Early diagnosis through clinical assessment and diagnostic evaluation
Preliminary Diagnosis through BP’s, oxygen saturation, hyperoxia test, pulse examination
Bedside RN first line during periods of Watch and Wait (ie- questions about arch but holding off on PGE administration to see if PDA declares it is necessary for systemic flow)
Early detection and intervention prior to episodes of extremis important for long-term outcome
Normal fetal circulation
Ductus venosus: highly oxygenated blood to inferior vena cava across foramen ovale to left atrium
Ductus arteriosus: majority of right ventricular output directed to descending aorta
Most highly oxygenated blood to brain (saturation 65%)
Very little blood flow to lungs (10% combined ventricular output)
Lowest oxygen-saturated blood returning from superior vena cava directed to lower half of body to return to placenta
With first breath lungs expand and pulmonary vascular resistance drops
All of right ventricular output enters pulmonary circulation
Increase in pulmonary venous return increases left atrial pressure and closes flap of foramen ovale
Direction of flow across ductus arteriosus reverses (aorta pulmonary artery)
Ductus arteriosus and ductus venosus begin to constrict
Once the baby takes the first breath, a number of changes occur in the infant's lungs and circulatory system:
Increased oxygen in the lungs causes a decrease in blood flow resistance to the lungs.
Blood flow resistance of the baby's blood vessels also increases.
Amniotic fluid drains or is absorbed from the respiratory system.
The lungs inflate and begin working on their own, moving oxygen into the bloodstream and removing carbon dioxide by breathing out (exhalation).
– directs assessment and diagnostic
Focus on physiology
Exact anatomy will be sorted out after stabilization
valuation
Communication
Organization
Class I- 48
Class II- 32
Class III- 14
Class IV-3
Other lesions without ductal-dependent systemic or pulmonary blood flow
Mixing of oxygenated and deoxygenated blood results in systemic saturations <95%
Not generally acutely ill, but may develop pulmonary overcirculation as pulmonary vascular resistance drops
Severe pulmonary valve stenosis including severe tetralogy of Fallot
Other complex malformations that include pulmonary valve atresia
Often component of heterotaxy syndrome
Small left atrium, mitral valve, left ventricle ascending aorta and aortic arch
Lower half of body perfused through PDA
Brain and coronary arteries perfused through PDA and retrograde flow in aortic arch
Pulmonary valve atresia
All blood flow to lungs supplied through PDA
Obligatory right-to-left shunting at atrial level: mild systemic desaturation (80s)
Hypoplastic right heart syndrome
Small tricuspid valve, right ventricle and pulmonary valve
May look normal while PDA open
Pulse oximetry in foot will often be <95%
Poor systemic cardiac output when PDA closes (usually within 1st 2 weeks of life)
Grey, mottled color
Weak or absent pulses
May not have pulse differential in coarctation of the aorta in the presence of poor cardiac output
May or may not have murmur
Tachypnea, grunting, respiratory distress
Similar appearance to sepsis
Cyanosis
Usually no significant respiratory distress
Good pulses and capillary refill
+/- murmur
Loud murmur means there is some pulmonary blood flow (pulmonary stenosis)
Absent murmur much more concerning for pulmonary atresia
Similar clinical appearance to meconium aspiration or severe bilateral pneumonia
Communication
Organization
Transposition of the great arteries
Aorta originates from right ventricle and carries desaturated blood back to body
Pulmonary artery originates from left ventricle and carries red blood back to lungs
Pulse oximetry: desaturated everywhere, possible higher saturations in feet
Chest x-ray:
Normal to slightly wet lung fields
No cardiomegaly
“Egg on a string”
ABG:
Low pO2
No significant metabolic acidosis unless profoundly cyanotic
In general with complete intracardiac mixing and no outflow tract obstruction saturations will be mid-80s initially.