Respiratory restriction and elevated pleural and esophageal pressures in morbid obesity

Abstract

To explore mechanisms of restrictive respiratory physiology and high pleural pressure (P(Pl)) in severe obesity, we studied 51 obese subjects (body mass index = 38-80.7 kg/m(2)) and 10 nonobese subjects, both groups without lung disease, anesthetized, and paralyzed for surgery. We measured esophageal and gastric pressures (P(Es), P(Ga)) using a balloon-catheter, airway pressure (P(AO)), flow, and volume. We compared P(Es) to another estimate of P(Pl) based on P(AO) and flow. Reasoning that the lungs would not inflate until P(AO) exceeded alveolar and pleural pressures (P(AO) > P(Alv) > P(Pl)), we disconnected subjects from the ventilator for 10-15 s to allow them to reach relaxation volume (V(Rel)) and then slowly raised P(AO) until lung volume increased by 10 ml, indicating the "threshold P(AO)" (P(AO-Thr)) for inflation, which we took to be an estimate of the lowest P(Alv) or P(Pl) to be found in the chest at V(Rel). P(AO-Thr) ranged from 0.6 to 14.0 cmH2O in obese and 0.2 to 0.9 cmH2O in control subjects. P(Es) at V(Rel) 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 P(AO-Thr) (R(2) = 0.16, P = 0.0015). Respiratory system compliance (C(RS)) 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 P(pl) throughout the chest. High P(Es) suggests high P(Pl) in such individuals. Lung and respiratory system compliances are low because of breathing at abnormally low lung volumes.

Figures

Fig. 1.

A: typical data from one experiment, illustrating the protocol (see text for explanation), showing airway pressure (PAO), gastric pressure (PGa), and esophageal pressure (PEs). Note the pressure rise when the balloon is withdrawn from stomach into the lower esophagus.B: third quasi-static inflation inA with expanded time scale and volume channel added. The gradual rise in PAO above the threshold airway pressure (PAO-Thr) causes lung inflation. PAO-Thr is 7.3 cmH2O in this example. (The threshold volume change of 10 ml is not visible at this scale.)

Fig. 2.

PEs at relaxation volume (PEs-Rel) plotted against PAO-Thr, with line of regression (R2 = 0.16, P= 0.0015).

Fig. 3.

PGa at end expiration and end inspiration plotted against the corresponding PEs, with regression lines showing correlations (R2 = 0.44, P< 0.0001, and R2 = 0.39,P < 0.0001, respectively). The majority of subjects have above-normal intra-abdominal pressure (IAP) (PGa at end expiration ≥ 10 cmH2O).

Fig. 4.

Dynamic respiratory system elastance (ERS) plotted against dynamic lung elastance (EL). ERS was principally determined by EL in our severely obese subjects (P< 0.0001).

Fig. 5.

PAO-Thr plotted against body mass index (BMI). PAO-Thr was not correlated with BMI in our obese subjects (R2 = 0.0002) but was weakly correlated when the control group was included in the regression (R2 = 0.068). (There are superimposed symbols in the control group.)

Fig. 6.

Quasi-static inflation PAO-lung volume (VL) curves of the lungs in morbidly obese subjects with the 5 lowest (A) and 5 highest (B) PAO-Thr. Curves of the subjects with the highest PAO-Thr exhibited a downward convexity (“knee”) early in inflation. FRC, functional residual capacity.

Fig. 7.

Hypothetical pressure-volume curves in normal (A) and obese (B) subjects, showing effects of increased pleural pressure (PPl) on lung behavior above FRC. In the normal respiratory system (RS; A), FRC is above closing volume, and the PAO-VL curve is relatively linear. In some obese subjects (B), the high PPl lowers FRC to closing volume. The normal lung appears noncompliant, and the inflation PAO-VL curve has a “knee.”