Transcript Clinical Update on Congenital Heart Defects

Neonatal Cardiology
Susan Hicks, RN
Nurse Manager, NICU/ICN
Madigan Healthcare System
Objectives
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Discuss the physiological adaptation from fetal
to newborn circulation
Describe how to perform a thorough cardiac
assessment on a neonate
Identify ductal dependent lesions and nursing
care for these infants
Identify the common Arrythmias in the
newborn period
Transition to Extrauterine Life
Placenta receives 50% of fetal cardiac
output and is the organ of gas exchange
in utero
 Low pulmonary blood flow (8-10% of
cardiac output) due to high pulmonary
vascular resistance
 Ductal patency is maintained by low
oxygen tension in utero and the
vasodilating effect of prostaglandin E2
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Fetal Circulation
Cardiopulmonary
Adaptation at Birth
Umbilical cord is clamped which
increases systemic vascular resistance
 The three major fetal shunts functionally
close during transition
 Surfactant is secreted into the amniotic
fluid by the fetal lung by about 20 weeks
gestation and increases in quantity
throughout gestation and can support
extrauterine breathing by about 34 weeks
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Ductal Closure
Increasing arterial oxygenation from the
lungs and decreasing prostaglandin
levels are potent stimulus’ to constrict the
ductus arteriosus
 Foramen ovale functionally closes related
to increase in left atrial and left
ventricular pressures
 Ductus venosus closes because of absent
umbilical venous return- becomes
ligimentum venosum
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Cardiac Assessment
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Heart Rate
– Cardiac output= Heart rate times stroke
volume
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Rhythm
– arrhythmias are common in the neonatal
period and are frequently benign
Murmur
Caused by turbulent blood flow
 Pathological vs. innocent
 Note location, intensity, radiation quality
and pitch
 Occur in 60% of neonates in the first 48
hours of life
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Murmurs
Grade 1- barely audible
 Grade 2- soft but immediately audible
 Grade 3- moderate intensity without a
thrill
 Grade 4- loud, can be heard with
stethoscope barely on the chest
 Grade 5- very loud, heard with
stethoscope slightly removed from the
chest
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Color/ Cyanosis
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Central vs. Peripheral
– assess central color on mucous membranes
paying attention to intrapartal history
– acrocyanosis common in newborn period
related to circulatory changes
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Cardiac vs. Pulmonary
– cyanosis not responsive to oxygenation
should bring suspicion of cardiac disease
Cardiac Assessment
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Perfusion
– Capillary Refill time
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Pulses
– Brachial, femoral (Central)
– tibial, radial (peripheral)
– right vs. left
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right preductal
left - postductal
– bounding common in premature infants
Blood Pressure
Use appropriate sized cuff for accuracy
 Norms dependent on weight, age
 Decreases 3-4 hours postnatally, increases
to plateau at 4-6 days of age
 Follow blood pressures for trending
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Cardiac Diagnosis
CXR- rule out pulmonary disease, assess
heart size
 EKG
 Cardiac Echo
 Blood Gas- low PaO2, normal CO2
 hyper-oxygen test- pre and post ductal
saturation
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Neonatal Cardiac Disease
Approximately 1% of infants born in the
United States each year have some form
of congenital heart disease.
 Major structural defects in the heart can
occur if there is an interference with the
maternal-placental fetal unit during the
first seven weeks of gestation when
cardiac development occurs
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Neonatal Cardiac Disease
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Causes of congenital heart disease
include chromosomal, genetic, maternal,
environmental, or multifactorial
Chromosomal Abnormalities
Many chromosomal abnormalities are
associated with structural heart defects.
 Almost half of the infants with Down’s
syndrome have some form of congenital
heart disease
 The most common defects in Down’s
include endocardial cushing defects and
ventral septal defects
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Maternal Factors
Maternal factors include maternal illness
and drug ingestion.
 Rubella during the first 7 weeks of
pregnancy carries a 50% risk of congenital
rubella with congenital defects of multiple
organ systems.
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Maternal Factors
Maternal drug use may also cause
congenital heart disease. Fifty percent of
newborns with Fetal Alcohol Syndrome
have some form of congenital heart
disease
 Infants of Diabetic Mothers have a 10%
chance of having and infant with a heart
defect,usually VSD and Transposition of
the Great Arteries
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Environmental Factors
Environmental factors as causes of
congenital heart disease have only
recently begun to be recognized
 More research is needed
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Cyanotic Heart Defects or
Ductal Dependent lesions
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Cyanotic heart defects are those that
produce a right-to-left shunt through the
heart, thus decreasing pulmonary blood
flow.
