COVID-19 has proven to be one of the deadliestrespiratory diseases present in the world today. While many infections result in a mild, self-limiting illness, patients with severe disease often require high level critical care. Despite our best life saving measures, patients with COVID-19 who are admitted to intensive care units (ICUs) have a significantly higher mortality ratecompared to patients admitted to ICUs for other respiratory illnesses. This review of the literature aims to describe a pathophysiologic mechanism that we believe contributes to high mortality in severely ill COVID-19 patients. Critical illness myopathy and polyneuropathy (CIMPN) is a poorly understood disease process that contributes to muscle and nerve damage in critically ill patients. In CIMPN, excessive systemic inflammation and changes in blood composition lead to damage of nerves and vasculature, which results in weakening of musculature. Damage to respiratory muscles can further exacerbate poor blood oxygenation causedbylung inflammation. Many of the same inflammatory markers seen in SARS-CoV-2 infections have also been shown to contribute to CIMPN. Additionally, high blood sugar levels caused by the bodys stress response can also contribute to CIMPN. Based on our findings, we recommend that future studies of critically ill COVID-19 patients focus on suppressing the cytokine TGF-beta and controllingblood sugar levels in order to combat the effects of CIMPN.