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Mechanical Properties of the Upper Airway

Kingman P. Strohl, James P. Butler, Atul Malhotra

10.1002/cphy.c110053

Source: Volume 2, Issue 3, July 2012

Published online: July 2012

Full Article on Wiley Online Library



Abstract

The importance of the upper airway (nose, pharynx, and larynx) in health and in the pathogenesis of sleep apnea, asthma, and other airway diseases, discussed elsewhere in the Comprehensive Physiology series, prompts this review of the biomechanical properties and functional aspects of the upper airway. There is a literature based on anatomic or structural descriptions in static circumstances, albeit studied in limited numbers of individuals in both health and disease. As for dynamic features, the literature is limited to studies of pressure and flow through all or parts of the upper airway and to the effects of muscle activation on such features; however, the links between structure and function through airway size, shape, and compliance remain a topic that is completely open for investigation, particularly through analyses using concepts of fluid and structural mechanics. Throughout are included both historically seminal references, as well as those serving as signposts or updated reviews. This article should be considered a resource for concepts needed for the application of biomechanical models of upper airway physiology, applicable to understanding the pathophysiology of disease and anticipated results of treatment interventions. © 2012 American Physiological Society. Compr Physiol 2:1853‐1872, 2012.

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Figure 1. Figure 1.

A drawing in the sagittal plane of the shape changes of the airway lumen and size and the location of valves (nasal, velopharyngeal, and glottic or laryngeal) encountered as air travels from the external nares to the trachea on inspiration or from the lungs in expiration.

Reprinted, with permission, from Proctor ([105]
Figure 2. Figure 2.

A midsagittal MRI plane view of the upper airways, showing the anatomy and position of important structural tissue features.
Figure 3. Figure 3.

An axial MRI image at the level of the velopharynx, showing the relative positions of the tongue and airway lumen.
Figure 4. Figure 4.

A cut‐away cartoon of a thick‐walled airway, showing the geometric arrangement in cylindrical coordinates of the tissue stresses in respectively the axial direction (Tzz), the radial direction (Trr), and the circumferential direction (). Shear stresses are not depicted. The internal and external radii are shown as a and b, respectively.
Figure 5. Figure 5.

Illustrations of the determination of Pcrit. (extrapolation, flow/pressure plots). The pressure‐flow plots including data from flow‐limited breaths that occur following drops in mask pressure (Pn is nasal pressure, analogous to Pao, which is airway opening pressure). is the maximum flow occurring during flow‐limited breathing. The active curve is acquired from data gathered during gradual progressive drops in Pn whereas the passive curve is from breaths following brief drops in Pn from a holding pressure. The passive curve is said to reflect the passive mechanics of the airway, whereas the active curve includes neuromuscular compensation and other factors. (Adapted, with permission, from Patil et al. [94])
Figure 6. Figure 6.

A schematic of the pressures and structural features promoting airway collapse and patency, respectively. Negative pharyngeal pressure during inspiration and various craniofacial abnormalities can promote pharyngeal collapse, whereas pharyngeal dilator muscle activation and caudal traction from increased end‐expiratory lung volume can promote pharyngeal patency. (Adapted, with permission, from Malhotra and White [71])
Figure 7. Figure 7.

Effects of lung volume on upper airway mechanics. Caudal traction promotes stiffening of the lower portion of the upper airways, contributing to changes in airflow. Reduced lung volume leads to diminished airflow ostensibly via reductions in caudal traction forces. (Adapted, with permission, from Owens et al. [91])
Figure 8. Figure 8.

A box diagram of the neural pathways for activation of muscles associated with upper airway motor output. Multiple different receptors are present at the hypoglossal motor nucleus yielding the possibility of pharmacological targets to increase upper airway tone. (Adapted, with permission, from Dempsey et al. [20])
Figure 9. Figure 9.

A Moody diagram showing the relationship between friction factor f, defined as the ratio of the pressure drop () to the Bernoulli term () and scaled by the length to diameter ratio (). Here, ρ is gas density and u is characteristic velocity. The Reynolds number is given by , where μ is gas viscosity. Both f and Re are dimensionless. Two characteristic regimes are displayed. For low Re, flow is laminar, pressure drops are linearly proportional to flow and gas viscosity. Beyond a transition region of , the flow becomes turbulent, and pressure drops become quadratic in flow, and proportional to gas density. The three curves above the transition correspond to different roughnesses of the airway, defined as the ratio of the magnitude of radial undulations in the lumen to the airway diameter. The dotted, dot‐dash, and dashed curves are for roughnesses of 0.05, 0.1, and 0.2, respectively. The detailed behavior in the transition region is difficult to define with any accuracy, as it is associated with fine details of airway geometry.
Figure 10. Figure 10.

