Complete airway closure in ARDS patients

Author: Jean-Michel Arnal, Intensivist, Hôpital Sainte Musse, Toulon, France, Reviewer: David Grooms, Süha Demirakca, Thomas Reimer

Complete airway closure is a frequent phenomenon in mechanically ventilated ARDS patients. While the location and mechanism of airway closure is still a topic of debate, it may add to the risk of ventilation-induced lung injuries. Detection is an important step in preventing it by optimizing ventilator settings.

Takeaway messages

  • Complete airway closure is frequent in mechanically ventilated ARDS patients and may add to the risk of ventilation-induced lung injuries.
  • Detection is an important step in preventing airway closure by optimizing ventilator settings.
  • In the case of complete airway closure, the total PEEP measured and the related calculations of driving pressures, static compliance, and recruitment-to-inflation ratio can be misleading.
  • A low-flow inflation curve can be used to detect airway closure and to determine the airway opening pressure as a basis for setting PEEP.

Distal airway closure is a physiologic phenomenon that occurs during forced expiration in awake, spontaneously breathing patients and explains why we can’t completely empty our lungs. In patients under anesthesia, complete airway closure in the dependent part of the lung is common (1). Airway closure is promoted by the decreased functional residual capacity and accentuated in obese patients, as well as in the case of the head-down position and/or pneumoperitoneum (2). The main mechanism is that pleural pressure at the end of expiration is higher than pressure inside the airway and induces a negative trans-mural pressure. The main consequence is post-operative atelectasis in the dependent part of the lung, which impairs gas exchange.

In ARDS patients, repeated closures of the airway with trapped gas have recently been described (3). The particularities of this airway closure are firstly, that it is not limited to the dependent part of the lung, but involves the entire lung, and secondly, it is not necessarily associated with complete lung collapse. The mechanism and actual location of the airway closure are not fully understood and do not seem to be related only to trans-airway pressure. Changes in surface tension, liquid distribution, and surfactant depletion may form the main mechanism of airway instability. The hypothesis is that a decrease in functional residual capacity and greater pleural pressure make the distal airways smaller. This increases surface tension and, at some point, an intra-bronchial liquid bridge appears that obstructs a segment of the distal airways. Some data suggest that a high level of surfactant depletion can favor airway closure by modifying the surface tension force in the distal airways (4). To reopen the closed airway, gas at high pressure progresses through the liquid and separates the bronchial walls. The airway opening pressure (AOP) is the airway pressure required to reopen the closed airways and start inflating the lung. Based on a computational model of the airway opening used to investigate the fluid-dynamic mechanism, it appears that the viscosity of lower-airway secretion dramatically increases the AOP (5); a fact which would support the use of active airway humidification. A recent case report using electrical impedance tomography demonstrated that AOP was evenly distributed between the ventral and dorsal regions (6).

Complete airway closure has been reported in 22% of obese, sedated patients with a normal lung (2), and 33% and 41% of ARDS patients (7,8). The incidence increases up to 65% in ARDS patients with a BMI ≥ 40 kg/m2 (8). In COVID-19 related ARDS, the reported incidence is between 24% and 44% (9).

There are several consequences of complete airway closure. First, cyclic airway closure affects the ventilation/perfusion ratio, which in turn impairs oxygenation of the blood. Poorly ventilated areas may eventually collapse, particularly if they are ventilated with a high fraction of oxygen. The result is absorption atelectasis, which induces shunt, further impairs blood oxygenation, and decreases lung compliance. Second, the amount of static airway pressure measured at end-expiration does not reflect alveolar pressure, because the alveoli are no longer communicating with the proximal airway. An end-expiratory occlusion usually shows a shape suggesting intrinsic PEEP, which corresponds with the pressure gradient between the distal airways upstream from the airway closure and the proximal airways (7). This “intrinsic PEEP” can be eliminated by prolonging the expiratory time; however, AOP is not affected by the expiratory time. Because the total PEEP measurement is not accurate, the calculations of driving pressure, static compliance, and recruitment-to-inflation ratio are affected (7, 8). Therefore, when AOP is higher than PEEP, AOP should be considered as the nearest measurable alveolar pressure and used instead of total PEEP in these calculations (7). Third, repeated opening and closing of distal airways may induce some inflammation and generate bronchiolar damage. Thus, complete airway closure is another possible cause of ventilation-induced lung injuries (10).

