Neonatal Cardiology

Neonatal Cardiology

Susan Hicks, RNNurse Manager, NICU/ICN

Madigan Healthcare System

ObjectivesObjectives

Discuss the physiological adaptation Discuss the physiological adaptation from fetal to newborn circulationfrom fetal to newborn circulation

Describe how to perform a thorough Describe how to perform a thorough cardiac assessment on a neonate cardiac assessment on a neonate

Identify ductal dependent lesions and Identify ductal dependent lesions and nursing care for these infantsnursing care for these infants

Identify the common Arrythmias in Identify the common Arrythmias in the newborn periodthe newborn period

Transition to Transition to Extrauterine LifeExtrauterine Life

Placenta receives 50% of fetal cardiac Placenta receives 50% of fetal cardiac output and is the organ of gas output and is the organ of gas exchange in utero exchange in utero

Low pulmonary blood flow (8-10% of Low pulmonary blood flow (8-10% of cardiac output) due to high cardiac output) due to high pulmonary vascular resistancepulmonary vascular resistance

Ductal patency is maintained by low Ductal patency is maintained by low oxygen tension in utero and the oxygen tension in utero and the vasodilating effect of prostaglandin E2vasodilating effect of prostaglandin E2

Fetal CirculationFetal Circulation

Cardiopulmonary Cardiopulmonary Adaptation at BirthAdaptation at Birth

Umbilical cord is clamped which Umbilical cord is clamped which increases systemic vascular resistanceincreases systemic vascular resistance

The three major fetal shunts The three major fetal shunts functionally close during transitionfunctionally close during transition

Surfactant is secreted into the amniotic Surfactant is secreted into the amniotic fluid by the fetal lung by about 20 weeks fluid by the fetal lung by about 20 weeks gestation and increases in quantity gestation and increases in quantity throughout gestation and can support throughout gestation and can support extrauterine breathing by about 34 extrauterine breathing by about 34 weeksweeks

Ductal ClosureDuctal Closure Increasing arterial oxygenation from Increasing arterial oxygenation from

the lungs and decreasing the lungs and decreasing prostaglandin levels are potent prostaglandin levels are potent stimulus’ to constrict the ductus stimulus’ to constrict the ductus arteriosusarteriosus

Foramen ovale functionally closes Foramen ovale functionally closes related to increase in left atrial and left related to increase in left atrial and left ventricular pressuresventricular pressures

Ductus venosus closes because of Ductus venosus closes because of absent umbilical venous return- absent umbilical venous return- becomes ligimentum venosumbecomes ligimentum venosum

Cardiac AssessmentCardiac Assessment

Heart RateHeart Rate– Cardiac output= Heart rate times Cardiac output= Heart rate times

stroke volumestroke volume Rhythm Rhythm

– arrhythmias are common in the arrhythmias are common in the neonatal period and are neonatal period and are frequently benignfrequently benign

MurmurMurmur

Caused by turbulent blood flowCaused by turbulent blood flow Pathological vs. innocentPathological vs. innocent Note location, intensity, Note location, intensity,

radiation quality and pitchradiation quality and pitch Occur in 60% of neonates in Occur in 60% of neonates in

the first 48 hours of lifethe first 48 hours of life

MurmursMurmurs Grade 1- barely audibleGrade 1- barely audible Grade 2- soft but immediately Grade 2- soft but immediately

audibleaudible Grade 3- moderate intensity without Grade 3- moderate intensity without

a thrilla thrill Grade 4- loud, can be heard with Grade 4- loud, can be heard with

stethoscope barely on the cheststethoscope barely on the chest Grade 5- very loud, heard with Grade 5- very loud, heard with

stethoscope slightly removed from stethoscope slightly removed from the chestthe chest

Color/ CyanosisColor/ Cyanosis

Central vs. PeripheralCentral vs. Peripheral– assess central color on mucous assess central color on mucous

membranes paying attention to membranes paying attention to intrapartal historyintrapartal history

