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Complete airway closure in ARDS patients

Article

Author: Jean-Michel Arnal, Intensivist, Hôpital Sainte Musse, Toulon, France

Date of first publication: 27.09.2021

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.
Complete airway closure in ARDS patients

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.

Atelectasis in the dependent lung

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 (Hedenstierna G, McCarthy GS. Airway closure and closing pressure during mechanical ventilation. Acta Anaesthesiol Scand. 1980;24(4):299-304. doi:10.1111/j.1399-6576.1980.tb01552.x1​). 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 (Grieco DL, Anzellotti GM, Russo A, et al. Airway Closure during Surgical Pneumoperitoneum in Obese Patients. Anesthesiology. 2019;131(1):58-73. doi:10.1097/ALN.00000000000026622​). 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.

Repeated airway closure with trapped gas

In ARDS patients, repeated closures of the airway with trapped gas have recently been described (Chen L, Del Sorbo L, Grieco DL, et al. Airway Closure in Acute Respiratory Distress Syndrome: An Underestimated and Misinterpreted Phenomenon. Am J Respir Crit Care Med. 2018;197(1):132-136. doi:10.1164/rccm.201702-0388LE3​). 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 (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(2):290-291. doi:10.1007/s00134-018-5501-54​). 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 (Chen Z, Zhong M, Jiang L, et al. 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;48(12):3003-3013. doi:10.1007/s10439-020-02648-05​); 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 (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;197(1):138-141. doi:10.1164/rccm.201706-1155LE6​).

Incidence and consequences

Complete airway closure has been reported in 22% of obese, sedated patients with a normal lung (Grieco DL, Anzellotti GM, Russo A, et al. Airway Closure during Surgical Pneumoperitoneum in Obese Patients. Anesthesiology. 2019;131(1):58-73. doi:10.1097/ALN.00000000000026622​), and 33% and 41% of ARDS patients (Chen L, Del Sorbo L, Grieco DL, et al. 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;201(2):178-187. doi:10.1164/rccm.201902-0334OC7​, Coudroy R, Vimpere D, Aissaoui N, et al. Prevalence of Complete Airway Closure According to Body Mass Index in Acute Respiratory Distress Syndrome. Anesthesiology. 2020;133(4):867-878. doi:10.1097/ALN.00000000000034448​). The incidence increases up to 65% in ARDS patients with a BMI ≥ 40 kg/m2 (Coudroy R, Vimpere D, Aissaoui N, et al. Prevalence of Complete Airway Closure According to Body Mass Index in Acute Respiratory Distress Syndrome. Anesthesiology. 2020;133(4):867-878. doi:10.1097/ALN.00000000000034448​). In COVID-19 related ARDS, the reported incidence is between 24% and 44% (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;64:141-143. doi:10.1016/j.jcrc.2021.04.0059​).

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 (Chen L, Del Sorbo L, Grieco DL, et al. 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;201(2):178-187. doi:10.1164/rccm.201902-0334OC7​). 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 (Chen L, Del Sorbo L, Grieco DL, et al. 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;201(2):178-187. doi:10.1164/rccm.201902-0334OC7​, Coudroy R, Vimpere D, Aissaoui N, et al. Prevalence of Complete Airway Closure According to Body Mass Index in Acute Respiratory Distress Syndrome. Anesthesiology. 2020;133(4):867-878. doi:10.1097/ALN.00000000000034448​). 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 (Chen L, Del Sorbo L, Grieco DL, et al. 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;201(2):178-187. doi:10.1164/rccm.201902-0334OC7​). 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 (Hedenstierna G, Chen L, Brochard L. Airway closure, more harmful than atelectasis in intensive care?. Intensive Care Med. 2020;46(12):2373-2376. doi:10.1007/s00134-020-06144-w10​).

Detection requires low-flow inflation curve

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 (Chen L, Del Sorbo L, Grieco DL, et al. 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;201(2):178-187. doi:10.1164/rccm.201902-0334OC7​, 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;64:141-143. doi:10.1016/j.jcrc.2021.04.0059​).

Complete airway closure can be alleviated by using recruitment maneuvers and setting PEEP to a value greater than the AOP (Hedenstierna G, Chen L, Brochard L. Airway closure, more harmful than atelectasis in intensive care?. Intensive Care Med. 2020;46(12):2373-2376. doi:10.1007/s00134-020-06144-w10​).

Using the P/V Tool® Pro on Hamilton Medical ventilators (Available as an option on HAMILTON-G5 and HAMILTON-C3/C6 ventilatorsA​, Standard on the HAMILTON-S1B​, Not all ventilators available in all marketsC​), 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.

