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Artificial Ventilation Can Create Germ Centers for Acute Respiratory Distress Syndrome

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Artificial ventilation can save lives but also strains lung tissue. If the lungs are already damaged, pressure ventilation can have undesirable effects. This primarily affects patients with Acute Respiratory Distress Syndrome (ARDS). In the attempt to keep the lungs open and enable gas exchange, the pressure from overdistending still intact lung areas can cause additional damage. Even less damaged lungs, where a smaller number of alveoli have collapsed and are no longer functional, can be susceptible to mechanical ventilation. In these collapsed alveoli, there is no longer any gas exchange of oxygen and carbon dioxide between the incoming air and the venous blood. Medicine refers to these mini-damages as micro-atelectasis. They cause the inhaled air to not be evenly distributed to all alveoli, which excessively strains the neighboring alveoli.

A team around DZL researcher Professor Dr. Lars Knudsen, specialist in Internal Medicine and Pulmonology at the Institute of Functional and Applied Anatomy of Hannover Medical School (MHH, DZL site BREATH), has now found that even clinically imperceptible small clusters of collapsed alveoli are sufficient to trigger ARDS under artificial ventilation. Furthermore, the researchers showed for the first time that the damage occurring under ventilation happens in the immediate vicinity of existing clusters of collapsed alveoli. As a result, the clusters grow and become clinically significant. DZL researcher Dr. Clemens Ruppert from the Justus Liebig University Giessen (DZL site UGMLC) also participated in this work. The results have been published in the journal "American Journal of Physiology."

Mechanical Stress Increases

When we breathe in, air flows into our lungs down to the alveoli. The alveoli increase in size by changing their shape and expanding. During gas exchange, oxygen from the inhaled air enters the bloodstream, and carbon dioxide from the blood is exhaled. Ideally, all alveoli expand evenly and without stress. If some alveoli are damaged due to illness or injury, they collapse and fail. Because alveoli resemble a sort of limp balloon with many folds and are interconnected like a fine net of rubber bands, the shrunken alveoli exert tensile forces on their neighbors and overextend them. "This mechanical stress apparently increases with artificial ventilation and sustainably damages the alveoli walls, which are only a few thousandths of a millimeter thick," explains Professor Knudsen.

Tiny Clusters Spread

In a mouse model, the research team provided experimental proof that clusters of collapsed alveoli are a key driver for the stealthy onset of ventilation-induced ARDS. "We inflicted a mild lung injury in the animal model," explains Professor Knudsen. The animals were clinically unremarkable, had normal oxygen saturation, and unremarkable lung function. "The only notable finding was that about 30 percent of the alveoli had collapsed at the end of the exhalation phase," the physician notes. These collapsed alveoli formed clusters with a radius of about 50 to 60 micrometers, comparable to the thickness of a human hair.

Very high pressures were required to reopen the collapsed alveoli, pressures not typically used during ventilation. When these lungs were ventilated under general anesthesia with a standard tidal volume, the animals initially had relatively stable lung function. However, after four to six hours of long-term ventilation, lung function deteriorated very rapidly, and isolated cases of lung failure occurred. "We could see under the microscope that the clusters of collapsed alveoli had grown larger and nearly doubled in radius," says the pulmonologist. Due to the progressive alveolar collapse near existing micro-atelectasis, the lungs lost an additional quarter of their open alveoli on average.

Search for ARDS Risk Markers

"Our data shows that alveoli near micro-atelectasis become unstable and that collapsed alveoli act as germ centers, causing further damage to the alveolar epithelium," says Professor Knudsen. Recognizing this damage early is difficult, as it does not reflect in standard lung function tests. Next, the researchers aim to use artificial intelligence to scan all collected data for potential markers indicating a risk for a fatal course under ventilation. Since both the structure of the mouse lung and the mechanisms of breathing have parallels with our lungs, the results can be extrapolated. However, the question of the conditions under which artificial ventilation causes the least lung damage remains open.

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Text: Stefan Zorn, Communications Department, Hannover Medical School


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