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Neonatal Cardiac assessment
Eric Towe, MD Pediatric Cardiology Avera Children’s Hospital University of South Dakota Sanford School of Medicine
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Objectives Incidence of congenital defects
Discuss types of congenital heart defects Outline clinical features of congenital heart defects Overview of specific congenital heart defect care
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Objectives Incidence of congenital defects
Discuss types of congenital heart defects Outline clinical features of congenital heart defects Overview of specific congenital heart defect care
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Congenital heart defects
Most common congenital defect Occur in 6-13/1000 live births Bicuspid aortic valve Ventricular septal defect (VSD) Atrial septal defect (ASD)
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Congenital heart defects
Cyanotic defects – 15% Pulse ox <80% Tetralogy of Fallot Critical defects – 25-33% Require surgical or cath intervention in first year of life
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Congenital heart defects
Leading cause of neonatal death prenatal diagnosis 58% Operator expertise Gestational age Fetal position Type of defect
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Congenital heart defects
Most infants identified soon after birth Some not until after discharge 30% critical Increased morbidity and mortality if delay
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Objectives Incidence of congenital defects
Discuss types of congenital heart defects Outline clinical features of congenital heart defects Overview of specific congenital heart defect care
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Neonatal cardiac anatomy
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classification Cyanotic congenital heart disease
Deoxygenated blood into systemic circulation shunts
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Ductal-dependent Circulation dependent of patent ductus arteriosus (PDA) Only source of blood to lungs or body Many cyanotic lesions are ductal dependent
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Critical congenital heart disease
Requires surgical repair or catheter intervention within first year Ductal-dependent, cyanotic, other less forms 25% of all chd
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Acyanotic heart disease
Congenital defect with normal pulse ox Wide range of severity
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Objectives Incidence of congenital defects
Discuss types of congenital heart defects Outline clinical features of congenital heart defects Overview of specific congenital heart defect care
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Initial diagnosis and evaluation
History Physical exam Chest x-ray Hyperoxia test EKG/echocardiogram
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history Risk factors Poor feeding Color change Irritability/sweating
Poor weight gain Excessive sleeping
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Risk factors Family history Multiple fetuses Genetic syndromes
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Genetic syndromes 7-12% congenital heart disease Most common
Trisomy 21 Turner syndrome Digeorge syndrome
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Risk factors Family history Multiple fetuses Genetic syndromes
Maternal factors
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Maternal factors Obesity Diabetes Medications NSAIDS Ace Retnoic acid
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Maternal factors Advanced maternal age Hypertension
Alcohol/substance abuse Epilepsy Infection – rubella, cmv, parvo b19, etc. Assisted reproductive technology
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Physical findings Can present shortly after birth Days after discharge
Shock, cyanosis, tachypnea, pulmonary edema
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shock Most common left heart obstructive lesions
Hypoplastic left heart Critical aortic valve stenosis Critical coarctation Interrupted aortic arch
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shock Infants present in shock as ductus arteriosus closes
Initiation of pge1 essential Must differentiate from septic shock Cardiomegaly and lack of response to volume – suggests cardiac
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Bluish skin tone caused by deoxygenated hemoglobin
cyanosis Bluish skin tone caused by deoxygenated hemoglobin Important sign in multiple types of CHD May not be seen Mild desaturations (>80%) Anemia Darker skin tones
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Ductal dependent lesions
cyanosis Ductal dependent lesions Right heart obstruction
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Pulmonary atresia
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Ductal dependent lesions
cyanosis Ductal dependent lesions Right heart obstruction Left heart obstruction
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Critical aortic valve stenosis
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Ductal dependent lesions
cyanosis Ductal dependent lesions Right heart obstruction Left heart obstruction Parallel circulations
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Transposition of the great arteries
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Ductal dependent lesions
cyanosis Ductal dependent lesions Right heart obstruction Left heart obstruction Parallel circulations Non-ductal dependent
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Differential cyanosis
Difference in pulse ox of >3% between right hand and lower extremity Pre versus post ductal Coarctation of the aorta
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Differential cyanosis
Difference in pulse ox of >3% between right hand and lower extremity Pre versus post ductal Coarctation of the aorta Persistent pulmonary hypertension of the newborn (PPHN)
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cyanosis Non-cardiac causes Pulmonary disorders Abnormal hemoglobin
Sepsis, hypoglycemia acrocyanosis Acrocyanosis – hands and feet – not oral mucosa
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Increased work of breathing Poor feeding
Respiratory symptoms Tachypnea Increased work of breathing Poor feeding Rapid increase in pulmonary blood flow Drop in pulmonary vascular resistance PDA in premature infants Truncus arteriosus
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Cardiac versus pulmonary disease
Further workup needed if: Persistently elevated respiratory rate (>60 bpm) Distress during feeding Cough and wheeze more likely pulmonary disease
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Physical exam Key component to neonatal assessment
Fails to detect more than half of infants with chd Subtle findings provide clues Findings may be absent in ductal dependent lesions if PDA still open
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Findings suggestive of CHD
Abnormal heart rate Abnormal precordial activity Abnormal splitting s2 Abnormal extra heart sounds Pathologic murmurs Hepatomegaly Diminished pulses in lower extremities Extracardiac abnormalities
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EKG best course for further evaluation if persistent
Abnormal heart rate Normal range bpm Up to six days of life Higher or lower rates EKG best course for further evaluation if persistent
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Abnormal precordial activity
