Adaptation to extrauterine life Flashcards
3 diff phases of lung development
- Canalicular phase
- Saccular phase
- Alveolar phase
Canalicular phase
- weeks
- Importance
17-27 weeks
Delineation of pulmonary acinus
Type II cells begin to differentiate, capillary network begins
Saccular phase
- weeks
- Importance
26-36 weeks
Thinning of interstitial space, closer association of endothelial and type I cells
Alveolar
- weeks
- Importance
36 weeks - 3 yrs
Presence of true alveoli
Lengthening and sprouting of capillary network
Surfactant
- what is it
- what does it do (4)
Phospholipid-protein complex (90% lipid, 10% protein)
Fxn:
- Lowers surface tension
- prevents alveolar collapse at end expiration
- Decreases work of breathing (improves compliance)
- Aids host defense
compliance - how ez it is to expand lungs. If you can change a lot of volume with very little effort - more compliant
What happens when you get the wind knocked out of you?
lose fxnal residual capacity
- normally, you dont empty your lungs completely
compliance
- Max compliance
how ez it is to expand lungs. If you can change a lot of volume with very little effort - more compliant
Max: max lung expansion for min effort
Where is surfactant made and how is it stored? How is it secreted? What does it do after it is secreted into the airspace?
Made in type II alveolar cells
- stored as lamellar bodies
- secreted as tubular myelin into airspace
- tubular myelin lines up along air-liquid interface in a multilayer fashion
(when air space collapses, the tails are densely packed, leading to mutual repulsion, opposing the collapse)
*good image in ppt
Role of surfactant in generating more pressure to get a lot of volume movement.
Without surfactant, you have to generate more negative pressure (or positive pressure if you are being ventilated) to move air into lung, to get a lot of volume movement.
Lung becomes poorly compliant. And lung loses FRC (air in lung after exhale)
X ray of surfactant deficiency
white out
CXR with diffuse microatelectasis (very poorly aerated)
Importance of FRC
Too low: lung underinflated, very noncompliant
Too high: (emphysema) lung over expanded to near lung capacity
Signs of surfactant deficiency aka (Hyaline membrane disease HMD)
- Premature or delayed maturity
- Increased work of breathing
- retractions
- grunting, flaring - Cyanosis in room air
- CXR with diffuse microatelectasis (very poorly aerated)
Treatment of surfactant deficiency
Oxygen
Improve lung inflation, establish FRC
- continuous PP airway (nasal CPAP)
- intubation and mechanical ventilation
- surfactant replacement
Lung fluid absorption
- what is it
- what needs to happen at birth
In the fetus, lungs are filled with fluid
- fluid is produced by the lung, comes from trachea, forms amniotic fluid
- fluid is secreted by lung epithelial cells, driven by active Cl- secretion
At birth, fluid needs to clear quickly to establish ventilation with air
- absorption depends on Na+ absorption
Clearance of fetal lung fluid
- Influence of maturity
Presence and activity of amilioride sensitive selective ENaC increase in late gestation, probably due to increased fetal production of cortisol.
- can be induced by exogenous GC and somewhat by catecholamines (stress of labor)
Clearance of fetal lung fluid
- Labor
Increased transpulmonary P
- uterine contractions squeeze fluid out at a greater rate than it is produced
- if no labor, more fluid remains to be removed after birth
At birth, what happens to FRC?
It increases a little bit with each effective inspiration
- but a big first inspiration is necessary to move air liquid interface more distally into air space –> interstitium –> circulation
- CPAP can help
In fetal life, is the flow of fluid bidirectionally?
No - always egressing
- ie: meconium aspiration –> inflammatory process
Failure of new born to breathe can be a result of:
- Primary apnea
- Secondary apnea
- Neuromuscular impairment
Primary apnea
stimulation (rubbing, drying) easily initiates cry
Secondary apnea
- what is it?
- When is it assumed?
Requires rescue with PPV to estab. lung inflation and begin regular respirations
*at birth, if HR is low and baby is not breathing, we assume its 2ndary apnea and intervene quickly w/ PPV
Issues in Neuromuscular impairment in new born making it difficult for them to breath
Due to:
- Maternal sedation, analgesia, MgSO4 during labor
- Primary neuromuscular problems in newborn:
myotonic dystrophy, congenital myopathies, SC injury, spinal muscular atrophy
At birth, and baby is not breathing, and not breathing when we dry them off, do we assume it will be primary or secondary or neuromuscular impairment related?
