>>13610561For a good overview of why COVID-19 is killing people on ventilators, see the following:
>https://www.ncbi.nlm.nih.gov/labs/pmc/articles/PMC7757048/>One of the characteristic changes in the blood parameters among the patients with COVID-19 includes leukocytosis with relative neutrophilia. Activation of neutrophils can trigger various cellular mechanisms, including the release of prostanoids, lysosomal enzymes, as well as highly reactive oxygen radicals and their intermediates. Myeloperoxidases released from the azurophil granules of neutrophils play a particularly critical role by participating in the synthesis of HOCl through a reaction involving H2O2 and chloride (Cl-). HOCl is highly reactive and not only causes lipid peroxidation of membranes, affecting their permeability; but also contributes to oxidative modification of free functional groups, inducing changes in the functionality of proteins. HOCl degrades heme with release of Fe2+, which in turn participates in generation of additional ROS. Furthermore, involvement of MPO and its related mechanisms result in a decrease in nitric oxide (NO), consequently leading to vasoconstriction. Taken together, these phenomena snugly fit into the clinical pathophysiology of severe/critical COVID-19 illness, which consist of alveolar capillary damage (secondary to the production of superoxide, H2O2 and HOCl), pulmonary vasoconstriction and pulmonary hypertension (secondary to NO depletion), elevated ferritin (following release of free iron secondary to heme-degradation), and deterioration of oxygen carrying capacity (secondary to heme degradation). 