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| EDITORIAL |
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| Year : 2021 | Volume
: 3
| Issue : 1 | Page : 16 |
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Complete Airway Closure
Xiumei Sun1, Lu Chen2, Jianxin Zhou1
1 Department of Critical Care Medicine, Beijing Tiantan Hospital, Capital Medical University, Beijing, China
2 Department of Critical Care, Keenan Research Centre and Li Ka Shing Institute, St. Michael's Hospital, Toronto, Ontario, Canada
| Date of Submission | 22-Sep-2021 |
| Date of Acceptance | 14-Nov-2021 |
| Date of Web Publication | 08-Dec-2021 |
Correspondence Address:
Prof. Jianxin Zhou
Department of Critical Care Medicine, Beijing Tiantan Hospital, Capital Medical University, No. 119 South 4th Ring West Road, Fengtai District, 100070 Beijing
China
 Source of Support: None, Conflict of Interest: None  | Check |
DOI: 10.4103/jtccm.jtccm_31_21
How to cite this article:
Sun X, Chen L, Zhou J. Complete Airway Closure. J Transl Crit Care Med 2021;3:16 |
Airway closure is defined as the lacking of communication between proximal airways and distal alveoli because of intermediate airways collapse, which was first proposed in 1967.[1] Recently, complete airway closure has been reported in 1/3 of patients with acute respiratory distress syndrome (ARDS) and in 22% of obese anesthetized patients with healthy lungs.[2],[3] For obese patients with ARDS, the incidence was even up to 65%.[4] When complete airway closure occurs, all alveoli do not communicate with the central airways.[5] Under this condition, no gas moves into the lung until the airway pressure reaches a critical level; the corresponding pressure is named as airway opening pressure (AOP), which varies from 5 to 20 cmH2O.[2-4]
At bedside, complete airway closure can be detected with a low flow pressure-volume (P-V) curve.[5] In a typical P-V curve without airway closure, the slope is consistently above the compliance of the breathing circuit even with the presence of a low inflection point due to lung collapse [Figure 1]a. As demonstrated by [Figure 1]b, in a patient with complete airway closure, the slope of the initial part of the P-V curve is complanate (that is the compliance of an occluded ventilator breathing circuit, approximate 1.5–2.5 ml/cmH2O) and there are no signs of cardiac oscillations. Then, the slope of this curve abruptly increases when pressure exceeds AOP accompanying gas entering alveoli, which represents the compliance of the respiratory system. In [Figure 1]c, the low flow pressure-impedance (P-I) curve derived from electric impedance tomography (EIT) shows a similar shape to the P-V curve from the same patient with [Figure 1]b. EIT monitoring further testified that there was not any gas moving into the lungs when the pressure was lower than AOP.[6] In addition, EIT can provide low flow P-V curves or P-I curves of different lung regions. In patients with asymmetrical ARDS (the difference of the ventilation distribution between left and right lung was more than 20%), regional P-V curves from the right and left lung derived from EIT both exhibited a complanate initial portion, but AOP of the left and right lung in the same patient was different, AOP of the more seriously injured lung was even 1.9 times higher than the other.[7] The traditional P-V curves derived from ventilator only reflected the global lung condition, for patients with asymmetrical ventilation, AOP estimated by the global P-V curve was closed to the unilateral lung with a lower AOP level since both lungs are connected in parallel.[7] | Figure 1: Typical low flow pressure-volume curves and a low flow pressure-impedance curve in patients with and without complete airway closure. (a) An example of traditional low flow pressure-volume curve in a patient without complete airway closure. It shows a low inflection point at approximate 5 cmH2O, the pressure to reopen partial collapsed alveoli. The slope of the curve is consistently higher than the compliance of the occluded breathing circuit (red line), and the zigzagging of the curve from beginning to end indicates cardiac oscillations. (b) Low flow pressure-volume curve in a patient with complete airway closure. The initial part of pressure-volume curve is without the signs of cardiac oscillations and the compliance is close to that of the occluded breathing circuit (red line) until airway pressure exceeds airway opening pressure (About 9 cmH2O in this patients). (c) Low flow pressure impedance curve from electric impedance tomography monitoring of the same patient in Figure b. The low flow pressure impedance curve shows a similar shape, and the ventilation map by electric impedance tomography further testified that there was no any gas entering lungs when airway pressure was lower than airway opening pressure
