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Neonatal Cardiac
Emergencies Jeffrey Moore, MD
Pediatric Cardiology
ProMedica Health System
Assistant Professor of Pediatrics/
Associate Clerkship Director
University of Toledo Medical School
Outline/Objectives
4 Cases
Will review signs and symptoms of both structural and electrical cardiac
causes of neonatal emergencies
Examine the pathophysiology behind these cardiac conditions
Will discuss life saving/stabilizing treatment for these emergencies
Introduction
Neonates: more common for structural heart disease to be the case of
emergency
Toddlers and young children: more common for dysrhythmia
Incidence of CHD: ~8/1000 live births and 1-2 of these patients will have
“critical” CHD
Accounts for ~10% of infant deaths
Timing and presentation depend on nature and severity of defect
Antenatal screening catches around 67% of neonatal cardiac
emergencies
Cardiovascular changes at birth
Fetal: lungs collapsed and filled with liquid high PVR
Placenta = gas exchange
Oxygenated blood is directed through the PFO to the left atrium (by the Eustachian valve)
Postnatal: first gasp of air causes lungs to expand and liquid to be reabsorbed
Lung expansion leads to drop in PVR
PDA will usually “functionally” close by 12 hour and anatomic closure in 2-3 weeks (becomes ligamentum arteriosum)
Most structural cardiac emergencies are secondary to ductal dependent lesions
Case #1
You are called to the nursery to evaluate an 8 hour old 37 week newborn
born to a 25 yo G2P2002. Pregnancy was complicated by pre-eclampsia.
APGARs were 8&9 at 1&5 minutes respectively. The nurse notes that the
patient has steadily become more tachypneic the last few hours. When
you arrive the patient has the following vitals: P 178, RR 48, BP (unable to
obtain), SpO2 98% on right hand. On exam, patient has is tachycardiac
with Grade II systolic murmur best heard between scapula (slightly L>R).
Pulses are 2+ brachial but thready in femoral.
Case #1
What is your next step in management?
A. Oxygen
B. Start IV and give bolus of fluids
C. Start IV and PGE1
D. Ibuprofen
E. EKG
The child improves with PGE administration and an echocardiogram is
ordered showing the following…
Neonatal Coarctation of the Aorta
(COA)
Neonatal Coarctation of the aorta
Coarctation of the aorta (COA) has a broad spectrum from asymptomatic
to severe in neonates depending on the severity of stenosis
Makes up about 7% of CHD
Severe COA, neonates are depending on ductal blood perfuse the
descending aorta
Narrowing of this leads to tissue hypoperfusion, acidosis, and potentially
shock
Acidosis = compensatory respiratory alkalosis (which can complicate the
exam)
Look for decrease pulses in lower extremity, delayed pulses, delayed cap
refill, blood pressure discrepancy (if able to obtain)
Aycanotic Congenital Heart Disease
Failure of adequate systemic flow
PDA often needed to maintain systemic flow
Examples includes severe COA, interrupted aortic arch, mitral stenosis,
aortic stenosis, Hypoplastic left heart syndrome
PGE PDA, will often work up to weeks later
Symptoms in a neonate are often nonspecific
Irritability
Poor feeding
Tachypnea
Acyanotic Congenital Heart Disease
Physical exam:
Poor pulses
Poor cap refill (>3s)
Tachypnea (acidosis)
Mottled skin
Murmur(s)
Aortic stenosis= systolic ejection murmur loudest at RUSB
Mitral stenosis= mid-diastolic murmur at apex
Acyanotic congenital heart disease
Prostaglandin saves lives
Prostagladin
Initial dose 0.05-0.1mcg/kg/min (high may be needed the older the
neonate)
Can titrate downwards if patient stabilizes
Apnea 10-12% of cases
Other adverse effects:
Fever (14%)
Cutaneous flush (10%)
Bradycardia (7%)
Seizures (4%)
Case 2
You are called to the bedside of a 1 hour old male infant for concerns of
cyanosis. Baby was born to a 37yo G6P4 mother with pregnancy complicated
by poor controlled maternal diabetes and poor prenatal compliance. APGARs
were 8&8 respectively. At bedside, Mother reports she tried to feed the baby
when he starting turning blue. On exam, you find a cyanotic appearing baby
with bluish appearance of the tongue. Vitals are P 178, RR 57, SpO2 70% (right
arm), 84% (right leg), BP’s (unable to obtain). On physical exam, patient is
tachypenic with mild retractions. Lungs are CTA and cardiac exam is only
significant for a prominent S2. Pulses are 2+ w/o delay.
Case 2
You start the baby on PGE which does not demonstrate significant
improvement. You order a stat CXR and echocardiogram which show
The patient was diagnosed with d-Transposition of the Great Arteries with
restrictive atrial septum. What is the next step in management?
