The latest research on the function of pulmonary surfactant, published in the journal Science, has challenged existing views and established that deep breaths (inhalation and exhalation) not only reduce tension but also restore the structural mechanics of the alveolar surface, which is crucial for optimal lung function.
Pulmonary surfactant is a vital fluid that coats the surface of the alveoli and facilitates breathing. Traditionally, its main role was thought to be the reduction of surface tension. Treatment based on this mechanism is successfully used to treat prematurely born infants who have a deficiency of this fluid.
However, as Professor Jan Vermant of ETH Zurich notes, the injection of this fluid is ineffective in adults with conditions such as Acute Respiratory Distress Syndrome (ARDS). This fact suggests that simply reducing surface tension is not enough to restore lung function. Professor Vermant and his group believe that not only chemical but also mechanical stresses play a critical role in lung function.
According to the study, a deep exhalation is critically important for the effective functioning of pulmonary surfactant. Such exhalations cause a change in the surfactant’s composition: the alveolar surface becomes enriched with special lipids (DPPC), which transforms the surfactant layer into a mechanically strong film.
Thanks to deep exhalation, the surfactant layer is strengthened. This strengthening creates a force in the lung called compressive stress. The results are that:
Overall stress is reduced: The tension acting on the lung surface is low. Lungs inflate easily: Low stress means that the lungs expand easily and fill with air.
The research also proved that this process requires constant repetition: if a deep exhalation does not occur, the harmful stress acting on the surface slowly increases and returns to its original, high level in about 45 minutes. This is why deep breaths are necessary for the lungs’ constant, normal operation. The study authors conclude that to maintain low stress, a deep breathing cycle should be performed approximately every 15 to 45 minutes. The study also emphasizes the need to increase (or periodically apply) the volume/pressure of inhaled air in intubated patients.
This new mechanism also explains why exogenous surfactant therapy is successful in treating Neonatal Respiratory Distress Syndrome (NRDS) but is less effective in Acute Respiratory Distress Syndrome (ARDS) in adults. The researchers suggest that in the case of ARDS, the problem is not merely a lack of surfactant. Damage (caused by inflammatory products or blood proteins) destroys the critical microstructure of the surfactant on the alveolar surface. As a result, the surfactant loses its mechanical function and can no longer provide the balance it acquires during deep exhalation, even though the fluid is physically present. Therefore, simply administering surfactant to the body no longer helps this damaged layer.
Based on the study results, the goal of future therapeutic methods should be not only to administer additional surfactant to the body but also to restore its mechanically active, multilayered structure. This includes optimizing lung ventilation strategy—determining the optimal frequency and volume of deep breaths during artificial ventilation to stiffen the structure—and also developing new medications that artificially restore the multilayered structure and induce compressive stresses, which are essential for lung stability.