– acrocyanosis common in newborn acrocyanosis common in newborn period related to circulatory changesperiod related to circulatory changes

Cardiac vs. PulmonaryCardiac vs. Pulmonary– cyanosis not responsive to oxygenation cyanosis not responsive to oxygenation

should bring suspicion of cardiac should bring suspicion of cardiac diseasedisease

Cardiac AssessmentCardiac Assessment

PerfusionPerfusion– Capillary Refill timeCapillary Refill time

PulsesPulses– Brachial, femoral (Central)Brachial, femoral (Central)– tibial, radial (peripheral)tibial, radial (peripheral)– right vs. leftright vs. left

right preductalright preductal left - postductalleft - postductal

– bounding common in premature infantsbounding common in premature infants

Blood Pressure Blood Pressure

Use appropriate sized cuff for Use appropriate sized cuff for accuracyaccuracy

Norms dependent on weight, ageNorms dependent on weight, age Decreases 3-4 hours postnatally, Decreases 3-4 hours postnatally,

increases to plateau at 4-6 days of increases to plateau at 4-6 days of ageage

Follow blood pressures for trendingFollow blood pressures for trending

Cardiac DiagnosisCardiac Diagnosis

CXR- rule out pulmonary CXR- rule out pulmonary disease, assess heart sizedisease, assess heart size

EKGEKG Cardiac EchoCardiac Echo Blood Gas- low PaO2, normal Blood Gas- low PaO2, normal

CO2CO2 hyper-oxygen test- pre and post hyper-oxygen test- pre and post

ductal saturationductal 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 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

Maternal Factors

Environmental Factors

Environmental factors as causes of congenital heart disease have only recently begun to be recognized

More research is needed

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.

Cyanotic Heart Defects or 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 FallotX-Ray Tetralogy of Fallot

Commonly thought Commonly thought to look “boot to look “boot shaped”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 AtresiaX-Ray of Pulmonary Atresia

Commonly with little Commonly with little vascular markings and vascular markings and may also be seen as may also be seen as “snowman”“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 AtresiaX-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 AnomalyEbstein’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 AnomalyEbstein’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 AnomalyX-Ray Ebstein’s Anomaly

Ductal Dependent LesionsDuctal Dependent Lesions

What will you see?What will you see?– Infant who is cyanotic and does NOT Infant who is cyanotic and does NOT

respond to O2.respond to O2.– Infant becomes increasingly cyanotic Infant becomes increasingly cyanotic

and/or tires easily with feedings in and/or tires easily with feedings in first few days as duct closesfirst few days as duct closes

– Usually appear comfortable but may Usually appear comfortable but may exhibit s/s of respiratory distressexhibit s/s of respiratory distress

– Xray may show CHF alreadyXray may show CHF already

Nursing CareNursing Care– Monitor VS very closelyMonitor VS very closely– Observe SaO2 closely – may not want Observe SaO2 closely – may not want

sats high d/t defect and shunting of bloodsats high d/t defect and shunting of blood– STRICT I&O!!! CHF can result easilySTRICT I&O!!! CHF can result easily– Pre/Post Sats may be orderedPre/Post Sats may be ordered– Sedate if necessary, Ventilate if Sedate if necessary, Ventilate if

necessary (may have underlying necessary (may have underlying respiratory issue also)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

Ductal Dependent Lesions

ArrythmiasBradycardia Etiology

– Usually secondary to respiratory or apnea

Clinical Signs– Decreased heart rate (<100), regular

QRS complex Treatment

– Treat underlying respiratory disorder (methylzanthines), stimulation

Etiology– Abnormal stimulation of the

AV node, heart disease usually not present

Supraventricular Tachycardia (SVT)

Treatment – Vagal stimulation (the diving

reflex) – Adenosine – Cardioversion - synchronized,

0.5-1.0 joules per kg

SVT

SVTSVT

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 mayfluctuate

>220, usually 250-350,rate constant

HX fever, volume loss,anemia

irritability, poorfeeding, vomiting,tachypnea, pallor

EKG regular EKG absent p waves