A. Balloon atrial septostomy
B. Arterial switch operation
C. Atrial switch operation (Mustard)
D. Heart transplant
E. Continue PGE and close observation
Restrictive atrial septum and balloon
atrial septostomy
May be needed to relieve pulmonary congestion
Hypoplastic left heart syndrome
Mitral stenosis
May be needed to relieve right sided congestion
Pulmonary atresia with intact ventricular septum
Tricuspid atresia
Total anomalous pulmonary venous connection/return
D-Transposition of the Great Arteries
Makes up 3% of all CHD and 20% of CHD
Restrictive atrial septum much more rare
PGE & PDA usually increase pulmonary flow Left atrial volume
increased L R oxygenated atrial shunting
Often does not carry a genetic predisposition (not familial or syndromic)
Infants of diabetic mothers have a 5x increased risk of CHD (d-TGA being
#1)
Critical Cyanotic Congenital Heart
Disease
Cyanosis = >5g/dL of deoxygenated hemoglobin
3 causes:
Incomplete oxygenation by the lungs
R L shunt through the heart (does not respond to 100%FiO2)
Abnormal Hg that cannot bind O2
Other examples of critical cyanotic CHD include Tetralogy of Fallot with
severe pulmonary stenosis, Tricuspid atresia with restrictive VSD, Pulmonary
atresia with intact ventricular septum, Total Anomalous Pulmonary Venous
Return (infracardiac)
Tricuspid Atresia
Prostaglandin saves lives
Case 3
You are seeing a 6d old female infant in your office for routine post-natal
follow up. Pt was a term SVD born to a 19 yo G1P1. Pregnancy was
complicated by no pre-natal care and home delivery. APGARs were 8&8
at 1&5 minutes. Mother is bottle feeding the infant and reports his volume
has decreased everyday where is now only taking 0.5oz q3h. He is also
breathing harder. You check his vitals and find P 188, RR 63, SpO2 75%, BP
(unable to obtain). On exam the infant is lethargic with rapid breathing and
retractions. He has poor pulses diffusely and with grey/bluish appearance
of his extremities. Cardiac exam is unremarkable. Cap refill is 5s. You call
911.
Case 3
What is the most likely diagnosis?
A. Large Malaligned Ventricular Septal Defect
B. Shone’s complex with severe sub-aortic stenosis
C. Tetralogy of Fallot with severe pulmonary stenosis
D. Truncus arteriosus
E. Hypoplastic Left Heart Syndrome
Hypoplastic Left Heart Syndrome
(HLHS)
Hypoplastic Left Heart Syndrome
(HLHS)
Accounts for 2-3% of all CHD
Fully “ductal dependent lesion” (required to maintain systemic circulation)
Most common single ventricle heart disease
If left untreated compromises 25-40% of all neonatal cardiac deaths
May also present with a restrictive atrial septum (like the previous case) and
require an atrial septostomy
Hypoplastic Left Heart Syndrome
(HLHS)
Signs/symptoms
Hypotension
Acidosis
Tachypnea
Respiratory distress
Cyanosis (large mixing lesion at baseline)
Poor feeding (increased systemic perfusion demand)
Often will have a normal cardiac exam
Case 4
A 2 week old male infant presents for routine follow-up. He was a 35 week
premature infant born to a 24 yo G2P2 who spent 5d in the NICU for
feeding concerns. Patient had no known pre-natal or postnatal issues.
Mother reports he has been very irritable over the last 12-24 hours and his
feeding has decreased from 3oz q3h to 1.5oz q3-4h. His vitals are P 247, RR
49, SpO2 95%, BP (you guessed it, unable to obtain). On exam patient is
crying with mild tachypnea and retractions. Lungs are CTAB and cardiac
exam is unremarkable outside of tachycardia. Pt has 2+ pulses, cap refill 2s,
and hepatomegaly ~1cm. You try ice to the face without significant
improvement in vitals. You obtain the following EKG.
What is your next step in
management?
A. Start IV and given adenosine
B. Start IV and give fluid bolus
C. Sedate and cardioversion
D. Defibrillation
E. Essential oils and relaxation therapy
Normal electrical conduction
SVT
Re-entrant SVT
Neonatal SVT
WPW can cause re-entrant SVT
Atrial fibrillation ventricular fibrillation not seen in neonates
Neonatal tachyarrhythmias
Other examples include atrial flutter, ectopic atrial tachycardia, ventricular
tachycardia
Atrial flutter:
common in fetus and newborns
once converted, rarely recurs
often well tolerate
Adenosine administration may distinguish flutter waves
Often have structurally normal hearts
Neonatal tachyarrhythmias
Ectopic atrial tachycardia
Abnormal p-wave morphology
Can lead to ventricular dysfunction over time, making it an emergency though
rare
Tend to only respond to anti-arrhythmics (as opposed to cardioversion)
Slow onset and offset
Ventricular tachycardia
Very rare in neonates
Adenosine has no effect
QRS complex may appear narrow
Ventricular Tachycardia
Neonatal tachyarrhythmias
Moral of the story…
Neonatal bradyarrhythmias
Bradycardia:
Sinus bradycardia (if severe, often non-cardiac)
Junctional bradycardia
AV block
Most common neonatal bradyarrhythmia is 3rd degree heart block
Often complication of maternal lupus (60-90%)
Caused by Ro/La antibodies
3rd degree heart block
Neonatal Bradyarrhythmias
Treatment
Epinephrine
Atropine
Transcutaneous/transvenous pacing
References
Recommended