Esophageal pressures in acute lung injury: do they represent artifact or useful information about transpulmonary pressure, chest wall mechanics, and lung stress?

Abstract

Acute lung injury can be worsened by inappropriate mechanical ventilation, and numerous experimental studies suggest that ventilator-induced lung injury is increased by excessive lung inflation at end inspiration or inadequate lung inflation at end expiration. Lung inflation depends not only on airway pressures from the ventilator but, also, pleural pressure within the chest wall. Although esophageal pressure (Pes) measurements are often used to estimate pleural pressures in healthy subjects and patients, they are widely mistrusted and rarely used in critical illness. To assess the credibility of Pes as an estimate of pleural pressure in critically ill patients, we compared Pes measurements in 48 patients with acute lung injury with simultaneously measured gastric and bladder pressures (Pga and P(blad)). End-expiratory Pes, Pga, and P(blad) were high and varied widely among patients, averaging 18.6 +/- 4.7, 18.4 +/- 5.6, and 19.3 +/- 7.8 cmH(2)O, respectively (mean +/- SD). End-expiratory Pes was correlated with Pga (P = 0.0004) and P(blad) (P = 0.0104) and unrelated to chest wall compliance. Pes-Pga differences were consistent with expected gravitational pressure gradients and transdiaphragmatic pressures. Transpulmonary pressure (airway pressure - Pes) was -2.8 +/- 4.9 cmH(2)O at end exhalation and 8.3 +/- 6.2 cmH(2)O at end inflation, values consistent with effects of mediastinal weight, gravitational gradients in pleural pressure, and airway closure at end exhalation. Lung parenchymal stress measured directly as end-inspiratory transpulmonary pressure was much less than stress inferred from the plateau airway pressures and lung and chest wall compliances. We suggest that Pes can be used to estimate transpulmonary pressures that are consistent with known physiology and can provide meaningful information, otherwise unavailable, in critically ill patients.

Figures

Fig. 1.

Esophageal pressure at end-expiratory occlusion (PesEEO) vs. end-expiratory gastric pressure (Pga) in all subjects. Pressures are of similar magnitudes and are correlated. Solid line, line of regression.

Fig. 2.

Difference between Pga and Pes (Pga − PesEEO) vs. Pga, all at end expiration. Dashed line, mean difference; solid horizontal line, line of regression. Pressure difference tended to be greater in atients with higher Pga, suggesting that greater tension in the passive diaphragm had caused greater transdiaphragmatic pressure.

Fig. 3.

Transpulmonary pressure at end-expiratory occlusion (Pl,esEEO) vs. simultaneously measured airway pressure [i.e., total positive end-expiratory pressure (PEEPT)]. Pl,esEEO is usually substantially less than PEEPT. Solid line, line of regression.

Fig. 4.

Possible mechanisms determining pressures in the thorax at end-expiratory (A) and end-inspiratory (B) occlusion. End-inspiratory and end-inspiratory CT scans at a level 7 cm below the carina in a patient with ARDS show extensive dependent consolidation of the lung, with large airways patent. Pressures shown in central airway (Paw) and esophagus (Pes) are the average measured values in all subjects. Possible local pressures are also shown for alveolar regions in upper, middle, and lower lung, including pleural pressure (Ppl), alveolar pressure (Palv), and elastic recoil pressure (Pel = Palv − Ppl). Ppl in middle lung determines effective transpulmonary pressure (Pl), which is shown below scans. Ppl at mid lung height is assumed to be 5 cmH2O lower than Pes, because gravity (G), acting on mediastinal contents, compresses the esophagus. Ppl values in upper and lower lung differ from Ppl at mid lung because of the gravitational pressure gradient, which is assumed to be 0.6 cmH2O/cm height throughout this edematous lung. In middle and upper lung, airways are open, Palv = Paw, and local elastic recoil pressure is equal to local transpulmonary pressure. In lower lung, small airways are closed and/or alveoli contain viscous fluid, preventing Palv from equilibrating with Paw, so Palv = Ppl, and local elastic recoil pressure is nil.

Fig. 5.

Estimated transpulmonary pressure at end-inspiratory occlusion (Pl,esEIO) vs. simultaneously measured airway pressure (Pplat). Pl,esEIO is substantially less than Pplat. Solid line, line of regression.

Fig. 6.

Static end-inspiratory transpulmonary pressure (Pl,esEIO = Pl,esEEO + El × Vt, where El is lung elastance and Vt is tidal volume), which is the parenchymal stress after inflation, plotted against the 3 parameters that together determine its value. Pl,esEIO is moderately correlated with Pl,esEEO (A), correlated with El (b), and not correlated with Vt (C).

Fig. 7.

Lung stress calculated using Eq. 2 of Chiumello et al. (7), ΔPl(stress), plotted against directly measured transpulmonary pressure (Pl,esEIO). ΔPl(stress) does not account for prestress before inflation and is much greater than Pl,esEIO.