Page 17 - Physiological based CPAP for preterm infants at birth Tessa Martherus

infant through its nose and mouth (14-16). So, active labour prior to delivery, contributes to the removal of some lung liquid before birth and before the first inhalation of air.
Once the infant is born, gas exchange needs to be established in the lungs for which the airway liquid needs to be cleared from the remaining liquid and aerated. Unless the infant is displaying constant and regular breathing, the larynx will be predominantly closed immediately after birth, but opens during each inspiration allowing air to enter the lung (17). The primary facilitator that drives air to flow into the lungs is transpulmonary pressure. With each inspiration, liquid leaves the airways and enters lung tissue, while air enters the lungs, and so lung liquid is cleared in a stepwise fashion, with each breath enhancing lung aeration (18, 19). At the beginning of this process, airway resistance is high due to the viscosity of liquid, compared to air, and its movement through the distal airways and across the distal airway wall. As a result, the liquid is forced to accumulate in the interstitial lung tissue (20, 21).
As the lungs become air-filled, this initiates many changes within the cardiopulmonary system. The viscosity of air is markedly lower than that of liquid and, therefore, airway resistance decreases and lung compliance increases as the lung aerates. The abrupt decrease in PVR and increase in PBF is intimately linked to lung aeration. An oxygen induced increase in nitric oxide and increased recoil of alveoli due to the creation of air/liquid surface tension (10) were thought to be primarily responsible for the decrease in PVR. However, recent evidence indicates that the accumulation of liquid in the interstitial tissue triggers a neural reflex, probably via juxta capillary receptors, causing a decrease in PVR and increase in PBF (22). Meanwhile, increased alveoli recoil increases the tendency of alveoli to collapse at end-expiration, which decreases the surface area for gas exchange and increases the required inspiratory effort (23). The liquid that accumulates in the interstitial tissue is replaced in the airways by air, which causes the chest wall to expand and the pressure in the interstitial tissue to rise. The interstitial tissue pressure remains high until the liquid is drained via the lymphatics and blood vessels hours after birth (16, 24, 25). This interstitial pressure causes a tendency for liquid to re-enter the airways during expiration, only to be cleared again during inspiration (18, 19, 26). Infants have several mechanisms to prevent alveolar collapse and to limit liquid re-entry into the lungs. During this phase of transition, the epithelial sodium channels continue to promote liquid absorption back into the interstitial tissue (26). In addition, alveolar type II cells continue to secrete surfactant after lung aeration, which lowers the surface tension, reduce lung recoil and improve lung compliance (27, 28). Infants also use expiratory braking manoeuvres to stop or slow down expiration. During expiration the larynx is (almost) closed while contracting their diaphragm, the airway pressure is increased while the expiratory time is prolonged to prevent airway collapse and liquid re-entry (19, 29-31). Once the infant has achieved a stable breathing pattern, the larynx will remain predominantly open to allow gas exchange (17).
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General introduction
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