The suggestion has been made that “The application of CPAP [continuous positive airway pressure]… may be crucial to help maintain airway patency in anesthetized infants.”1Before this suggestion can be applied, there is additional crucial information that must be obtained. The effect of CPAP on respiratory control in the awake state may be quite different than that in the anesthetized state. As the authors have pointed out, infants are dependent on neural input for airway maintenance. However, no data have been presented about the effect of loss of neural input (i.e. , the anesthetized state) and its effect on control of respiration in the presence of CPAP. End-tidal carbon dioxide increased from 41 to 46 mmHg in the study with increasing depth of propofol anesthesia, with “no further change resulting from the application of CPAP.” If ventilation is depressed and there is an increase in dead space ventilation (VD/VT), due to decreased tidal volume, end-tidal carbon dioxide may not change when in fact arterial carbon dioxide tension is increasing. One can see this unchanged or decreased end-tidal carbon dioxide when CPAP is applied to a spontaneously breathing patient anesthetized with an inhalation agent. In the exhaled breaths after the release of CPAP applied for only a minute or so, there is a large outpouring of carbon dioxide. Studies of CPAP in spontaneously breathing infants should include data on arterial carbon dioxide tension.

Columbia University, New York.

Crawford MW, Rohan D, Macgowan CK, Yoo SJ, Macpherson BA: Effect of propofol anesthesia and continuous positive airway pressure on upper airway size and configuration in infants. Anesthesiology 2006; 105:45–50