CARDIOPULMONARY CHANGES AT BIRTH AND PRINCIPLES OF NEWBORN RESUSCITATION Flashcards
T/F: Before birth the lungs take no part in gas exchange
T
Before birth the future airways of the lungs are liquid-filled and the lungs take no part in gas exchange, which instead occurs across the placenta
Pulmonary blood flow (PBF) is low because pulmonary vascular resistance (PVR) is high, redirecting the majority of right ventricular output (RVO) through the — and into the systemic circulation
ductus arteriosus (DA)
Conversion of the fetal to adult circulation requires —, — and —
Elimination the umbilical – placental circulation
Increase of pulmonary blood flow to a level necessary for adequate gas exchange
Separation of the left sides of the heart by the closure of fetal channels
T ventilation comprises two components —- and —
Physical expansion of the lungs with gas
Elimination of fluid in the alveoli and increase in alveolar concentration associated with breathing air
T/F: Removal of placental circulation facilitates closure of the foramen ovale and causes a small decrease in right atrial pressure
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T/F: Removal of placental circulation enables functional closure of ductus arteriosus resulting in elimination of flow from the pulmonary trunk to the aorta
T
T/F: In fetal life small pulmonary arteries have a thick MEDIAL layer composed predominantly of smooth muscle cells
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T/F: In fetal life the pulmonary vessels constrict markedly with hypoxia and dilate with an increase in PO2
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T/F: Following the immediate fall in pulmonary vascular resistance following birth, morphologic changes in the pulmonary vessels result in a PERMANENT fall in pulmonary vascular resistance
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T/F: The decrease in the thickness of the smooth muscle layer in the small arteries results in a gradual further decrease in pulmonary vascular resistance and pulmonary arterial pressure within 2-3 weeks after birth
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T/F: Within 2 -3wks after birth there a gradual further decrease in pulmonary vascular resistance and pulmonary arterial pressure
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4 conditions that can result from persistence of any fetal shunts/physiology
- Persistent Ductus Arteriosus
- Patent Foramen Ovale
- Persistent Pulmonary
hypertension of the Newborn - Transient Tachypnea of the newborn
After birth functional closure of the ductus arteriosus occurs when
10 -15 hrs after birth by constriction of the medial smooth muscle
T/F: Both functional and anatomic closure of the DA occur at the same time
F
Anatomic closure is completed by 2-3 weeks of age by permanent changes in the endothelium and the sub-intimal layers of the ductus
Anatomic closure of the DA is completed at — wks after birth
2 -3 wks
What causes the anatomic closure of the DA
permanent changes in the endothelium and the sub-intimal layers of the ductus
Permanent changes in the – and – causes the anatomic closure of the DA
Endothelium and sub-intimal layers of the ductus
% of PDA seen in all CHD
5 - 10%
T/F: PDA can be asymptomatic
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Usually asymptomatic when DA is small
Persistent patency of the DA leaves a communication between the DA and —
Left pulmonary artery
T/F: Large shunt PDA may cause CHF and recurrent pneumonia
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— disease may develop if large PDA with pulmonary hypertension is left untreated
Pulmonary vascular obstructive disease
% of newborns with failure of functional closure of the foramen ovale
75%
T/F: Patent foramen ovale causes a left-to-right shunt
T
T/F: ASD is commoner in males
F.
Has a female preponderance
The 3 types of ASD
Primum defect
Secundum defect
Sinus venosus defect
The most common of the ASDs
Secundum defect
Location of the primum defect
Antero-inferior atrial septum
Location of the secundum defect
Middle portion of atrial septum
Location of the sinus venosus defect
Postero-superior atrial septum
Defect in the middle portion of atrial septum
Secundum defect
Defect in the antero-inferior atrial septum
Primum defect
Defect in the postero-superior atrial septum
Sinus venosus defect
% of children with PFO/ASD that will experience spontaneous closure in the first 4 years of life
40%
T/F: If a large PFO/ASD defect is untreated, CHF and pulmonary HTN may develop in the 1st decade of life
F
2nd or 3rd decade of life
If a large PFO/ASD defect is untreated, — and —may develop in the 2nd or 3rd decade of life
CHF and pulmonary HTN