Neonatal Cardiac Emergencies

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)


(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


(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

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


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


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

Neonatal Cardiac Emergencies

Documents

Transcript of Neonatal Cardiac Emergencies