The impact of anatomic manipulations on pharyngeal collapse: results from a computational model of the normal human upper airway

Abstract

Obstructive sleep apnea (OSA) is a common disease with important neurocognitive and cardiovascular sequelae. Existing therapies are unsatisfactory, leading investigators to seek alternative forms of anatomic manipulation to influence pharyngeal mechanics. We have developed a two-dimensional computational model of the normal human upper airway based on signal averaging of MRI. Using the finite element method, we can perform various anatomic perturbations on the structure in order to assess the impact of these manipulations on pharyngeal mechanics and collapse. By design, the normal sleeping upper airway model collapses at -13 cm H2O. This closing pressure becomes more negative (ie, less collapsible) when we perform mandibular advancement (-21 cm H2O), palatal resection (-18 cm H2O), or palatal stiffening (-17 cm H2O). Where clinical data are available in the literature, the results of our model correspond reasonably well. Furthermore, our model provides information regarding the site of obstruction and provides hypotheses for clinical studies that can be undertaken in the future (eg, combination therapies). We believe that, in the future, finite element modeling will provide a useful tool to help advance our understanding of OSA and its response to various therapies.

Figure 1

MRI is provided as a reference for the labeling of our model. Below, left to right: An airway with normal sleeping muscle activation that collapses, as described above, at −13 cm H₂O epiglottic pressure. The sleeping airway with 1-cm mandibular advancement and normal activation is widely patent. The sleeping airway with 1-cm mandibular advancement and normal muscle activity now has a Pclose of −21 cm H₂O. If muscle activation is reduced by 50%, the upper airway remains widely patent at −13 cm H₂O. EMG = electromyogram.

Figure 2

Left to right: An airway during sleep with intact uvula at −13 cm H₂O epiglottic pressure, and the airway during sleep without the uvula at 0, −13, and −18 cm H₂O, respectively. All deformations are with normal sleeping muscle activation. The dashed line shows the initial tissue locations at zero pressure with or without the uvula. The solid line shows the structural position at a given epiglottic pressure with or without the uvula. Uvula removal makes the upper airway less collapsible and changes the site of obstruction.

Figure 3

The impact of the Restore Medical palatal implant on pharyngeal mechanics. The implant (18 mm in length, 2 mm in width including scar) was given a Young’s modulus (stiffness) of 1.3 MPa and inserted into the soft palate (stiffness or Young’s modulus [E] of 25,000 Pa). With normal genioglossal muscle contraction during sleeping conditions, the implant leads to a less collapsible pharyngeal airway (based on a more negative Pclose from −11.5 at baseline to −7 cm H₂O after implant).