Yes, COVID-19 can cause atelectasis, a condition where part of the lung collapses and can no longer fill with air. In one study of hospitalized patients with COVID pneumonia, about 24% showed some degree of atelectasis on chest CT scans. The virus damages the lungs in ways that make this complication more likely than with many other respiratory infections, and larger areas of collapse are linked to significantly worse outcomes.
How COVID-19 Causes Lung Collapse
The connection between COVID-19 and atelectasis starts at the cellular level. SARS-CoV-2 specifically targets a type of cell deep in the lungs called type II alveolar cells. These cells have a critical job: they produce pulmonary surfactant, a thin coating that lines the inside of the tiny air sacs (alveoli) where oxygen enters your blood. Surfactant reduces surface tension and keeps those air sacs open. Without it, they stick together and collapse, like a wet plastic bag that seals shut.
When the virus infects and damages these surfactant-producing cells, a chain reaction follows. Researchers using electron microscopy have mapped out the sequence: first the cells are injured, then surfactant production drops, then the air sacs become unstable and begin to close. This creates tiny pockets of collapsed lung tissue called microatelectasis. As surfactant levels fall further, the collapse can spread, leading to fluid buildup in the lungs, poor oxygen exchange, and respiratory failure. This process is a major driver of the severe breathing difficulty seen in COVID-related ARDS (acute respiratory distress syndrome).
The virus also disrupts surfactant at a genetic level, interfering with the genes responsible for producing key surfactant proteins. So the damage isn’t just from killing cells directly. It also reprograms surviving cells to produce less of the substance your lungs need to stay inflated.
Mucus Plugging Adds a Second Path to Collapse
Surfactant loss isn’t the only mechanism. COVID-19 triggers intense inflammation that causes the airways to produce excessive, abnormally thick mucus. This mucus can physically block smaller airways, preventing air from reaching the air sacs beyond the blockage. When trapped air in those sacs gets absorbed into the bloodstream with no fresh air replacing it, the tissue collapses.
Autopsy studies of COVID-19 patients have found mucus plugs not only in the larger airways but also deep in the small airways and alveoli. Infected immune cells in the lungs release a flood of inflammatory signals that worsen this cycle, driving more mucus production, more plugging, and more collapse. In severe cases, this contributes to the dangerous drop in blood oxygen levels that sends patients to the ICU.
Who Is at Higher Risk
Obesity is a significant risk factor for developing atelectasis during COVID-19. Excess weight compresses the lower portions of the lungs even under normal conditions, making those regions more prone to collapse. Obesity also creates a baseline state of increased inflammation in lung tissue, which compounds the inflammatory damage from the virus itself.
A related and often overlooked factor is obstructive sleep apnea, which is common in people with obesity but frequently undiagnosed. Sleep apnea involves repeated airway obstruction that generates mechanical stress on the lungs and promotes chronic inflammation. Research suggests that this pre-existing lung inflammation may prime the lungs for worse injury once COVID infection takes hold. The repeated airway closures during sleep can also worsen active lung injury through shear forces on already damaged tissue. Patients who are overweight, have sleep apnea, or both appear to face a compounded risk for severe lung complications including atelectasis.
How Atelectasis Affects Recovery
The size of the collapsed area matters enormously. In a CT-based study of COVID pneumonia patients, those with small areas of atelectasis (19% of the total group) had outcomes roughly comparable to patients with no collapse at all. Only about 7% of the small-atelectasis group needed ICU admission. But among the 5% of patients with large areas of atelectasis, 75% required ICU care. Larger collapse means less functional lung tissue, worse oxygen levels, and a harder path to recovery.
On imaging, atelectasis in COVID patients often appears alongside the ground-glass opacities and consolidation typical of viral pneumonia, which can make it tricky to identify. Radiologists look for specific clues like visible airway outlines within consolidated lung tissue and “fibrosis-like stripes,” which may actually represent collapsed sub-segments of lung. As the infection resolves, these areas of collapse can gradually reopen, with follow-up scans showing the consolidated regions shrinking over time and eventually leaving behind only thin fibrous bands.
Treatment in the Hospital
For patients sick enough to be hospitalized, one of the most effective strategies for reopening collapsed lung tissue is prone positioning, which simply means lying face down. This shifts the weight of the heart and abdomen off the back portions of the lungs, where collapse is most common. In COVID-related ARDS, combining prone positioning with carefully adjusted ventilator pressure produces significantly better results than either approach alone, with notably greater improvement in airflow to the collapsed back portions of the lungs compared to non-COVID ARDS patients.
For patients on mechanical ventilation, doctors use positive pressure settings to keep unstable air sacs from repeatedly opening and closing with each breath, which can cause additional tissue damage. However, the right pressure level varies from person to person. Lungs that are highly “recruitable,” meaning they have a lot of collapsed tissue that can potentially reopen, benefit from higher pressure. Lungs with less recruitability can actually be harmed by too much pressure, which over-inflates the healthy portions instead of opening the collapsed ones. Clinicians assess this by monitoring how oxygen levels and lung flexibility respond to pressure changes.
Recovery After Discharge
For patients recovering at home or in outpatient settings, incentive spirometry is a common tool used to help re-expand collapsed lung areas. This is a simple handheld device that encourages slow, deep breathing. Protocols used in studies of post-COVID patients typically involve 10 to 20 repetitions performed two or more times daily, continued for around four weeks. Some programs extend to eight weeks with sessions lasting 10 to 15 minutes twice a day.
The evidence for incentive spirometry in post-COVID recovery suggests it can improve lung function measurements, though results have been inconsistent across studies. It remains a low-risk, accessible option that can be used at home. Deep breathing exercises, staying as physically active as your condition allows, and avoiding prolonged time lying flat on your back all help promote lung re-expansion. Most small areas of atelectasis from COVID resolve on their own as inflammation subsides and surfactant production recovers, but larger areas of collapse may take weeks to months to fully clear.