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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.
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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.

Footnotes

  • A. Available as an option on HAMILTON-G5 and HAMILTON-C3/C6 ventilators
  • B. Standard on the HAMILTON-S1
  • C. Not all ventilators available in all markets

References

  1. 1. Hedenstierna G, McCarthy GS. Airway closure and closing pressure during mechanical ventilation. Acta Anaesthesiol Scand. 1980;24(4):299-304. doi:10.1111/j.1399-6576.1980.tb01552.x
  2. 2. Grieco DL, Anzellotti GM, Russo A, et al. Airway Closure during Surgical Pneumoperitoneum in Obese Patients. Anesthesiology. 2019;131(1):58-73. doi:10.1097/ALN.0000000000002662
  3. 3. Chen L, Del Sorbo L, Grieco DL, et al. Airway Closure in Acute Respiratory Distress Syndrome: An Underestimated and Misinterpreted Phenomenon. Am J Respir Crit Care Med. 2018;197(1):132-136. doi:10.1164/rccm.201702-0388LE
  4. 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;45(2):290-291. doi:10.1007/s00134-018-5501-5
  5. 5. Chen Z, Zhong M, Jiang L, et al. 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;48(12):3003-3013. doi:10.1007/s10439-020-02648-0
  6. 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;197(1):138-141. doi:10.1164/rccm.201706-1155LE
  7. 7. Chen L, Del Sorbo L, Grieco DL, et al. 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;201(2):178-187. doi:10.1164/rccm.201902-0334OC
  8. 8. Coudroy R, Vimpere D, Aissaoui N, et al. Prevalence of Complete Airway Closure According to Body Mass Index in Acute Respiratory Distress Syndrome. Anesthesiology. 2020;133(4):867-878. doi:10.1097/ALN.0000000000003444
  9. 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;64:141-143. doi:10.1016/j.jcrc.2021.04.005
  10. 10. Hedenstierna G, Chen L, Brochard L. Airway closure, more harmful than atelectasis in intensive care?. Intensive Care Med. 2020;46(12):2373-2376. doi:10.1007/s00134-020-06144-w

Airway closure and closing pressure during mechanical ventilation.

Hedenstierna G, McCarthy GS. Airway closure and closing pressure during mechanical ventilation. Acta Anaesthesiol Scand. 1980;24(4):299-304. doi:10.1111/j.1399-6576.1980.tb01552.x

Six subjects without clinical evidence of lung disease were investigated for airway closure and airway closing pressure before and during fentanyl-thiopentone anesthesia with mechanical ventilation. Airway closure was measured by single breath and FRC by multiple breath nitrogen washout. Airway closing pressure was taken to be the transpulmonary pressure at which airway closure commenced. Airway closure occurred within a normal breath in two out of six subjects breathing spontaneously, but in all during mechanical ventilation. Closing capacity was the same in both the awake and anesthetized states while FRC was reduced by 0.41 when anesthesia was instituted. Transpulmonary pressure FRC was on average 1.5 cmH2O (0.15 kPa) and airway closing pressure 4.5 cmH2O (0.44 kPa) greater during anesthesia than in the awake state. Compliance of the lung, calculated both during a vital capacity maneuver and during a tidal breath, was lower with anesthesia. The results of this study suggest that the airways are less stable during mechanical ventilation. But, since lung compliance is lower during anesthesia, a higher transpulmonary pressure is required to maintain a given lung volume. Hence, airway closure occurs at the same lung volume in the anesthetized compared to the non-anesthetized subject.

Airway Closure during Surgical Pneumoperitoneum in Obese Patients.

Grieco DL, Anzellotti GM, Russo A, et al. Airway Closure during Surgical Pneumoperitoneum in Obese Patients. Anesthesiology. 2019;131(1):58-73. doi:10.1097/ALN.0000000000002662



BACKGROUND

Airway closure causes lack of communication between proximal airways and alveoli, making tidal inflation start only after a critical airway opening pressure is overcome. The authors conducted a matched cohort study to report the existence of this phenomenon among obese patients undergoing general anesthesia.

METHODS

Within the procedures of a clinical trial during gynecological surgery, obese patients underwent respiratory/lung mechanics and lung volume assessment both before and after pneumoperitoneum, in the supine and Trendelenburg positions, respectively. Among patients included in this study, those exhibiting airway closure were compared to a control group of subjects enrolled in the same trial and matched in 1:1 ratio according to body mass index.

