The mastoid as a functional rate-limiter of middle ear pressure change.

INTRODUCTION: The physiological function of the mastoid air cell system (MACS) with respect to middle ear (ME) pressure-regulation remains controversial because predictive mathematical models and experimental data to formulate and test hypotheses are lacking.
OBJECTIVE: A mathematical description of MACS volume effects on the rate of ME pressure change is presented; the agreement between published data and model prediction is examined for consistency with the hypothesis that the MACS acts as a functional rate-limiter of ME pressure change, and an explanation for the relationship between MACS volume and otitis media is discussed.
METHODS: The mathematical description shows that the value of a single, free parameter, termed the "MACS buffering efficiency" (M) determines if MACS volume affects the rate of ME pressure change caused by diffusive gas exchange. The MACS serves no rate-limiting function for M=0, acts as a gas sink for M>1 and acts as a gas reserve (rate-limiter) for M<1.
RESULTS: Fitting the model equation to published adult human data yielded an estimate for M of 0.2. This implies that larger MACS volumes are associated with lesser rates of change in ME pressure caused by diffusive gas exchange and lesser required frequencies of effective Eustachian tube openings to maintain near ambient ME pressures.
CONCLUSION: If well-controlled studies confirm M<1 for children and adults, larger MACS volumes will increase the time required to develop sufficient ME underpressures to cause otitis media by hydrops ex vacuo during transient or prolonged periods of Eustachian tube dysfunction.