Quantifying the potential of infant bedding to limit CO2 dispersal and factors affecting rebreathing in bedding

Rebreathing may impair ventilation and lead to sudden death among sleeping infants. To estimate the potential for rebreathing imposed by an infant's sleep microenvironment, we developed a mechanical model to assess the rate of CO2 dispersal away from an infant's face. We compared the mechanical model results with changes in arterial blood gases of rabbits. The rabbits breathed into the same microenvironments used for the model studies. In the rabbits, rebreathing (documented by capnometry) caused hypercarbia and in some cases death. The mechanical model consisted of the mannequin head positioned as in the rabbit studies and connected to a 100-ml syringe filled with CO2. CO2 was washed out of the system using 30-ml "breaths" (rate = 15/min). The half times (t1/2) for CO2 dispersal served to quantify the rebreathing potential of 16 items of bedding. The t1/2 values correlated with increments in the rabbits' arterial PCO2 (r = 0.789). The threshold for the increase in the rabbits' arterial PCO2 corresponded to t1/2 values of > or = 18.7 s; the 90% point for lethality in the rabbit model was 28.1 s. The mechanical model was also used to show the independent effects of softness and porosity of bedding on its rebreathing potential. By describing the potential for rebreathing within bedding, the mechanical model should be useful in future quantitative studies of infants' respiratory adaptation to sleep microenvironments.