Airway closure during mechanical ventilation of acute respiratory distress syndrome patients

With interest we read the article “Phenotypes of esophageal pressure response to the change of positive end-expiratory pressure in patients with moderate acute respiratory distress syndrome” by Cheng et al. (1). The peripheral airway closure might be the underlying mechanism explaining the two types of esophageal pressure (P_es) response phenotypes.

Cheng’s findings underscore once again the prevalent underestimation and misinterpretation of peripheral airway closure (2), particularly evident during the ventilation of patients with the acute respiratory distress syndrome (ARDS).

This misinterpretation can be attributed directly to the internationally used definition of transpulmonary pressure which equates to airway pressure (P_aw) minus pleural pressure (P_pl). The more accurate definition should be the pressure within the lung (alveolar pressure) minus P_pl. These definitions remain congruent as long the airways remain open and all alveoli are connected to the main airway. Yet, as demonstrated by Dollfuss et al. (3) in 1967 a phenomenon termed “peripheral airway closure” occurs when P_pl rises. Peripheral airways close at a transmural pressure higher than that of the alveolus, thus safeguarding against alveolar collapse.

In Dollfuss’ experiments, volunteers increased P_pl by exhaling deeper than their functional residual capacity (FRC), which led to closure of peripheral airways. Hedenstierna et al. (4) demonstrated that in 50% of standard mechanically ventilated surgery patients, peripheral airway closure occurs above the level of FRC. When P_pl rises to higher levels, as often happens with obese patients in a supine position, peripheral airway closure can become a total lung closure (5). Under these conditions, airflow into the lung begins at the airway opening pressure (AOP). When P_aw decreases, airflow stops at a pressure close to the AOP (by some hysteresis).

The high incidence of total lung closure during mechanical ventilation of ARDS patients is evident from measured end-expiratory P_pl and P_aw. Normally, the end-expiratory transpulmonary pressure at FRC is about 5 cmH₂O (with P_aw at 0 and P_pl at about −5 cmH₂O or lower). During mechanical ventilation of ARDS patients, this end-expiratory transpulmonary pressure is at least 5 cmH₂O due to added lung volume and decreased lung compliance from illness. The P_pl during mechanical ventilation, even with a normal thoracic compliance, rises substantially to pressures above 15 cmH₂O in both obese healthy individuals and those with ARDS.

For instance, if P_pl is determined to be 15 cmH₂O, then alveolar pressure must be at least 20 cmH₂O. If positive end-expiratory pressure (PEEP) is set at 12 cmH₂O (and there is no flow at end-expiration), it indicates total airway closure where there is no connection between the airway and alveoli. This observation of airway closure is often overlooked because expiratory flow is not monitored as P_aw decreases, which would reveal that flow stops at an AOP much higher than PEEP.

This phenomenon explains the observed relationship between P_es and PEEP noted by Cheng et al. If PEEP+3 remains below the AOP, there is no P_es dependence on PEEP (all investigated PEEP levels are below AOP). However, if AOP is lower than PEEP+3, there will be dependence, indicating that expiratory flow did not reach zero.

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