then q 30 min.
Observe for bleeding at site
NV checks distal to insertion site
Monitor IV fluids
Increase fluids to help flush out dye
Dehydration + polycythemia = clot
Fluid Overload
Strict I & O
Observe for reactions to dye (vomiting, rash, increased creatinine, decreased urinary output)

Major Complications of Congenital Heart Defects
Failure to Thrive (FTT)
Congestive Heart Failure (CHF)
Polycythemia with risk of stroke
Manifestations of
difficulty feeding/decreased appetite
failure to gain weight
abnormal cardiac rhythm known as a gallop
periorbital and facial edema
neck vain distention
decreased peripheral perfusion
decreased UOP
clubbing of fingers
Shea, Jake, Cullin, Jubry, & Liora Stoffregen
Clubbing of Fingers
Risk for CVA
Increases viscosity of blood
Hypoxemia leads to compensatory increase in formation of RBCs

Most Important Drug Used For HF: Digoxin
Cardiac glycoside
Increases cardiac output by:
Strengthening the force of ventricular contraction
Slowing heart rate and allows the ventricles more time to fill with blood
Therapeutic Levels
0.8 to 2 ng/mL

Signs & Symptoms of Digoxin Toxicity
Vomiting (do NOT repeat dose)
Caregiver Education
Explanation of Disorder
S&S to report
Frequent small feedings
High calorie formula
Do not allow to cry for long periods

Level of activity
Most children self-limit
Teach to observe for S&S of activity intolerance
Treat minor illnesses promptly
Medication Regimens

also present in indigenous populations within developed countries (Alaskan natives and native Americans in the U.S.)
however it is still endemic worldwide where overcrowding is an issue
nearly disappeared from the United States and other developed countries
Diagnosis and Management
prolonged P-R interval
presence of at least one physical manifestation
evidence of recent streptococcal infection (strep culture, positive antistreptolysin O titer - ASO titer)
presence of at least two minor manifestations
elevated ESR
positive C-reactive protein
aimed at eradication of the strep and treatment of other symptoms
children susceptible to recurrent attacks risking further cardiac damage - require prophylaxis
PCN drug of choice - monthly injections (or oral dose BID) after initial 10-day course of therapy
bed rest during acute phase
assess for cardiac symptoms throughout hospitalization
high fever unresponsive to antibiotic treatment
bilateral conjunctivitis
strawberry tongue
cracked lips
swelling of hands & feet
erythema of palms & soles followed by desquamation (peeling)
Beau's lines (deep grooves in nails)
Thrombus formation
Myocardial Infarction

Recovery & Prognosis
Death can result from blood clots forming in the coronary arteries
Poorer prognosis if therapy started after a coronary artery aneurysm has developed
Typically complete recovery within 4-8 weeks with early detection and treatment

High dose IV immune globulin (IVIG) in combination with aspirin has been shown to lower the prevalence of coronary artery abnormalities when given within
10 days
of fever onset.
Give aspirin with
food or milk
Avoid live vaccines (MMR, Varicella) for 11 months after receiving IVIG!!!
"Tet Spell"
Hypercyanotic episode
Squatting or putting the child in the knee-chest position:
• Traps blood in legs
• decreases systemic venous return
• breaks the overload-hypoxia cycle.

Take Apical Pulse for 1 full minute.
Withhold & notify healthcare provider if
HR is:
<100 bpm infants & toddlers
rate varies for older children & adolescents. If rate isn't specified in orders, hold dose and notify physician if rate is decreasing or is markedly lower than previous rates.
Nursing Care and Caregiver Education
Nursing Care and
observe and document peripheral perfusion by palpating peripheral pulses
note temperature, color changes, capillary refill time
weigh infant/child daily - USE SAME SCALE
give digoxin bid - morning and evening - 20-30 min before a feeding
if child vomits, DO NOT REPEAT DOSE. If vomiting continues, or if child vomits two doses in a row, NOTIFY PHYSICIAN!!!
Acquired Heart Disease
Rheumatic Fever
Kawasaki Disease
Toxicity is usually seen at > 2 ng/mL
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