Coronavirus disease 2019 (COVID-19) is a contagious respiratory and vascular diseases causes severe acute respiratory syndrome (SARS-Co V -2). The first case was identified in Wuhan China in December 2019. Common symptoms of COVID-19 include fever, cough, fatigue, breathing difficulties, and loss of smell and taste. Symptoms begin one to fourteen days after exposure to the virus. While most people have mild symptoms, some people develop acute respiratory distress syndrome (ARDS). ARDS can be precipitated cytokine storm, multiorgan failure, septic shock and blood clots. Longer-term damage to organs (in particular, the lungs and heart) has been observed.

Person-to-person transmission of SARS-Co V -2 has gained global attention and extensive measures to effectively control the outbreak and treatment of COVID-19. COVID19 due to SARS-Co V -2 involves multiple organs and lung injury is one of the most clinical manifestations. The entry route of SARS-Co V -2 into the human cells is mainly facilitated by the angiotensin-converting enzyme 2 (ACE2) receptors, which seem to be expressed by type 2 pneumocytes .The binding of SARS-CoV-2 to the ACE2 receptors could arise into acute systemic inflammatory responses and cytokine storm, consequentially leading to lung-resident dendritic cells (rDCs) activation, and to T lymphocytes production and release antiviral cytokines into the alveolar septa and interstitial compartments . However, the knowledge about the sequelae of SARS-Co V -2 infection remains limited.

Interstitial inflammation, diffuse alveolar damage, and necrotizing bronchitis,bronchiolitis are general histopathological findings of lung in respiratory viral infections . Diffuse alveolar damage is the most commonly observed finding with respiratory virus infections both in acute and late (organizing) stages. The characteristic features of acute diffuse alveolar damage are intra-alveolar oedema. Fibrin deposition and formation of hyaline membranes lining the alveolar walls follow. Late diffuse alveolar damage stages are Type II pneumocyte proliferation, granulation tissue formation, followed by collagen deposition.

The lung pathology of fatal COVID-19 was dominated by diffuse alveolar damage with fibrin rich hyaline membranes and a few multinucleated giant cells. The aberrant wound healing may lead to severe scaring and fibrosis. Preliminary evidence suggests impaired lung function in coronavirus pneumonia could be last for several months or even years, with the impairment of diffusing capacity (DLCO) as the most common abnormality, followed by total lung capacity and restrictive ventilatory defects.

In post COVID patients there is impaired respiratory muscle performance. While impaired respiratory muscle performance is considered to be rare . It is more frequently seen in patients possessing poor health characteristics, in particular chronic lung diseases. Patients infected with COVID-19 may suffer musculoskeletal consequences due to the inflammatory process aggravated by the loss of muscle mass from immobilism, generating motor disabilities that are not yet quantifiable. There are studies underway for muscular strength assessment in post covid pneumonia patients.

With this background we have designed this study to assess pulmonary functions and symptoms in patients with post covid pneumonia.