Transcript Clinical Update on Congenital Heart Defects
Neonatal Cardiology
Susan Hicks, RN Nurse Manager, NICU/ICN Madigan Healthcare System
Objectives
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
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
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
Cardiac Assessment
Heart Rate
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Cardiac output= Heart rate times stroke volume
Rhythm
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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
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
Color/ Cyanosis
Central vs. Peripheral
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assess central color on mucous membranes paying attention to intrapartal history
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acrocyanosis common in newborn period related to circulatory changes
Cardiac vs. Pulmonary
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cyanosis not responsive to oxygenation should bring suspicion of cardiac disease
Cardiac Assessment
Perfusion
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Capillary Refill time
Pulses
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Brachial, femoral (Central)
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tibial, radial (peripheral) right vs. left
right preductal
left - postductal
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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
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
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
Neonatal Cardiac Disease
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
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.
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
Environmental Factors
Environmental factors as causes of congenital heart disease have only recently begun to be recognized
More research is needed
Cyanotic Heart Defects or Ductal Dependent lesions
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
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 repair
Transposition of the Great Arteries
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
Most common cyanotic heart lesion Pulmonary stenosis, VSD, Aorta overrides VSD, right ventricular hypertrophy Dynamics depend on degree of pulmonary stenosis Surgical repair
X-Ray Tetralogy of Fallot
Commonly thought to look “boot shaped”
Pulmonary Atresia
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
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
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
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Massive heart noted at birth if severe
•
18% of symptomatic newborns dies the neonatal period
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30% die before 10 yrs of age
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Median age of death is about 20 yrs.
X-Ray Ebstein’s Anomaly
Ductal Dependent Lesions
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
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
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
Etiology
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Usually secondary to respiratory or apnea
Clinical Signs
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Decreased heart rate (<100), regular QRS complex
Treatment
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Treat underlying respiratory disorder (methylzanthines), stimulation
Supraventricular Tachycardia (SVT)
Etiology
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Abnormal stimulation of the AV node, heart disease usually not present
SVT
Treatment
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Vagal stimulation (the diving reflex)
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Adenosine
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Cardioversion - synchronized, 0.5-1.0 joules per kg
SVT
Clinical Signs
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Heart rate persistently >200-220
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Heart rate does not change based on infant’s activity
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Usually absent p waves on EKG
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Signs of circulatory collapse and decreased cardiac output
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Eventually, congestive heart failure
Arrythmias
Sinus Tachycardia SVT HR HX 180-215, rate may fluctuate fever, volume loss, anemia EKG regular EKG >220, usually 250-350, rate constant irritability, poor feeding, vomiting, tachypnea, pallor absent p waves