Preoxygenation: comparison of maximal breathing and tidal volume techniques.

To the Editor;-Baraka et al. recently demonstrated that preoxygenation using eight deep breaths within 60 s (8 DB/60 s) at an oxygen flow of 10 L/min can produce arterial oxygen tension (PaO2) values comparable to those obtained using normal tidal volume breathing (TVB) for 3 min. In addition, they showed that this technique significantly dekdyed the onset of apnea-induced hemoglobin desaturation. Before this new method becomes widely accepted, several issues need to be clarified. First, we wonder What role the baseline values for Pao2 played in the delayed hemoglobin desaturation after 8 DB/60 s. For this portion of their study, Baraka et al. used a separate group of subjects, group B, in whom baseline Pa,)2 values were 407 -+ 53 mmHg after 3 min of TVB and 434 2 45 mmHg after 8 DB/60 s. Both values were higher than those of subjects in group A, in whom 3 min of TVB yielded a Pao2 higher than 392 2 72 mmHg uersus 369 -+ 69 mmHg after 8 DB/60 s. It cannot be ruled out that the higher Pa,,, values observed in in group B after 8 DB/60 s contributed to the delay in hemoglobin desaturation. If subjects from group A were subjected to apnea, the benefit of 8 DW6O s may not have been evident, or at least may not have been as dramatic. Second, we think that reporting this technique as eight breaths in 60 s underestimates the number of breaths and the time of preoxygenation. If we understand the protocol correctly, after the eight breaths, a rapid-sequence induction of anesthesia was carried out. During this period, face-mask oxygenation was continued until apnea ensued, a period described as 15 to 30 s during which an additional 2 to 4 deep breaths occurred. Thus, it appears that Baraka eC al. actually evaluated the efficacy of 10 to 12 breaths during a 75 to 90 s period rather than eight deep breaths in 60 s. The authors proposed two possible mechanisms for the delayed decrease in hemoglobin saturation during 8 DB/60 s: (1) that the extra 15 to 30 s provided more alveolar oxygenation in patients breathing deeply for 60 s than during W; and (2) that continued deep breathing during this extra time may have opened collapsed airways or lung tissue, with a consequent increase in oxygen store in the functional residual capacity. In his editorial, Benumof' proposed other explanations, including a leftward shift of oxyhemoglobin dissociation curve secondary to hyperventilation-induced reductions in Pa,;,,2. We propose that by extending the duration of deep breathing beyond 60 s (Le., to 75-90 s) may have enhanced the potential influence of this factor. A delay in desaturation caused by a leftward shift of the oxyhemoglobin dissociation curve would not necessarily favor improved oxygen transport. Because the authors presented only values for Paoz, the role of changes in arterial carbon dioxide tension and arterial pH must remain speculative.