Congenital Heart Disease Flashcards
Photo of fetal circulation (maybe a hot spot Q?)
The Placenta is a large low resistance vascular bed – PVR > SVR
CO is combined ventricular output, the RV is thicker and has 2/3rds of output, and LV is only 1/3rd
3 shunts of the fetal heart
- Ductus Arteriosus
- Foramen Ovale
- Ductus Venosus
Ductus Arteriosus
largest vessel – protects the lungs against circulatory overload –> RV strengthens which increases pulmonary vascular resistance and decreases blood flow
- should close within 24 hours of birth, yet can take 2 -3 weeks
How to close or keep ductus arteriosus open
Small opening: prostaglandin inhibitors (Indamethacin) to close … larger = surgery
if baby needs the shunt to get O2 rich blood –> PGE1 and bradykinin to KEEP DILATED
meconium aspiration
would continue PVR increase and fetal circulation to persist –> PULM HTN –> ECMO
worsened with hypoxia, acidosis, and hypothermia
Newborn Heart- Foramen Ovale
function: to shunt highly O2 rich blood from the RA to the LA
- Functional closure occurs in the first few hours after birth as the LAP > RAP
Probe patent foramen ovale = PFO
- 50% of 5 year olds
- 25% of 20 year olds
CONCERNED about: Paradoxical embolus
to prevent … SVR > PVR
Ductus Venosus
Connects the umbillical vein to the inferior vena cava … flow is regulated though a eustachian valve
Fetal Blood Flow
Blood enters from two areas: the IVC and SVC …
IVC from Moms blood (more O2) and SVC replies on patent foramen ovale and ductus arterosis d/t mixing of blood
Fate of Shunts
First few days –> weeks is unstable circulation, PVR is still increased yet sensitive to changes
1st breath will DECREASE PVR
HPV is marked
PVR normalizes in 6wks ~ adult
Newborn heart- Ventricular tissue
Fewer myocytes - 30%
Greater proportion of connective tissue
Relative RVH
- Decreased compliance
- More sensitive to preload
Ventricular interdependence
- Relatively noncompliant
- Relatively restricted in ability to change SV
- Cardiac output is more rate dependent
- By age 2-3 yrs CV system essentially that of a fit adult
Autonomic Nervous System
PNS essentially complete at birth
SNS innervation of heart and vasculature incomplete - more bradycardia esp with stress (hypothermia, hypoxia, and acidosis)
Greater dependence on adrenal-circulating catecholamine system
Vagal tone predominates
normal neonate pressures
PEARLs about the preterm infant heart
More sensitive to depressant effects of inhaled agents - CO can decrease
Decreased responsive to catecholamines
Relatively high PVR persists
Pulmonary vasculature more sensitive to vasoconstriction by
* Hypoxia
* Acidosis
* Hypercarbia
Acyanotic Lesions
L – R shunt
Atrial septal defect (ASD)
Ventricular septal defect (VSD)
Atrioventricular Septal defect (AV Canal)
Patent ductus arteriosus (PDA)
Types of Atrial Septal Defects
1 Secundum ASD – at the Fossa Ovalis, most common.
There are 3 major types:
ASD Clinical Signs & Symptoms
Rarely presents with signs of CHF or cyanosis
Increased fatigability
Mild failure to thrive, can’t suck well
May have associated pulmonary hypertension –>cyanosis
Hyperactive precordium – RV heave – fixed split S2
II-III/VI systolic ejection murmur @LSB
Mid-diastolic murmur @LLSB
- afib if overloaded d/t stretch of atrial fiber muscles
Treatment of ASD
Surgical or Cath closure for secundum ASD with Qp:Qs (flow) ratio > 2:1
Closure performed electively 2-5 years
Surgical correction earlier in children with CHF or pulmonary hypertension
Mortality <1%
Ventricular Septal Defect Types
- Perimembranous (or membranous) – Most common.
- Infundibular (subpulmonary or supracristal VSD) – involves the RV outflow tract.
- Muscular VSD – can be single or multiple.
- AVSD – inlet VSD, almost always involves AV valvular abnormalities.
VSD Signs and Symptoms
Elevated RV & Pulmonary pressure
Hypertrophy
Small – moderate VSD usually asymptomatic – 50% will close by 2 years
Moderate – large VSD – symptomatic – surgical repair
II-III/VI harsh holosystolic murmur @ LSB
Prominent P2 – diastolic murmur
CHF – Respiratory failure
seen from birth - 6 mo.
VSD Treatment
Small = no surgical intervention
Symptomatic = initial medical treatment with diuretics and afterload reducers
Surgical closure
Large VSD
Ages 6 – 12 mos. large VSD & pulmonary HTN
Ages > 24 mos. With Qp:Qs ratio > 2:1
Supracristal VSD of any size (aortic valve involvement)
Atrioventricular Septal Defect
Complete
Low primum ASD continuous with posterior VSD
Cleft in both septal leaflets of TV/MV
Large L – R shunt
TR/MR – pulmonary HTN
Incomplete
Primum ASD with cleft in MV & small VSD
Hemodynamics are dependent on lesion
AVSD – Signs & Symptoms
Incomplete may be indistinguishable from ASD
CHF
Recurrent pulmonary infection
Failure to thrive
Easy fatigability
Late cyanosis from pulmonary vascular disease w R to L shunt
Hyperactive precordium
Accentuate 1st heart sound
Wide splitting of S2
Pulmonary systolic ejection murmur w/thrill
Holosystolic murmur at apex w/radiation to axilla
Mid-diastolic rumbling murmur @ LSB
Marked cardiac enlargement on CX-ray
AVSD Treatment
Treat CHF symptoms
Surgery is always required
Pulmonary banding may be required in premature infants or infants < 5Kg
Mortality low w/incomplete 1 – 2%
Mortality w/complete 5%
Patent ductus arteriosus (PDA) Signs and Symptoms
Small - asymptomatic
Large – may have symptoms of CHF – FTT – growth retardation
Bounding arterial pulses
Widened pulse pressure
Enlarged heart – prominent apical impulse
Continuous systolic murmur
Mid-diastolic murmur at apex
PAP = systolic pressures with larger PDA