Abstract
Mechanical properties of the liquid-filled fetal lung are similar to those of the adult lung in so far as pulmonary tissue offers little resistance to volume change, but not to liquid flow, throughout its volume range. Contrary to what has been held, fetal lungs are not highly plastic. As fetal development progresses, tissue elastance probably falls as tissue-to-potential airspace density decreases. At the same time, liquid in future airspaces is enriched with phospholipid surfactants secreted by maturing type 2 saccular epithelial cells. When air-breathing begins at birth, dispersion of air into surfactant-rich liquid ofmature lungs results in formation of stable bubbles, the films of which achieve surface tension near-zero. Saccules are distended by the air-containing bubbles as well as by “free” air in direct communication with the airways. Stable bubbles establish immediate formation of functional residual capacity, continued gas exchange throughout the respiratory cycle, and saccular resistance to collapse as a result of the near-zero surface tension of and the structural stability provided by bubble films. This process produces the mature volume-pressure diagram, both in vivo and in vitro, which is characterized by relatively low opening pressure, high maximal volume, wide hysteresis and retention of large volumes at end-deflation or end-expiration. High expiratory pressures in vivo probably enhance production and distribution of bubbles. Surfactant-poorimmature lungs do not have the capacity to produce stable bubbles. As a consequence, initial aeration requires high opening pressure, achieves proportionately small maximal volume, and results in little hysteresis and gas retention during deflation. This is the underlying pathophysiologic derangement of neonatal respiratory distress syndrome.
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