extrauterine life Flashcards
Canalicular phase of lung development
17-27 weeks. Delineation of pulmonary acinus. Type II cells begin to differentiate, capillary network begins
Saccular phase of lung development
26-36 weeks. Thinning of interstitial space, closer association of endothelial and type I cells
Alveolar phase of lung development
36 weeks – 3 years. Presence of true alveoli. Lengthening and sprouting of capillary network
when is the limit of viability for lung development
23-24 weeks
surfactant functions
Phospholipid-protein complex (90% lipid, 10% protein). Lowers surface tension. Prevents alveolar collapse at end expiration. Decreases work of breathing (improves compliance, DV/DP). Aids host defense
Surfactant Metabolism
Made in Type II alveolar cells, stored as lamellar bodies. Secreted as tubular myelin into the alveolar space. Molecules line up in the presence of surfactant proteins and phospholipids into a monolayer-multilayer film along the liquid-air interface
Hyaline membrane disease
surfactant deficiency
Signs of Surfactant Deficiency
Prematurity or delayed maturity (infant of diabetic mother), increased work of breathing (retractions, grunting, flaring), cyanosis on room air, CXR shows diffuse microatelectasis
Treatment of Surfactant Deficiency
oxygen, CPAP. Intubation/ mechanical ventilation, surfactant replacement
fetal lungs before birth
filled with fluid- produced by lung epithelial cells, egresses from trachea and forms amniotic fluid. At birth, fluid clears to establish ventilation
How is fetal lung fluid cleared
amiloride-sensitive selective epithelial Na channels (ENaC) increases in late gestation and is induced by glucocorticoids and catecholamines (labor). Also increased transpulmonary pressure during labor squeezes out the fluid
lung inflation after birth
Distal airways are either collapsed or filled with fluid prior to first breath. Air-liquid interface moves distally with each inspiration, if inspiration is strong, and little or no fluid re-enters during exhalation
Transient Tachypnea of the Newborn
Retained fetal lung fluid due to air spaces not well inflated causes respiratory distress. Can be caused by Rapid labor, no labor (elective C/S), maternal b-blockers (at least in theory). Also ineffective lung inflation ue to poor muscle tone, overly compliant chest wall, prematurity
fetal vs neonatal breathing
Fetal “breathing” inconsistent, shallow, no net movement of fluid in. Fetal gasping occurs with asphyxia, can result in movement of liquid into the fetal lung before birth-Example: Meconium aspiration. At birth, onset of regular, consistent respirations. Mild asphyxia and hypercarbia of normal labor
Causes of failure to breathe at birth
- primary apnea- stimulation (drying, rubbing) initiates cry easily. 2. Secondary apnea- Requires rescue with positive pressure ventilation to establish lung inflation and begin regular respirations. 3. Neuromuscular impairment- hypotonia
Causes of neuromuscular impairment at birth
Maternal sedation, analgesia, MgSO4 during labor. Primary neuromuscular problems in newborn: such as myotonic dystrophy, congenital myopathies, spinal cord injury, spinal muscular atrophy
compare HR and BP in primary vs secondary apnea
primary: HR and BP maintained. Secondary: HR and BP fall quickly. Always assume it is secondary apnea and intervene quickly
Apgar Scores
Rapid description of newborn condition at birth and after resuscitation. 0-2 points assigned for each of 5 categories: maximum 10, minimum 0 (dead). Assigned at 1 and 5 minutes, then every 5 minutes until > 6. Score does NOT predict long-term outcome unless very low (0-2) for more than 10-15 minutes
components of apgar scores
heart rate (none, 100), respiration (absent, irregular/gasping, regular/ crying), tone (limp, some flexion, active motion), response to suction (none, grimace, cough/sneeze/cry), color (pale/blue, acrocyanosis, completely pink)
fetal circulation
oxygenated blood from umbilical vein bypasses liver via ductus venosus. Pulmonary vascular resistance is high, so pulmonary blood flow is very low (vasoconstriction). Blood is shunted from RA to LA across foramen ovale, and from Pulmonary Artery to Aorta across ductus arteriosus
Importance of Lung Inflation to Cardiovascular Transition
Lung inflation: 1. etablishes functional residual capacity and lung volume. 2. Increased alveolar oxygen decreases pulmonary vascular resistance, leading to increased pulmonary artery blood flow and O2. Ductus arteriosus constricts. Increased left atrial volume closes foramen ovale.
Factors contribting to closure of ductus arteriosus
Increased PaO2, change in local conc. Of prostaglandins and NO production
Persistent Pulmonary Hypertension of the Newborn
PVR remains high, SVR fails to increase. Blood continues to flow R to L across foramen ovale. Ductus remains open, blood continues to flow R to L (from PA to Aorta), bypassing the lungs
Causes of Persistent Pulmonary Hypertension of the Newborn
- Abnormally constricted pulmonary vessels- parenchymal lung dz, sepsis, acidosis (reversible with lung inflation, correction of acidosis). 2. Remodeled pulmonary vascular tree (abnormal musculature)- premature closure of DA, maternal NSAID use. Not easily reversible. 3. Hypoplastic pulmonary vascular tree- hypoplastic lungs due to diaphragmatic hernia, renal agenesis, prolonged oligohydramnios. Not completely reversible
Differential Oxygenation
If shunting across ductus arteriosus, the right arm and face will be oxygenated and the rest of the body will be hypoxic b/c the ductus arteriosus location on the aorta. Pre-ductal blood is well oxygenated (head and right arm), post ductal blood is loss oxygenated (descending aorta)
Factors that maintain high vs low PVR
High PVR: low O2, low pH, high CO2, elevated leukotrienes and endothelin. Low PVR: alveolar distension, elevated O2, high pH, low CO2, elevated NO and prostacyclin
How do respirations change from fetal to neonate life
Tachypnea (>60/min), rales, mild retractions, grunting common during first hour. Periodic breathing (pauses of several seconds, without bradycardia or cyanosis) common in first days. Normal rate is 40-60/min, easy and without retractions
How does HR change during first days of life
Initially is 150-180 bpm, decreasing to 100-120 bpm by 30-60 min after birth, with excellent skin perfusion. Heart rate may dip to 75-80 bpm during sleep, always with good color. Murmurs are common during first day.
Average BP at birth
BP is 60-90/30-60 (mean 50-55) mmHg
Glucose Homeostasis following birth
Continuous supply of glucose cut off at birth. Insulin decreases. Glucose initially maintained by mobilization of hepatic glycogen stores. Then, gluconeogenesis from amino acids, glycerol (fat) and lactate.
who is at risk for Neonatal Hypoglycemia
Infants with : Intrauterine growth restriction (IUGR), premature, IDM, and polycythemia (plethoric).
Neonatal hypoglycemia signs and diagnosis
signs: : jittery, irritable, lethargy, apnea, seizures. Diagnosis: Blood sugar < 45mg% with symptoms. Blood sugar < 35-40mg% with risk factors, but no symptoms
Neonatal hypoglycemia treatment
Formula if baby is able and interested. IV glucose if not able to feed, not improved after feeding, glucose is very low (<25-30), or life threatening sx
Temperature adaptations of newborn
Non-shivering thermogenesis (brown fat). Inability to maintain temperature may occur if infection, CNS abnormality, IUGR, prematurity
Calcium adaptations of newborn
Fetal calcium levels exceed mother’s; fetal PTH suppressed and calcitonin levels high. Continuous Ca supply to fetus ends abruptly, levels fall. Risk in IDM, asphyxia and prematurity. Signs: jttery, seizures
