Esophageal and transpulmonary pressures in acute respiratory failure

Abstract

Objective: Pressure inflating the lung during mechanical ventilation is the difference between pressure applied at the airway opening (Pao) and pleural pressure (Ppl). Depending on the chest wall's contribution to respiratory mechanics, a given positive end-expiratory and/or end-inspiratory plateau pressure may be appropriate for one patient but inadequate or potentially injurious for another. Thus, failure to account for chest wall mechanics may affect results in clinical trials of mechanical ventilation strategies in acute respiratory distress syndrome. By measuring esophageal pressure (Pes), we sought to characterize influence of the chest wall on Ppl and transpulmonary pressure (PL) in patients with acute respiratory failure.

Design: Prospective observational study.

Setting: Medical and surgical intensive care units at Beth Israel Deaconess Medical Center.

Patients: Seventy patients with acute respiratory failure.

Interventions: Placement of esophageal balloon-catheters.

Measurements and main results: Airway, esophageal, and gastric pressures recorded at end-exhalation and end-inflation Pes averaged 17.5 +/- 5.7 cm H2O at end-expiration and 21.2 +/- 7.7 cm H2O at end-inflation and were not significantly correlated with body mass index or chest wall elastance. 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). Although PL at end-expiration was significantly correlated with positive end-expiratory pressure (p < .0001), only 24% of the variance in PL was explained by Pao (R = .243), and 52% was due to variation in Pes.

Conclusions: In patients in acute respiratory failure, elevated esophageal pressures suggest that chest wall mechanical properties often contribute substantially and unpredictably to total respiratory impedance, and therefore Pao may not adequately predict PL or lung distention. Systematic use of esophageal manometry has the potential to improve ventilator management in acute respiratory failure by providing more direct assessment of lung distending pressure.

Figure 1

Changes in airway opening pressure (ΔP_ao) and esophageal pressure (ΔP_es) 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 in P_es correspond closely to changes in P_ao (R² = .937, p < .0001), suggesting that the esophageal balloon is correctly positioned.

Figure 2

Esophageal pressures (P_es) as a function of airway pressure (P_ao). P_es was not significantly correlated with P_ao at end-expiration (R² = .054, p = .055) but it was at end-inspiration (R² = .188, p = .0002).

Figure 3

The relationship between estimated transpulmonary pressure (P_L) and pressure at the airway opening (P_ao). P_L was correlated with P_ao both at end-expiration (R² = .243, p < .0001) and end-inspiration (R² = .45, p < .0001). There was, however, an inconsistent and unpredictable underestimation of P_L by the P_ao as evidenced by the offset from the line of identity. P_L at end-inflation was higher in passively ventilated patients than in those making active respiratory efforts, possibly because sicker patients with stiffer lungs were more likely to be deeply sedated or paralyzed and thus passive.

Figure 4

Transpulmonary pressure (P_L) at the end-inspiratory hold as a function of tidal volume. There was no significant correlation.

Figure 5

Esophageal pressure (P_es) as a function of chest wall elastance. P_es at end-expiration was not significantly correlated with stiffness of the chest wall as estimated by chest wall elastance from P_es at zero flow during tidal ventilation (R² = .011, p = .05), although P_es at end-inflation was (R² = .43, p < .0001).

Figure 6

The relationship between esophageal pressure (P_es) and gastric pressure (P_ga). Esophageal pressure at end-expiration was significantly correlated with Pga (R² = .354, p < .0001).