The emergence of the “baby lung”: a mechanical consequence of positive pressure ventilation and reduced pulmonary compliance

Introduction

Acute respiratory distress syndrome (ARDS) is defined by diffuse alveolar damage, pulmonary edema, and severely reduced lung compliance. Positive pressure ventilation (PPV) is often essential for survival, yet it concentrates mechanical stress on the limited portion of aerated parenchyma—the “baby lung” (1). This conventional concept, however, underestimates the role of chest wall mechanics and elevated pleural pressure (P_pl) (2) and airway pressure (P_aw).

Mechanical perspective on PPV in low-compliance lungs

In healthy lungs during spontaneous breathing, end-expiratory P_pl is negative (~−6 cmH₂O), keeping alveoli open. In ARDS, under mechanical ventilation, P_pl may become markedly positive (3-5) (+15 to +20 cmH₂O), especially in dependent regions. When P_aw is increased to maintain ventilation [including positive end-expiratory pressure (PEEP)], P_pl rises in parallel.

Tissue compression and alveolar interdependence

Lung tissue compression depends not on transpulmonary pressure (P_tp = P_aw − P_pl) but on mean wall pressure. The parenchyma is “sandwiched” between P_pl and P_aw; thus, the mean of both, (P_aw + P_pl)/2, determines compressive load. Increases in both P_aw and P_pl preserve P_tp but elevate interstitial pressure, favouring collapse of gravity-dependent alveoli.

Non-dependent alveoli, exposed to lower P_pl are more expanded at rest and therefore less compliant. When two alveolar units experience the same pressure change, the more compliant unit will show the largest volume change. This asymmetry drives redistribution under positive pressure: gas leaves compliant dependent alveoli toward stiffer non-dependent regions, worsening heterogeneity.

Surfactant dynamics reinforce this: as an alveolus shrinks, its radius decreases, surfactant layer thickens, and compliance rises, making collapse more likely. Expansion has the opposite effect. Thus, regional shifts accelerate and contribute to the “baby lung” phenomenon.

Given that the dependent regions of the lung (those in the lower parts with respect to gravity) generally have higher compliance, the drop in P_pl during natural inspiration preferentially inflates these lower regions. This compensates partly for their gravitational disadvantage and contributes to a more homogeneous distribution of natural ventilation (6). In contrast, if P_aw and P_pl both increase—such as during inspiration in PPV or increased external pressure (such as obesity)—the opposite occurs: the dependent regions are compressed, and ventilation is diverted toward the non-dependent, already better-ventilated lung zones, further aggravating ventilation heterogeneity.

Prone positioning and P_pl

Prone positioning is often said to homogenize P_pl gradients, yet the gravitational gradient, determined by height and specific weight of the air-filled lung tissue, remains unchanged. What improves is the mean P_pl: properly performed prone positioning, with support under the shoulders and pelvis, evoking a “hanging belly”, reduces diaphragmatic compression, lowers P_pl, and reopens collapsed dorsal alveoli.

Gattinoni et al. (7) showed that prone positioning shifts the “baby lung” from ventral to dorsal regions and increases its size. Thus, the “baby lung” is not a fixed anatomical region but a dynamic volume, shaped by P_pl. Reduction of P_pl in the prone position facilitates recruitment and improves ventilation homogeneity.

Negative pressure ventilation (NPV) versus PPV: experimental insights

In a study by Klassen et al. (8), porcine lungs with pleural defects were ventilated alternately with PPV and NPV using identical tidal volumes. PPV required nearly twice the driving pressure. However, air leakage through pleural defects was almost five times greater during NPV. This suggests that NPV more effectively reaches peripheral lung regions, whereas PPV promotes peripheral airway collapse and preferentially ventilates central areas—a distribution reminiscent of the “baby lung” phenomenon observed in ARDS.

Airway resistance dynamics

PPV raises P_aw to drive inspiration, simultaneously increasing P_pl, thereby compressing lung tissue and airways. This results in elevated airway resistance and may even cause airway closure during inspiration and early expiration, when P_aw falls rapidly fast below a still-elevated P_pl. Initial air trapping may occur due to peripheral airway closure during expiration followed by atelectasis from reduced inspiratory filling and gas resorption in the dependent regions. In contrast, NPV (or spontaneous breathing) lowers external pressure during inspiration, reducing airway compression and resistance. Inspiratory flow is facilitated, and dependent regions are preferentially ventilated and recruited.

