My previous post regarding pressure and tidal volume (VT) was a vast oversimplification. A little more info: VT can be divided into at least 2 fractions. Fraction 1 is deadspace ventilation; this is ventilation of tissues that DO NOT participate in gas exchange. Such tissues are the naso- and oro- pharynx, larynx, trachea, bronchi, bronchioles, etc. The second fraction is alveolar ventilation. This is where gas exchange occurs. Think of the lungs as one big balloon covered by a mesh of lichens. These lichens represent the pulmonary capillaries. Gas exchange occurs at the alveolar-pulmonary capillary interface. As the alveoli expand and contract with inspiration and expiration, the pressure in the alveoli is transmitted to the surrounding pulmonary capillaries. If the intra-alveolar pressure and resulting distention is great enough, flow through the pulmonary capillaries can decrease or even stop. This may convert alveolar ventilation (good for CO2 washout) into deadspace ventilation (good for CO2 retention). At what pressure does this conversion occur? Very variable but likely to be somewhere in the 8 cmH2O to 20 cmH2O pressure range. Beginning to see how this works?
Straight CPAP and CPAP with lower EPR values (1 cmH2O relief) MAY promote increased deadspace ventilation and CO2 retention. CPAP with higher EPR values (3 cm H2O) MAY promote increased alveolar ventilation and CO2 washout resulting in increased central apnea (normal response to decreased CSF and arterial pH). Mask volume and flow in the mask has little to do with this UNLESS the fresh gas flow into the mask is too low to prevent rebreathing of exhaled CO2; very unlikely.
Hope this helps. Sorry for the long post.