In utero, the fetal lungs are illed with amnionic luid, which must be cleared quickly for air breathing. This clearance occurs through various means, and the contributions of these mechanisms may depend on gestational age and mode of delivery. First, a large release of fetal adrenaline late in labor stimulates pulmonary epithelial cells to stop secreting and instead to start reabsorbing lung liquid as a result of sodium-channel activation (te Pas, 2008). The contribution of this mechanism is unlikely to be major, as blockade of the receptors for sodium channel activation reduces or delays but does not prevent lung liquid clearance at birth (O'Brodovich, 1990).
As a second method, mechanical forces aid lung fluid clearance during labor. Early reports described compression of the fetal thorax and abdomen as they passed through the birth canal leading to lung liquid expulsion (Karl berg, 1962; Saunders, 1978). By this mechanism, up to a third of lung liquid is expelled in a jet of luid from the nose and mouth once the respiratory tract is exposed to the lower outside pressure.
The Newborn 607
However, it may be that uterine contractions force a change in fetal posture leading to compression of the thorax and increased intrathoracic pressures. his prompts expulsion of lung liquid early in labor more so than the "vaginal squeeze" theory (Lines, 1997; te Pas, 2008; Vyas, 1981).
In a third mechanism, a significant amount of lung liquid is cleared after birth (Hooper, 2016). In animal studies, most lung aeration occurs during inspiration-within three to ive breaths after birth. But, no liquid clears between breaths (Hooper, 2007). Speciically, the transpulmonary pressure gradient during inspiration promotes movement of fluid into the interstitial tissue. From here, it is gradually cleared, probably by the pulmonary circulation and lymphatic vessls. It is possible for lung interstitial tissue pressure to rise to a point that luid can actually move back into the airspaces during expiration unless positive end-expiratory pressure opposes liquid reentry (Siew, 2009a,b). This may be a contributing factor in the development of transient tachypnea of the newborn.
As fluid is replaced by air, compression of the pulmonary vasculature is reduced considerably, and in turn, resistance to blood flow is lowered. With the fall in pulmonary arterial blood pressure, the ductus arteriosus normally closes.
High, negative intrathoracic pressures are required to permit the initial entry of air into the fluid-illed alveoli. Normally, from the irst breath after birth, progressively more residual air accumulates in the lung. And, with each successive breath, lower pulmonary opening pressure is required. In the normal mature newborn, by approximately the ifth breath, pressurevolume changes achieved with each respiration are very similar to those of the adult. hus, the breathing pattern shifts from shallow episodic inspirations characteristic of the fetus to regular, deeper inhalations (Chap. 17, p. 333).
As a last mechanism, surfactant, which is synthesized by the type II pneumocytes, lowers alveolar surface tension and helps maintain lung inlation by preventing alveolar collapse. Insuficient surfactant, which is common in preterm neonates, leads promptly to respiratory distress syndrome (Chap. 34, p. 636).
In utero, umbilical venous retun is the main source of preload for the left ventricle, particularly as fetal pulmonary blood flow is very low due to high pulmonary vascular resistance and is unable to provide suicient venous return to maintain left ventricular output (Hooper, 2015).