TY - CHAP M1 - Book, Section TI - Chapter 61. Special Intensive Care A1 - Parker, Thomas A. A2 - Rudolph, Colin D. A2 - Rudolph, Abraham M. A2 - Lister, George E. A2 - First, Lewis R. A2 - Gershon, Anne A. PY - 2011 T2 - Rudolph's Pediatrics, 22e AB - Respiratory failure is one of the most common problems requiring admission to the neonatal intensive care unit. Respiratory failure is often the final result of restrictive lung disease with regional or global alveolar collapse or consolidation. In order to achieve optimal alveolar gas exchange, the lung needs to be inflated at end expiration (at functional residual capacity) and have sufficient tidal and minute ventilation to eliminate carbon dioxide.1 Under optimal conditions, several factors help prevent the collapse of alveoli at the end of expiration and thereby maintain an adequate functional residual capacity. Surfactant, which is produced in the type II cells of the lung, dramatically reduces surface tension and opposes the tendency of alveoli to collapse when lung volume is at its lowest. In addition, the rigidity of the chest wall opposes lung collapse. In comparison to the adult, several factors present disadvantages for the neonate’s capacity to maintain optimal lung volumes. The neonatal chest is highly compliant, which limits its ability to oppose elastic recoil and collapse during expiration and increases the potential for the development of collapse. This problem is greatly exacerbated in the setting of surfactant deficiency or inactivation, in which unopposed surface tension dramatically increases the chance of alveolar collapse during expiration. Lastly, although the small diameter of the neonatal tracheobronchial tree generally is sufficient to provide unimpeded airflow, further small reductions in its diameter can dramatically increase resistance and adversely affect gas entry and egress. SN - PB - The McGraw-Hill Companies CY - New York, NY Y2 - 2024/04/19 UR - accesspediatrics.mhmedical.com/content.aspx?aid=6736591 ER -