RESULTS

Eleven of 50 patients (22%) showed airway closure after intubation, with a median (interquartile range) airway opening pressure of 9 cm H2O (6 to 12). With pneumoperitoneum, airway opening pressure increased up to 21 cm H2O (19 to 28) and end-expiratory lung volume remained unchanged (1,294 ml [1,154 to 1,363] vs. 1,160 ml [1,118 to 1,256], P = 0.155), because end-expiratory alveolar pressure increased consistently with airway opening pressure and counterbalanced pneumoperitoneum-induced increases in end-expiratory esophageal pressure (16 cm H2O [15 to 19] vs. 27 cm H2O [23 to 30], P = 0.005). Conversely, matched control subjects experienced a statistically significant greater reduction in end-expiratory lung volume due to pneumoperitoneum (1,113 ml [1,040 to 1,577] vs. 1,000 ml [821 to 1,061], P = 0.006). With airway closure, static/dynamic mechanics failed to measure actual lung/respiratory mechanics. When patients with airway closure underwent pressure-controlled ventilation, no tidal volume was inflated until inspiratory pressure overcame airway opening pressure.

CONCLUSIONS

In obese patients, complete airway closure is frequent during anesthesia and is worsened by Trendelenburg pneumoperitoneum, which increases airway opening pressure and alveolar pressure: besides preventing alveolar derecruitment, this yields misinterpretation of respiratory mechanics and generates a pressure threshold to inflate the lung that can reach high values, spreading concerns on the safety of pressure-controlled modes in this setting.

Airway Closure in Acute Respiratory Distress Syndrome: An Underestimated and Misinterpreted Phenomenon.

Chen L, Del Sorbo L, Grieco DL, et al. Airway Closure in Acute Respiratory Distress Syndrome: An Underestimated and Misinterpreted Phenomenon. Am J Respir Crit Care Med. 2018;197(1):132-136. doi:10.1164/rccm.201702-0388LE

Mechanism of airway closure in acute respiratory distress syndrome: a possible role of surfactant depletion.

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(2):290-291. doi:10.1007/s00134-018-5501-5

Effects of the Lower Airway Secretions on Airway Opening Pressures and Suction Pressures in Critically Ill COVID-19 Patients: A Computational Simulation.

Chen Z, Zhong M, Jiang L, et al. 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;48(12):3003-3013. doi:10.1007/s10439-020-02648-0

In patients with critically ill COVID-19 pneumonia, lower airways are filled with plenty of highly viscous exudates or mucus, leading to airway occlusion. The estimation of airway opening pressures and effective mucus clearance are therefore two issues that clinicians are most concerned about during mechanical ventilation. In this study we retrospectively analyzed respiratory data from 24 critically ill patients with COVID-19 who received invasive mechanical ventilation and recruitment maneuver at Jinyintan Hospital in Wuhan, China. Among 24 patients, the mean inspiratory plateau pressure was 52.4 ± 4.4 cmH2O (mean ± [SD]). Particularly, the capnograms presented an upward slope during the expiratory plateau, indicting the existence of airway obstruction. A computational model of airway opening was subsequently introduced to investigate possible fluid dynamic mechanisms for the extraordinarily high inspiratory plateau pressures among these patients. Our simulation results showed that the predicted airway opening pressures could be as high as 40-50 cmH2O and the suction pressure could exceed 20 kPa as the surface tension and viscosity of secretion simulants markedly increased, likely causing the closures of the distal airways. We concluded that, in some critically ill patients with COVID-19, limiting plateau pressure to 30 cmH2O may not guarantee the opening of airways due to the presence of highly viscous lower airway secretions, not to mention spontaneous inspiratory efforts. Active airway humidification and effective expectorant drugs are therefore strongly recommended during airway management.

Airway Closure Could Be Confirmed by Electrical Impedance Tomography.

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;197(1):138-141. doi:10.1164/rccm.201706-1155LE

Potential for Lung Recruitment Estimated by the Recruitment-to-Inflation Ratio in Acute Respiratory Distress Syndrome. A Clinical Trial.