Airway pressure release ventilation (APRV) was once promoted as a means to maintain alveolar recruitment by keeping the lung at a high mean P_aw with brief release phases for CO₂ elimination. However, in patients with reduced compliance and heterogeneous time constants, a sudden drop in P_aw during the release phase may promote peripheral air trapping rather than uniform deflation. From a mechanical standpoint, such rapid pressure transitions may increase regional stress within the “baby lung” and potentially aggravate ventilator-induced injury. Although APRV attracted considerable interest two decades ago, it has largely fallen out of favour and is not recommended as a standard mode in current ARDS guidelines.

Recent insights from Nieman et al. are consistent with this view (9). They emphasize that ventilation strategies such as time-controlled adaptive ventilation (TCAV) can reduce driving pressure by improving compliance and maintaining alveolar recruitment. In our interpretation, lowering the driving pressure simultaneously reduces both P_pl and P_aw—particularly the latter—thereby relieving tissue compression and mitigating airway closure.

Interestingly, the concept of “protecting the baby lung” remains embedded in current ARDS guidelines, though its meaning varies with clinical context. For instance, the 2023 European Society of Intensive Care Medicine (ESICM) guidelines (10) recommend low tidal volume and low plateau pressure both as preventive measures in patients without established lung injury and as therapeutic measures in those with advanced, inhomogeneous injury—the so-called “baby lung”, representing the remaining ventilatable lung tissue. However, in most guidelines, the term serves more as a metaphor than as a mechanistic framework. Recognizing this dual role of lung-protective ventilation highlights the importance of mechanistic approaches, such as considering how P_aw-driven tissue compression contributes to both the development and progression of injury.

Breaking the vicious cycle of oxygenation failure by reconsidering PEEP: a case for negative end-expiratory pressure (NEEP)

Clinicians often counter desaturation by increasing the fraction of inspired oxygen (FiO₂) and PEEP, yet high FiO₂ accelerates absorption atelectasis as oxygen is absorbed from poorly ventilated alveoli, causing collapse (11). High PEEP, in turn, raises P_pl, compresses dependent regions, and worsens ventilation-perfusion mismatch. This vicious cycle drives further increases in FiO₂ and PEEP, thereby exacerbating lung injury. Recruitment manoeuvres with high P_aw may transiently reopen collapsed areas, but only extreme PEEP levels can sustain this—at the cost of regional and global perfusion and overall hemodynamic stability. We therefore propose replacing PEEP with continuous negative extrathoracic pressure (NEEP). By restoring physiological negative P_pl, NEEP relieves parenchymal compression, recruits dependent regions without excessive P_aw or FiO₂, and reduces overdistension in non-dependent regions, thereby promoting more homogeneous ventilation and potentially breaking the cycle of iatrogenic oxygenation failure.

Clinical accessibility

Negative, or biphasic, pressure ventilation and NEEP are now easily available for clinical use, both in the intensive care unit (ICU) and in the perioperative setting (12) (http://airwaymanagement.dk/cuirass_for_airway_surgery).

Conclusions

The “baby lung” in ARDS is best understood as a mechanical artefact by PPV in a compressed, non-compliant lung rather than purely anatomical consolidation. Elevating P_aw and P_pl together concentrates ventilation in a limited region, increasing the risk of volutrauma. Shifting to NEEP could restore physiological mechanics and protect the lung. Further studies are warranted to explore this approach.

Acknowledgments

None.

Footnote

Provenance and Peer Review: This article was a standard submission to the journal. The article has undergone external peer review.

Peer Review File: Available at https://jtd.amegroups.com/article/view/10.21037/jtd-2025-1693/prf

Funding: None.

Conflicts of Interest: All authors have completed the ICMJE uniform disclosure form (available at https://jtd.amegroups.com/article/view/10.21037/jtd-2025-1693/coif). J.P.M. reports board memberships (BSAR, ESPCOP, Montanus, Exovent), charity involvement with the Exovent Developing Group (no honoraria), equipment support from Medec International (unrelated to this work), payments or honoraria from MSD, Medtronic, and Medec International outside the submitted work, and co-founder status of MT4L outside the submitted work. The other authors have no conflicts of interest to declare.

Ethical Statement: The authors are accountable for all aspects of the work in ensuring that questions related to the accuracy or integrity of any part of the work are appropriately investigated and resolved.

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