Alveolar instability (atelectrauma) is not identified by arterial oxygenation predisposing the development of an occult ventilator-induced lung injury

Abstract

Background: Improperly set mechanical ventilation (MV) with normal lungs can advance lung injury and increase the incidence of acute respiratory distress syndrome (ARDS). A key mechanism of ventilator-induced lung injury (VILI) is an alteration in alveolar mechanics including alveolar instability or recruitment/derecruitment (R/D). We hypothesize that R/D cannot be identified by PaO2 (masking occult VILI), and if protective ventilation is not applied, ARDS incidence will increase.

Methods: Sprague-Dawley rats (n = 8) were anesthetized, surgically instrumented, and placed on MV. A thoracotomy was performed and an in vivo microscope attached to the pleural surface of the lung with baseline dynamic changes in alveolar size during MV recorded. Alveolar instability was induced by intra-tracheal instillation of Tween and alveolar R/D identified as a marked change in alveolar size from inspiration to expiration with increases in positive end-expiratory pressure (PEEP) levels.

Results: Despite maintaining a clinically acceptable PaO2 (55-80 mmHg), the alveoli remained unstable with significant R/D at low PEEP levels. Although PaO2 consistently increased with an increase in PEEP, R/D did not plateau until PEEP was >9 cmH2O.

Conclusions: PaO2 remained clinically acceptable while alveolar instability persisted at all levels of PEEP (especially PEEP <9 cmH2O). Therefore, PaO2 levels cannot be used reliably to guide protective MV strategies or infer that VILI is not occurring. Using PaO2 to set a PEEP level necessary to stabilize the alveoli could underestimate the potential for VILI. These findings highlight the need for more accurate marker(s) of alveolar stability to guide protective MV necessary to prevent VILI.

Fig. 1

In vivo microscopy showing alveolar inflation of non-injured (PEEP 12) and injured (PEEP 18) lungs at end-inspiration and end-expiration

Fig. 2

Stepwise increases in low levels of PEEP (3–9 cmH₂O) led to an increase in both alveolar stability and arterial oxygenation as measured by pO₂. High levels of PEEP (12–18 cmH₂O), however, improved arterial oxygenation in a stepwise fashion without a concomitant increase in alveolar stability

Fig. 3

Experimental timeline: Following instrumentation, lung injury, and thoracotomy, PEEP titrations were \incrementally increased by 3 cmH₂O until 18 cmH₂O was reached. Arterial blood gas (ABG) and in vivo microscopy at inspiration and expiration was recorded after a 5-min equilibration