Precordial palpation for normal placement Left side of chest Right side – dextrocardia Complex CHD Cardiac enlargement + respiratory symptoms = likely chd Order chest x-ray if concerned
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Cardiac auscultation is key component to evaluation
Abnormal heart sounds Cardiac auscultation is key component to evaluation Timing of murmur S1/S2 Extra heart sounds Pathologic murmurs
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Cardiac cycle Systole diastole
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S2 normally splits with inspiration
Abnormal splitting s2 S2 normally splits with inspiration S2 splitting reduces likelihood of CHD Infant heart rate often too high to hear 80 of newborns by 48 hours <150 bpm
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Defects with Abnormal s2
Single s2 Aortic atresia Pulmonary atresia Tetralogy of fallot Pulmonary hypertension Wide fixed split s2 ASD (not all)
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Presence of heart murmurs often associated with CHD
Not all CHD has a heart murmur 80% of children will have a heart murmur 1% pathologic
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Sound of blood moving through heart
Heart murmurs Sound of blood moving through heart Turbulent flow Pressure difference Ventricular function
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Timing Systolic Early Mid Late Pan Diastolic Continuous
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Heart murmurs Systolic 1-6/6
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Intensity Grade + Thrill - Thrill LOUDEST, Stethoscope off chest
Louder, Edge of stethoscope Intensity Grade 1 2 3 4 5 6 Loud, Palpable thrill 6 Easily heard, Intermediate intensity 5 Faint, Heard immediately 4 + Thrill - Thrill Faint, with concentration 3 2 1
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Heart murmurs Systolic 1-6/6 Diastolic 1-4/4 Never innocent
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Location Aortic area Pulmonic area A P Mitral area Tricuspid area T M
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Normal liver edge 1-3 cm below right costal margin Enlarged liver
Hepatomegaly Normal liver edge 1-3 cm below right costal margin Enlarged liver Heart failure Increased central venous pressure
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Diminished pulses Cool/mottled lower extremities
Essential part of evaluation Decreased or absent pulses lower extremity Coarctation Aortic arch obstruction Usually accompanied with bounding pulses in upper extremities Cool/mottled lower extremities
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Blood pressure Monitor upper and lower extremities
Gradient > 10 mmHg (upper>lower) Appropriate cuff size Neonatal hypertension
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Extracardiac abnormalities
22% of infants with chd – extracardiac defects Skeletal Hand or arm Chromosomal abnormalities 12.3% of infants with CHD had chromosomal abnormality Down syndrome Turners Digeorge
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Pulse ox screening
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Pulse ox screening Performed after 24 hours or as late as possible if early discharge Measure right hand (pre-ductal) and either foot Positive screen based on AAP: SpO2 < 90% in either extremity SpO2 < 95% in both upper and lower extremities on 3 measurements – one hour apart SpO2 difference > 3% between upper and lower on 3 measurements – one hour apart
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Reduces diagnostic gap to 5-10%
Pulse ox screening Positive screen Identify cause of hypoxia Echocardiography Consultation with pediatric cardiologist Reduces diagnostic gap to 5-10% Ductal dependent lesions
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Diagnostic approach Presence or absence of symptoms determines approach Symptomatic infants Urgent consultation Physical exam Pulse ox/Hyperoxia test Chest x-ray Echocardiogram
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Differentiate between cardiac and pulmonary
Chest x-ray chd Differentiate between cardiac and pulmonary Obtain in cyanosis/respiratory symptoms Findings consistent with chd Cardiomegaly Dextrocardia Abnormal cardiac silhouette Arch sidedness (right) 20% TOF right sided aortic arch
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Abnormal cardiac silhouette
Boot shaped heart Tetralogy of Fallot
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Abnormal cardiac silhouette
Egg on a String Transposition of the Great Arteries
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Abnormal cardiac silhouette
Egg on a String Transposition of the Great Arteries
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Abnormal cardiac silhouette
Wall to Wall or Basketball Ebstein Abnormality
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Hyperoxia test Distinguish cardiac from non-cardiac causes of cyanosis
Measure arterial PaO2 right radial artery (preductal) and foot Taken during room air and after 10 minutes on 100% FiO2 If systemic PaO2 >150 mmHg after O2 administration - more likely pulmonary Abnormal PaO2 doesn’t “rule in” CHD Should not use pulse ox as surrogate to PaO2
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Echocardiography Definitive diagnosis of chd
Consult pediatric cardiology Shock not responsive to volume Cyanosis Failed hyperoxia test Abnormal CXR Physical findings Abnormal pulse ox screening Genetic Disorder or extracardiac malformation
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Diagnostic approach Asymptomatic infants
Presence or absence of symptoms determines approach Symptomatic infants Urgent consultation Physical exam Pulse ox/Hyperoxia test Chest x-ray Echocardiogram Asymptomatic infants
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Asymptomatic infants Pulse ox screening Careful physical examination Careful history If questions/concerns - call
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Objectives Incidence of congenital defects
Discuss types of congenital heart defects Outline clinical features of congenital heart defects Overview of specific congenital heart defect care
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Initial management Cyanotic infants require immediate assessment and general supportive care Airway management IV access Vital Signs Antibiotics if other cause cannot be identified Prostaglandin E1 Keeps ductus open Starting dose 0.05 mcg/kg/min Can cause apnea – have ET tube at bedside CXR, Echo if possible Consult Cardiology/Transport to tertiary care center
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Initial management Heart murmur but otherwise asymptomatic Close clinical observation Vital signs Careful history and complete physical Pulse Ox screening Consider CXR/EKG/Echo Contact with any questions/Concerns
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Summary Congenital heart disease is the most common congenital defect
Careful history and physical exam is key Pulse Ox screening improves detection Most neonates present while in hospital Some present after discharge Careful history and physical – feeding, respiratory issues, cyanosis
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Summary Consider CXR, hyperoxia test or echocardiogram if concerns Cyanotic infants require immediate care Airway/IV access Antibiotics PGE1 Echocardiogram Transfer/Cardiology consultation
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Questions?
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Thank you
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