Chen L, Del Sorbo L, Grieco DL, et al. 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;201(2):178-187. doi:10.1164/rccm.201902-0334OC

Rationale: Response to positive end-expiratory pressure (PEEP) in acute respiratory distress syndrome depends on recruitability. We propose a bedside approach to estimate recruitability accounting for the presence of complete airway closure.Objectives: To validate a single-breath method for measuring recruited volume and test whether it differentiates patients with different responses to PEEP.Methods: Patients with acute respiratory distress syndrome were ventilated at 15 and 5 cm H2O of PEEP. Multiple pressure-volume curves were compared with a single-breath technique. Abruptly releasing PEEP (from 15 to 5 cm H2O) increases expired volume: the difference between this volume and the volume predicted by compliance at low PEEP (or above airway opening pressure) estimated the recruited volume by PEEP. This recruited volume divided by the effective pressure change gave the compliance of the recruited lung; the ratio of this compliance to the compliance at low PEEP gave the recruitment-to-inflation ratio. Response to PEEP was compared between high and low recruiters based on this ratio.Measurements and Main Results: Forty-five patients were enrolled. Four patients had airway closure higher than high PEEP, and thus recruitment could not be assessed. In others, recruited volume measured by the experimental and the reference methods were strongly correlated (R2 = 0.798; P < 0.0001) with small bias (-21 ml). The recruitment-to-inflation ratio (median, 0.5; range, 0-2.0) correlated with both oxygenation at low PEEP and the oxygenation response; at PEEP 15, high recruiters had better oxygenation (P = 0.004), whereas low recruiters experienced lower systolic arterial pressure (P = 0.008).Conclusions: A single-breath method quantifies recruited volume. The recruitment-to-inflation ratio might help to characterize lung recruitability at the bedside.Clinical trial registered with www.clinicaltrials.gov (NCT02457741).

Prevalence of Complete Airway Closure According to Body Mass Index in Acute Respiratory Distress Syndrome.

Coudroy R, Vimpere D, Aissaoui N, et al. Prevalence of Complete Airway Closure According to Body Mass Index in Acute Respiratory Distress Syndrome. Anesthesiology. 2020;133(4):867-878. doi:10.1097/ALN.0000000000003444



BACKGROUND

Complete airway closure during expiration may underestimate alveolar pressure. It has been reported in cases of acute respiratory distress syndrome (ARDS), as well as in morbidly obese patients with healthy lungs. The authors hypothesized that complete airway closure was highly prevalent in obese ARDS and influenced the calculation of respiratory mechanics.

METHODS

In a post hoc pooled analysis of two cohorts, ARDS patients were classified according to body mass index (BMI) terciles. Low-flow inflation pressure-volume curve and partitioned respiratory mechanics using esophageal manometry were recorded. The authors' primary aim was to compare the prevalence of complete airway closure according to BMI terciles. Secondary aims were to compare (1) respiratory system mechanics considering or not considering complete airway closure in their calculation, and (2) and partitioned respiratory mechanics according to BMI.

RESULTS

Among the 51 patients analyzed, BMI was less than 30 kg/m2 in 18, from 30 to less than 40 in 16, and greater than or equal to 40 in 17. Prevalence of complete airway closure was 41% overall (95% CI, 28 to 55; 21 of 51 patients), and was lower in the lowest (22% [3 to 41]; 4 of 18 patients) than in the highest BMI tercile (65% [42 to 87]; 11 of 17 patients). Driving pressure and elastances of the respiratory system and of the lung were higher when complete airway closure was not taken into account in their calculation. End-expiratory esophageal pressure (ρ = 0.69 [95% CI, 0.48 to 0.82]; P < 0.001), but not chest wall elastance, was associated with BMI, whereas elastance of the lung was negatively correlated with BMI (ρ = -0.27 [95% CI, -0.56 to -0.10]; P = 0.014).

CONCLUSIONS

Prevalence of complete airway closure was high in ARDS and should be taken into account when calculating respiratory mechanics, especially in the most morbidly obese patients.

EDITOR’S PERSPECTIVE

 

Positive end-expiratory pressure in COVID-19-related ARDS: Do not forget the airway closure.

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;64:141-143. doi:10.1016/j.jcrc.2021.04.005

Airway closure is a physiological phenomenon in which the distal airways are obstructed when the airway pressure drops below the airway opening pressure. We assessed this phenomenon in 27 patients with coronavirus disease 2019-related acute respiratory distress syndrome. Twelve (44%) patients had an airway opening pressure above 5 cmH2O. The median airway opening pressure was 8 cmH2O (interquartile range, 7-10), with a maximum value of 17 cmH2O. Three patients had a baseline positive end-expiratory pressure lower than the airway opening pressure.

Airway closure, more harmful than atelectasis in intensive care?

Hedenstierna G, Chen L, Brochard L. Airway closure, more harmful than atelectasis in intensive care?. Intensive Care Med. 2020;46(12):2373-2376. doi:10.1007/s00134-020-06144-w

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