Respiratory restriction and elevated pleural and esophageal pressures in morbid obesity

Abstract

To explore mechanisms of restrictive respiratory physiology and high pleural pressure (PPl) in severe obesity, we studied 51 obese subjects (body mass index = 38–80.7 kg/m2) and 10 nonobese subjects, both groups without lung disease, anesthetized, and paralyzed for surgery. We measured esophageal and gastric pressures (PEs, PGa) using a balloon-catheter, airway pressure (PAO), flow, and volume. We compared PEs to another estimate of PPl based on PAO and flow. Reasoning that the lungs would not inflate until PAO exceeded alveolar and pleural pressures (PAO > PAlv > PPl), we disconnected subjects from the ventilator for 10–15 s to allow them to reach relaxation volume (VRel) and then slowly raised PAO until lung volume increased by 10 ml, indicating the “threshold PAO” (PAO-Thr) for inflation, which we took to be an estimate of the lowest PAlv or PPl to be found in the chest at VRel. PAO-Thr ranged from 0.6 to 14.0 cmH2O in obese and 0.2 to 0.9 cmH2O in control subjects. PEs at VRel was higher in obese than control subjects (12.5 ± 3.9 vs. 6.9 ± 3.1 cmH2O, means ± SD; P = 0.0002) and correlated with PAO-Thr ( R2 = 0.16, P = 0.0015). Respiratory system compliance (CRS) was lower in obese than control (0.032 ± 0.008 vs. 0.053 ± 0.007 l/cmH2O) due principally to lower lung compliance (0.043 ± 0.016 vs. 0.084 ± 0.029 l/cmH2O) rather than chest wall compliance (obese 0.195 ± 0.109, control 0.223 ± 0.132 l/cmH2O). We conclude that many severely obese supine subjects at relaxation volume have positive Ppl throughout the chest. High PEs suggests high PPl in such individuals. Lung and respiratory system compliances are low because of breathing at abnormally low lung volumes.