Expiratory Diaphragm Activity Reduces Atelectasis Formation

Objective We hypothesized that the major inspiratory muscle, the diaphragm, also acts during expiration as a brake to maintain lung aeration and prevent collapse. We tested this hypothesis in a porcine model of surfactant‐depleted lung. Methods Acute lung injury was induced in 8 anesthetized, tracheostomized pigs by repeated lung lavages, targeting a PaO 2 /FiO 2 of 250 mmHg. After stabilization, the animals were switched to spontaneous breathing (SB) and underwent a decremental continuous positive end‐expiratory pressure (PEEP) trial of 15, 12, 9, 6, 3 and 0 cmH 2 O. Diaphragmatic electric activity during ongoing expiration (EAdi exp ) and at no‐flow end‐expiration (EAdi min ) (six electrodes esophageal‐gastric catheter) and the trans‐diaphragmatic pressure (gastric minus esophageal pressure, Pdi) were measured. Para‐diaphragmatic dynamic‐CT scans (dCTs) were obtained. The dCT scans were collected at end‐expiration and the amount of collapse (atelectasis) in that cut was calculated. The atelectatic tissue was defined as the sum of voxels with a density between −100 and +100 Hounsfield Units. In 4 pigs, the same protocol was repeated during mechanical pressure control ventilation (PCV) after complete muscle paralysis. Results In spontaneously breathing pigs, a linear correlation was found between expiratory EAdi and expiratory Pdi (R 2 > 0.82, p < 0.01). During mechanical ventilation (PCV) with muscle paralysis, no electrical activity of the diaphragm was seen. When PEEP was lowered, with concomitant decrease in lung volume, the EAdi exp increased significantly throughout the expiration. The EAdi min increased when PEEP was reduced from 12 to 0 cmH 2 O. Gas flow was lower at any given time point of expiration during SB without muscle paralysis than during PCV with muscle paralysis. Atelectasis increased in size with the lowering of PEEP but significantly more so during PCV than during SB so that the difference between SB and PCV increased with decreasing PEEP ( Figure 1). Conclusions Our findings show that the diaphragm electrical activity is well related to the diaphragmatic muscle force and that the diaphragm acts as an expiratory brake to limit the fall in end‐expiratory lung volume and to prevent lung collapse. Thus, the diaphragm is an active muscle also during expiration and loss of its function, as during mechanical ventilation and muscle paralysis, may be a contributing factor to unsuccessful respiratory support. We also speculate that expiratory work of breathing may be an additional component of work, added to the inspiratory work that contributes to respiratory muscle fatigue. Support or Funding Information Supported by grants from the Swedish Research Council, the Swedish Heart and Lung Fund, and institutional funds at Uppsala and Bari Universities