Pneumolysis in COVID-19: A Novel Concept Derived from High Altitude Physiology

Abstract

The COVID-19 pandemic surprised everyone with a severe lung compromise giving rise to gasping and death from respiratory insufficiency. The understanding of lung compromise is essential to advances in the field of pneumology. It is well known that the SARS-CoV-2 adheres through its spikes to the ACE-2 receptors of type II pneumocytes and introduces its RNAm material in search of its reproduction. Pneumolysis, defined as “lung destruction”, is the mechanism whereby the virus utilizes the alveolar cells to reproduce itself and destroys them in the process. The viral “attack” leads to dysfunction of the alveolar type II cells that work in conjunction with the type I alveolar cells, and a specialized thin oxygen and carbon dioxide permeable membrane. Once the virus is inside the cell, the organism’s immune system attempts to attack the virus, causing significant inflammatory reactions with remarkable ineffectiveness. The following destruction of the alveoli gives rise to a shunt, uneven ventilation-perfusion, and alteration of diffusion, generating a rapidly progressive hypoxemia that is often lethal.