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Research Papers

Airway Transmural Pressures in an Airway Tree During Bronchoconstriction in Asthma

[+] Author and Article Information
Tilo Winkler

Department of Anesthesia,
Critical Care and Pain Medicine,
Massachusetts General Hospital
and Harvard Medical School,
55 Fruit Street,
Boston, MA 02114
e-mail: twinkler@mgh.harvard.edu

Manuscript received August 31, 2018; final manuscript received December 20, 2018; published online February 13, 2019. Assoc. Editor: Chun Seow.

ASME J of Medical Diagnostics 2(1), 011005 (Feb 13, 2019) (6 pages) Paper No: JESMDT-18-1047; doi: 10.1115/1.4042478 History: Received August 31, 2018; Revised December 20, 2018

Airway transmural pressure in healthy homogeneous lungs with dilated airways is approximately equal to the difference between intraluminal and pleural pressure. However, bronchoconstriction causes airway narrowing, parenchymal distortion, dynamic hyperinflation, and the emergence of ventilation defects (VDefs) affecting transmural pressure. This study aimed to investigate the changes in transmural pressure caused by bronchoconstriction in a bronchial tree. Transmural pressures before and during bronchoconstriction were estimated using an integrative computational model of bronchoconstriction. Briefly, this model incorporates a 12-generation symmetric bronchial tree, and the Anafi and Wilson model for the individual airways of the tree. Bronchoconstriction lead to the emergence of VDefs and a relative increase in peak transmural pressures of up to 84% compared to baseline. The highest increase in peak transmural pressure occurred in a central airway outside of VDefs, and the lowest increase was 27% in an airway within VDefs illustrating the heterogeneity in peak transmural pressures within a bronchial tree. Mechanisms contributing to the increase in peak transmural pressures include increased regional ventilation and dynamic hyperinflation both leading to increased alveolar pressures compared to baseline. Pressure differences between intraluminal and alveolar pressure increased driven by the increased airway resistance and its contribution to total transmural pressure reached up to 24%. In conclusion, peak transmural pressure in lungs with VDefs during bronchoconstriction can be substantially increased compared to dilated airways in healthy homogeneous lungs and is highly heterogeneous. Further insights will depend on the experimental studies taking these conditions into account.

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Figures

Grahic Jump Location
Fig. 1

Integrative model of bronchoconstriction in an airway tree incorporating the dynamic single-airway model from Anafi and Wilson into a symmetrically bifurcating tree with 12 airway generations. That computational model involves calculations of airflow, pressure, volume, and parenchymal forces for each individual airway with high time resolution. Airway radii are updated breath-by-breath in response to airway smooth muscle activation and the airway's peak transmural pressure during the breathing cycle. The schematic of single-airway model illustrates the effects of different components on peak transmural pressure defined as the difference between intraluminal and peribronchial pressures. The peribronchial pressure on the outside of the airway is affected by the alveolar pressure (PA) and the parenchymal tethering. The tethering forces (black arrows) increase when the airway narrows or the airflow (Vaw, light gray arrows) increases the alveolar volume (VA). The peak transmural pressure during the breathing cycle is a force opposing the constriction of the airway smooth muscle (ASM, medium gray arrows). All airways interact with each other according to the pressures and airflows within the bronchial tree.

Grahic Jump Location
Fig. 2

Regional ventilation map and corresponding peak transmural pressures (Ptm) of all airways of the bronchial tree. (a) Map of relative regional ventilation showing the ventilation defects (VDefs) that emerged during bronchoconstriction. (b) Schematic bronchial tree corresponding to the ventilation map with gray airways on the left where most airways are outside of VDefs, and black airways on the right side where airways are in a region dominated by VDefs. (c) Increase in peak transmural pressure relative to baseline versus airway generation. The central airway generation is zero. The connectivity among the airways with the bronchial tree is visualized by gray and black lines corresponding to the location of the airways in panel B. (d) Same data as in panel C but focusing on the magnitude of changes. Gray dots correspond to gray airways and black dot to black airways in panel B. Small offsets were added to the airway generation of each airway to reduce the overlap among dots. In general, peak transmural pressures were higher in regions outside of VDefs. But the low peak transmural pressures of the terminal airways linked to the small VDefs on the left side (gray dots) are similar to the peak transmural pressures of the terminal airways in the larger VDefs on the right side (black dots).

Grahic Jump Location
Fig. 3

Effect of bronchoconstriction on the alveolar pressures as contributing factor to peak transmural pressure of the airways: (a) Relative change in peak alveolar pressures at the time points of the peak in the airway's transmural pressure during the breathing cycle and (b) change in peak alveolar pressure relative to the change in transmural pressure caused by bronchoconstriction. Gray and black dots correspond to the location of airways in Fig. 2.

Grahic Jump Location
Fig. 4

Contribution of the pressure difference between intraluminal and local alveolar pressure relative to the peak transmural pressure of the individual airways. The contributions are visualized across airway generations. There is a gradient in the difference between intraluminal and alveolar pressure caused by airway resistance, but the severe airway narrowing and closure within VDefs has a much larger effect on the contribution of the intraluminal-to-alveolar pressure difference to peak transmural pressure. Gray and black dots correspond to the location of airways in Fig. 2.

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