Cyanosis is usually present within the first
few days of life and worsens with the closure
of the PDA as blood supply is bypassing the
lungs. These are then referred to as Ductal
Dependent Lesions.
Coarctation of the Aorta
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Constriction of the
aorta distal to the left
subclavian artery,
usually at insertion
site of the Ductus
Left to right shunt.
Decreased pulses and
BP in lower
extremities
Treat CHF, surgical
Transposition of the Great Arteries
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Position of the great
arteries are reversed.
Oxygenated blood from
lungs enters left heart
and goes back to lungs
via Pulmonary artery.
Desaturated blood
enters the right atrium
and leaves via the aorta.
Left to right mixing is
required for survival.
PGE, septostomy,
surgical repair.
X-Ray Transpositon of the Great
Arteries
Commonly referred
to as an “egg lying
on it’s side”
Tetralogy of Fallot
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Most common
cyanotic heart lesion
Pulmonary stenosis,
VSD, Aorta overrides
VSD, right
ventricular
hypertrophy
Dynamics depend on
degree of pulmonary
stenosis
X-Ray Tetralogy of Fallot
Commonly thought
to look “boot
shaped”
Pulmonary Atresia
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Complete obstruction
of the pulmonary
valve resulting in
hypoplastic Right
ventricle and
tricuspid valve atresia
Right to left shunt via
the foramen ovale
Dependent on PDA
for mixing
X-Ray of Pulmonary Atresia
Commonly with little
vascular markings and
may also be seen as
“snowman”
Tricuspid Atresia
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Failure of tricuspid
valve to develop
Right to left shut via
the foramen ovale
If VSD present, some
blood from the left to
the right ventricle and
to lungs
PGE to create mixing
via the PDA
Surgical correction,
good survival rate
X-Ray Tricuspid Atresia
Little vascular
marking, heart
appears smaller
than normal.
Persistent Pulmonary
Hypertension of the Newborn
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Hypoxia and acidosis
create pulmonary
vasoconstriction
lungs become high
resistance
blood flows path of
least resistance
Treatment-correct
acidosis, ventilate,
NO
Ebstein’s Anomaly
•Anomaly of the tricuspid
valve – occurs in less than
1% of all congenital heart
defects
•Downward displacement
of the Tricuspid valve
into the RV.
•Portion of RV is
incorporated into the RA.
•A PFO or ASD with a
right-to-left shunt present
Ebstein’s Anomaly
•Massive heart noted at birth if
severe
•18% of symptomatic newborns
dies the neonatal period
•30% die before 10 yrs of age
•Median age of death is about
20 yrs.
X-Ray Ebstein’s Anomaly
Ductal Dependent Lesions
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What will you see?
– Infant who is cyanotic and does NOT
respond to O2.
– Infant becomes increasingly cyanotic
and/or tires easily with feedings in first
few days as duct closes
– Usually appear comfortable but may
exhibit s/s of respiratory distress
– Xray may show CHF already
Ductal Dependent Lesions
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Nursing Care
– Monitor VS very closely
– Observe SaO2 closely – may not want sats high
d/t defect and shunting of blood
– STRICT I&O!!! CHF can result easily
– Pre/Post Sats may be ordered
– Sedate if necessary, Ventilate if necessary (may
have underlying respiratory issue also)
Ductal Dependent Lesions
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Nursing Treatment includes
– medications (prostaglandin infusion, inotrops,
and correction of metabolic acidosis)
– surgical intervention (balloon septostomy) to
maintain mixing between the right and left heart
thus increasing pulmonary blood flow
– corrective surgical repair
Bottom line: When in doubt start prostagland!
Transport these infants asap to a cardiac care
center
Arrythmias
Bradycardia
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Etiology
– Usually secondary to respiratory or apnea
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Clinical Signs
– Decreased heart rate (<100), regular QRS
complex
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Treatment
– Treat underlying respiratory disorder
(methylzanthines), stimulation
Supraventricular
Tachycardia (SVT)
Etiology
– Abnormal stimulation of the AV node,
heart disease usually not present
SVT
Treatment
– Vagal stimulation (the diving reflex)
– Adenosine
– Cardioversion - synchronized, 0.5-1.0
joules per kg
SVT
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Clinical Signs
– Heart rate persistently >200-220
– Heart rate does not change based on infant’s
activity
– Usually absent p waves on EKG
– Signs of circulatory collapse and decreased
cardiac output
– Eventually, congestive heart failure
Arrythmias
Sinus Tachycardia
SVT
HR
180-215, rate may
fluctuate
>220, usually 250-350,
rate constant
HX
fever, volume loss,
anemia
EKG
regular EKG
irritability, poor
feeding, vomiting,
tachypnea, pallor
absent p waves