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In ten patients requiring respiratory support for an episode of acute respiratory failure (ARF), the best therapeutic level of PEEP was determined by measurement of changes in lung and chest wall compliance (CT) during a PEEP challenge from 0 to 20 cm H2O. During this challenge, hemodynamic monitoring combined with thermodilution measurement of right ventricular (RV) ejection fraction (EF) and two-dimensional echocardiographic measurement of RV size permitted assessment of the effects of increasing levels of PEEP on RV function. RV preload, as reflected by RV end-diastolic volume (EDV) and two-dimensional RV end-diastolic area (EDA), remained unchanged and RV diastolic compliance progressively decreased. On the other hand, RV systolic function, as assessed by RVEF and two-dimensional RV fractional area contraction (FAC), was progressively depressed. Substantial deleterious effects of PEEP were noted at high levels of PEEP including reduced CT and augmented pulmonary vascular resistance. Inadequate increase in RV preload to compensate for increased RV afterload resulted in depressed RV systolic function and contributed to the reduction in cardiac output. Finally, two-dimensional echocardiography proved to be more sensitive than fast-response thermodilution to evaluate change in RV function.

Nineteen patients with acute respiratory failure were divided into three groups according to their total compliance (CT). Transmission of airway pressure to the pleural space was then evaluated by measurement of esophageal pressure at both end-expiration and end-inspiration, and at three levels of PEEP. Chest wall (CW) and lung complicance (CL) were also calculated from simultaneous measurements of lung volume changes induced by tidal delivery. In group 1 (CT greater than 45 ml/cmH2O), 37 percent of airway pressure was transmitted to pleural space. In group 2 (CT between 45 and 30 ml/cmH2O), 32 percent of airway pressure was transmitted to the pleural space. In group 3 (CT less than 30 ml/cmH2O), only 24 percent of airway pressure was transmitted to the pleural space. These differences are statistically significant (p less than 0.001) and illustrate the influence of a progressive increase in lung stiffness (CL = 100.3 +/- 17.2 ml/cmH2O in group 1, CL = 45.0 +/- 6.3 ml/cmH2O in group 2, and CL = 28.6 +/- 8.9 ml/cmH2O in group 3) on transmission of airway pressure to the pleural space. Despite lesser transmission of airway pressure to the pleural space in the most damaged lungs, no significant difference was found between groups with regard to transmural venous pressure changes throughout the study.