Respiratory Flashcards
Normal Neonatal ABG: normal pO2
50-70 (term infant)
45-65 (preterm infant)
LEFT shift in the oxyhemoglobin dissociation curve
hypothermia, hypocapnia, alkalosis, and decreasing 2-3 DPG
(think frost bite - blue fingers and toes (no o2 or perfusion in those cold extremities) )
RIGHT shift in the oxyhemoglobin dissociation curve
hyperthermia, acidosis (think hot), hypercapnia, increased levels of 2-3, DPG (when skin is hot, it flushes with blood and oxygen, increased perfusion)
Embryology: Embryonic Phase
3-6 weeks; lung bud develops ; single lung buds divide into the right and left lung buds and into trachea
some airway branching; pulmonary vein, pulmonary artery formation occurs
abnormal development: Tracheal agenesis, tracheal stenosis, TEF, pulmonary sequestration
Embryology: Psuedoglandular phase
6-16 weeks
conducting airways are formed
abnormal development: congenital lobar emphysema, congenital diaphragmatic hernia
Embryology: cannicular phase
16-26 weeks
the acinar or respiratory units form; Cuboidal cells develop into Type 1 Cells (those responsible for gas exchange) and Type 2 cells (those capable of surfactant production)
embryology: terminal sac or saccular phase
weeks 26-36
saccules develop which will eventually turn into alveoli; Type 2 cells increase in production and release of surfactant
infants delivered in this stage may have RDS, pulmonary insufficiency, PIE, BPD
factors that facilitate alveolarization
vitamin A
thyroxin
Fetal lung fluid production
produced at 4-5 ml/kg/hr
is facilitated by active transport of chloride from the interstitium
L-S ratio
lecithin-sphyngomyelin ratio of 2:1 is indicative of fetal lung maturity
its use is not accurate in infants of diabetic mothers
PG ratio (phosphatidyglycerol levels)
used to assess fetal lung maturity; more useful in IDM; increases in production at around 35 weeks, its presence indicates lung maturity
Fetal breathing movements
can be seen as early as 11 weeks
Role of antenatal steroids
maximum benefit is at 48 hours after administration with a result in the increase in production of proteins that control the manufacture of surfactant by type 2 cells
pulmonary hypoplasia
pulmonary underdevelopment;
- primary - intrinsic failure of resp. development
- secondary - result of abnormal processes that interfere with lung development;
- oligo r/t renal anomalies
- IUGR
- space occupying lesions (CHD, Cardiomegaly, cystic lung disease)
Pulmonary Hypoplasia Diagnosis & Management
- Diagnosis:
- CXR shows decrease lung volume
- Management
- abnormal pulmonary vasculature may result in PPHN
- poor lung compliance requires higher pressures to ventilate
- minimize over expansion (consider HFOV)
- admin surfactant
- consider iNO if PPHN present
Congenital Diaphragmatic Hernia
diaphragm defect allows herniation of bowel contents into chest; creates a mass effect → impedes resp. development
posterolateral defects most common; anterior 2nd
left side more commonly affected
presentation: severe resp. distress, scaphoid abdomen, cyanosis
avoid bag-mask and CPAP; immediate intubation required
use of cuffed ETT tubes may reduce gaseous distention
Tracheoesophageal Fistula / esophageal fistula
EA - anatomic interruption of the esophagus
TEF - combined anomalies of esophagus and trachea due to abnormal development of the embryonic foregut
male predisposition
TE/ EA associations
association with Trisomy 13,18,21, pierre-robin, digeorge, fanconi, polysplenia
higher incidence of VACTERL Association and CHARGE
TEF/EA Types
- A - isolated EA no fistula
- B - Proximal TEF with Distal EA
- C - Ea with Distal TEF - most common
- D - Both proximal and distal TEF - least common
- E - Isolated TEF (aka H type)
Absence of air in the abdomen indicates a pure ___ or an _____ with isolated _____.
pure EA or EA with isolated upper pouch TEF
Presence of air in the abdomen indicates a ________.
TEF patent to the distal esophagus.
TEF / EA management
avoid intubation if possible - may cause abdominal distention; if necessary - HFOV
Repogle on continuous suction to minimize secretion and aspiration
elevate HOB to minimize reflux
RDS
surfactant deficiency;
pulmonary edema from serum proteins leaking into the alveoli contibutes to the loss of FRC, alters ventilation:perfusion ratio
increased fetal insulin production in response to maternal diabetes inhibits proteins critical for surfactant production
Early onset Pneumonia organisms (common)
GBS, E. Coli, Klebsiella
E Coli(most common bacterial isolate)
Late onset pneumonia organism
Staphylococcus, Coagulase negative Staphylococci, Staph Aureus
Pneumonia on CXR
unilateral or bilateral, alveolar infiltrates, areas of confluent opacities, diffuse interstitial pattern, and pleural effusions
ground glass and air bronchograms may also be present
Treatment of early onset pneumonia
ampicillin and gentamicin
treatment of late onset pneumonia
vanc and gent
TTN CXR
pulmonary marking with perihilar streaking
hyperaeration with widened intercostal spaces, mild cardiomegaly, mild pleural effusion; flat diaphragm
TTN management
CPAP with or without supplemental oxygen to improve lung recruitment;
withholding feedings if tachypnea >60-80 bpm. , restricting fluid intake may decrease duration of support
usually self limiting within 72 hours
Risk factors for MAS
post-term, SGA, fetal distress, placental insufficiency, oligo, cord compression, intrauterine hypoxia
MAS patho
meconium can inactivate surfactant, inhibit production, cause obstruction, resulting in resp. distress, impaired exchange