Rationale. If the diaphragm, known as the major inspiratory muscle, is active also during expiration, it will limit closure of the small
airways as well as cyclic opening and closing of airways and alveoli. We investigated the expiratory role of the diaphragm in conditions
that promote lung collapse.
Methods. Acute lung injury was induced in 8 anesthetized, tracheostomized pigs by repeated lung lavages, targeting a PaO2/FiO2 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 cmH2O. During steady state conditions, para-diaphragmatic dynamic-CT scans
(dCTs) were obtained together with measurements of respiratory variables. In 4 pigs, the same protocol was repeated during mechanical
pressure control ventilation (PCV) in fully muscle-paralyzed animals. The electrical diaphragmatic activity was continuously recorded
during the expiration (EAdiexp) and during apnea (EAdimin). The EAdiexp recording from end-inspiration to end-expiration was divided
into 4 quartiles (Q1, Q2, Q3, Q4) and the mean value for each of them was expressed as percentage of the EAdi peak. During SB and PCV,
the dCT scans collected at end-expiration and half-expiration were identified 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.
Results. When, during spontaneous breathing, PEEP was lowered from 15 to 6 cmH2O, the EAdiexp increased significantly in all 4
quartiles of the expiratory curve (see Figure, left panel). The EAdimin increased when PEEP was reduced from 12 to 0 cmH2O. However,
atelectasis did not increase in size until PEEP was below 9 cmH2O. Larger atelectasis was seen during PCV (with no measurable EAdi) than
during SB at PEEP levels from 9 to 0 cmH2O. This was seen not only at end-expiration, but already half way down the expiration (see
Figure, right panels).
Conclusions. The increasing diaphragm activity with decreasing airway pressure during the expiration will protect against atelectasis
formation. The effects of the diaphragmatic activity are visible already half way down the expiration. These findings have potential
implications how to design ventilatory support strategies in a wide range of pathological lung conditions, from chronic obstructive
pulmonary disease to acute lung injury.