COVID-19, caused by the SARS-CoV-2 virus, is primarily known as a respiratory illness. Shortness of breath is a common and serious symptom. This discomfort arises from a series of complex biological processes that affect the lungs’ ability to function properly. Understanding these underlying mechanisms helps to explain why breathing becomes so challenging for many individuals battling the virus.
Viral Attack and Lung Inflammation
The SARS-CoV-2 virus targets cells lining the lungs. It achieves this by binding to the angiotensin-converting enzyme 2 (ACE2) receptor, which is abundant on the surface of type II alveolar cells within the lungs. The virus uses its spike (S) glycoproteins to attach to these ACE2 receptors, gaining entry into the host cells. Once inside, the virus replicates, damaging the delicate air sacs, known as alveoli, which are responsible for gas exchange.
This viral damage triggers a robust immune response. While the immune system aims to clear the infection, it can sometimes become overactive, leading to excessive inflammation. This uncontrolled inflammatory response is often referred to as a “cytokine storm,” characterized by a dysregulated release of pro-inflammatory signaling molecules like IL-6, IL-1β, IFN-γ, and TNF-α. This inflammation causes fluid and cellular debris to accumulate within the alveoli and lung tissue. This fluid buildup significantly impairs normal lung function.
Compromised Oxygen Transfer
The inflammation and fluid accumulation within the lungs directly impede the transfer of oxygen into the bloodstream. The delicate alveoli, where gas exchange occurs, become compromised. The alveolar-capillary membrane, a very thin barrier through which oxygen diffuses from the air sacs into the surrounding capillaries, becomes thickened by the inflammatory fluid and damaged cells.
This thickening makes it harder for oxygen to efficiently pass from the inhaled air into the blood. Simultaneously, the removal of carbon dioxide from the blood into the lungs for exhalation is also hindered. The impaired gas exchange results in lower-than-normal oxygen levels in the blood, a condition known as hypoxemia, which directly contributes to the sensation of shortness of breath.
Blood Clotting in the Lungs
Beyond viral damage and inflammation, COVID-19 can also induce a state where the blood becomes more prone to clotting. This “hypercoagulable state” increases the risk of blood clot formation within the lungs. Microclots can form within the small blood vessels of the lungs, known as the pulmonary microvasculature.
These microclots obstruct blood flow to specific areas of the lung, further disrupting oxygen uptake. Even if an alveolus is clear of fluid and inflammation, it cannot effectively exchange gases if its blood supply is blocked. This phenomenon represents a distinct mechanism contributing to the severe respiratory distress experienced by patients.
Persistent Lung Changes
For some individuals with severe COVID-19, the extensive inflammation and damage can lead to lasting structural changes in the lungs. One such change is pulmonary fibrosis, involving the development of scar tissue within the lung tissue. This scarring reduces the elasticity and overall capacity of the lungs.
These persistent alterations can result in chronic or lingering shortness of breath, a common symptom associated with “long COVID”. The presence of scar tissue can lead to ongoing lung dysfunction and reduced oxygen levels, impacting a person’s ability to perform daily activities.