4.6 Article

Esophageal and transpulmonary pressures in acute respiratory failure

Journal

CRITICAL CARE MEDICINE
Volume 34, Issue 5, Pages 1389-1394

Publisher

LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1097/01.CCM.0000215515.49001.A2

Keywords

lung injury; pleural pressure; ventilator; positive end-expiratory pressure; acute respiratory distress syndrome

Funding

  1. NHLBI NIH HHS [R01 HL073146, R01 HL052586, R01 HL073146-01, HL 52586] Funding Source: Medline
  2. NIA NIH HHS [K23 AG024837, K23 AG024837-02] Funding Source: Medline

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Objective: Pressure inflating the lung during mechanical ventilation is the difference between pressure applied at the airway opening (P-ao) and pleural pressure (P-pi). 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 (P-es) we sought to characterize influence of the chest wall on P-pI and transpulmonary pressure (P-L) 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 P-es 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 P-L 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 P-L at end-expiration was significantly correlated with positive end-expiratory pressure (p <.0001), only 24% of the variance in P-L was explained by P-ao (R-2 =.243), and 52% was due to variation in P-es. 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 P-ao may not adequately predict P-L 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.

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