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Now, the mechanism and anatomical location of complete airway closure are not clear yet. The structural collapse of airway walls may be the main reason for airway closure.[8],[9] The obesity and head down position may promote airway closure by applying more pressure on airway walls. Moreover, the relaxation of tracheal smooth muscle during anesthesia also can make airways more easily closed.[10] Besides, surfactant depletion leads to airway instable by affecting surface tension at the liquid-gas interface and contributes to airway closure.[11] Expiratory flow limitation seems to be related to complete airway closure, the incidence of complete airway closure in patients with expiratory flow limitation was higher than those without expiratory flow limitation,[12] but these two phenomena were not the same thing. The prolonged expiration before the P-V curve can eliminate expiratory flow limitation and auto-PEEP, but AOP stayed unchanged.[2] Perhaps, some factors play an important role in both and the relationship needs further to be discussed. The computed tomography (CT) during complete airway closure did not find total lung collapse, suggesting that alveoli were still inflated and the location of closure was airways, but the specific location is still unknown.[5] Recently, the synchrotron radiation phase-contrast CT was used to directly observe individual airways characters in an ARDS model of rabbits and could visualize small airways with diameters of 600–1400 μ. The airway closure mainly occurred in the 18th generation airways and even might appear at more than one site along the airway.[8] These evidence support that small airways can occur closure, but if complete airway closure is located in small airways, it will need hundreds or thousands of small airways to be closed simultaneously, so may the large airway or even trachea be the real site of complete airway closure? The fiber-optic bronchoscopy found that third-level bronchus appeared closed during expiration and reopened during inspiration in a severe ARDS patient with complete airway closure (AOP = 9 cmH2O).[13] Hence, the sites of complete airway closure are probably not only in the terminal bronchioles but also more in the main bronchi or even the trachea, it needs further to be explored.
The complete airway closure could bring several relevant clinical consequences. First, airway pressure is not able to reflect actual alveolar pressure in case of complete airway closure even if an end-expiratory occlusion being performed, that makes a misinterpretation of respiratory mechanics.[3] Second, complete airway closure could induce denitrogenation atelectasis due to intermittently open or continuously closed airways, especially in high fraction inspired oxygen.[14] The lung atelectasis can cause ventilation/perfusion mismatch and impair oxygenation. Third, cyclic opening and closing might result in inflammatory reactions and bronchiolar damages when the PEEP setting is lower than AOP.[15] Therefore, the PEEP setting is recommended to be higher than AOP.
In conclusion, complete airway closure often occurs in ARDS and anesthesia obese patients, but it is easy to be ignored except for performing a low flow P-V curve and might increase the risk of ventilation-induced lung injury.
| References | |  |
| 1. | Dollfuss RE, Milic-Emili J, Bates DV. Regional ventilation of the lung studied with boluses of 133 xenon. Respir Physiol 1967;2:234-46.  |
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| 3. | Grieco DL, Anzellotti GM, Russo A, Bongiovanni F, Costantini B, D'Indinosante M, et al. Airway closure during surgical pneumoperitoneum in obese patients. Anesthesiology 2019;131:58-73. |
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| 7. | Rozé H, Boisselier C, Bonnardel E, Perrier V, Repusseau B, Brochard L, et al. Electrical impedance tomography to detect airway closure heterogeneity in asymmetrical acute respiratory distress syndrome. Am J Respir Crit Care Med 2021;203:511-5. |
| 8. | Broche L, Pisa P, Porra L, Degrugilliers L, Bravin A, Pellegrini M, et al. Individual airway closure characterized in vivo by phase-contrast CT imaging in injured rabbit lung. Crit Care Med 2019;47:e774-81. |
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| 11. | Coudroy R, Lu C, Chen L, Demoule A, Brochard L. Mechanism of airway closure in acute respiratory distress syndrome: A possible role of surfactant depletion. Intensive Care Med 2019;45:290-1. |
| 12. | Guérin C, Terzi N, Galerneau LM, Mezidi M, Yonis H, Baboi L, et al. Lung and chest wall mechanics in patients with acute respiratory distress syndrome, expiratory flow limitation, and airway closure. J Appl Physiol (1985) 2020;128:1594-603. |
| 13. | Malatesta C, Mele F, Menga LS, Bello G, Grieco DL, Antonelli M. Airway closure and fiberoptic evidence of bronchial collapse during the acute respiratory distress syndrome. Intensive Care Med 2019;45:1838-9. |
| 14. | Derosa S, Borges JB, Segelsjö M, Tannoia A, Pellegrini M, Larsson A, et al. Reabsorption atelectasis in a porcine model of ARDS: Regional and temporal effects of airway closure, oxygen, and distending pressure. J Appl Physiol (1985) 2013;115:1464-73. |
| 15. | Tsuchida S, Engelberts D, Peltekova V, Hopkins N, Frndova H, Babyn P, et al. Atelectasis causes alveolar injury in nonatelectatic lung regions. Am J Respir Crit Care Med 2006;174:279-89. |
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