Physiologic Adaptations to Extrauterine Life Flashcards
1
Q
Pulmonary adaptation to extrauterine life is determined …
A
Pulmonary adaptation to extrauterine life is determined by 3 factors:
Lung growth & development
Respiratory drive
Physiologic maturation
2
Q
Characteristics of Lung Growth & Development
A
- Canalicular Phase:
- 17-27 weeks.
- Type II cells begin to differentiate and capillary network begins to form.
- Saccular Phase:
- 26-36 weeks.
- Thinning of interstitial space allowing closer association of capillaries to air spaces and type I cells.
- Alveolar Phase:
- 36 weeks to 3 or more years.
- True alveoli present.
- Take home message: Prior to 24 weeks the capacity for ventilation is limited by lack of true air spaces and the distance of capillaries from rudimentary air spaces. This is the limit of viability for a fetus.
3
Q
Characteristics of fetal==> infant respiratory drive
A
Respiratory Drive
Fetal “breathing” movements are inconsistent, no net movement of fluid into lungs
Fetal gasping occurs with asphyxia, can result in fluid aspiration (e.g. meconium aspiration) prior to birth
At birth, onset of regular, consistent respirations occurs in response to:
Sensory stimulation: cold, light, touch, noise
Mild asphyxia and hypercarbia as the blood flow to the baby is not great during contractions
4
Q
Characteristics of failure to breathe
A
- Primary apnea:
- Apnea is brief in duration
- Stimulation easily initiates cry
- Followed by gasping respirations
- HR and BP relatively maintained
- Secondary apnea:
- When original gasping ceases, secondary apnea ensues;
- Requires positive pressure ventilation to establish lung inflation and begin regular respirations
- Stimulation alone is ineffective
- HR and BP fall quickly
- Death occurs without rescue ventilation
- Therefore, if the infant is apneic at birth, we assume it’s secondary apnea and intervene quickly
5
Q
Physiologic maturation of fetal pulmonary system
A
- Surfactant is a phospholipid-protein complex that coats the inside of air sacs and allows air to remain in the air sac on expiration called the functional residual capacity.
- Lower surface tension within air spaces.
- Prevent alveolar closure at the end of expiration.
- Composition:
- 90% lipid: phosphatidylcholine + phosphatidylglycerol.
- 10% protein: Proteins A, B, C, D and phospholipids are important for spreading surfactant as a mono-multilayer film and fighting infection.
- The surfactant mono-multilayer enables the formation of the Functional Residual capacity, FRC, and the ΔV / ΔP, which is the optimal compliance.
- Macrophages recycle 90%.
- Secreted by Type II alveolar cells. Stored as lamellar bodies. Extruded as tubular myelin into the airspace after fusing with cell membrane.
6
Q
Describe the importance of lung inflation.
A
- Establishes lung volume, FRC (functional residual capacity)
- Sets the stage for easy tidal breathing
- Increased alveolar oxygen:
- Decreases pulmonary vascular resistance and increases pulmonary blood flow
- Increases arterial pO2 leading to constriction of ductus arteriosus
- Increases pulmonary blood flow leading to increased left atrial volume closure of foramen ovale flap
- Take home: Lung inflation is the key to cardiovascular transition as well.
7
Q
Describe the importance of adequate lung fluid absorption.
A
- Within the amniotic sac, the fetal lungs are filled with fluid, and the pulmonary epithelium secretes fluid by active Cl- secretion, while Na+ absorption is limited. The fluid exits via the trachea into the amniotic space. This is the basis for testing amniotic fluid for lung maturity.
- At birth the fluid needs to be cleared quickly so that ventilation with air can be established.
- Corticosteroids cause an ↑ Amiloride-Sensitive Selective Epithelial Na+ channels, ENac, during late gestation. Causing fluid absorption.
- ↑ Intrathoracic pressure during labor results in more egress of fluid from the trachea; less emptying occurs during C-section without labor.
- Hydrostatic forces move the fluid distally through the airways and into the interstitium with inspiration, no return to the air space during exhalation. FRC builds during inspiration.
8
Q
Consequences of failure to absorb fluid @ lungs
A
- Failure of fluid absorption = retained fetal lung fluid also called Transient Tachypnea of the Newborn, TTN.
- If excessive fluid / delayed absorption by the vasculature and lymph from the interstitium, oxygen is required.
- Observed in: C-section without labor, maternal β-blocker therapy, ineffective inspirations.
- Generally seen in term and late preterm infants, mild respiratory distress, short course, well-inflated but wet-looking lungs on CXR.
- Can progress to severe respiratory failure.
