Pediatric Cardiology Flashcards
What does heart failure look like in an infant
Respiratory distress, especially with feeding
poor feeding
poor growth
hepatomegaly and rales
What is the foramen ovale
Right atrium to left atrium hole
what is ductus arteriosus
pulmonary artery to aorta
What is ductus venosis
umbilical verin to IVC (bypasses liver)
what happens to lead to the closure of ductus arteriosus
decreased level of prostaglandin E2
What is the leading cause of birth-defect related perinatal and infant death and disease
Congenital heart disease
What are the types of congenital heart disease
Acyanotic heart disease
obstructive lesions
cyanotic heart disease
What is the most common heart defect
Bicuspid aortic valve
often unknown until adulthood
What are risk factors for CHD
prematurity: 2-3x higher
family history: 3 fold increase if first degree relative
genetic syndrome
maternal factors: diabetes, HTN, obesity, PKU, thyroid, smoking, alcohol use
in utero infection: TORCH
What are TORCH infections
in utero infection
rubella, flu-like illness, CMV, HHV6, HSV, parvovirus, toxoplasmosis
What is Acyanotic heart disease
L>R shunts
Patent ductus arteriosus (PDA)
Ventricular septal defect (VSD)
Atrial septal defect (ASD)
What is the classic murmur description of PDA
continuous machine-like murmur LUSB or left infra-clavicular area
What is a PDA
failure of DA to close
more common in babies born < 30 weeks
how are PDA’s diagnosed
clinical findings (murmur)
ECHO
What is the management of a PDA
mod-severe or signs of CHF/PHN: surgical or percutaneous (preferred) closure
what is the management of premature infants with PDA
prostaglandin inhibitors tried first
-indomethacin, ibuprofen
(does not work in term neonates and older infants)
What is a VSD
ventricular septal defect
common congenital heart disease - 50% of all congenital heart disease have VSD as a component
what are symptoms of VSD
diaphoresis, particularly with feeds
difficulty feeding
failure to thrive
CHF
irreversible pulmonary vascular changes within 6-12 months
What is the classic sign of VSD
holosystolic murmur heard best a the mid to LLSB
what confirms the diagnosis of a VSD
ECHO - size and location confirmation
What is the management of VSD
35% will close spontaneously
small defects - will close by age 2
moderate or large: asymptomatic: regular follow ups, symptomatic depends
what is the treatment for moderate or severe symptomatic VSD
mild: oral diuretics (lasix), neutritional support
Moderate: lasiz +/- aldactone; maximize caloric intake
Severe: inpatient, IV diuretics, max nutritional suppport, stabilize condition for surgery
What are the types of ASD
Primum
Secundum
Sinus venosus
What is primum ASD
septrum primum doesnt fuse with the endocardial cushions
usually associated iwth other abnormalities
What is secundum ASD
hole near the foramen ovale
females> males
usu. isolated; can be associated with genetic disorders
what is sinus venosus ASD
malposition of insertion of vena cava
What is the clinical presentation of ASD
usu no symptomatic early, normally come to attention on PE
impact depends on size/location
infants with larger ASD can present with CHF, FTT
What is the classic findings with ASD
wide, fixed split S2 (vs only on inspiration)
mid-systolic ejection murmur
how is ASD diagnosed
clinical suspicion with murmur
EKG may show RBBB
ECHO confirms diagnosis
MRI can be helpful
what is the managment of ASD
many spontaneously close in infancy/early childhood
untreated, with persistent shunt: R sided heart failure afe 30-40
repair if R heart enlargement
surgical
What are Acyanotic Obstructive defects
Coarctation of the Aorta (COA)
Aortic Stenosis (AS)
Pulmonary stenosis (PS)
What is Coarctation of the Aorta
narrowin of descending oarta, distal to LSCA
symptoms depend on degree of obstruction
what are the classic findings with COA
hypertension in UEs, low-unobtainable BPs in LE
decreased/delayed femoral pulses
possible murmur caused by collateral blood flow
how is COA diagnosed
prenatal difficulties due to low CO via aorta
ECHO
what is the management of COA
imperative to identify critical COA in neonates: rapid initiation of prostaglandin E > once stable, surgery
balloon angioplasty preferred