Transcript CONGENITAL CARDIAC DEFECTS

The Child with
Cardiovascular
Dysfunction
Chapter 25
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Fetal Circulation Structures
• Umbilical vein; umbilical arteries
• Foramen ovale
• Ductus arteriosus
• Ductus venosus
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Changes at Birth
• (Note to instructor: Image available in
Electronic Image Collection)
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Pediatric Indicators
of Cardiac Dysfunction
• Poor feeding/SOB/fatigue/cyanosis
• Tachypnea/ tachycardia/diaphoresis
• Syncope/chest pain/dizziness/palpitations
• Failure to thrive/poor weight gain/activity
intolerance/ hx frequent respiratory infections
• Developmental delays
• + Prenatal history—maternal exposure to
infection, drugs, birth complications
• + Family history of cardiac disease
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Diagnostics: Cardiac
Catheterization
• May be diagnostic or interventional
• May be left or right-sided
• Pre-procedure interventions:
– Education—procedure and touch senses
– Assessment
– Accurate ht & wt
– Allergies
– Mark pulses
– Pulse ox
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Cardiac Cath cont’d
• Postprocedure interventions:
– Keep extremity straight 4-6h
– Assess 6 Ps
– Routine postop VS (apical)
– I&O d/t contrast
– Pulse ox
– Observe for hematoma or hemorrhage
– Home care p. 894
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Two Types of Cardiac Defects
• Congenital
– Anatomic anomalies present at birth that
result in abnormal cardiac function
• Acquired
– Disease process after birth
•
Infection
•
Autoimmune response
•
Environmental factors
•
Familial tendencies
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Causes of CHD
• Chromosomal/genetic = 10%-12%
• Maternal or environmental = 1%-2%
– Maternal drug use
• Fetal alcohol syndrome—50% have CHD
– Maternal illness
• Rubella in 1st 7 wks of pregnancy→50% risk of
defects including PDA and pulmonary branch
stenosis
• CMV, toxoplasmosis, other viral illnesses>>
cardiac defects
• Mothers with chronic illness such as DM or lupus
are more likely to have babies with CHDs
• Multifactorial = 85%
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CHD
• Incidence: 5-8 per 1000 live births
– About 2-3 of these are symptomatic in
first year of life
– Major cause of death in first year of
life (after prematurity)
– Most common anomaly is VSD
– 28% of kids with CHD have another
recognized anomaly (trisomy 21, 13,
18, +++ )
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Classification of CHD
• Hemodynamic characteristics
– Increased pulmonary blood flow
(patent ductus arteriosus)
– Decreased pulmonary blood flow
(Tetralogy of Fallot)
– Obstruction of blood flow out of the
heart (coarctation of aorta)
– Mixed blood flow (transposition of
great arteries)
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Patent Ductus Arteriosus (PDA)
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PDA cont’d
• Failure to close within first weeks of life
• Causes left to right shunt
• Additional blood is re-circulated thru lungs and
comes back to left side
• Causes increased workload on both ventricles
• May have S/S CHF; machinery–like murmur;
wide pulse pressure; bounding pulses
• Treated medically with indomethacin IV;
placement of a coil thru interventional cardiac
cath; or surgically with VATS and placing a clip
on the ductus
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Tetralogy of Fallot (TOF)
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TOF cont’d
• 4 defects: VSD, pulmonic stenosis, overriding
aorta, right ventricular hypertrophy
• Blood mixes in ventricles but depending on large
vessel resistance, shunt could be either direction
• Blood from both ventricles is distributed
systemically
• Infant/Child has tet spells which are relieved by
squatting or knee chest position (915). Will also
have murmur.
• Complete surgical repair is tx of choice—repair
of VSD, resection of stenosis with pericardial
patch over surgical site to enlarge ventricle
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Coarctation of Aorta (COA)
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COA cont’d
• Narrowing of aorta near PDA
• Increased pressure in head and upper
extremities; decreased in lower
• S/S include HBP and bounding pulses in
arms, LBP and weak or absent pulses in
legs; CHF; dizziness, HA, syncope,
epistaxis
• Tx: angioplasty, resection with
anastomosis, grafting
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Transposition of Great Vessels
(TGV or TGA)
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TGV cont’d
• PA comes from LV, goes to lungs and back to LV;
aorta comes from RV goes to body and back to
RV
• No communication between the pulmonary and
systemic circulation
• Patent foramen ovale or VSD must be present to
sustain life, but will cause CHF
• S/S range from moderately to severely cyanotic
depending on size of septal defect; CHF sx,
murmur
• Tx includes prostaglandin E1 and septostomy
(Rashkind procedure) to increase mixing until
surgery; arterial switch is surgery of choice
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CHF in Children
• Impaired myocardial function
– Tachycardia, fatigue, weakness, restless,
pale, cool extremities, diaphoresis, decrease
BP, decrease urine output, gallop rhythm
• Pulmonary congestion
– Tachypnea, dyspnea, respiratory distress
(grunting, flaring, retractions), exercise
intolerance, cyanosis
• Systemic venous congestion
– Peripheral and periorbital edema, weight
gain, ascites, hepatomegaly, JVD
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CHF cont’d
• Treatment goals are to decrease fluid overload,
increase oxygenation, improve output, decrease
O2 demand of heart
– Lasix—decreases overload
– Digoxin—improves output—need to double
check dosage with another nurse—infants
rarely receive > 1 mL (50 mcg)
– ACEIs, bedrest, nutritional support—
decreases O2 demand
– Oxygen therapy
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CHF—Nursing interventions
• VS, heart and lung sounds, pulses
• Monitor tissue perfusion, O2 tx
• Maintain rest, nutrition
• Monitor fluid status
– Edema, dehydration, fontanels
– JVD, hepatomegaly, periorbital and
peripheral edema
– I&O, daily wts, specific gravity
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