Application of positive end-expiratory pressure during induction of general anesthesia in morbidly obese patients prevents atelectasis formation and improves oxygenation. Therefore, this technique should be considered for anesthesia induction in morbidly obese patients.

By use of the technique of rapid airway occlusion, the effects of inspiratory flow, volume, and time on lung and chest wall mechanics were investigated in 10 chronic obstructive pulmonary disease (COPD) patients mechanically ventilated for acute respiratory failure. We measured the interrupter resistance (Rint), which in humans reflects airway resistance; the additional resistances due to time constant inequality and viscoelastic pressure dissipations within the lungs (delta RL) and the chest wall; and the static and dynamic elastances of lung and chest wall. We observed that 1) static elastances of lung and chest wall in COPD patients were similar to those of normal subjects; 2) Rint of the lung was markedly increased and flow dependent in COPD patients, whereas Rint of the chest wall was negligible as in normal subjects; and 3) in COPD patients, delta RL was markedly increased at all inflation flows and volumes, reflecting increased time constant inequalities within the lungs and/or altered viscoelastic behavior. The results imply increased dynamic work due to Rint and delta RL and marked time dependency of pulmonary resistance and elastance in COPD patients.

In 10 sedated paralyzed mechanically ventilated chronic obstructive pulmonary disease (COPD) patients, we measured the inspiratory mechanical work done per breath on the respiratory system (WI,rs). We measured the tracheal and esophageal pressures to assess the lung (L) and chest wall (W) components of WI and used the technique of rapid airway occlusion during constant-flow inflation to partition WI into static work [Wst, including work due to intrinsic positive end-expiratory pressure (WPEEPi)], dynamic work due to airway resistance, and the additional resistance offered by the respiratory tissues. Although the patients were hyperinflated, the slope of the static volume-pressure relationships of the lung did not decrease with inflation volume up to 0.8 liter. WI,W was similar in COPD patients and normal subjects. All components of WI,L were higher in COPD patients. The increase in Wst,rs was due entirely to WPEEPi. Our data suggest that, during spontaneous breathing, COPD patients would probably develop inspiratory muscle fatigue, unless continuous positive airway pressure were applied to reduce WPEEPi.