Our patients had characteristics typical of patients with acute respiratory failure at an academic medical center (). The overall mortality rate was 29%, consistent with values reported in the literature for mixed medical/surgical populations with ARDS (5
). Initial ventilator settings included tidal volume 487 ± 124 mL or 7.4 ± 1.9 mL/kg ideal body weight (n = 67), frequency 24.7 ± 13.9 min−1
, and PEEP 14.2 ± 4.5 cm H2
O (n = 69). Tidal volume tended to be slightly lower in patients who died, perhaps as a result of more conservative ventilator management in the sicker patients, but the results did not reach significance (6.90 ± 0.45 vs. 7.56 ± 0.26 mL/kg, p
Baseline patient characteristics
Esophageal balloon position was assessed retrospectively in the 20 patients who were making respiratory efforts during the end-expiratory occlusion (). Efforts against the occlusion produced similar changes in Pao and Pes, indicating proper balloon position. In five patients, we tested the dependence of Pes on balloon air volume by inflating the esophageal balloon sequentially with 0.5 and 1.0 mL of air. The increase in Pes associated with the higher balloon volume was 1–3 cm H2O, indicating a moderate sensitivity of Pes to balloon air volume.
Figure 1 Changes in airway opening pressure (ΔPao) and esophageal pressure (ΔPes) during an inspiratory effort against an occluded airway at end-expiration in 20 patients who were active during the maneuvers. Line is the line of identity. Changes (more ...)
Pes averaged 17.5 ± 5.7 cm H2O at end-expiration and 21.2 ± 7.7 cm H2O at end-inflation (n = 69) and was not different in passive patients and those making active respiratory efforts (p = .64 and .33, respectively). Pes at end-expiration was not significantly correlated with PEEP (R2 = .054, p = .055, n = 69), and at end-inspiration Pes was weakly correlated with Pao (R2 = .188, p = .0002, n = 69, ).
Esophageal pressures (Pes) as a function of airway pressure (Pao). Pes was not significantly correlated with Pao at end-expiration (R2 = .054, p = .055) but it was at end-inspiration (R2 = .188, p = .0002).
Estimated PL was 1.5 ± 6.3 cm H2O at end-expiration, 21.4 ± 9.3 cm H2O at end-inflation, and 18.4 ± 10.2 cm H2O (n = 40) during an end-inspiratory hold (plateau). PL at end-expiration was, as would be expected, significantly correlated with both PEEP and Pes. However, only 24% of the variance in PL was explained by Pao (R2 = .243, p < .0001, n = 69), whereas 51% was explained by Pes (R2 = .508, p < .0001, n = 69, ). As shown in , at any given value of Pao, there was a substantial range of PL, and it was therefore not possible to accurately predict PL from Pao. Nor could PL be predicted from tidal volume; PL during the end-inspiratory hold was not correlated with tidal volume (R2 = .036, p = .257, n = 38, ).
Figure 3 The relationship between estimated transpulmonary pressure (PL) and pressure at the airway opening (Pao). PL was correlated with Pao both at end-expiration (R2 = .243, p < .0001) and end-inspiration (R2 = .45, p < .0001). There was, however, (more ...)
Transpulmonary pressure (PL) at the end-inspiratory hold as a function of tidal volume. There was no significant correlation.
PL at end-expiration was not different between passive and actively breathing patients, but both PL and Pao at end-inflation were lower among patients who were actively breathing (17.8 vs. 24.9 cm H2O, p < .001 for PL, and 33.1 vs. 42.2 cm H2O, p < .0001 for Pao). These differences probably reflect the fact that the sicker patients, who had stiffer lungs, were more likely to be deeply sedated and/or paralyzed and thus passive ().
Pes was not correlated with obesity as assessed by body mass index at end-expiration (R2 = .051, p = .069) or at end-inspiration (R2 = .032, p = .152, n = 66). Similarly, chest wall stiffness, as indicated by ECWTV, was not significantly correlated with body mass index (R2 < .001, p = .975, n = 32).
Pes at end-expiration was not significantly correlated with stiffness of the chest wall as estimated by ECWTV (R2 = .011, p = .052, n = 35), although Pes was correlated with ECWTV at end-inflation (R2 = .43, p < .0001, n = 35, ).
Figure 5 Esophageal pressure (Pes) as a function of chest wall elastance. Pes at end-expiration was not significantly correlated with stiffness of the chest wall as estimated by chest wall elastance from Pes at zero flow during tidal ventilation (R2 = .011, p (more ...)
Gastric pressure at end-expiration (16.6 ± 6.8 cm H2O, n = 44) was similar to esophageal pressure (17.5 ± 5.7 cm H2O), and esophageal pressure was significantly correlated with gastric pressure (R2 = .354, p < .0001, n = 44, ).
The relationship between esophageal pressure (Pes) and gastric pressure (Pga). Esophageal pressure at end-expiration was significantly correlated with Pga (R2 = .354, p < .0001).