extrauterine life

Question 1

Canalicular phase of lung development

Answer 1

17-27 weeks. Delineation of pulmonary acinus. Type II cells begin to differentiate, capillary network begins

Question 2

Saccular phase of lung development

Answer 2

26-36 weeks. Thinning of interstitial space, closer association of endothelial and type I cells

Question 3

Alveolar phase of lung development

Answer 3

36 weeks – 3 years. Presence of true alveoli. Lengthening and sprouting of capillary network

Question 4

when is the limit of viability for lung development

Answer 4

23-24 weeks

Question 5

surfactant functions

Answer 5

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

Question 6

Surfactant Metabolism

Answer 6

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

Question 7

Hyaline membrane disease

Answer 7

surfactant deficiency

Question 8

Signs of Surfactant Deficiency

Answer 8

Prematurity or delayed maturity (infant of diabetic mother), increased work of breathing (retractions, grunting, flaring), cyanosis on room air, CXR shows diffuse microatelectasis

Question 9

Treatment of Surfactant Deficiency

Answer 9

oxygen, CPAP. Intubation/ mechanical ventilation, surfactant replacement

Question 10

fetal lungs before birth

Answer 10

filled with fluid- produced by lung epithelial cells, egresses from trachea and forms amniotic fluid. At birth, fluid clears to establish ventilation

Question 11

How is fetal lung fluid cleared

Answer 11

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

Question 12

lung inflation after birth

Answer 12

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

Question 13

Transient Tachypnea of the Newborn

Answer 13

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

Question 14

fetal vs neonatal breathing

Answer 14

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

Question 15

Causes of failure to breathe at birth

Answer 15

1. 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

Question 16

Causes of neuromuscular impairment at birth

Answer 16

Maternal sedation, analgesia, MgSO4 during labor. Primary neuromuscular problems in newborn: such as myotonic dystrophy, congenital myopathies, spinal cord injury, spinal muscular atrophy

Question 17

compare HR and BP in primary vs secondary apnea

Answer 17

primary: HR and BP maintained. Secondary: HR and BP fall quickly. Always assume it is secondary apnea and intervene quickly

Question 18

Apgar Scores

Answer 18

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

Question 19

components of apgar scores

Answer 19

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)

Question 20

fetal circulation

Answer 20

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

Question 21

Importance of Lung Inflation to Cardiovascular Transition

Answer 21

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.

Question 22

Factors contribting to closure of ductus arteriosus

Answer 22

Increased PaO2, change in local conc. Of prostaglandins and NO production

Question 23

Persistent Pulmonary Hypertension of the Newborn

Answer 23

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

Question 24

Causes of Persistent Pulmonary Hypertension of the Newborn

Answer 24

1. 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

Question 25

Differential Oxygenation

Answer 25

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)

Question 26

Factors that maintain high vs low PVR

Answer 26

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

Question 27

How do respirations change from fetal to neonate life

Answer 27

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

Question 28

How does HR change during first days of life

Answer 28

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.

Question 29

Average BP at birth

Answer 29

BP is 60-90/30-60 (mean 50-55) mmHg

Question 30

Glucose Homeostasis following birth

Answer 30

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.

Question 31

who is at risk for Neonatal Hypoglycemia

Answer 31

Infants with : Intrauterine growth restriction (IUGR), premature, IDM, and polycythemia (plethoric).

Question 32

Neonatal hypoglycemia signs and diagnosis

Answer 32

signs: : jittery, irritable, lethargy, apnea, seizures. Diagnosis: Blood sugar < 45mg% with symptoms. Blood sugar < 35-40mg% with risk factors, but no symptoms

Question 33

Neonatal hypoglycemia treatment

Answer 33

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

Question 34

Temperature adaptations of newborn

Answer 34

Non-shivering thermogenesis (brown fat). Inability to maintain temperature may occur if infection, CNS abnormality, IUGR, prematurity

Question 35

Calcium adaptations of newborn

Answer 35

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