Pediatric Alterations in

Cardiac Function
Congenital Heart Defects
Laura M. Hernandez,
DNP, ARNP
NWCNHS

Congenital Heart Dz.

(Chpt.34)

5-8 in 1000 live births

Major cause of death other than
prematurity in the 1st year of life
90% etiology is unknown
KNOW fetal circulation
Pressure changes
Flow changes
Foramen ovale/PDA
CHF

Pediatric Indicators of Cardiac

Dysfunction
Poor feeding
Tachypnea/ Tachycardia
Failure to thrive/poor weight
gain/activity intolerance
Developmental delays
+ Prenatal history
+ Family history of cardiac disease

Understanding Heart
Defects

Blood flows b/c pressure of gradients in

different parts of the body & the hearts
pumping ax.
Blood flo=Hi to lo, taking path of least resis.
Blood rate=hi pressure=fast vice versa hi
resistance=slow (not always)
Normal=Rt sided pressure<than Lt
Aorta (circ)=hi & PA (lung)=lo

Understanding Heart
Defects

If this directional flo is interrupted with a

septal defect then the pressure changes
and switches the flo backwards e.g. left
to right shunting
Blood returning to heart via SVC & IVC
has lowest sat leaving venous blood desat
Sats are = in RA,RV, and PA
Blood entering Lt from lungs is fully sat.
Sat & desat blood should not mix

Defects of Increased
Pulmonary Blood Flow

All

have CHF
Cyanosis, clubbing possible
ASD
VSD
AVC
PDA
Coarct.
AS,PS
TOF

Of Aorta

Defects of Increased
Pulmonary Blood Flow-ASD

ASD-abnormal opening b/w

atria, allowing blood from the hi
left to enter the lo rt
Repair: Surgical patch/open
repair before school age

Defects of Increased
Pulmonary Blood Flow-VSD

VSD-abnormal opening b/w the rt and Lt

ventricles
Most common of anomalies
Varies from pinhole to absence of septum
Assct with other defects
20-60% close spontaneously in 1st y
Repair: banding , cath closure, surgical

AVC defect
Incomplete fusion of endocardial
cushions
Lo ASD and clefts of the mitral and
tricuspid valves, creating a large AV
valve that allows blood to flo b/w all
four chambers
Most common anomaly in DS
Repair: banding, patch & reconstruct

PDA
Failure of the fetal ductus arteriosus
to close within the first weeks of life
Repair: Indomethicin (prostaglandin
inhibitor), ligation via Lt
thoracotomy, or VATS-visual assisted
thorascopic surgery, coils via cath,
full surgery

Obstructed Defects
COA
AS
PS

Coarctation of Aorta
Localized narrowing near the
insertion of the DA, resulting in
increased pressure proximal to the
defect (head and UE) and decreased
pressure distal to the obstruction
(body and LE)
Repair: Resex and end to end anas.
Of aorta, balloon angioplasty

Aortic/Pulmonic Stenosis
Narrowed entrance at respective
valves
AS surgical repair rarely results in a
normal valve e.g. limit physical
activity
Repair: balloon angio

Defects of Decreased
Pulmonary Blood Flow
TOF
Tricuspid

Atresia

Tetralogy of Fallot
Four defects: VSD, PS, Overriding
Aorta, Rt. Ventricular Hypertrophy
Tet Spells (p.1488), pan systolic
murmur
Aorta receives blood from both
ventricles
Repair:BT shunt, median sternotomy
and CP bypass

Mixed Blood Flow

Defects
Transposition

of Great

Vessels
Total anomalous
pulmonary venous
connection
Truncus Arteriosus
Hypo plastic Lt. Heart
Syndrome

Transposition of the great

vessels
The PA leaves the LV with no
communication b/w the systemic
and pulmonary circulations
Need VSD and ASD in order to
survive
Complex surgical procedures:
arterial switch performed in the 1st
weeks of life, creating a new aorta

Hypo plastic Lt.Heart

Syndrome
Underdevelopment of the Lt. Side
resulting in a hypo plastic Lt.
Ventricle and aortic atresia.
Surgical repair: 1st stage:Norwood
procedure 2nd stage: bidirectional
Glenn shunt @6-9 m. to relieve
cyanosis and reduce the volume load
on the rt. Ventricle 3rd stage:
modified Fontan procedure.

Common Medical Treatment

Medications

Procedures & Diagnostics

Prostaglandins

Cardiac Catheterization

Digoxin

Oxygen

Lasix

CPT

Heparin

Chest Tubes

Indocin (Indomethacin)

Pacing

Aldactone (Spironolactone)

EKG

Antibiotics (PCN, EES)

Echo (ECG)

Antihypertensives

Exercise Stress Test

ACE inhibitors

Hemoglobin

Beta Blockers

Hematocrit

Apresoline

CBG (pO2)

Rheumatic Fever (RF)

RF
Inflammatory disease occurs after
group A
-hemolytic streptococcal pharyngitis
Self-limiting

Affects joints, skin, brain, serous surfaces,

and heart

Clinical Manifestation of RF

Clinical manifestation:

Carditis
Polyarthritis
Erythema marginatum

Transitory rash on trunk and proximal extremities

Nonpruritic

Subcutaneous nodules

Occur in crops over bony prominences

Arthralgia, fever, epistaxis, abdominal pain

St. Vitus Dance
5th Manifestation

RF Management

Primary prevention
(cure group A beta
strep) throat
cx/PCN
Prevent cardiac
damage
Palliation of other
symptoms (ASA,
prednisone)
Prevent recurrence

Encourage
compliance of ABX
esp. long term

Bed rest-helps
with heart load

Nutrition

Chorea-provide
safety

Kawasaki Disease

Acute systemic vasculitis, unknown

cause
Duration 6-8 weeks, self-limiting
Without treatment of KD, 20%-25%
have cardiac complications

Dilation of coronary arteries (ectasia)

Coronary artery aneurysms (giant
aneurysms > 8 mm)

Acute, subacute, convalescent phases

Usually younger than age 5 (toddlers)

Clinical Manifestations

High feverunresponsive to antipyretics/ antibiotics

4/5 signs (rash, redness/swelling of hands and feet,
cracked lips/strawberry tongue, red eyes, unilateral
lymphadenopathy, irritability)
Abdominal pain
CBC: anemia, WBC, Platelets, ESR, CRP-elevation
>1.5 cm cervical lympadenopathy

A Four-year-old boy
with the typical
features of Kawasakis
disease:

bilateral
nonexudative
conjunctivitis (A);
dry, fissured,
erythematous lips
and a strawberry
tongue ( A and B);
erythematous and
edematous hands
and feet (C and
D);
an erythematous
truncal rash (E);
a desquamating
perineal rash (F).

www. neim.org

Management

Echocardiogram
Aspirin and Immunoglobulin administration
Monitor Cardiac status, promote comfort, and education
Assess heart for tachy, gallop, uo, resp. distress, and
temperature
ASA toxicity: HA, confusion, dizziness, tinnitus (Reyes
Syndrome)
Avoid NSAIDS
No live vaccines for 9-12 months after IVIG therapy

ASA 80-100 mg/kg/day

fever
Then 3-5 mg/kg/day
antiplatelet

Baby
Aspirin

Things to Know
A Fall in serum K+
enhances the effects of
Digoxin, increasing digoxin
toxicity
Digoxin toxicity: vomiting,
lethargy
Oxygen: a drug
administered w/ appropriate
order, can be detrimental
Infants rarely receive more
than 1 ml in one dose
Hold Digoxin: if heart rate:
I: <90 , C: <70, A: <60