(A and B). Illustration of flow tracings demonstrating the phenomenon of negative effort dependence. Shown are plots of flow and epiglottic pressure as a function of time. Panel A shows flows significantly decreasing with substantial drops in epiglottic pressure. This finding is in contrast to the classic Starling resistor in which flow is constant across a range of driving pressures. Panel B shows that this type of behavior can also occur even within a breath whereby flow peaks in early inspiration and decreases despite increasing driving pressure later in inspiration. The magnitude of these effects is considerable as compared with the relatively modest reductions in airflow previously described secondary to gas compression during forced expiration.


Figure 1.

A drawing in the sagittal plane of the shape changes of the airway lumen and size and the location of valves (nasal, velopharyngeal, and glottic or laryngeal) encountered as air travels from the external nares to the trachea on inspiration or from the lungs in expiration.

Reprinted, with permission, from Proctor ([105]


Figure 2.

A midsagittal MRI plane view of the upper airways, showing the anatomy and position of important structural tissue features.



Figure 3.

An axial MRI image at the level of the velopharynx, showing the relative positions of the tongue and airway lumen.



Figure 4.

A cut‐away cartoon of a thick‐walled airway, showing the geometric arrangement in cylindrical coordinates of the tissue stresses in respectively the axial direction (Tzz), the radial direction (Trr), and the circumferential direction (). Shear stresses are not depicted. The internal and external radii are shown as a and b, respectively.



Figure 5.

Illustrations of the determination of Pcrit. (extrapolation, flow/pressure plots). The pressure‐flow plots including data from flow‐limited breaths that occur following drops in mask pressure (Pn is nasal pressure, analogous to Pao, which is airway opening pressure). is the maximum flow occurring during flow‐limited breathing. The active curve is acquired from data gathered during gradual progressive drops in Pn whereas the passive curve is from breaths following brief drops in Pn from a holding pressure. The passive curve is said to reflect the passive mechanics of the airway, whereas the active curve includes neuromuscular compensation and other factors. (Adapted, with permission, from Patil et al. [94])



Figure 6.

A schematic of the pressures and structural features promoting airway collapse and patency, respectively. Negative pharyngeal pressure during inspiration and various craniofacial abnormalities can promote pharyngeal collapse, whereas pharyngeal dilator muscle activation and caudal traction from increased end‐expiratory lung volume can promote pharyngeal patency. (Adapted, with permission, from Malhotra and White [71])



Figure 7.

Effects of lung volume on upper airway mechanics. Caudal traction promotes stiffening of the lower portion of the upper airways, contributing to changes in airflow. Reduced lung volume leads to diminished airflow ostensibly via reductions in caudal traction forces. (Adapted, with permission, from Owens et al. [91])



Figure 8.

A box diagram of the neural pathways for activation of muscles associated with upper airway motor output. Multiple different receptors are present at the hypoglossal motor nucleus yielding the possibility of pharmacological targets to increase upper airway tone. (Adapted, with permission, from Dempsey et al. [20])



Figure 9.

A Moody diagram showing the relationship between friction factor f, defined as the ratio of the pressure drop () to the Bernoulli term () and scaled by the length to diameter ratio (). Here, ρ is gas density and u is characteristic velocity. The Reynolds number is given by , where μ is gas viscosity. Both f and Re are dimensionless. Two characteristic regimes are displayed. For low Re, flow is laminar, pressure drops are linearly proportional to flow and gas viscosity. Beyond a transition region of , the flow becomes turbulent, and pressure drops become quadratic in flow, and proportional to gas density. The three curves above the transition correspond to different roughnesses of the airway, defined as the ratio of the magnitude of radial undulations in the lumen to the airway diameter. The dotted, dot‐dash, and dashed curves are for roughnesses of 0.05, 0.1, and 0.2, respectively. The detailed behavior in the transition region is difficult to define with any accuracy, as it is associated with fine details of airway geometry.



Figure 10.

(A and B). Illustration of flow tracings demonstrating the phenomenon of negative effort dependence. Shown are plots of flow and epiglottic pressure as a function of time. Panel A shows flows significantly decreasing with substantial drops in epiglottic pressure. This finding is in contrast to the classic Starling resistor in which flow is constant across a range of driving pressures. Panel B shows that this type of behavior can also occur even within a breath whereby flow peaks in early inspiration and decreases despite increasing driving pressure later in inspiration. The magnitude of these effects is considerable as compared with the relatively modest reductions in airflow previously described secondary to gas compression during forced expiration.

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Article Title: Mechanical Properties of the Upper Airway
 

How to Cite

Kingman P. Strohl, James P. Butler, Atul Malhotra. Mechanical Properties of the Upper Airway. Compr Physiol 2012, 2: 1853-1872. doi: 10.1002/cphy.c110053