Airway closure is usually not detected during tidal ventilation, regardless of the ventilation mode used, and requires a low-flow inflation curve to be performed (see Figure 1). The initial part of the inflation shows either no or only a small volume increase because the airways are closed. Then, at a certain pressure corresponding to the AOP, inflation starts. This point has been wrongly interpreted as a low inflection point, intrinsic PEEP, or the pressure where regional transpulmonary pressure would become positive. AOP measurements report values of between 5 and 20 cmH2O (7, 9).

Complete airway closure can be alleviated by using recruitment maneuvers and setting PEEP to a value greater than the AOP (10).

Using the P/V Tool® Pro on Hamilton Medical ventilators*, a low-flow pressure-volume curve can be used to assess the presence of complete airway closure, measure the AOP, and perform a recruitment maneuver.

Figure 1: Low-flow inflation PV curve from 5 to 25 cmH2O in a patient without airway closure (left panel). Volume increases as soon as pressure increases, and cardiac oscillations can be seen throughout the whole PV curve. Low-flow inflation PV curve in a patient with complete airway closure (right panel). Volume increases only when airway pressure reaches AOP (arrow). Cardiac oscillations can only be seen above AOP.

*Available as an option on HAMILTON-G5 and HAMILTON-C3/C6 ventilators; standard on the HAMILTON-S1. Not all ventilators available in all markets.


  1.  Hedenstierna G, McCarthy. Airway closure and closing pressure during mechanical ventilation. Acta Anaesthesiol Scand. 1980 Aug;24(4):299-304.
  2. Grieco DL, Anzellotti GM, Russo A, Bongiovanni F, Costantini B, D'Indinosante M, Varone F, Cavallaro F, Tortorella L, Polidori L, Romanò B, Gallotta V, Dell'Anna AM, Sollazzi L, Scambia G, Conti G, Antonelli M. Airway Closure during Surgical Pneumoperitoneum in Obese Patients. Anesthesiology. 2019 Jul;131(1):58-73. 
  3. Chen L, Del Sorbo L, Grieco DL, Shklar O, Junhasavasdikul D, Telias I, Fan E, Brochard L. Airway Closure in Acute Respiratory Distress Syndrome: An Underestimated and Misinterpreted Phenomenon. Am J Respir Crit Care Med. 2018 Jan 1;197(1):132-136
  4. 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 Feb;45(2):290-291.
  5. Chen Z, Zhong M, Jiang L, Chen N, Tu S, Wei Y, Sang L, Zheng X, Zhang C, Tao J, Deng L, Song Y. Effects of the Lower Airway Secretions on Airway Opening Pressures and Suction Pressures in Critically Ill COVID-19 Patients: A Computational Simulation. Ann Biomed Eng. 2020 Dec;48(12):3003-3013.
  6. Sun XM, Chen GQ, Zhou YM, Yang YL, Zhou JX. Airway Closure Could Be Confirmed by Electrical Impedance Tomography. Am J Respir Crit Care Med. 2018 Jan 1;197(1):138-141
  7. Chen L, Del Sorbo L, Grieco DL, Junhasavasdikul D, Rittayamai N, Soliman I, Sklar MC, Rauseo M, Ferguson ND, Fan E, Richard JM, Brochard L. Potential for Lung Recruitment Estimated by the Recruitment-to-Inflation Ratio in Acute Respiratory Distress Syndrome. A Clinical Trial. Am J Respir Crit Care Med. 2020 Jan 15;201(2):178-187.
  8. Coudroy R, Vimpere D, Aissaoui N, Younan R, Bailleul C, Couteau-Chardon A, Lancelot A, Guerot E, Chen L, Brochard L, Diehl JL. Prevalence of Complete Airway Closure According to Body Mass Index in Acute Respiratory Distress Syndrome. Anesthesiology. 2020 Oct 1;133(4):867-878.
  9. Brault C, Zerbib Y, Kontar L, Carpentier M, Maizel J, Slama M. Positive end-expiratory pressure in COVID-19-related ARDS: Do not forget the airway closure. J Crit Care. 2021 Aug;64:141-143.
  10. Hedenstierna G, Chen L, Brochard L. Airway closure, more harmful than atelectasis in intensive care? Intensive Care Med. 2020 Dec;46(12):2373-2376. 

Related Articles

airway closure, distal airway closure, airway opening pressure, PEEP, VILI, low-flow curve, inflation limb, recruitment maneuver, surfactant

Date of Printing: 30.06.2022
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Date of Printing: 30.06.2022
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