Page 582 - Clinical Application of Mechanical Ventilation
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548    Chapter 17


                                            to better visualize the vocal cords and advance the ETT through the vocal cords
                          The vocal cord marking   under direct vision. If the cords are closed, wait for them to open before attempting
                        on the ETT should stop at
                        or slightly beyond the vocal   to advance the ETT. Hold the tube against the baby’s palate while removing the
                        cords.              laryngoscope blade and stylette (if used) and securing the ETT (AAP/NRP, 2005).
                                             If the tube has a vocal cord marking, it should be at or slightly beyond the vocal
                                            cords. If the tube does not have a vocal cord marking, a rule to estimate the depth of
                                            intubation is to add 6 to the body weight in kilograms (kg). For example, the depth
                          A rule to estimate the   of ETT for a 2-kg infant should be 8 cm (6 1 2) at the lips.
                        depth of intubation is to
                        add 6 to the body weight in   Listen for breath sounds over both lung fields and place a CO  detector on the ETT
                                                                                                2
                        kilograms.
                                            and verify change in color. However, a CO  detector should not be used when intu-
                                                                               2
                                            bating for meconium removal. After confirming endotracheal placement, the tube is
                                            taped securely. A chest radiograph is done to confirm the depth of ETT placement.


                      SURFACTANT REPLACEMENT THERAPY



                                            It has long been understood that the primary dysfunction in respiratory distress
                          The primary cause of RDS   syndrome (RDS) is abnormally high alveolar surface tension resulting from a lack
                        is surfactant deficiency.
                                            of pulmonary surfactant. Thus it became an item of major interest in the scientific
                                            community to develop a surfactant that can be administered to an infant to replace
                      surfactant: A natural phospholipid   that which is lacking (Robertson & Halliday, 1998).
                      that lowers the surface tension of   Naturally occurring surfactant is composed of several phospholipids and lipids, and
                      the lungs. Deficiency of surfactant
                      causes high surface tension in the   four or more specific apoproteins. Each component appears to have its own distinct
                      lungs and increases the work of   characteristics with regard to production, secretion, and removal (Jobe & Ilkegami,
                      breathing.
                                            1993). These factors have made it difficult to produce an ideal replacement surfactant.
                                             Approximately  90%  of  surfactant  is  phospholipid,  with  phosphatidylcholine
                                            (PC) comprising 85% of the total amount. Roughly 60% of the PC is dipalmitoyl
                                            phosphatidylcholine (DPPC). It is the DPPC that allows surfactant to lower the
                                            surface tension of alveoli (Holm & Waring, 1993). The remaining phospholipids
                                            are phosphatidylglycerol (PG) and phosphatidylinositol (PI). Cholesterol is the pre-
                                            dominant neutral lipid in surfactant. The four proteins found in surfactant, given
                                            the names of surfactant proteins A, B, C, and D (SP-A, etc.), make up 5% to 10%
                                            of the total. While small in quantity, their presence is essential for proper activity of
                                            pulmonary surfactant (Holm & Waring, 1993).


                                            History


                                            Early studies were discouraging because researchers could not find the right com-
                                            bination of components that formed an effective surfactant. Effective dosages and
                                            ideal method of delivery were two other questions that hindered the development
                                            of surfactant replacement therapy.
                      surfactant replacement: Direct
                      instil lation of synthetic surfactant   Early surfactants were made with DPPC and were nebulized into the trachea.
                      (Surfaxin) or natural surfactant   This type of surfactant alone and method of delivery did not produce the desired
                      (Survanta, Infasurf) into the trachea.
                                            results. Continued research and later studies of surfactant and its biochemical and
                                            biophysical properties illustrated the important role of the other proteins and lipids.






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