![]() ![]() Another important pathophysiologic process is that of nitric oxide (NO).Oxygen produces damage-associated molecular pattern molecules (DAMPs) that stimulate an inflammatory response in the lungs, which damages the alveolar epithelial cells and thus perpetuates a vicious cycle of producing more inflammatory cytokines.Oxygen produces reactive oxygen species (ROS) that increases cell apoptosis, or cell death by directly damaging the mitochondria, which we know as the “powerhouse” of the cell.While the biochemistry and physiological pathways bring back nightmares from our science classes, it is important to review the role oxygen plays at a cellular level to further understand the damage it can potentially do in our patients. First, let’s get into the pathophysiology. We will review several studies and articles that have been published in the recent years outlining the data behind the effects of hyperoxia and how this affects patient mortality and outcomes. There have been multiple studies and evidence that have adjusted guidelines based on hypoxemic states, but there are no guidelines that give recommendations on how to avoid or manage hyperoxia. This increases the partial pressure of arterial oxygen (PaO2). ![]() Hyperoxia is a state where the cells and tissues of the body are exposed to an excessive amount of oxygen, usually from oxygen supplementation via nasal cannula or mechanical ventilation. Providing supplemental oxygen increases oxygen delivery in HYPOXEMIC patients, but it can actually damage tissues in NON-HYPOXEMIC patients. Up to 86% of hospitalized patients receive some sort of oxygen therapy – whether it is via nasal cannula or mechanical ventilation. ![]() Oxygen was introduced into anesthesiology practice in the 1930s, and it is now one of the most widely used “drugs” in hospitalized patients. ![]()
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