Secondary apnea
- immediately give PPV
Apgar score: Max points: How is it measured: Does it predict long term outcome? Does it dx asphyxia?
Max points: 10 min
How is it measured:
- assigned at 1 and 5 min
- then every 5 min until 20 min until score is 7
Does it predict long term outcome? No (but
Apgar score
measures what categories?
Heart rate Respiration Muscle tone Response to suction Color
(points are 0-2 for each)
How does lung inflation help with cardiovascular transition?
Sets stage for ez tidal breathing (FRC)
Resultant increased alveolar oxygen
- decrease pulmonary vascular resistance –>
Increases pulmonary blood flow
- Increased arterial pO2 –> constriction of ductus arteriosus
- Increased pulmonary bf –> increases LA volume –>
closes foramen ovale flap
*LUNG INFLATION IS KEY TO CV TRANSITION
Trace flow of blood from placenta to systemic system (brain + heart)
Mom --> Placenta --> Umbilical vein --> Ductus venosus --> IVC --> RA --> (because of the way the blood streams into RA, it preferentially shoots thru foramen ovale) --> LA --> LV --> Ascending aorta --> Brain + heart (best oxygenated blood) - organs most resistant to hypoxic insult
Trace flow of blood from fetus body to
placenta
SVC --> RA --> RV --> Pulmonary artery --> (but since there is a ductus arteriosus that is huge in the fetus and the vascular resistance is high in lungs, and low systemically because placenta is still in systemic circuit, blood goes from pulmonary artery --> aorta --> adrenal glands, pancreas (rest of body)
Postnatal circulation:
biggest change
- PLacenta is removed, cord is clamped
- systemic vascular resistance increases - Body is cold and wet
- systemic vasoconstriction - Lung expands
- PVR drops
- Pulm bf increases
- PaO2 increases - Ductus arteriosis ad venosis constricts
- Venous return from lung increases:
- Foramen ovale flap closes
*ALL REVERSIBLE
Response to delivery:
Umbilical artery
Umbilical vein
Umbilical artery
- vasoconstrict with increasing oxygenation
Umbilical vein
- collapse with absent blood flow from (now absent) placenta
Response to delivery:
Ductus arteriosis
Ductus venosus
Ductus arteriosis
- fxnally closes w/ increased oxygenation and loss of PGE2 from placenta
Ductus venosus
- collapse with absent blood flow
Response to delivery:
Foramen ovale
Pulmonary arteries
Foramen ovale
- closes when systemic pressure (LA) is > than pulmonary P (RA)
Pulmonary arteries
- vasodilate with elevated oxygen lvls
3 birth abnormalities that can cause Persistent pulmonary HTN of newborn (PPHN)
abnml:
1. PVR remains elevated
(+/- SVR fails to increase)
2. Blood continues to flow R–>L across foramen ovale
3. Ductus arteriosis remains open, blood cont to flow R –> L (PA to Aorta) and bypassing the lungs
Differential oxygenation
Pre-ductal blood (head + R arm) well oxygenated
Post ductal blood (descending aorta) is less well oxygenated (mixed)
Similar to PPHN
3 main categories of PPHN
- Abnormally constricted pulmonary vessels
- Remodeled pulmonary vascular tree (abnl musculature)
- Hypoplastic pulmonary vascular tree
Factors that decrease PVR
things that cause alveolar distention:
- INcrease Po2
- INcrease pH
- INcrease NO
- Increase Prostacyclin
- Decrease Pco2
Signs of neonatal hypoglycemia
jittery irritable lethargy apnea seizures
dx: blood sugar
Factors that maintain pulmonary vasoconstriction
and increase PVR) (5
- low pO2
- low pH
- high pCO2
- Leukotrienes
- Endothelin
Factors that maintain pulmonary vasoconstriction
and increase PVR) (5
- low pO2
- low pH
- high pCO2
- Leukotrienes
- Endothelin
