How to interpret the two phenotypes of esophageal pressure response to the positive end expiratory pressure change?

We read the comments on our recently published paper with interest and are delighted with the inspiring discussion (1).

Two different types of esophageal pressure (Pes) responses to positive end expiratory pressure (PEEP) changes were found in our study. Complete airway closure might be an underlying mechanism for PEEP-independent Pes phenotype, and peripheral airway closure could be underestimated and misinterpreted especially in the ventilated acute respiratory distress syndrome (ARDS) patients (2).

However, the incidence of complete airway closure might not be high (3). In our study, two-third of the enrolled moderate ARDS patients was taken as PEEP-dependent Pes, and this was consistent with Coudroy et al.’s finding (4). The prevalence of complete airway closure in ARDS patients was 41% overall and was significantly associated with high body mass index (BMI). Data from another study (2) also suggested that complete airway closure occurred in one-quarter to one-third of moderate to severe ARDS patients who received mechanical ventilation. The median airway opening pressure (AOP) in these two studies were 9.6 cmH₂O (4) and 13 cmH₂O (2) respectively. The initial empirical PEEP setting in our study was 12 cmH₂O and ranged from 10 to 14 cmH₂O. Therefore, the different Pes responses could not be entirely attributed to complete airway closure.

Another potential mechanism of the two Pes phenotypes was airway pressure transmission. Airway pressure could transmit to pleura and lung stiffness influenced the transmission due to the damping effect (5). Different severity of the “baby” ARDS lung caused variances of respiratory system compliance, and even without the presence of complete airway closure, airway pressure could rarely transmit to pleura in patients with lower compliance, manifesting Pes independent to PEEP changes.

From another point of view, due to the flaw of esophageal manometry, the airway pressure transmission could not be detected by Pes. The pathophysiology of ARDS determines that the lung lesion was heterogeneous, and lesion was much more severe in dependent regions. Pes values reflects the pleural pressure in the dependent to middle lung regions adjacent to the esophageal balloon (6). If the lung injury in the dependent regions was severe enough, the end-expiratory airway pressure changes mostly transmitted to the independent regions and no changes could be detected from Pes values.

In summary, two Pes phenotypes were identified at the PEEP trial. Patients in the PEEP-dependent group has higher respiratory system compliance and lower BMI, complete airway closure does not occur and airway pressure could transmit to pleura and Pes responded to the change. For these patients, identification of Pes phenotype could be beneficial for avoiding lung overdistension caused by higher PEEP application during Pes-guided PEEP titration. As for the PEEP-independent patients, in one hand, because of existence of complete airway closure, airway pressure could not transmit to pleura, and AOP should be demonstrated; on the other hand, due to the heterogeneity of ARDS lung, airway pressure transmitted to the pleura in independent regions, and Pes remained constant as its values correlated well with pleural pressure in the middle to dependent regions. Moreover, electrical impedance tomography could facilitate the differentiation of these two situations. A conceptual protocol of interpret Pes phenotypes during PEEP trial was summarized in Figure 1. Further study is required to investigate how Pes phenotypes impact optimal PEEP setting based on the Pes values.

Figure 1 Identification and interpretations of Pes phenotypes. *, the PEEP-dependent type was defined as ΔPes ≥30% ΔPEEP during both series of PEEP adjustment and the PEEP-independent type was defined as ΔPes <30% ΔPEEP in any series. PEEP, positive end expiratory pressure; Pes, esophageal pressure; ΔPes, Pes changes; ΔPEEP, PEEP changes; RS, respiratory system; BMI, body mass index; AOP, airway opening pressure.

Acknowledgments

Funding: None.

Footnote

Provenance and Peer Review: This article was commissioned by the editorial office, Journal of Thoracic Disease. The article did not undergo external peer review.

Conflicts of Interest: Both authors have completed the ICMJE uniform disclosure form (available at https://jtd.amegroups.com/article/view/10.21037/jtd-24-704/coif). The authors have no conflicts of interest to declare.

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