Rehabilitación respiratoria oportuna y precoz en pacientes con neumonía COVID 19 en un hospital referencial

Abstract

SARS-CoV-2 is a beta-coronavirus of the same subgenus as SARS and MERS viruses, they share the same gene binding receptor, angiotensin converting enzyme (ACE2). (1) The spectrum of disease severity is varied, with the mild form being the most frequent (81%), and severe disease present in 14% of cases, with critical presentation being present in 5%, with a mortality of 2.3%.(2) The post-pneumonia respiratory sequela caused by beta-Coronaviruses is diffuse alveolar damage with fibrotic lesions; the pathophysiological mechanism is multifactorial, which involves activation of transforming growth factor beta (TGF-β)(3), IL1, IL6, MCP1 and TNF-α secondary to epithelial injury and subsequent inflammation. In addition, exposure to high O2 concentrations and effects of barotrauma, caused by advanced oxygen/ventilatory support, activate the pro-fibrotic TGF-β pathway, resulting in aberrant repair characterized by exaggerated deposition of fibroblasts, myofibroblasts and collagen. Forty-seven percent and 25% of patients who survive moderate to severe COVID-19 pneumonia have decreased carbon monoxide diffusion and predicted total lung capacity, respectively. (4)