9
Q
What are signs and treatment of surfactant deficiency?
A
- Signs of surfactant deficiency:
- CXR with diffuse reticulogranular pattern of microatelectasis which appears like a “whiteout” → can’t see the heart on CXR.
- Macromolecular proteinaceous pulmonary edema called hyaline membrane disease.
- Poor lung compliance (ΔV/ΔP)
- Prematurity or delayed maturity, e.g. infant of diabetic mother.
- Signs of respiratory distress such as retractions, nasal flaring, and grunting.
- Grunting keeps airspaces open via positive end expiratory pressure, PEEP.
- Cyanotic on room air.
- Treatment:
- Mother is given betamethasone.
- Oxygen for the baby
- Positive end expiratory pressure (CPAP, PEEP) to improve lung inflation and FRC
- Intubation and mechanical ventilation
- Surfactant replacement via endotracheal tube
10
Q
Characteristics of fetal circulation
A
- placenta is the organ of gas exchange, with the best-oxygenated blood coming to the fetus through the umbilical vein, shunting through the ductus venosus bypassing the liver to the right atrium (RA)
- The placenta has very low vascular resistance, creating a very low systemic vascular resistance as blood returns to it from the fetal aorta through the umbilical arteries
- Conversely the pulmonary vascular resistance is very high in the fetus, and the pulmonary blood flow is very low due to active pulmonary vasoconstriction
- Local hypoxemia, acidosis, fluid-filled lungs, and possibly leukotrienes maintain the vasoconstriction
- Blood is shunted from the right atrium (RA) to the left atrium (LA) through the foramen ovale, and from the pulmonary artery (PA, high resistance) to the aorta (Ao, low resistance) through the ductus arteriosus (DA)
- In utero, < 10% of combined ventricular output goes to the lungs
- In utero, the right ventricle (RV) is the systemic (main) ventricle as very little blood flow returns from the lungs to the left atrium and left ventricle (LA, LV) for exit out the Ao
- In utero, the pulmonary and systemic circulations are connected but parallel
11
Q
Circulation changes after cutting of umbilical cord
A
- Following birth, the lungs expand with air, the placenta is removed from the circuit (the cord is cut), and the circulation changes dramatically
- With lung expansion, pulmonary vascular resistance begins to fall
- Pulmonary blood flow increases, PaO2 increases
- Venous return to the LA increases
- With cord clamping and cold stress/vasoconstriction, systemic vascular resistance increases
- Pressures in the LA become greater than in the RA, and the foramen ovale flap closes
- With increased PaO2, and ↓ in local prostaglandin and NO production, the DA constricts
- The circulations are now in series (as in the adult): blood enters RA, goes to RV, through PA to lungs, returns to LA, through LV and out to Aorta; 50% of combined ventricular output now goes to lungs
12
Q
Reversible changes in circulation
A
- The DA constricts but is not anatomically closed for days to weeks
- The foramen ovale flap can reopen to allow blood to flow from RA to LA if RA pressure > LA
- Normal transitional circulation is a balance between pulmonary vascular resistance and systemic vascular resistance: blood flows from higher to lower resistance across these reversible fetal channels
- In the case of increased pulmonary vascular resistance, often accompanied by or aggravated by decreased systemic vascular resistance (hypotension), R to L shunting at foramen ovale + DA can recur or continue: known as Persistent Pulmonary Hypertension of the Newborn (PPHN)
13
Q
Unique features of fetal circulation
A
- ductus venosus
- foramen ovale
- ductus arteriosus
14
Q
Factors that modulate pulmonary vascular (PVR) resistance
A
- Normally following birth, lung expansion causes PVR to fall. Additionally, ↑ PO2, ↑ pH, ↓ PCO2, ↑ NO, ↑ Prostacyclin all contribute to a lower PVR.
- The opposite factors cause the PVR to remain high, for example:
- Lung disease, and inadequate lung inflation
- Surfactant deficiency
- Retained fetal lung fluid
- Inadequate inflation at birth
- Chronic intrauterine hypoxemia which leads to vascular remodeling
- Acidosis, sepsis, other stressors which cause pulmonary vasoconstriction
15
Q
When might persistent pulmonary hypertension (PPHN) in the newborn be expected to occur?
A
- 3 main categories of PPHN:
- Abnormally constricted pulmonary vessels as with parenchymal lung disease, poor lung inflation following birth
- Abnormal pulmonary vascular musculature remodeled, as with antenatal closure of DA, maternal NSAID use, chronic intrauterine hypoxemia
- Hypoplastic pulmonary vasculature as with pulmonary hypoplasia from any cause – decreased vascular cross-sectional area
