Barotrauma during air travel: predictions of a mathematical model

Abstract

Middle ear barotrauma during flight is a painful disorder experienced by passengers who cannot properly regulate their middle ear pressure in response to the changing cabin pressures during ascent and descent. Previous reports emphasized the important role of poor eustachian tube function in disease pathogenesis but paid little attention to other moderating factors. Here we describe a mathematical model of middle ear pressure regulation and simulate the pressure response to the changes in cabin pressure experienced over typical flights. The results document buffering mechanisms that decrease the requisite efficiency of active, muscle-assisted eustachian tube opening for disease-free flight. These include the relative difference between destination and departure elevations and the ratio of maximum tympanic membrane volume displacement to middle ear volume, where greater absolute values require lesser efficiencies for disease-free flight. Also, the specific type of functional deficit is important since ears with a completely obstructed eustachian tube can be less susceptible to barotrauma than those with a eustachian tube that passively opens but fails to dilate in response to muscle activity. These buffering systems can explain why some children and adults with poor eustachian tube function do not experience middle ear barotrauma.

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

“…This phenomenon is a valid physical property of all similarly constructed pressure systems but, with few isolated exceptions conditioned by an extremely high ratio of tympanic membrane displacement volume to total ME volume (e.g. hyper-compliant tympanic membrane in a low volume ME can protect from barotitis or delay the onset of ME pressure change caused by diffusive, transmucosal gas exchange [15]), is not relevant to explaining the relationship between MACS volume and otitis media risk. In contrast, EQ2b describes the effect on ME pressure of adding or removing gas to a ME system with fixed volume as for example during diffusive gas exchange between the ME and adjacent compartments (See Below).…”

“…For an individual ear, volume gas flow (Q ET =δN/ET opening) is a function of the extant total pressure gradient and the values of relatively fixed structural and functional parameters of the Eustachian tube [15]. From EQ3, the change in ME pressure effected by each Eustachian tube opening is an inverse function of ME volume and a direct function of volume gas flow that, in turn, depends on the above listed factors.…”

“…While the physiological mechanism underlying MACS gas generation is not well developed [3,5,13] and experimental evidences supporting that possibility have alternative explanations [14], ME pressure-buffering is easily demonstrated. There, pressure-buffering can be decomposed into two effects, a magnitudelimiting effect on pressure change under conditions where ME cavity volume is changed (Boyle's Law) [15] and a rate-limiting effect on pressure change under conditions where the contained volume of ME gas is changed (General Gas Law) [16]. Confusion between the consequences of changing ME volume and changing ME gas volume is common in the published literature and this underlies much of the existing controversies regarding the functional role of the MACS in ME pressure-regulation [4,17].…”

Eustachian tube–Tensor veli palatini muscle–cranial base relationships in children and adults: An osteological study

“…Numerous past studies related the development and/or persistence of that disease to a deficiency in middle ear (ME) pressure-regulation, defined as an imbalance between the gas supplied to the ME by the Eustachian tube (ET) and the gas loss from the ME secondary to passive transmucosal diffusion of N 2 from ME to local blood [2, 3]. In turn, this imbalance causes the development of subambient ME pressures that results in a conductive hearing loss and OME by hydrops ex vacuo [4, 5].…”

Eustachian tube function in young children without a history of otitis media evaluated using a pressure chamber protocol

“…This “gradient effect” was demonstrated consistently in past studies that used other response measures and different types of tests to evaluate active ET function in children and adults with and without ME disease 16-18 , though the mechanism previously proposed to explain the phenomenon, “locking of the valve region” 19,20 , is unsatisfactory, and without anatomical (identification of an “ET valve”) or physiological (“locking”) foundation. A complete explanation for this phenomenon is beyond the scope of this presentation and requires a detailed analysis of the extant forces acting on the ET lumen under the various conditions 21 . Nonetheless, the similarity of this “gradient effect” on the response measure used in this study and on those used in earlier studies confirms that PGE captures similar information to other measures of ET opening efficiency.…”